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Source: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/erss.cgi?rss_guid=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU

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<title>lipid</title>
<link>https://pubmed.ncbi.nlm.nih.gov/rss-feed/?feed_id=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&v=2.18.0.post9+e462414&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&utm_source=Feedvalidator&ff=20240518072257&utm_medium=rss</link>
<description>lipid: Latest results from PubMed</description>
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<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
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<title>Brain-targeted drug delivery - nanovesicles directed to specific brain cells by brain-targeting ligands</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760847/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>Neurodegenerative diseases are characterized by extensive loss of function or death of brain cells, hampering the life quality of patients. Brain-targeted drug delivery is challenging, with a low success rate this far. Therefore, the application of targeting ligands in drug vehicles, such as lipid-based and polymeric nanoparticles, holds the promise to overcome the blood-brain barrier (BBB) and direct therapies to the brain, in addition to protect their cargo from degradation and metabolization....</description>
<content:encoded><![CDATA[<div>J Nanobiotechnology. 2024 May 17;22(1):260. doi: 10.1186/s12951-024-02511-7.ABSTRACTNeurodegenerative diseases are characterized by extensive loss of function or death of brain cells, hampering the life quality of patients. Brain-targeted drug delivery is challenging, with a low success rate this far. Therefore, the application of targeting ligands in drug vehicles, such as lipid-based and polymeric nanoparticles, holds the promise to overcome the blood-brain barrier (BBB) and direct therapies to the brain, in addition to protect their cargo from degradation and metabolization. In this review, we discuss the barriers to brain delivery and the different types of brain-targeting ligands currently in use in brain-targeted nanoparticles, such as peptides, proteins, aptamers, small molecules, and antibodies. Moreover, we present a detailed review of the different targeting ligands used to direct nanoparticles to specific brain cells, like neurons (C4-3 aptamer, neurotensin, Tet-1, RVG, and IKRG peptides), astrocytes (Aquaporin-4, D4, and Bradykinin B2 antibodies), oligodendrocytes (NG-2 antibody and the biotinylated DNA aptamer conjugated to a streptavidin core Myaptavin-3064), microglia (CD11b antibody), neural stem cells (QTRFLLH, VPTQSSG, and NFL-TBS.40-63 peptides), and to endothelial cells of the BBB (transferrin and insulin proteins, and choline). Reports demonstrated enhanced brain-targeted delivery with improved transport to the specific cell type targeted with the conjugation of these ligands to nanoparticles. Hence, this strategy allows the implementation of high-precision medicine, with reduced side effects or unwanted therapy clearance from the body. Nevertheless, the accumulation of some of these nanoparticles in peripheral organs has been reported indicating that there are still factors to be improved to achieve higher levels of brain targeting. This review is a collection of studies exploring targeting ligands for the delivery of nanoparticles to the brain and we highlight the advantages and limitations of this type of approach in precision therapies.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760847/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760847</a> | DOI:<a href=https://doi.org/10.1186/s12951-024-02511-7>10.1186/s12951-024-02511-7</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760847</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Ricardo Moreira</dc:creator>
<dc:creator>Clévio Nóbrega</dc:creator>
<dc:creator>Luís Pereira de Almeida</dc:creator>
<dc:creator>Liliana Mendonça</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Journal of nanobiotechnology</dc:source>
<dc:title>Brain-targeted drug delivery - nanovesicles directed to specific brain cells by brain-targeting ligands</dc:title>
<dc:identifier>pmid:38760847</dc:identifier>
<dc:identifier>doi:10.1186/s12951-024-02511-7</dc:identifier>
</item>
<item>
<title>Effects of gender-affirming hormone therapy on body fat: a retrospective case‒control study in Chinese transwomen</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760846/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>CONCLUSION: After receiving GAHT, total body fat and regional fat increased in Chinese transwomen, and the body fat distribution changed from masculine to feminine, especially during the first two years. However, neither the increase in total body fat percentage nor the decrease in visceral fat content didn't bring about significant changes in the incidence of obesity, nor did triglycerides or low-density lipoprotein-cholesterol.</description>
<content:encoded><![CDATA[<div>Lipids Health Dis. 2024 May 17;23(1):146. doi: 10.1186/s12944-024-02131-y.ABSTRACTBACKGROUND: There is insufficient research on how gender-affirming hormone therapy (GAHT) affects body fat modifications in transwomen from China. It is unclear whether hormone therapy affects the prevalence of obesity and blood lipid levels within this population. The current research aimed to assess how GAHT and treatment duration had an impact on the change in and redistribution of body fat in Chinese transwomen.METHODS: This study included 40 transwomen who had not received GAHT and 59 who had. Body fat, blood lipid, and blood glucose levels were measured. GAHT is mainly a pharmacologic (estrogen and anti-androgen) treatment. The study also stratified participants based on the duration of GAHT to assess its impact on body fat distribution. The duration of GAHT was within one year, one to two years, two to three years, or more than three years.RESULTS: After receiving GAHT, total body fat increased by 19.65%, and the percentage of body fat increased by 17.63%. The arm, corrected leg, and leg regions showed significant increases in fat content (+ 24.02%, + 50.69%, and + 41.47%, respectively) and percentage (+ 25.19%, + 34.90%, and + 30.39%, respectively). The total visceral fat content decreased (-37.49%). Based on the diagnostic standards for a body mass index ≥ 28 or total body fat percentage ≥ 25% or 30%, the chance of developing obesity did not change significantly. Blood glucose levels significantly increased (+ 12.31%). Total cholesterol levels (-10.45%) decreased significantly. Fat changes in those who received GAHT for one to two years were significantly different from those who did not receive GAHT.CONCLUSION: After receiving GAHT, total body fat and regional fat increased in Chinese transwomen, and the body fat distribution changed from masculine to feminine, especially during the first two years. However, neither the increase in total body fat percentage nor the decrease in visceral fat content didn't bring about significant changes in the incidence of obesity, nor did triglycerides or low-density lipoprotein-cholesterol.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760846/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760846</a> | DOI:<a href=https://doi.org/10.1186/s12944-024-02131-y>10.1186/s12944-024-02131-y</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760846</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Qin Pei</dc:creator>
<dc:creator>Yuwei Song</dc:creator>
<dc:creator>Zhongwei Huang</dc:creator>
<dc:creator>Hongkun Yu</dc:creator>
<dc:creator>Hao Xu</dc:creator>
<dc:creator>Xunda Ye</dc:creator>
<dc:creator>Lvfen Gao</dc:creator>
<dc:creator>Jian Gong</dc:creator>
<dc:creator>Xiaoying Tian</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Lipids in health and disease</dc:source>
<dc:title>Effects of gender-affirming hormone therapy on body fat: a retrospective case‒control study in Chinese transwomen</dc:title>
<dc:identifier>pmid:38760846</dc:identifier>
<dc:identifier>doi:10.1186/s12944-024-02131-y</dc:identifier>
</item>
<item>
<title>Imaging and blood flow characteristics of cerebrovascular fenestration malformation and its relationship with the occurrence of ischemic cerebrovascular disease</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760844/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>CONCLUSION: Cerebrovascular fenestration malformation is most common in the basilar artery. Cerebrovascular fenestration malformation may also be associated with other cerebrovascular malformations. Standardized antiplatelet and statin lipid-lowering and plaque-stabilizing drugs are suitable for patients with cerebral infarction complicated with fenestration malformation. The relationship between cerebral blood flow changes in basilar artery fenestration malformation and the occurrence of...</description>
<content:encoded><![CDATA[<div>Eur J Med Res. 2024 May 17;29(1):289. doi: 10.1186/s40001-024-01853-0.ABSTRACTOBJECTIVE: To explore the imaging and transcranial Doppler cerebral blood flow characteristics of cerebrovascular fenestration malformation and its relationship with the occurrence of ischemic cerebrovascular disease.METHODS: A retrospective analysis was conducted on the imaging data of 194 patients with cerebrovascular fenestration malformation who visited the Heyuan People's Hospital from July 2021 to July 2023. The location and morphology of the fenestration malformation blood vessels as well as the presence of other cerebrovascular diseases were analyzed. Transcranial Doppler cerebral blood flow detection data of patients with cerebral infarction and those with basilar artery fenestration malformation were also analyzed.RESULTS: A total of 194 patients with cerebral vascular fenestration malformation were found. Among the artery fenestration malformation, basilar artery fenestration was the most common, accounting for 46.08% (94/194). 61 patients (31.44%) had other vascular malformations, 97 patients (50%) had cerebral infarction, of which 30 were cerebral infarction in the fenestrated artery supply area. 28 patients with cerebral infarction in the fenestrated artery supply area received standardized antiplatelet, lipid-lowering and plaque-stabilizing medication treatment. During the follow-up period, these patients did not experience any symptoms of cerebral infarction or transient ischemic attack again. There were no differences in peak systolic flow velocity and end diastolic flow velocity, pulsatility index and resistance index between the ischemic stroke group and the no ischemic stroke group in patients with basal artery fenestration malformation (P > 0.05).CONCLUSION: Cerebrovascular fenestration malformation is most common in the basilar artery. Cerebrovascular fenestration malformation may also be associated with other cerebrovascular malformations. Standardized antiplatelet and statin lipid-lowering and plaque-stabilizing drugs are suitable for patients with cerebral infarction complicated with fenestration malformation. The relationship between cerebral blood flow changes in basilar artery fenestration malformation and the occurrence of ischemic stroke may not be significant.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760844/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760844</a> | DOI:<a href=https://doi.org/10.1186/s40001-024-01853-0>10.1186/s40001-024-01853-0</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760844</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Weifang Xing</dc:creator>
<dc:creator>Wensheng Zhang</dc:creator>
<dc:creator>Minzhen Zhu</dc:creator>
<dc:creator>Yangchun Wen</dc:creator>
<dc:creator>Yunqiang Huang</dc:creator>
<dc:creator>JinZhao He</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>European journal of medical research</dc:source>
<dc:title>Imaging and blood flow characteristics of cerebrovascular fenestration malformation and its relationship with the occurrence of ischemic cerebrovascular disease</dc:title>
<dc:identifier>pmid:38760844</dc:identifier>
<dc:identifier>doi:10.1186/s40001-024-01853-0</dc:identifier>
</item>
<item>
<title>Associations between serum ferritin baselines and trajectories and the incidence of metabolic dysfunction-associated steatotic liver disease: a prospective cohort study</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760825/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>CONCLUSIONS: Not only a higher baseline SF but also SF changing trajectory are significantly associated with risk of new-onset MASLD. SF could be a predictor of the occurrence of MASLD.</description>
<content:encoded><![CDATA[<div>Lipids Health Dis. 2024 May 17;23(1):141. doi: 10.1186/s12944-024-02129-6.ABSTRACTBACKGROUND AND AIMS: Evidence from prospective cohort studies on the relationship between metabolic dysfunction-associated steatotic liver disease (MASLD) and longitudinal changes in serum ferritin (SF) still limited. This study aimed to investigate the associations of SF baselines and trajectories with new-onset MASLD and to present a MASLD discriminant model.METHODS: A total of 1895 participants who attended health examinations at least three times in a hospital in Dalian City between 2015 and 2022 were included. The main outcome was the incidence of MASLD. The associations between SF baselines and trajectories with the risk of MASLD were analyzed by Cox proportional hazards regression, restricted cubic spline (RCS) analysis and time-dependent receiver operating characteristic (ROC) curve analysis. In addition, a MASLD discrimination model was established using logistic regression analyses.RESULTS: Among the 1895 participants, 492 developed MASLD during follow-up. Kaplan-Meier analysis indicated that participants in the low-stable trajectory group had a longer MASLD-free time compared with participants in other groups. Compared with those in the low-stable trajectory group, the adjusted hazard ratios (HRs) with 95% confidence intervals (CIs) for the risk of new-onset MASLD in the medium-high, high-stable and high-high trajectory groups were 1.54(1.18-2.00), 1.77(1.35-2.32) and 1.55(1.07-2.26), respectively (Ptrend < 0.001). The results were robust in subgroup and sensitivity analyses. Multivariate Cox proportional regression showed that SF was an independent risk factor of MASLD (HR = 1.002, 95%CI: 1.000-1.003, P = 0.003). The restricted cubic spline demonstrated a nonlinear relationship between SF and the risk of MASLD. The 8-variable model had high discriminative performance, good accuracy and clinical effectiveness. The ROC curve results showed that AUC was greater than that of the FLI, HSI and ZJU models (all P < 0.01).CONCLUSIONS: Not only a higher baseline SF but also SF changing trajectory are significantly associated with risk of new-onset MASLD. SF could be a predictor of the occurrence of MASLD.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760825/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760825</a> | DOI:<a href=https://doi.org/10.1186/s12944-024-02129-6>10.1186/s12944-024-02129-6</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760825</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Ziping Song</dc:creator>
<dc:creator>Xinlei Miao</dc:creator>
<dc:creator>Xiaoling Xie</dc:creator>
<dc:creator>Guimin Tang</dc:creator>
<dc:creator>Jiayi Deng</dc:creator>
<dc:creator>Manling Hu</dc:creator>
<dc:creator>Shuang Liu</dc:creator>
<dc:creator>Song Leng</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Lipids in health and disease</dc:source>
<dc:title>Associations between serum ferritin baselines and trajectories and the incidence of metabolic dysfunction-associated steatotic liver disease: a prospective cohort study</dc:title>
<dc:identifier>pmid:38760825</dc:identifier>
<dc:identifier>doi:10.1186/s12944-024-02129-6</dc:identifier>
</item>
<item>
<title>Association between omega-3 polyunsaturated fatty acids and osteoarthritis: results from the NHANES 2003-2016 and Mendelian randomization study</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760818/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>CONCLUSIONS: Omega-3 PUFAs were inversely associated with OA in adults aged 40 ∼ 59. However, MR studies did not confirm a causal relationship between the two.</description>
<content:encoded><![CDATA[<div>Lipids Health Dis. 2024 May 17;23(1):147. doi: 10.1186/s12944-024-02139-4.ABSTRACTBACKGROUND: Omega-3 polyunsaturated fatty acids (omega-3 PUFAs) exhibit potential as therapeutics for a variety of diseases. This observational and Mendelian randomization (MR) study aims to explore the relationship between omega-3 PUFAs and osteoarthritis (OA).METHODS: Excluding individuals under 20 years old and those with missing data on relevant variables in the National Health and Nutrition Examination Survey (NHANES) spanning from 2003 to 2016, a total of 22 834 participants were included in this cross-sectional study. Weighted multivariable-adjusted logistic regression was used to estimate the association between omega-3 PUFAs and OA in adults. Moreover, restricted cubic splines were utilized to examine the dose-response relationship between omega-3 PUFAs and OA. To further investigate the potential causal relationship between omega-3 PUFAs and OA risk, a two-sample MR study was conducted. Furthermore, the robustness of the findings was assessed using various methods.RESULTS: Omega-3 PUFAs intake were inversely associated with OA in adults aged 40 ∼ 59 after multivariable adjustment [Formula: see text], with a nonlinear relationship observed between omega-3 PUFAs intake and OA [Formula: see text]. The IVW results showed there was no evidence to suggest a causal relationship between omega-3 PUFAs and OA risk [Formula: see text].CONCLUSIONS: Omega-3 PUFAs were inversely associated with OA in adults aged 40 ∼ 59. However, MR studies did not confirm a causal relationship between the two.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760818/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760818</a> | DOI:<a href=https://doi.org/10.1186/s12944-024-02139-4>10.1186/s12944-024-02139-4</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760818</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Yuxuan Liu</dc:creator>
<dc:creator>Feichao Song</dc:creator>
<dc:creator>Muchun Liu</dc:creator>
<dc:creator>Xi Huang</dc:creator>
<dc:creator>Shuyan Xue</dc:creator>
<dc:creator>Xuanyu Zhang</dc:creator>
<dc:creator>Huiqin Hao</dc:creator>
<dc:creator>Junfeng Zhang</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Lipids in health and disease</dc:source>
<dc:title>Association between omega-3 polyunsaturated fatty acids and osteoarthritis: results from the NHANES 2003-2016 and Mendelian randomization study</dc:title>
<dc:identifier>pmid:38760818</dc:identifier>
<dc:identifier>doi:10.1186/s12944-024-02139-4</dc:identifier>
</item>
<item>
<title>Fatty Liver Index (FLI) is the best score to predict MASLD with 50% lower cut-off value in women than in men</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760802/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>CONCLUSIONS: In this study, we found that FLI is the best non-invasive predictor of both liver steatosis and MASLD. The finding that in women FLI cut-off value for MASLD detection is 50% lower than in men suggests the need of a sex-specific personalized program of screening and prevention of dysmetabolism-related liver diseases, despite outwardly healthy biomarkers profile.</description>
<content:encoded><![CDATA[<div>Biol Sex Differ. 2024 May 17;15(1):43. doi: 10.1186/s13293-024-00617-z.ABSTRACTBACKGROUND: Metabolic dysfunction-associated steatotic liver disease (MASLD) is defined by the presence of hepatic steatosis, detected on ultrasonography (US) imaging or histology, and at least one of criteria for Metabolic Syndrome diagnosis. Simple non-invasive tests (NITs) have been proposed as an acceptable alternative when US and biopsy are not available or feasible but have not been validated for MASLD. In this observational study, we investigated the reliability of NITs for MASLD detection and whether sex-differences in screening methods should be considered.METHODS: We included 1069 individuals (48% males and 52% females) who underwent their first clinical examination for Metabolic Syndrome in the period between January 2015 and December 2022. Liver steatosis was detected through US and anthropometric and clinical parameters were recorded.RESULTS: Liver steatosis was detected in 648 patients and MASLD was diagnosed in 630 subjects (355 males; 275 females). Women with MASLD showed better metabolic profile and lower prevalence of Metabolic Syndrome criteria than men. Among NITs, Fatty Liver Index (FLI) showed the best ability for detection of MASLD, with a cut-off value of 44 (AUC = 0.82). When considering the two sexes for MASLD detection via FLI, despite no substantial differences regarding FLI correlations with metabolic biomarkers except for age, women showed marked lower FLI cut-off value (32; AUC = 0.80) than men (60; AUC = 0.80).CONCLUSIONS: In this study, we found that FLI is the best non-invasive predictor of both liver steatosis and MASLD. The finding that in women FLI cut-off value for MASLD detection is 50% lower than in men suggests the need of a sex-specific personalized program of screening and prevention of dysmetabolism-related liver diseases, despite outwardly healthy biomarkers profile.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760802/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760802</a> | DOI:<a href=https://doi.org/10.1186/s13293-024-00617-z>10.1186/s13293-024-00617-z</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760802</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Lucilla Crudele</dc:creator>
<dc:creator>Carlo De Matteis</dc:creator>
<dc:creator>Fabio Novielli</dc:creator>
<dc:creator>Ersilia Di Buduo</dc:creator>
<dc:creator>Stefano Petruzzelli</dc:creator>
<dc:creator>Alessia De Giorgi</dc:creator>
<dc:creator>Gianfranco Antonica</dc:creator>
<dc:creator>Elsa Berardi</dc:creator>
<dc:creator>Antonio Moschetta</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Biology of sex differences</dc:source>
<dc:title>Fatty Liver Index (FLI) is the best score to predict MASLD with 50% lower cut-off value in women than in men</dc:title>
<dc:identifier>pmid:38760802</dc:identifier>
<dc:identifier>doi:10.1186/s13293-024-00617-z</dc:identifier>
</item>
<item>
<title>Association between metabolic syndrome and kidney cancer risk: a prospective cohort study</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760801/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>CONCLUSIONS: Both pre-MetS and MetS status were positively associated with kidney cancer risk. The risk associated with kidney cancer varied by combinations of MetS components. These findings may offer novel perspectives on the aetiology of kidney cancer and assist in designing primary prevention strategies.</description>
<content:encoded><![CDATA[<div>Lipids Health Dis. 2024 May 17;23(1):142. doi: 10.1186/s12944-024-02138-5.ABSTRACTBACKGROUND: Kidney cancer has become known as a metabolic disease. However, there is limited evidence linking metabolic syndrome (MetS) with kidney cancer risk. This study aimed to investigate the association between MetS and its components and the risk of kidney cancer.METHODS: UK Biobank data was used in this study. MetS was defined as having three or more metabolic abnormalities, while pre-MetS was defined as the presence of one or two metabolic abnormalities. Hazard ratios (HRs) and 95% confidence intervals (CIs) for kidney cancer risk by MetS category were calculated using multivariable Cox proportional hazards models. Subgroup analyses were conducted for age, sex, BMI, smoking status and drinking status. The joint effects of MetS and genetic factors on kidney cancer risk were also analyzed.RESULTS: This study included 355,678 participants without cancer at recruitment. During a median follow-up of 11 years, 1203 participants developed kidney cancer. Compared to the metabolically healthy group, participants with pre-MetS (HR= 1.36, 95% CI: 1.06-1.74) or MetS (HR= 1. 70, 95% CI: 1.30-2.23) had a significantly greater risk of kidney cancer. This risk increased with the increasing number of MetS components (P for trend < 0.001). The combination of hypertension, dyslipidemia and central obesity contributed to the highest risk of kidney cancer (HR= 3.03, 95% CI: 1.91-4.80). Compared with participants with non-MetS and low genetic risk, those with MetS and high genetic risk had the highest risk of kidney cancer (HR= 1. 74, 95% CI: 1.41-2.14).CONCLUSIONS: Both pre-MetS and MetS status were positively associated with kidney cancer risk. The risk associated with kidney cancer varied by combinations of MetS components. These findings may offer novel perspectives on the aetiology of kidney cancer and assist in designing primary prevention strategies.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760801/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760801</a> | DOI:<a href=https://doi.org/10.1186/s12944-024-02138-5>10.1186/s12944-024-02138-5</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760801</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Lin Wang</dc:creator>
<dc:creator>Han Du</dc:creator>
<dc:creator>Chao Sheng</dc:creator>
<dc:creator>Hongji Dai</dc:creator>
<dc:creator>Kexin Chen</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Lipids in health and disease</dc:source>
<dc:title>Association between metabolic syndrome and kidney cancer risk: a prospective cohort study</dc:title>
<dc:identifier>pmid:38760801</dc:identifier>
<dc:identifier>doi:10.1186/s12944-024-02138-5</dc:identifier>
</item>
<item>
<title>Low expression of ELOVL6 may be involved in fat loss in white adipose tissue of cancer-associated cachexia</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760797/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>CONCLUSION: Overall, the expression of ELOVL6 was decreased in the WAT of CAC patients. Decreased expression of ELOVL6 might induce fat loss in CAC patients by potentially altering the fatty acid composition of adipocytes. These findings suggest that ELOVL6 may be used as a valuable biomarker for the early diagnosis of CAC and may hold promise as a target for future therapies.</description>
<content:encoded><![CDATA[<div>Lipids Health Dis. 2024 May 17;23(1):144. doi: 10.1186/s12944-024-02126-9.ABSTRACTBACKGROUND: Cancer-associated cachexia (CAC) arises from malignant tumors and leads to a debilitating wasting syndrome. In the pathophysiology of CAC, the depletion of fat plays an important role. The mechanisms of CAC-induced fat loss include the enhancement of lipolysis, inhibition of lipogenesis, and browning of white adipose tissue (WAT). However, few lipid-metabolic enzymes have been reported to be involved in CAC. This study hypothesized that ELOVL6, a critical enzyme for the elongation of fatty acids, may be involved in fat loss in CAC.METHODS: Transcriptome sequencing technology was used to identify CAC-related genes in the WAT of a CAC rodent model. Then, the expression level of ELOVL6 and the fatty acid composition were analyzed in a large clinical sample. Elovl6 was knocked down by siRNA in 3T3-L1 mouse preadipocytes to compare with wild-type 3T3-L1 cells treated with tumor cell conditioned medium.RESULTS: In the WAT of patients with CAC, a significant decrease in the expression of ELOVL6 was found, which was linearly correlated with the extent of body mass reduction. Gas chromatographic analysis revealed an increase in palmitic acid (C16:0) and a decrease in linoleic acid (C18:2n-6) in these tissue samples. After treatment with tumor cell-conditioned medium, 3T3-L1 mouse preadipocytes showed a decrease in Elovl6 expression, and Elovl6-knockdown cells exhibited a reduction in preadipocyte differentiation and lipogenesis. Similarly, the knockdown of Elovl6 in 3T3-L1 cells resulted in a significant increase in palmitic acid (C16:0) and a marked decrease in oleic acid (C18:1n-9) content.CONCLUSION: Overall, the expression of ELOVL6 was decreased in the WAT of CAC patients. Decreased expression of ELOVL6 might induce fat loss in CAC patients by potentially altering the fatty acid composition of adipocytes. These findings suggest that ELOVL6 may be used as a valuable biomarker for the early diagnosis of CAC and may hold promise as a target for future therapies.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760797/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760797</a> | DOI:<a href=https://doi.org/10.1186/s12944-024-02126-9>10.1186/s12944-024-02126-9</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760797</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Chenyang Jin</dc:creator>
<dc:creator>Shuangjie Wang</dc:creator>
<dc:creator>Xiangyu Sui</dc:creator>
<dc:creator>Qingyang Meng</dc:creator>
<dc:creator>Guohao Wu</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Lipids in health and disease</dc:source>
<dc:title>Low expression of ELOVL6 may be involved in fat loss in white adipose tissue of cancer-associated cachexia</dc:title>
<dc:identifier>pmid:38760797</dc:identifier>
<dc:identifier>doi:10.1186/s12944-024-02126-9</dc:identifier>
</item>
<item>
<title>Nitrogen starvation causes lipid remodeling in Rhodotorula toruloides</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760782/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>CONCLUSIONS: Integrative analysis identified the specific biosynthetic pathways that are differentially regulated during lipid remodeling. This insight into the mechanisms of lipid accumulation can lead to the success of future metabolic engineering strategies for overproduction of oleochemicals.</description>
<content:encoded><![CDATA[<div>Microb Cell Fact. 2024 May 17;23(1):141. doi: 10.1186/s12934-024-02414-0.ABSTRACTBACKGROUND: The oleaginous yeast Rhodotorula toruloides is a promising chassis organism for the biomanufacturing of value-added bioproducts. It can accumulate lipids at a high fraction of biomass. However, metabolic engineering efforts in this organism have progressed at a slower pace than those in more extensively studied yeasts. Few studies have investigated the lipid accumulation phenotype exhibited by R. toruloides under nitrogen limitation conditions. Consequently, there have been only a few studies exploiting the lipid metabolism for higher product titers.RESULTS: We performed a multi-omic investigation of the lipid accumulation phenotype under nitrogen limitation. Specifically, we performed comparative transcriptomic and lipidomic analysis of the oleaginous yeast under nitrogen-sufficient and nitrogen deficient conditions. Clustering analysis of transcriptomic data was used to identify the growth phase where nitrogen-deficient cultures diverged from the baseline conditions. Independently, lipidomic data was used to identify that lipid fractions shifted from mostly phospholipids to mostly storage lipids under the nitrogen-deficient phenotype. Through an integrative lens of transcriptomic and lipidomic analysis, we discovered that R. toruloides undergoes lipid remodeling during nitrogen limitation, wherein the pool of phospholipids gets remodeled to mostly storage lipids. We identify specific mRNAs and pathways that are strongly correlated with an increase in lipid levels, thus identifying putative targets for engineering greater lipid accumulation in R. toruloides. One surprising pathway identified was related to inositol phosphate metabolism, suggesting further inquiry into its role in lipid accumulation.CONCLUSIONS: Integrative analysis identified the specific biosynthetic pathways that are differentially regulated during lipid remodeling. This insight into the mechanisms of lipid accumulation can lead to the success of future metabolic engineering strategies for overproduction of oleochemicals.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760782/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760782</a> | DOI:<a href=https://doi.org/10.1186/s12934-024-02414-0>10.1186/s12934-024-02414-0</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760782</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Shekhar Mishra</dc:creator>
<dc:creator>Anshu Deewan</dc:creator>
<dc:creator>Huimin Zhao</dc:creator>
<dc:creator>Christopher V Rao</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Microbial cell factories</dc:source>
<dc:title>Nitrogen starvation causes lipid remodeling in Rhodotorula toruloides</dc:title>
<dc:identifier>pmid:38760782</dc:identifier>
<dc:identifier>doi:10.1186/s12934-024-02414-0</dc:identifier>
</item>
<item>
<title>Metabolomics reveals metabolites associated with hair follicle cycle in cashmere goats</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760765/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>CONCLUSIONS: The expression patterns of metabolites such as sugars, lipids, amino acids, and nucleotides in skin tissue affect hair follicle growth, in which 2'-deoxyadenosine, L-valine, 2'-deoxyuridine, riboflavin, cytidine, deoxyguanosine, L-tryptophan, and guanosine-5'-monophosphate may regulate the hair follicle cycle by participating in ABC transporters. Feeding practices may regulate hair follicle cycles by influencing the amount of hormones and vitamins expressed in the skin of cashmere...</description>
<content:encoded><![CDATA[<div>BMC Vet Res. 2024 May 17;20(1):208. doi: 10.1186/s12917-024-04057-0.ABSTRACTBACKGROUND: The hair follicle is a skin accessory organ that regulates hair development, and its activity varies on a regular basis. However, the significance of metabolites in the hair follicle cycle has long been unknown.RESULTS: Targeted metabolomics was used in this investigation to reveal the expression patterns of 1903 metabolites in cashmere goat skin during anagen to telogen. A statistical analysis was used to investigate the potential associations between metabolites and the hair follicle cycle. The findings revealed clear changes in the expression patterns of metabolites at various phases and in various feeding models. The majority of metabolites (primarily amino acids, nucleotides, their metabolites, and lipids) showed downregulated expression from anagen (An) to telogen (Tn), which was associated with gene expression, protein synthesis and transport, and cell structure, which reflected, to some extent, that the cells associated with hair follicle development are active in An and apoptotic in An-Tn. It is worth mentioning that the expression of vitamin D3 and 3,3',5-triiodo-L-thyronine decreased and then increased, which may be related to the shorter and longer duration of outdoor light, which may stimulate the hair follicle to transition from An to catagen (Cn). In the comparison of different hair follicle development stages (An, Cn, and Tn) or feeding modes (grazing and barn feeding), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis revealed that common differentially expressed metabolites (DEMs) (2'-deoxyadenosine, L-valine, 2'-deoxyuridine, riboflavin, cytidine, deoxyguanosine, L-tryptophan, and guanosine-5'-monophosphate) were enriched in ABC transporters. This finding suggested that this pathway may be involved in the hair follicle cycle. Among these DEMs, riboflavin is absorbed from food, and the expression of riboflavin and sugars (D-glucose and glycogen) in skin tissue under grazing was greater and lower than that during barn feeding, respectively, suggesting that eating patterns may also alter the hair follicle cycle.CONCLUSIONS: The expression patterns of metabolites such as sugars, lipids, amino acids, and nucleotides in skin tissue affect hair follicle growth, in which 2'-deoxyadenosine, L-valine, 2'-deoxyuridine, riboflavin, cytidine, deoxyguanosine, L-tryptophan, and guanosine-5'-monophosphate may regulate the hair follicle cycle by participating in ABC transporters. Feeding practices may regulate hair follicle cycles by influencing the amount of hormones and vitamins expressed in the skin of cashmere goats.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760765/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760765</a> | DOI:<a href=https://doi.org/10.1186/s12917-024-04057-0>10.1186/s12917-024-04057-0</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760765</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Shengchao Ma</dc:creator>
<dc:creator>Wenzhi Cao</dc:creator>
<dc:creator>Xiaolin Ma</dc:creator>
<dc:creator>Xiaofang Ye</dc:creator>
<dc:creator>Chongkai Qin</dc:creator>
<dc:creator>Bin Li</dc:creator>
<dc:creator>Wenna Liu</dc:creator>
<dc:creator>Qingwei Lu</dc:creator>
<dc:creator>Cuiling Wu</dc:creator>
<dc:creator>Xuefeng Fu</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>BMC veterinary research</dc:source>
<dc:title>Metabolomics reveals metabolites associated with hair follicle cycle in cashmere goats</dc:title>
<dc:identifier>pmid:38760765</dc:identifier>
<dc:identifier>doi:10.1186/s12917-024-04057-0</dc:identifier>
</item>
<item>
<title>High-density lipoprotein mimetic nano-therapeutics targeting monocytes and macrophages for improved cardiovascular care: a comprehensive review</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760755/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>The prevalence of cardiovascular diseases continues to be a challenge for global health, necessitating innovative solutions. The potential of high-density lipoprotein (HDL) mimetic nanotherapeutics in the context of cardiovascular disease and the intricate mechanisms underlying the interactions between monocyte-derived cells and HDL mimetic showing their impact on inflammation, cellular lipid metabolism, and the progression of atherosclerotic plaque. Preclinical studies have demonstrated that...</description>
<content:encoded><![CDATA[<div>J Nanobiotechnology. 2024 May 17;22(1):263. doi: 10.1186/s12951-024-02529-x.ABSTRACTThe prevalence of cardiovascular diseases continues to be a challenge for global health, necessitating innovative solutions. The potential of high-density lipoprotein (HDL) mimetic nanotherapeutics in the context of cardiovascular disease and the intricate mechanisms underlying the interactions between monocyte-derived cells and HDL mimetic showing their impact on inflammation, cellular lipid metabolism, and the progression of atherosclerotic plaque. Preclinical studies have demonstrated that HDL mimetic nanotherapeutics can regulate monocyte recruitment and macrophage polarization towards an anti-inflammatory phenotype, suggesting their potential to impede the progression of atherosclerosis. The challenges and opportunities associated with the clinical application of HDL mimetic nanotherapeutics, emphasize the need for additional research to gain a better understanding of the precise molecular pathways and long-term effects of these nanotherapeutics on monocytes and macrophages to maximize their therapeutic efficacy. Furthermore, the use of nanotechnology in the treatment of cardiovascular diseases highlights the potential of nanoparticles for targeted treatments. Moreover, the concept of theranostics combines therapy and diagnosis to create a selective platform for the conversion of traditional therapeutic medications into specialized and customized treatments. The multifaceted contributions of HDL to cardiovascular and metabolic health via highlight its potential to improve plaque stability and avert atherosclerosis-related problems. There is a need for further research to maximize the therapeutic efficacy of HDL mimetic nanotherapeutics and to develop targeted treatment approaches to prevent atherosclerosis. This review provides a comprehensive overview of the potential of nanotherapeutics in the treatment of cardiovascular diseases, emphasizing the need for innovative solutions to address the challenges posed by cardiovascular diseases.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760755/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760755</a> | DOI:<a href=https://doi.org/10.1186/s12951-024-02529-x>10.1186/s12951-024-02529-x</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760755</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Juan Zhen</dc:creator>
<dc:creator>Xiangjun Li</dc:creator>
<dc:creator>Haitao Yu</dc:creator>
<dc:creator>Bing Du</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Journal of nanobiotechnology</dc:source>
<dc:title>High-density lipoprotein mimetic nano-therapeutics targeting monocytes and macrophages for improved cardiovascular care: a comprehensive review</dc:title>
<dc:identifier>pmid:38760755</dc:identifier>
<dc:identifier>doi:10.1186/s12951-024-02529-x</dc:identifier>
</item>
<item>
<title>Association of lipid-lowering drug targets with risk of cutaneous melanoma: a mendelian randomization study</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760735/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>CONCLUSION: The study concludes that PCSK9 plays a significant role in the development of CM, and its inhibition is linked to a reduced risk of the disease.</description>
<content:encoded><![CDATA[<div>BMC Cancer. 2024 May 17;24(1):602. doi: 10.1186/s12885-024-12366-8.ABSTRACTBACKGROUND: Melanoma proliferation is partly attributed to dysregulated lipid metabolism. The effectiveness of lipid-lowering drugs in combating cutaneous melanoma (CM) is a subject of ongoing debate in both in vitro and clinical studies.METHOD: This study aims to evaluate the causal relationship between various lipid-lowering drug targets, namely 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR, targeted by statins), Proprotein convertase subtilisin/kexin type 9 (PCSK9, targeted by alirocumab and evolocumab), and Niemann-Pick C1-like 1 (NPC1L1, targeted by ezetimibe), and the outcomes of cutaneous melanoma. To mimic the effects of lipid-lowering drugs, we utilized two genetic tools: analysis of polymorphisms affecting the expression levels of drug target genes, and genetic variations linked to low-density lipoprotein cholesterol levels and drug target genes. These variations were sourced from genome-wide association studies (GWAS). We applied Summary-data-based Mendelian Randomization (SMR) and Inverse Variance Weighted Mendelian Randomization (IVW-MR) to gauge the effectiveness of these drugs.RESULTS: Our findings, with SMR results showing an odds ratio (OR) of 1.44 (95% CI: 1.08-1.92; P = 0.011) and IVW-MR results indicating an OR of 1.56 (95% CI: 1.10-2.23; P = 0.013), demonstrate a positive correlation between PCSK9 expression and increased risk of CM. However, no such correlations were observed in other analyses.CONCLUSION: The study concludes that PCSK9 plays a significant role in the development of CM, and its inhibition is linked to a reduced risk of the disease.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760735/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760735</a> | DOI:<a href=https://doi.org/10.1186/s12885-024-12366-8>10.1186/s12885-024-12366-8</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760735</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Lusheng Miao</dc:creator>
<dc:creator>Taosheng Miao</dc:creator>
<dc:creator>Ying Zhang</dc:creator>
<dc:creator>Jin Hao</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>BMC cancer</dc:source>
<dc:title>Association of lipid-lowering drug targets with risk of cutaneous melanoma: a mendelian randomization study</dc:title>
<dc:identifier>pmid:38760735</dc:identifier>
<dc:identifier>doi:10.1186/s12885-024-12366-8</dc:identifier>
</item>
<item>
<title>Characterization of the gut microbiota in polycystic ovary syndrome with dyslipidemia</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760705/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>CONCLUSIONS: The gut microbiota characterizations in patients with PCOS.D differ from those in patients with PCOS and controls, and those might also be related to clinical parameters. This may have the potential to become an alternative therapy to regulate the clinical lipid levels of patients with PCOS in the future.</description>
<content:encoded><![CDATA[<div>BMC Microbiol. 2024 May 17;24(1):169. doi: 10.1186/s12866-024-03329-x.ABSTRACTBACKGROUND: Polycystic ovary syndrome (PCOS) is an endocrinopathy in childbearing-age females which can cause many complications, such as diabetes, obesity, and dyslipidemia. The metabolic disorders in patients with PCOS were linked to gut microbial dysbiosis. However, the correlation between the gut microbial community and dyslipidemia in PCOS remains unillustrated. Our study elucidated the different gut microbiota in patients with PCOS and dyslipidemia (PCOS.D) compared to those with only PCOS and healthy women.RESULTS: In total, 18 patients with PCOS, 16 healthy females, and 18 patients with PCOS.D were enrolled. The 16 S rRNA sequencing in V3-V4 region was utilized for identifying the gut microbiota, which analyzes species annotation, community diversity, and community functions. Our results showed that the β diversity of gut microbiota did not differ significantly among the three groups. Regarding gut microbiota dysbiosis, patients with PCOS showed a decreased abundance of Proteobacteria, and patients with PCOS.D showed an increased abundance of Bacteroidota compared to other groups. With respect to the gut microbial imbalance at genus level, the PCOS.D group showed a higher abundance of Clostridium_sensu_stricto_1 compared to other two groups. Furthermore, the abundances of Faecalibacterium and Holdemanella were lower in the PCOS.D than those in the PCOS group. Several genera, including Faecalibacterium and Holdemanella, were negatively correlated with the lipid profiles. Pseudomonas was negatively correlated with luteinizing hormone levels. Using PICRUSt analysis, the gut microbiota community functions suggested that certain metabolic pathways (e.g., amino acids, glycolysis, and lipid) were altered in PCOS.D patients as compared to those in PCOS patients.CONCLUSIONS: The gut microbiota characterizations in patients with PCOS.D differ from those in patients with PCOS and controls, and those might also be related to clinical parameters. This may have the potential to become an alternative therapy to regulate the clinical lipid levels of patients with PCOS in the future.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760705/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760705</a> | DOI:<a href=https://doi.org/10.1186/s12866-024-03329-x>10.1186/s12866-024-03329-x</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760705</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Tianjin Yang</dc:creator>
<dc:creator>Guanjian Li</dc:creator>
<dc:creator>Yuping Xu</dc:creator>
<dc:creator>Xiaojin He</dc:creator>
<dc:creator>Bing Song</dc:creator>
<dc:creator>Yunxia Cao</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>BMC microbiology</dc:source>
<dc:title>Characterization of the gut microbiota in polycystic ovary syndrome with dyslipidemia</dc:title>
<dc:identifier>pmid:38760705</dc:identifier>
<dc:identifier>doi:10.1186/s12866-024-03329-x</dc:identifier>
</item>
<item>
<title>Association between lipid accumulation product and psoriasis among adults: a nationally representative cross-sectional study</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760661/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>CONCLUSIONS: This study found that the LAP index and adult psoriasis were positively correlated, especially in young males without comorbidities. Therefore, it is proposed that LAP may serve as a biomarker for early diagnosis of psoriasis and tracking the effectiveness of treatment.</description>
<content:encoded><![CDATA[<div>Lipids Health Dis. 2024 May 17;23(1):143. doi: 10.1186/s12944-024-02123-y.ABSTRACTBACKGROUND: Lipid accumulation product (LAP) is an accessible and relatively comprehensive assessment of obesity that represents both anatomical and physiological lipid accumulation. Obesity and psoriasis are potentially related, according to previous research. Investigating the relationship between adult psoriasis and the LAP index was the goal of this study.METHODS: This is a cross-sectional study based on data from the National Health and Nutrition Examination Survey (NHANES) 2003-2006 and 2009-2014. The association between LAP and psoriasis was examined using multivariate logistic regression and smoothed curve fitting. To verify whether this relationship was stable across populations, subgroup analyses and interaction tests were performed.RESULTS: The LAP index showed a positive correlation with psoriasis in 9,781 adult participants who were 20 years of age or older. A 27% elevated probability of psoriasis was linked to every unit increase in ln LAP in the fully adjusted model (Model 3: OR 1.27, 95% CI 1.06-1.52). In comparison with participants in the lowest ln LAP quartile, those in the highest quartile had an 83% greater likelihood of psoriasis (Model 3: OR 1.83, 95% CI 1.08-3.11). This positive correlation was more pronounced for young males, participants who had never smoked, non-drinkers, participants who exercised little, as well as non-hypertensive and non-diabetic participants.CONCLUSIONS: This study found that the LAP index and adult psoriasis were positively correlated, especially in young males without comorbidities. Therefore, it is proposed that LAP may serve as a biomarker for early diagnosis of psoriasis and tracking the effectiveness of treatment.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760661/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760661</a> | DOI:<a href=https://doi.org/10.1186/s12944-024-02123-y>10.1186/s12944-024-02123-y</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760661</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Caiyun Zhang</dc:creator>
<dc:creator>Xiaoping Dong</dc:creator>
<dc:creator>Jun Chen</dc:creator>
<dc:creator>Fang Liu</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Lipids in health and disease</dc:source>
<dc:title>Association between lipid accumulation product and psoriasis among adults: a nationally representative cross-sectional study</dc:title>
<dc:identifier>pmid:38760661</dc:identifier>
<dc:identifier>doi:10.1186/s12944-024-02123-y</dc:identifier>
</item>
<item>
<title>Nonlinear association of triglyceride-glucose index with hyperuricemia in US adults: a cross-sectional study</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760656/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>CONCLUSION: Additional prospective studies are required to corroborate the current findings, which indicate a strong positive connection between TyG and hyperuricemia among adults in the United States.</description>
<content:encoded><![CDATA[<div>Lipids Health Dis. 2024 May 17;23(1):145. doi: 10.1186/s12944-024-02146-5.ABSTRACTBACKGROUND: Despite abundant evidence on the epidemiological risk factors of metabolic diseases related to hyperuricemia, there is still insufficient evidence regarding the nonlinear relationship between triglyceride-glucose (TyG) index and hyperuricemia. Thus, the purpose of this research is to clarify the nonlinear connection between TyG and hyperuricemia.METHODS: From 2011 to 2018, a cross-sectional study was carried out using data from the National Health and Nutrition Examination Survey (NHANES). This study had 8572 participants in all. TyG was computed as Ln [triglycerides (mg/dL) × fasting glucose (mg/dL)/2]. The outcome variable was hyperuricemia. The association between TyG and hyperuricemia was examined using weighted multiple logistic regression, subgroup analysis, generalized additive models, smooth fitting curves, and two-piecewise linear regression models.RESULTS: In the regression model adjusting for all confounding variables, the OR (95% CI) for the association between TyG and hyperuricemia was 2.34 (1.70, 3.21). There is a nonlinear and reverse U-shaped association between TyG and hyperuricemia, with a inflection point of 9.69. The OR (95% CI) before the inflection point was 2.64 (2.12, 3.28), and after the inflection point was 0.32 (0.11, 0.98). The interaction in gender, BMI, hypertension, and diabetes analysis was statistically significant.CONCLUSION: Additional prospective studies are required to corroborate the current findings, which indicate a strong positive connection between TyG and hyperuricemia among adults in the United States.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760656/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760656</a> | DOI:<a href=https://doi.org/10.1186/s12944-024-02146-5>10.1186/s12944-024-02146-5</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760656</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Linjie Qiu</dc:creator>
<dc:creator>Yan Ren</dc:creator>
<dc:creator>Jixin Li</dc:creator>
<dc:creator>Meijie Li</dc:creator>
<dc:creator>Wenjie Li</dc:creator>
<dc:creator>Lingli Qin</dc:creator>
<dc:creator>Chunhui Ning</dc:creator>
<dc:creator>Jin Zhang</dc:creator>
<dc:creator>Feng Gao</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Lipids in health and disease</dc:source>
<dc:title>Nonlinear association of triglyceride-glucose index with hyperuricemia in US adults: a cross-sectional study</dc:title>
<dc:identifier>pmid:38760656</dc:identifier>
<dc:identifier>doi:10.1186/s12944-024-02146-5</dc:identifier>
</item>
<item>
<title>Long-term (11 Years) Results of Laparoscopic Gastric Bypass: Changes in Weight, Blood Levels of Sugar and Lipids, and Late Adverse Effects : Laparoscopic Gastric Bypass Results</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760651/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>CONCLUSION: After surgery, there is a significant and durable loss of weight, with a tendency for late Recurrent Weight Gain. Furthermore, the improvement in biochemical parameters is sustained over time, but surgery's adverse effects may appear later.</description>
<content:encoded><![CDATA[<div>Obes Surg. 2024 May 17. doi: 10.1007/s11695-024-07249-7. Online ahead of print.ABSTRACTPURPOSE: Laparoscopic Roux-en-Y Gastric Bypass (LRYGB) remains the most effective procedure to treat severe obesity with proven short- and intermediate-term benefits. The main goal is to describe the effects on weight and biochemical laboratory tests after long-term follow-up (11 years).MATERIALS AND METHODS: A prospective cohort of adults with obesity treated with LRYGB between 2004 and 2010 in one center were studied. Patients with prior bariatric or upper digestive tract surgery, hiatal hernia >4 cm, alcoholism, or decompensated conditions were excluded. The study enrolled 123 patients, with a mean follow-up of 133±29 months and a 14% loss of participants.RESULTS: The percentage of Total Weight Loss (%TWL) at one, five, and eleven years was 30.3±8.4%, 29.1±6.9%, and 23.4±7%, respectively. Of the patients, 61.3% (65/106) maintained a %TWL≥20 after eleven years. Recurrent Weight Gain (RWG) at five and eleven years was 2.6±11.4% and 11 ±11.5%, respectively. At the end of the follow-up, 31.1% (33/106) of patients had RWG≥15%. Hypercholesterolemia and hypertriglyceridemia improved in 85.7% (54/63) and 90.2% (7/61) of the cohort, respectively. Remission of diabetes occurred in 80% of this subgroup. Gallstones developed in 28% of patients, and bowel obstruction due to internal hernia occurred in 9.4%. Anemia due to iron deficiency appeared in 25 patients.CONCLUSION: After surgery, there is a significant and durable loss of weight, with a tendency for late Recurrent Weight Gain. Furthermore, the improvement in biochemical parameters is sustained over time, but surgery's adverse effects may appear later.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760651/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760651</a> | DOI:<a href=https://doi.org/10.1007/s11695-024-07249-7>10.1007/s11695-024-07249-7</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760651</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>L Deycies Gaete</dc:creator>
<dc:creator>J Attila Csendes</dc:creator>
<dc:creator>A Tomás González</dc:creator>
<dc:creator>P Álvaro Morales</dc:creator>
<dc:creator>Benjamín Panza</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Obesity surgery</dc:source>
<dc:title>Long-term (11 Years) Results of Laparoscopic Gastric Bypass: Changes in Weight, Blood Levels of Sugar and Lipids, and Late Adverse Effects : Laparoscopic Gastric Bypass Results</dc:title>
<dc:identifier>pmid:38760651</dc:identifier>
<dc:identifier>doi:10.1007/s11695-024-07249-7</dc:identifier>
</item>
<item>
<title>Integrative multi-omics profiling in human decedents receiving pig heart xenografts</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760586/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>In a previous study, heart xenografts from 10-gene-edited pigs transplanted into two human decedents did not show evidence of acute-onset cellular- or antibody-mediated rejection. Here, to better understand the detailed molecular landscape following xenotransplantation, we carried out bulk and single-cell transcriptomics, lipidomics, proteomics and metabolomics on blood samples obtained from the transplanted decedents every 6 h, as well as histological and transcriptomic tissue profiling. We...</description>
<content:encoded><![CDATA[<div>Nat Med. 2024 May 17. doi: 10.1038/s41591-024-02972-1. Online ahead of print.ABSTRACTIn a previous study, heart xenografts from 10-gene-edited pigs transplanted into two human decedents did not show evidence of acute-onset cellular- or antibody-mediated rejection. Here, to better understand the detailed molecular landscape following xenotransplantation, we carried out bulk and single-cell transcriptomics, lipidomics, proteomics and metabolomics on blood samples obtained from the transplanted decedents every 6 h, as well as histological and transcriptomic tissue profiling. We observed substantial early immune responses in peripheral blood mononuclear cells and xenograft tissue obtained from decedent 1 (male), associated with downstream T cell and natural killer cell activity. Longitudinal analyses indicated the presence of ischemia reperfusion injury, exacerbated by inadequate immunosuppression of T cells, consistent with previous findings of perioperative cardiac xenograft dysfunction in pig-to-nonhuman primate studies. Moreover, at 42 h after transplantation, substantial alterations in cellular metabolism and liver-damage pathways occurred, correlating with profound organ-wide physiological dysfunction. By contrast, relatively minor changes in RNA, protein, lipid and metabolism profiles were observed in decedent 2 (female) as compared to decedent 1. Overall, these multi-omics analyses delineate distinct responses to cardiac xenotransplantation in the two human decedents and reveal new insights into early molecular and immune responses after xenotransplantation. These findings may aid in the development of targeted therapeutic approaches to limit ischemia reperfusion injury-related phenotypes and improve outcomes.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760586/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760586</a> | DOI:<a href=https://doi.org/10.1038/s41591-024-02972-1>10.1038/s41591-024-02972-1</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760586</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Eloi Schmauch</dc:creator>
<dc:creator>Brian Piening</dc:creator>
<dc:creator>Maedeh Mohebnasab</dc:creator>
<dc:creator>Bo Xia</dc:creator>
<dc:creator>Chenchen Zhu</dc:creator>
<dc:creator>Jeffrey Stern</dc:creator>
<dc:creator>Weimin Zhang</dc:creator>
<dc:creator>Alexa K Dowdell</dc:creator>
<dc:creator>Jacqueline I Kim</dc:creator>
<dc:creator>David Andrijevic</dc:creator>
<dc:creator>Karen Khalil</dc:creator>
<dc:creator>Ian S Jaffe</dc:creator>
<dc:creator>Bao-Li Loza</dc:creator>
<dc:creator>Loren Gragert</dc:creator>
<dc:creator>Brendan R Camellato</dc:creator>
<dc:creator>Michelli F Oliveira</dc:creator>
<dc:creator>Darragh P O'Brien</dc:creator>
<dc:creator>Han M Chen</dc:creator>
<dc:creator>Elaina Weldon</dc:creator>
<dc:creator>Hui Gao</dc:creator>
<dc:creator>Divya Gandla</dc:creator>
<dc:creator>Andrew Chang</dc:creator>
<dc:creator>Riyana Bhatt</dc:creator>
<dc:creator>Sarah Gao</dc:creator>
<dc:creator>Xiangping Lin</dc:creator>
<dc:creator>Kriyana P Reddy</dc:creator>
<dc:creator>Larisa Kagermazova</dc:creator>
<dc:creator>Alawi H Habara</dc:creator>
<dc:creator>Sophie Widawsky</dc:creator>
<dc:creator>Feng-Xia Liang</dc:creator>
<dc:creator>Joseph Sall</dc:creator>
<dc:creator>Alexandre Loupy</dc:creator>
<dc:creator>Adriana Heguy</dc:creator>
<dc:creator>Sarah E B Taylor</dc:creator>
<dc:creator>Yinan Zhu</dc:creator>
<dc:creator>Basil Michael</dc:creator>
<dc:creator>Lihua Jiang</dc:creator>
<dc:creator>Ruiqi Jian</dc:creator>
<dc:creator>Anita S Chong</dc:creator>
<dc:creator>Robert L Fairchild</dc:creator>
<dc:creator>Suvi Linna-Kuosmanen</dc:creator>
<dc:creator>Minna U Kaikkonen</dc:creator>
<dc:creator>Vasishta Tatapudi</dc:creator>
<dc:creator>Marc Lorber</dc:creator>
<dc:creator>David Ayares</dc:creator>
<dc:creator>Massimo Mangiola</dc:creator>
<dc:creator>Navneet Narula</dc:creator>
<dc:creator>Nader Moazami</dc:creator>
<dc:creator>Harvey Pass</dc:creator>
<dc:creator>Ramin S Herati</dc:creator>
<dc:creator>Adam Griesemer</dc:creator>
<dc:creator>Manolis Kellis</dc:creator>
<dc:creator>Michael P Snyder</dc:creator>
<dc:creator>Robert A Montgomery</dc:creator>
<dc:creator>Jef D Boeke</dc:creator>
<dc:creator>Brendan J Keating</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Nature medicine</dc:source>
<dc:title>Integrative multi-omics profiling in human decedents receiving pig heart xenografts</dc:title>
<dc:identifier>pmid:38760586</dc:identifier>
<dc:identifier>doi:10.1038/s41591-024-02972-1</dc:identifier>
</item>
<item>
<title>Restoration of HMGCS2-mediated ketogenesis alleviates tacrolimus-induced hepatic lipid metabolism disorder</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760545/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>Tacrolimus, one of the macrolide calcineurin inhibitors, is the most frequently used immunosuppressant after transplantation. Long-term administration of tacrolimus leads to dyslipidemia and affects liver lipid metabolism. In this study, we investigated the mode of action and underlying mechanisms of this adverse reaction. Mice were administered tacrolimus (2.5 mg·kg^(-1)·d^(-1), i.g.) for 10 weeks, then euthanized; the blood samples and liver tissues were collected for analyses. We showed that...</description>
<content:encoded><![CDATA[<div>Acta Pharmacol Sin. 2024 May 17. doi: 10.1038/s41401-024-01300-0. Online ahead of print.ABSTRACTTacrolimus, one of the macrolide calcineurin inhibitors, is the most frequently used immunosuppressant after transplantation. Long-term administration of tacrolimus leads to dyslipidemia and affects liver lipid metabolism. In this study, we investigated the mode of action and underlying mechanisms of this adverse reaction. Mice were administered tacrolimus (2.5 mg·kg-1·d-1, i.g.) for 10 weeks, then euthanized; the blood samples and liver tissues were collected for analyses. We showed that tacrolimus administration induced significant dyslipidemia and lipid deposition in mouse liver. Dyslipidemia was also observed in heart or kidney transplantation patients treated with tacrolimus. We demonstrated that tacrolimus did not directly induce de novo synthesis of fatty acids, but markedly decreased fatty acid oxidation (FAO) in AML12 cells. Furthermore, we showed that tacrolimus dramatically decreased the expression of HMGCS2, the rate-limiting enzyme of ketogenesis, with decreased ketogenesis in AML12 cells, which was responsible for lipid deposition in normal hepatocytes. Moreover, we revealed that tacrolimus inhibited forkhead box protein O1 (FoxO1) nuclear translocation by promoting FKBP51-FoxO1 complex formation, thus reducing FoxO1 binding to the HMGCS2 promoter and its transcription ability in AML12 cells. The loss of HMGCS2 induced by tacrolimus caused decreased ketogenesis and increased acetyl-CoA accumulation, which promoted mitochondrial protein acetylation, thereby resulting in FAO function inhibition. Liver-specific HMGCS2 overexpression via tail intravenous injection of AAV8-TBG-HMGCS2 construct reversed tacrolimus-induced mitochondrial protein acetylation and FAO inhibition, thus removing the lipid deposition in hepatocytes. Collectively, this study demonstrates a novel mechanism of liver lipid deposition and hyperlipidemia induced by long-term administration of tacrolimus, resulted from the loss of HMGCS2-mediated ketogenesis and subsequent FAO inhibition, providing an alternative target for reversing tacrolimus-induced adverse reaction.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760545/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760545</a> | DOI:<a href=https://doi.org/10.1038/s41401-024-01300-0>10.1038/s41401-024-01300-0</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760545</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Sen-Lin Li</dc:creator>
<dc:creator>Hong Zhou</dc:creator>
<dc:creator>Jia Liu</dc:creator>
<dc:creator>Jian Yang</dc:creator>
<dc:creator>Li Jiang</dc:creator>
<dc:creator>Hui-Min Yuan</dc:creator>
<dc:creator>Meng-Heng Wang</dc:creator>
<dc:creator>Ke-Shan Yang</dc:creator>
<dc:creator>Ming Xiang</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Acta pharmacologica Sinica</dc:source>
<dc:title>Restoration of HMGCS2-mediated ketogenesis alleviates tacrolimus-induced hepatic lipid metabolism disorder</dc:title>
<dc:identifier>pmid:38760545</dc:identifier>
<dc:identifier>doi:10.1038/s41401-024-01300-0</dc:identifier>
</item>
<item>
<title>Isobutyric acid enhances the anti-tumour effect of anti-PD-1 antibody</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760458/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>The low response rate of immune checkpoint inhibitors (ICIs) is a challenge. The efficacy of ICIs is influenced by the tumour microenvironment, which is controlled by the gut microbiota. In particular, intestinal bacteria and their metabolites, such as short chain fatty acids (SCFAs), are important regulators of cancer immunity; however, our knowledge on the effects of individual SCFAs remains limited. Here, we show that isobutyric acid has the strongest effect among SCFAs on both immune...</description>
<content:encoded><![CDATA[<div>Sci Rep. 2024 May 17;14(1):11325. doi: 10.1038/s41598-024-59677-1.ABSTRACTThe low response rate of immune checkpoint inhibitors (ICIs) is a challenge. The efficacy of ICIs is influenced by the tumour microenvironment, which is controlled by the gut microbiota. In particular, intestinal bacteria and their metabolites, such as short chain fatty acids (SCFAs), are important regulators of cancer immunity; however, our knowledge on the effects of individual SCFAs remains limited. Here, we show that isobutyric acid has the strongest effect among SCFAs on both immune activity and tumour growth. In vitro, cancer cell numbers were suppressed by approximately 75% in humans and mice compared with those in controls. Oral administration of isobutyric acid to carcinoma-bearing mice enhanced the effect of anti-PD-1 immunotherapy, reducing tumour volume by approximately 80% and 60% compared with those in the control group and anti-PD-1 antibody alone group, respectively. Taken together, these findings may support the development of novel cancer therapies that can improve the response rate to ICIs.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760458/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760458</a> | DOI:<a href=https://doi.org/10.1038/s41598-024-59677-1>10.1038/s41598-024-59677-1</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760458</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Masakazu Murayama</dc:creator>
<dc:creator>Masahiro Hosonuma</dc:creator>
<dc:creator>Atsuo Kuramasu</dc:creator>
<dc:creator>Sei Kobayashi</dc:creator>
<dc:creator>Akiko Sasaki</dc:creator>
<dc:creator>Yuta Baba</dc:creator>
<dc:creator>Yoichiro Narikawa</dc:creator>
<dc:creator>Hitoshi Toyoda</dc:creator>
<dc:creator>Junya Isobe</dc:creator>
<dc:creator>Eiji Funayama</dc:creator>
<dc:creator>Kohei Tajima</dc:creator>
<dc:creator>Aya Sasaki</dc:creator>
<dc:creator>Yuki Maruyama</dc:creator>
<dc:creator>Yoshitaka Yamazaki</dc:creator>
<dc:creator>Midori Shida</dc:creator>
<dc:creator>Kazuyuki Hamada</dc:creator>
<dc:creator>Yuya Hirasawa</dc:creator>
<dc:creator>Toshiaki Tsurui</dc:creator>
<dc:creator>Hirotsugu Ariizumi</dc:creator>
<dc:creator>Tomoyuki Ishiguro</dc:creator>
<dc:creator>Risako Suzuki</dc:creator>
<dc:creator>Ryotaro Ohkuma</dc:creator>
<dc:creator>Yutaro Kubota</dc:creator>
<dc:creator>Atsushi Horiike</dc:creator>
<dc:creator>Takehiko Sambe</dc:creator>
<dc:creator>Mayumi Tsuji</dc:creator>
<dc:creator>Satoshi Wada</dc:creator>
<dc:creator>Shinichi Kobayashi</dc:creator>
<dc:creator>Toshikazu Shimane</dc:creator>
<dc:creator>Takuya Tsunoda</dc:creator>
<dc:creator>Hitome Kobayashi</dc:creator>
<dc:creator>Yuji Kiuchi</dc:creator>
<dc:creator>Kiyoshi Yoshimura</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Scientific reports</dc:source>
<dc:title>Isobutyric acid enhances the anti-tumour effect of anti-PD-1 antibody</dc:title>
<dc:identifier>pmid:38760458</dc:identifier>
<dc:identifier>doi:10.1038/s41598-024-59677-1</dc:identifier>
</item>
<item>
<title>Comparison of HIIT and MICT and further detraining on metabolic syndrome and asprosin signaling pathway in metabolic syndrome model of rats</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760452/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>Physical activity promotes various metabolic benefits by balancing pro and anti-inflammatory adipokines. Recent studies suggest that asprosin might be involved in progression of metabolic syndrome (MetS), however, the underlying mechanisms have not been understood yet. This study aimed to evaluate the effects of high-intensity interval training (HIIT), moderate-intensity continuous training (MICT), and further detraining on MetS indices, insulin resistance, serum and the liver levels of...</description>
<content:encoded><![CDATA[<div>Sci Rep. 2024 May 17;14(1):11313. doi: 10.1038/s41598-024-61842-5.ABSTRACTPhysical activity promotes various metabolic benefits by balancing pro and anti-inflammatory adipokines. Recent studies suggest that asprosin might be involved in progression of metabolic syndrome (MetS), however, the underlying mechanisms have not been understood yet. This study aimed to evaluate the effects of high-intensity interval training (HIIT), moderate-intensity continuous training (MICT), and further detraining on MetS indices, insulin resistance, serum and the liver levels of asprosin, and AMP-activated protein kinase (AMPK) pathway in menopause-induced MetS model of rats. A total of 64 Wistar rats were used in this study and divided into eight groups: Sham1, OVX1 (ovariectomized), Sham2, OVX2, OVX + HIIT, OVX + MICT, OVX + HIIT + Det (detraining), and OVX + MICT + Det. Animals performed the protocols, and then serum concentrations of asprosin, TNF-α, insulin, fasting blood glucose, and lipid profiles (TC, LDL, TG, and HDL) were assessed. Additionally, the liver expression of asprosin, AMPK, and P-AMPK was measured by western blotting. Both HIIT and MICT caused a significant decrease in weight, waist circumference, BMI (P = 0.001), and serum levels of glucose, insulin, asprosin (P = 0.001), triglyceride, total cholesterol, low-density lipoprotein (LDL), and TNF-α (P = 0.001), but an increase in the liver AMPK, P-AMPK, and P-AMPK/AMPK (P = 0.001), compared with OVX2 noexercised group. MICT was superior to HIIT in reducing serum asprosin, TNF-a, TG, LDL (P = 0.001), insulin, fasting blood glucose, HOMA-IR, and QUEKI index (P = 0.001), but an increase in the liver AMPK, and p-AMPK (P = 0.001). Although after two months of de-training almost all indices returned to the pre exercise values (P < 0.05). The findings suggest that MICT effectively alleviates MetS induced by menopause, at least partly through the activation of liver signaling of P-AMPK and the reduction of asprosin and TNF-α. These results have practical implications for the development of exercise interventions targeting MetS in menopausal individuals, emphasizing the potential benefits of MICT in mitigating MetS-related complications.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760452/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760452</a> | DOI:<a href=https://doi.org/10.1038/s41598-024-61842-5>10.1038/s41598-024-61842-5</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760452</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Hiwa Ahmed Rahim</dc:creator>
<dc:creator>Arsalan Damirchi</dc:creator>
<dc:creator>Parvin Babaei</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Scientific reports</dc:source>
<dc:title>Comparison of HIIT and MICT and further detraining on metabolic syndrome and asprosin signaling pathway in metabolic syndrome model of rats</dc:title>
<dc:identifier>pmid:38760452</dc:identifier>
<dc:identifier>doi:10.1038/s41598-024-61842-5</dc:identifier>
</item>
<item>
<title>Synthesis and characterization of iron oxide nanoparticles from Lawsonia inermis and its effect on the biodegradation of crude oil hydrocarbon</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760417/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>Crude oil hydrocarbons are considered major environmental pollutants and pose a significant threat to the environment and humans due to having severe carcinogenic and mutagenic effects. Bioremediation is one of the practical and promising technology that can be applied to treat the hydrocarbon-polluted environment. In this present study, rhamnolipid biosurfactant (BS) produced by Pseudomonas aeruginosa PP4 and green synthesized iron nanoparticles (G-FeNPs) from Lawsonia inermis was used to...</description>
<content:encoded><![CDATA[<div>Sci Rep. 2024 May 17;14(1):11335. doi: 10.1038/s41598-024-61760-6.ABSTRACTCrude oil hydrocarbons are considered major environmental pollutants and pose a significant threat to the environment and humans due to having severe carcinogenic and mutagenic effects. Bioremediation is one of the practical and promising technology that can be applied to treat the hydrocarbon-polluted environment. In this present study, rhamnolipid biosurfactant (BS) produced by Pseudomonas aeruginosa PP4 and green synthesized iron nanoparticles (G-FeNPs) from Lawsonia inermis was used to evaluate the biodegradation efficiency (BE) of crude oil. The surface analysis of G-FeNPs was carried out by using FESEM and HRTEM to confirm the size and shape. Further, the average size of the G-FeNPs was observed around 10 nm by HRTEM analysis. The XRD and Raman spectra strongly confirm the presence of iron nanoparticles with their respective peaks. The BE (%) of mixed degradation system-V (PP4+BS+G-FeNPs) was obtained about 82%. FTIR spectrum confirms the presence of major functional constituents (C=O, -CH3, C-O, and OH) in the residual oil content. Overall, this study illustrates that integrated nano-based bioremediation could be an efficient approach for hydrocarbon-polluted environments. This study is the first attempt to evaluate the G-FeNPs with rhamnolipid biosurfactant on the biodegradation of crude oil.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760417/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760417</a> | DOI:<a href=https://doi.org/10.1038/s41598-024-61760-6>10.1038/s41598-024-61760-6</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760417</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Balakrishnan Muthukumar</dc:creator>
<dc:creator>Ramanathan Duraimurugan</dc:creator>
<dc:creator>Punniyakotti Parthipan</dc:creator>
<dc:creator>Rajaram Rajamohan</dc:creator>
<dc:creator>Rajakrishnan Rajagopal</dc:creator>
<dc:creator>Jayaraman Narenkumar</dc:creator>
<dc:creator>Aruliah Rajasekar</dc:creator>
<dc:creator>Tabarak Malik</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Scientific reports</dc:source>
<dc:title>Synthesis and characterization of iron oxide nanoparticles from Lawsonia inermis and its effect on the biodegradation of crude oil hydrocarbon</dc:title>
<dc:identifier>pmid:38760417</dc:identifier>
<dc:identifier>doi:10.1038/s41598-024-61760-6</dc:identifier>
</item>
<item>
<title>Combination of UGT1A1 polymorphism and baseline plasma bilirubin levels in predicting the risk of antipsychotic-induced dyslipidemia in schizophrenia patients</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760414/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>The prolonged usage of atypical antipsychotic drugs (AAPD) among individuals with schizophrenia often leads to metabolic side effects such as dyslipidemia. These effects not only limit one's selection of AAPD but also significantly reduce compliance and quality of life of patients. Recent studies suggest that bilirubin plays a crucial role in maintaining lipid homeostasis and may be a potential pre-treatment biomarker for individuals with dyslipidemia. The present study included 644...</description>
<content:encoded><![CDATA[<div>Schizophrenia (Heidelb). 2024 May 17;10(1):52. doi: 10.1038/s41537-024-00473-1.ABSTRACTThe prolonged usage of atypical antipsychotic drugs (AAPD) among individuals with schizophrenia often leads to metabolic side effects such as dyslipidemia. These effects not only limit one's selection of AAPD but also significantly reduce compliance and quality of life of patients. Recent studies suggest that bilirubin plays a crucial role in maintaining lipid homeostasis and may be a potential pre-treatment biomarker for individuals with dyslipidemia. The present study included 644 schizophrenia patients from two centers. Demographic and clinical characteristics were collected at baseline and 4 weeks after admission to investigate the correlation between metabolites, episodes, usage of AAPDs, and occurrence of dyslipidemia. Besides, we explored the combined predictive value of genotypes and baseline bilirubin for dyslipidemia by employing multiple PCR targeted capture techniques to sequence two pathways: bilirubin metabolism-related genes and lipid metabolism-related genes. Our results indicated that there existed a negative correlation between the changes in bilirubin levels and triglyceride (TG) levels in patients with schizophrenia. Among three types of bilirubin, direct bilirubin in the baseline (DBIL-bl) proved to be the most effective in predicting dyslipidemia in the ROC analysis (AUC = 0.627, p < 0.001). Furthermore, the odds ratio from multinomial logistic regression analysis showed that UGT1A1*6 was a protective factor for dyslipidemia (ß = -12.868, p < 0.001). The combination of baseline DBIL and UGT1A1*6 significantly improved the performance in predicting dyslipidemia (AUC = 0.939, p < 0.001). Schizophrenia patients with UGT1A1*6 mutation and a certain level of baseline bilirubin may be more resistant to dyslipidemia and have more selections for AAPD than other patients.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760414/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760414</a> | DOI:<a href=https://doi.org/10.1038/s41537-024-00473-1>10.1038/s41537-024-00473-1</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760414</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Chenquan Lin</dc:creator>
<dc:creator>Shuangyang Zhang</dc:creator>
<dc:creator>Ping Yang</dc:creator>
<dc:creator>Bikui Zhang</dc:creator>
<dc:creator>Wenbin Guo</dc:creator>
<dc:creator>Renrong Wu</dc:creator>
<dc:creator>Yong Liu</dc:creator>
<dc:creator>Jianjian Wang</dc:creator>
<dc:creator>Haishan Wu</dc:creator>
<dc:creator>Hualin Cai</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Schizophrenia (Heidelberg, Germany)</dc:source>
<dc:title>Combination of UGT1A1 polymorphism and baseline plasma bilirubin levels in predicting the risk of antipsychotic-induced dyslipidemia in schizophrenia patients</dc:title>
<dc:identifier>pmid:38760414</dc:identifier>
<dc:identifier>doi:10.1038/s41537-024-00473-1</dc:identifier>
</item>
<item>
<title>Deficiency of ADAR2 ameliorates metabolic-associated fatty liver disease via AMPK signaling pathways in obese mice</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760406/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>Non-alcoholic fatty liver disease (NAFLD) is a chronic disease caused by hepatic steatosis. Adenosine deaminases acting on RNA (ADARs) catalyze adenosine to inosine RNA editing. However, the functional role of ADAR2 in NAFLD is unclear. ADAR2^(+/+)/GluR-B^(R/R) mice (wild type, WT) and ADAR2^(-/-)/GluR-B^(R/R) mice (ADAR2 KO) mice are fed with standard chow or high-fat diet (HFD) for 12 weeks. ADAR2 KO mice exhibit protection against HFD-induced glucose intolerance, insulin resistance, and...</description>
<content:encoded><![CDATA[<div>Commun Biol. 2024 May 17;7(1):594. doi: 10.1038/s42003-024-06215-4.ABSTRACTNon-alcoholic fatty liver disease (NAFLD) is a chronic disease caused by hepatic steatosis. Adenosine deaminases acting on RNA (ADARs) catalyze adenosine to inosine RNA editing. However, the functional role of ADAR2 in NAFLD is unclear. ADAR2+/+/GluR-BR/R mice (wild type, WT) and ADAR2-/-/GluR-BR/R mice (ADAR2 KO) mice are fed with standard chow or high-fat diet (HFD) for 12 weeks. ADAR2 KO mice exhibit protection against HFD-induced glucose intolerance, insulin resistance, and dyslipidemia. Moreover, ADAR2 KO mice display reduced liver lipid droplets in concert with decreased hepatic TG content, improved hepatic insulin signaling, better pyruvate tolerance, and increased glycogen synthesis. Mechanistically, ADAR2 KO effectively mitigates excessive lipid production via AMPK/Sirt1 pathway. ADAR2 KO inhibits hepatic gluconeogenesis via the AMPK/CREB pathway and promotes glycogen synthesis by activating the AMPK/GSK3β pathway. These results provide evidence that ADAR2 KO protects against NAFLD progression through the activation of AMPK signaling pathways.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760406/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760406</a> | DOI:<a href=https://doi.org/10.1038/s42003-024-06215-4>10.1038/s42003-024-06215-4</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760406</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Mei-Lang Kung</dc:creator>
<dc:creator>Siao Muk Cheng</dc:creator>
<dc:creator>Yun-Han Wang</dc:creator>
<dc:creator>Kai-Pi Cheng</dc:creator>
<dc:creator>Yu-Lin Li</dc:creator>
<dc:creator>Yi-Tsen Hsiao</dc:creator>
<dc:creator>Bertrand Chin-Ming Tan</dc:creator>
<dc:creator>Yun-Wen Chen</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Communications biology</dc:source>
<dc:title>Deficiency of ADAR2 ameliorates metabolic-associated fatty liver disease via AMPK signaling pathways in obese mice</dc:title>
<dc:identifier>pmid:38760406</dc:identifier>
<dc:identifier>doi:10.1038/s42003-024-06215-4</dc:identifier>
</item>
<item>
<title>Evaluation of CSF 8-iso-prostaglandin F2α and erythrocyte anisocytosis as prognostic biomarkers for delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760404/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>Delayed cerebral ischemia (DCI) is a serious, life-threatening, complication affecting patients who have survived the initial bleeding from a ruptured intracranial aneurysm. Due to the challenging diagnosis, potential DCI prognostic markers should be of value in clinical practice. According to recent reports isoprostanes and red blood cell distribution (RDW) showed to be promising in this respect. We conducted a prospective study of 27 aSAH patients and control group (n = 8). All patients from...</description>
<content:encoded><![CDATA[<div>Sci Rep. 2024 May 17;14(1):11302. doi: 10.1038/s41598-024-61956-w.ABSTRACTDelayed cerebral ischemia (DCI) is a serious, life-threatening, complication affecting patients who have survived the initial bleeding from a ruptured intracranial aneurysm. Due to the challenging diagnosis, potential DCI prognostic markers should be of value in clinical practice. According to recent reports isoprostanes and red blood cell distribution (RDW) showed to be promising in this respect. We conducted a prospective study of 27 aSAH patients and control group (n = 8). All patients from the study group were treated within the first day of the initial bleeding. We collected data regarding clinical status and results of biochemical, and radiological examinations. We measured cerebrospinal fluid (CSF) concentration of 8-iso-prostaglandin F2α (F2-IsoP) and RDW on days 1, 3, and 5. Both CSF F2-IsoP level and RDW-SD measured on day 1 were significant predictors of DCI. The receiver operating characteristics curve for DCI prediction based on the multivariate model yielded an area under the curve of 0.924 (95% CI 0.824-1.000, p < 0.001). In our study, the model based on the combination of RDW and the level of isoprostanes in CSF on the first day after the initial bleeding showed a prognostic value for DCI prediction. Further studies are required to validate this observation.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760404/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760404</a> | DOI:<a href=https://doi.org/10.1038/s41598-024-61956-w>10.1038/s41598-024-61956-w</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760404</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Karol Wiśniewski</dc:creator>
<dc:creator>Karol Zaczkowski</dc:creator>
<dc:creator>Bartosz M Szmyd</dc:creator>
<dc:creator>Marta Popęda</dc:creator>
<dc:creator>Michał Bieńkowski</dc:creator>
<dc:creator>Bartłomiej Posmyk</dc:creator>
<dc:creator>Ernest J Bobeff</dc:creator>
<dc:creator>Dariusz J Jaskólski</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Scientific reports</dc:source>
<dc:title>Evaluation of CSF 8-iso-prostaglandin F2α and erythrocyte anisocytosis as prognostic biomarkers for delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage</dc:title>
<dc:identifier>pmid:38760404</dc:identifier>
<dc:identifier>doi:10.1038/s41598-024-61956-w</dc:identifier>
</item>
<item>
<title>High-throughput mechanical phenotyping and transcriptomics of single cells</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760380/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>The molecular system regulating cellular mechanical properties remains unexplored at single-cell resolution mainly due to a limited ability to combine mechanophenotyping with unbiased transcriptional screening. Here, we describe an electroporation-based lipid-bilayer assay for cell surface tension and transcriptomics (ELASTomics), a method in which oligonucleotide-labelled macromolecules are imported into cells via nanopore electroporation to assess the mechanical state of the cell surface and...</description>
<content:encoded><![CDATA[<div>Nat Commun. 2024 May 17;15(1):3812. doi: 10.1038/s41467-024-48088-5.ABSTRACTThe molecular system regulating cellular mechanical properties remains unexplored at single-cell resolution mainly due to a limited ability to combine mechanophenotyping with unbiased transcriptional screening. Here, we describe an electroporation-based lipid-bilayer assay for cell surface tension and transcriptomics (ELASTomics), a method in which oligonucleotide-labelled macromolecules are imported into cells via nanopore electroporation to assess the mechanical state of the cell surface and are enumerated by sequencing. ELASTomics can be readily integrated with existing single-cell sequencing approaches and enables the joint study of cell surface mechanics and underlying transcriptional regulation at an unprecedented resolution. We validate ELASTomics via analysis of cancer cell lines from various malignancies and show that the method can accurately identify cell types and assess cell surface tension. ELASTomics enables exploration of the relationships between cell surface tension, surface proteins, and transcripts along cell lineages differentiating from the haematopoietic progenitor cells of mice. We study the surface mechanics of cellular senescence and demonstrate that RRAD regulates cell surface tension in senescent TIG-1 cells. ELASTomics provides a unique opportunity to profile the mechanical and molecular phenotypes of single cells and can dissect the interplay among these in a range of biological contexts.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760380/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760380</a> | DOI:<a href=https://doi.org/10.1038/s41467-024-48088-5>10.1038/s41467-024-48088-5</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760380</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Akifumi Shiomi</dc:creator>
<dc:creator>Taikopaul Kaneko</dc:creator>
<dc:creator>Kaori Nishikawa</dc:creator>
<dc:creator>Arata Tsuchida</dc:creator>
<dc:creator>Takashi Isoshima</dc:creator>
<dc:creator>Mayuko Sato</dc:creator>
<dc:creator>Kiminori Toyooka</dc:creator>
<dc:creator>Kentaro Doi</dc:creator>
<dc:creator>Hidekazu Nishikii</dc:creator>
<dc:creator>Hirofumi Shintaku</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Nature communications</dc:source>
<dc:title>High-throughput mechanical phenotyping and transcriptomics of single cells</dc:title>
<dc:identifier>pmid:38760380</dc:identifier>
<dc:identifier>doi:10.1038/s41467-024-48088-5</dc:identifier>
</item>
<item>
<title>Liver ACOX1 regulates levels of circulating lipids that promote metabolic health through adipose remodeling</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760332/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>The liver gene expression of the peroxisomal β-oxidation enzyme acyl-coenzyme A oxidase 1 (ACOX1), which catabolizes very long chain fatty acids (VLCFA), increases in the context of obesity, but how this pathway impacts systemic energy metabolism remains unknown. Here, we show that hepatic ACOX1-mediated β-oxidation regulates inter-organ communication involved in metabolic homeostasis. Liver-specific knockout of Acox1 (Acox1-LKO) protects mice from diet-induced obesity, adipose tissue...</description>
<content:encoded><![CDATA[<div>Nat Commun. 2024 May 17;15(1):4214. doi: 10.1038/s41467-024-48471-2.ABSTRACTThe liver gene expression of the peroxisomal β-oxidation enzyme acyl-coenzyme A oxidase 1 (ACOX1), which catabolizes very long chain fatty acids (VLCFA), increases in the context of obesity, but how this pathway impacts systemic energy metabolism remains unknown. Here, we show that hepatic ACOX1-mediated β-oxidation regulates inter-organ communication involved in metabolic homeostasis. Liver-specific knockout of Acox1 (Acox1-LKO) protects mice from diet-induced obesity, adipose tissue inflammation, and systemic insulin resistance. Serum from Acox1-LKO mice promotes browning in cultured white adipocytes. Global serum lipidomics show increased circulating levels of several species of ω-3 VLCFAs (C24-C28) with previously uncharacterized physiological role that promote browning, mitochondrial biogenesis and Glut4 translocation through activation of the lipid sensor GPR120 in adipocytes. This work identifies hepatic peroxisomal β-oxidation as an important regulator of metabolic homeostasis and suggests that manipulation of ACOX1 or its substrates may treat obesity-associated metabolic disorders.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760332/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760332</a> | DOI:<a href=https://doi.org/10.1038/s41467-024-48471-2>10.1038/s41467-024-48471-2</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760332</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Dongliang Lu</dc:creator>
<dc:creator>Anyuan He</dc:creator>
<dc:creator>Min Tan</dc:creator>
<dc:creator>Marguerite Mrad</dc:creator>
<dc:creator>Amal El Daibani</dc:creator>
<dc:creator>Donghua Hu</dc:creator>
<dc:creator>Xuejing Liu</dc:creator>
<dc:creator>Brian Kleiboeker</dc:creator>
<dc:creator>Tao Che</dc:creator>
<dc:creator>Fong-Fu Hsu</dc:creator>
<dc:creator>Monika Bambouskova</dc:creator>
<dc:creator>Clay F Semenkovich</dc:creator>
<dc:creator>Irfan J Lodhi</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Nature communications</dc:source>
<dc:title>Liver ACOX1 regulates levels of circulating lipids that promote metabolic health through adipose remodeling</dc:title>
<dc:identifier>pmid:38760332</dc:identifier>
<dc:identifier>doi:10.1038/s41467-024-48471-2</dc:identifier>
</item>
<item>
<title>Effect of Ambient Conditions on Acoustic Activation of the Perfluoropropane Droplets Within the Infarct Zone</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760280/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>CONCLUSIONS: Selective IZ enhancement with AA of intravenous PDs is possible, but temperature sensitive. Thermal activation appears to occur when PDs are given at higher temperatures, preventing AA, and increasing unwanted bioeffects.</description>
<content:encoded><![CDATA[<div>Ultrasound Med Biol. 2024 May 16:S0301-5629(24)00188-1. doi: 10.1016/j.ultrasmedbio.2024.04.011. Online ahead of print.ABSTRACTBACKGROUND: Acoustically activated perfluoropropane droplets (PD) formulated from lipid encapsulated microbubble preparations produce a delayed myocardial contrast enhancement that preferentially highlights the infarct zones (IZ). Since activation of PDs may be temperature sensitive, it is unclear what effect body temperature (BT) has on acoustic activation (AA).OBJECTIVE: We sought to determine whether the microvascular retention and degree of myocardial contrast intensity (MCI) would be affected by BT at the time of intravenous injection.METHODS: We administered intravenous (IV) PD in nine rats following 60 min of ischemia followed by reperfusion. Injections in these rats were given at temperatures above and below 36.5°C, with high MI activation in both groups at 3 or 6 min following IV injection (IVI). In six additional rats (three in each group), IV PDs were given only at one temperature (<36.5°C or ≥36.5°C), permitting a total of 12 comparisons of different BT. Differences in background subtracted MCI at 3-6 min post-injection were compared in the infarct zone (IZ) and remote zone (RZ). Post-mortem lung hematoxylin and eosin (H&E) staining was performed to assess the effect potential thermal activation on lung tissue.RESULTS: Selective MCI within the IZ was observed in 8 of 12 rats who received IVI of PDs at <36.5°C, but none of the 12 rats who had IVI at the higher temperature (p < 0.0001). Absolute MCI following droplet activation was significantly higher in both the IZ and RZ when given at the lower BT. H&E indicated significant red blood extravasation in 5/7 rats who had had IV injections at higher BT, and 0/7 rats who had IV PDs at <36.5°C.CONCLUSIONS: Selective IZ enhancement with AA of intravenous PDs is possible, but temperature sensitive. Thermal activation appears to occur when PDs are given at higher temperatures, preventing AA, and increasing unwanted bioeffects.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760280/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760280</a> | DOI:<a href=https://doi.org/10.1016/j.ultrasmedbio.2024.04.011>10.1016/j.ultrasmedbio.2024.04.011</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760280</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Shouqiang Li</dc:creator>
<dc:creator>Cheng Chen</dc:creator>
<dc:creator>John Lof</dc:creator>
<dc:creator>Elizabeth A Stolze</dc:creator>
<dc:creator>Jiri Sklenar</dc:creator>
<dc:creator>Xucai Chen</dc:creator>
<dc:creator>John J Pacella</dc:creator>
<dc:creator>Flordeliza S Villanueva</dc:creator>
<dc:creator>Terry O Matsunaga</dc:creator>
<dc:creator>E Carr Everbach</dc:creator>
<dc:creator>Stanley J Radio</dc:creator>
<dc:creator>Sherry Westphal</dc:creator>
<dc:creator>Feng Xie</dc:creator>
<dc:creator>Xiaoping Leng</dc:creator>
<dc:creator>Thomas R Porter</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Ultrasound in medicine & biology</dc:source>
<dc:title>Effect of Ambient Conditions on Acoustic Activation of the Perfluoropropane Droplets Within the Infarct Zone</dc:title>
<dc:identifier>pmid:38760280</dc:identifier>
<dc:identifier>doi:10.1016/j.ultrasmedbio.2024.04.011</dc:identifier>
</item>
<item>
<title>Menopause and metabolic dysfunction-associated steatotic liver disease</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760254/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>Nonalcoholic fatty liver disease, recently proposed to be renamed metabolic dysfunction-associated steatotic liver disease, is a highly prevalent disease (25-30 % of the global general population) whose prevalence increases after menopause. Apart from the rates of simple steatosis, the severity of the disease (e.g., hepatic fibrosis) increases after menopause. Menopause is associated with higher abdominal adiposity and dysmetabolism of carbohydrate and lipid metabolism, which may contribute to...</description>
<content:encoded><![CDATA[<div>Maturitas. 2024 May 14:108024. doi: 10.1016/j.maturitas.2024.108024. Online ahead of print.ABSTRACTNonalcoholic fatty liver disease, recently proposed to be renamed metabolic dysfunction-associated steatotic liver disease, is a highly prevalent disease (25-30 % of the global general population) whose prevalence increases after menopause. Apart from the rates of simple steatosis, the severity of the disease (e.g., hepatic fibrosis) increases after menopause. Menopause is associated with higher abdominal adiposity and dysmetabolism of carbohydrate and lipid metabolism, which may contribute to the development and severity of metabolic dysfunction-associated steatotic liver disease and the higher cardiovascular risk observed after menopause. The association between menopause and metabolic dysfunction-associated steatotic liver disease renders menopausal hormone therapy an appealing way to reverse hepatic disease in parallel with the benefits of menopausal hormone therapy in other tissues. In this regard, most animal studies have shown a beneficial effect of estrogens on metabolic dysfunction-associated steatotic liver disease. Still, clinical studies are few, and their data are conflicting. The effect of menopausal hormone therapy on metabolic dysfunction-associated steatotic liver disease may be distinct among estrogen monotherapies and the combinations of estrogens and progestogens. It may also depend on the type of progestogen and the route of administration. However, more studies specifically designed for these aims are needed to draw secure conclusions. This review summarizes the data related to the association between menopause and metabolic dysfunction-associated steatotic liver disease, as well as between menopausal hormone therapy and metabolic dysfunction-associated steatotic liver disease, with a special focus on clinical studies.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760254/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760254</a> | DOI:<a href=https://doi.org/10.1016/j.maturitas.2024.108024>10.1016/j.maturitas.2024.108024</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760254</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Stergios A Polyzos</dc:creator>
<dc:creator>Dimitrios G Goulis</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Maturitas</dc:source>
<dc:title>Menopause and metabolic dysfunction-associated steatotic liver disease</dc:title>
<dc:identifier>pmid:38760254</dc:identifier>
<dc:identifier>doi:10.1016/j.maturitas.2024.108024</dc:identifier>
</item>
<item>
<title>Exploring the relationship between starch structure and physicochemical properties: The impact of extrusion on highland barley flour</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760145/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>Highland barley (HB) is an intriguing plateau cereal crop with high nutrition and health benefits. However, abundant dietary fiber and deficient gluten pose challenges to the processing and taste of whole HB products. Extrusion technology has been proved to be effective in overcoming these hurdles, but the association between the structure and physicochemical properties during extrusion remains inadequately unexplored. Therefore, this study aims to comprehensively understand the impact of...</description>
<content:encoded><![CDATA[<div>Food Res Int. 2024 May;183:114226. doi: 10.1016/j.foodres.2024.114226. Epub 2024 Mar 13.ABSTRACTHighland barley (HB) is an intriguing plateau cereal crop with high nutrition and health benefits. However, abundant dietary fiber and deficient gluten pose challenges to the processing and taste of whole HB products. Extrusion technology has been proved to be effective in overcoming these hurdles, but the association between the structure and physicochemical properties during extrusion remains inadequately unexplored. Therefore, this study aims to comprehensively understand the impact of extrusion conditions on the physicochemical properties of HB flour (HBF) and the multi-scale structure of starch. Results indicated that the nutritional value of HBF were significantly increased (soluble dietary fiber and β-glucan increased by 24.05%, 19.85% respectively) after extrusion. Typical underlying mechanisms based on starch structure were established. High temperature facilitated starch gelatinization, resulting in double helices unwinding, amylose leaching, and starch-lipid complexes forming. These alterations enhanced the water absorption capacity, cold thickening ability, and peak viscosity of HBF. More V-type complexes impeded amylose rearrangement, thus enhancing resistance to retrogradation and thermal stability. Extrusion at high temperature and moisture exhibited similarities to hydrothermal treatment, partly promoting amylose rearrangement and enhancing HBF peak viscosity. Conversely, under low temperature and high moisture, well-swelled starch granules were easily broken into shorter branch-chains by higher shear force, which enhanced the instant solubility and retrogradation resistance of HBF as well as reduced its pasting viscosity and the capacity to form gel networks. Importantly, starch degradation products during this condition were experimentally confirmed from various aspects. This study provided some reference for profiting from extrusion for further development of HB functional food and "clean label" food additives.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760145/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760145</a> | DOI:<a href=https://doi.org/10.1016/j.foodres.2024.114226>10.1016/j.foodres.2024.114226</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760145</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Fei Ge</dc:creator>
<dc:creator>Yue Sun</dc:creator>
<dc:creator>Chenxi Yang</dc:creator>
<dc:creator>Weiwei Cheng</dc:creator>
<dc:creator>Zhenjiong Wang</dc:creator>
<dc:creator>Xifeng Xia</dc:creator>
<dc:creator>Di Wu</dc:creator>
<dc:creator>Xiaozhi Tang</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Food research international (Ottawa, Ont.)</dc:source>
<dc:title>Exploring the relationship between starch structure and physicochemical properties: The impact of extrusion on highland barley flour</dc:title>
<dc:identifier>pmid:38760145</dc:identifier>
<dc:identifier>doi:10.1016/j.foodres.2024.114226</dc:identifier>
</item>
<item>
<title>Electrostatic spray drying: A new alternative for drying of complex coacervates</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760128/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>Complex coacervation can be used for controlled delivery of bioactive compounds (i.e., flaxseed oil and quercetin). This study investigated the co-encapsulation of flaxseed oil and quercetin by complex coacervation using soluble pea protein (SPP) and gum arabic (GA) as shell materials, followed by innovative electrostatic spray drying (ES). The dried system was analyzed through encapsulation efficiency (EE) and yield (EY), morphological and physicochemical properties, and stability for 60 days....</description>
<content:encoded><![CDATA[<div>Food Res Int. 2024 May;183:114189. doi: 10.1016/j.foodres.2024.114189. Epub 2024 Mar 4.ABSTRACTComplex coacervation can be used for controlled delivery of bioactive compounds (i.e., flaxseed oil and quercetin). This study investigated the co-encapsulation of flaxseed oil and quercetin by complex coacervation using soluble pea protein (SPP) and gum arabic (GA) as shell materials, followed by innovative electrostatic spray drying (ES). The dried system was analyzed through encapsulation efficiency (EE) and yield (EY), morphological and physicochemical properties, and stability for 60 days. Small droplet size emulsions were produced by GA (in the first step of complex coacervation) due to its greater emulsifying activity than SPP. Oil EY and EE, moisture, and water activity in dried compositions ranged from 75.7 to 75.6, 76.0-73.4 %, 3.4-4.1 %, and 0.1-0.2, respectively. Spherical microcapsules were created with small and aggregated particle size but stable for 60 days. An amount of 8 % of quercetin remained in the dried coacervates after 60 days, with low hydroperoxide production. In summary, when GA is used as the emulsifier and SPP as the second biopolymer in the coacervation process, suitable coacervates for food applications are obtained, with ES being a novel alternative to obtain coacervates in powder, with improved stability for encapsulated compounds. As a result, this study helps provide a new delivery system option and sheds light on how the characteristics of biopolymers and the drying process affect coacervate formation.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760128/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760128</a> | DOI:<a href=https://doi.org/10.1016/j.foodres.2024.114189>10.1016/j.foodres.2024.114189</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760128</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Talita A Comunian</dc:creator>
<dc:creator>Laura G Gómez-Mascaraque</dc:creator>
<dc:creator>Audrey Maudhuit</dc:creator>
<dc:creator>Guillaume Roelens</dc:creator>
<dc:creator>Denis Poncelet</dc:creator>
<dc:creator>Stephan Drusch</dc:creator>
<dc:creator>André Brodkorb</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Food research international (Ottawa, Ont.)</dc:source>
<dc:title>Electrostatic spray drying: A new alternative for drying of complex coacervates</dc:title>
<dc:identifier>pmid:38760128</dc:identifier>
<dc:identifier>doi:10.1016/j.foodres.2024.114189</dc:identifier>
</item>
<item>
<title>Metabolomics analysis of physicochemical properties associated with freshness degradation in frozen Antarctic krill (Euphausia superba)</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760127/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>This study aimed to determine the effect of different frozen temperatures during storage on the quality of Antarctic krill (Euphausia superba) and assess the change at the metabolite level via a combination of physicochemical property analysis, liquid chromatography-tandem mass spectrometry (LC-MS) based non-targeted metabolomics profiling. Regarding samples stored at -20 °C, the expressions of 7055 metabolites were elevated, while 2313 were downregulated. Lipids and lipid molecules had the...</description>
<content:encoded><![CDATA[<div>Food Res Int. 2024 May;183:114190. doi: 10.1016/j.foodres.2024.114190. Epub 2024 Mar 3.ABSTRACTThis study aimed to determine the effect of different frozen temperatures during storage on the quality of Antarctic krill (Euphausia superba) and assess the change at the metabolite level via a combination of physicochemical property analysis, liquid chromatography-tandem mass spectrometry (LC-MS) based non-targeted metabolomics profiling. Regarding samples stored at -20 °C, the expressions of 7055 metabolites were elevated, while 2313 were downregulated. Lipids and lipid molecules had the highest proportion of differential metabolites. A total of 432 discriminatory metabolites with Kyoto Encyclopedia of Genes and Genomes (KEGG) IDs was obtained. We also observed that the concentrations of differential bitter free amino acids (FAAs) and oxidation products of arachidonic and linoleic acid increased. Moreover, as the storage temperature increased, the freshness, umami, and sweetness components were considerably reduced. Furthermore, results indicated that the color, pH and water-holding capacity (WHC) were potential indicators of quality deterioration, while inosinic acid was a probable biomarker for umami degradation of frozen Antarctic krill. In conclusion, this study demonstrates that storage at lower temperatures can be beneficial for maintaining the freshness of Antarctic krill from macro and micro perspectives.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760127/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760127</a> | DOI:<a href=https://doi.org/10.1016/j.foodres.2024.114190>10.1016/j.foodres.2024.114190</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760127</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Ling Ni</dc:creator>
<dc:creator>Chaojun Jiang</dc:creator>
<dc:creator>Quanyou Guo</dc:creator>
<dc:creator>Hai Chi</dc:creator>
<dc:creator>Chengqi Fan</dc:creator>
<dc:creator>Jiangao Shi</dc:creator>
<dc:creator>Na Lin</dc:creator>
<dc:creator>Zhidong Liu</dc:creator>
<dc:creator>Shengjun Chen</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Food research international (Ottawa, Ont.)</dc:source>
<dc:title>Metabolomics analysis of physicochemical properties associated with freshness degradation in frozen Antarctic krill (Euphausia superba)</dc:title>
<dc:identifier>pmid:38760127</dc:identifier>
<dc:identifier>doi:10.1016/j.foodres.2024.114190</dc:identifier>
</item>
<item>
<title>The prescription of valproate: risk of harm</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760090/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>No abstract</description>
<content:encoded><![CDATA[<div>Lancet Neurol. 2024 Jun;23(6):557-558. doi: 10.1016/S1474-4422(24)00141-8.NO ABSTRACTPMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760090/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760090</a> | DOI:<a href=https://doi.org/10.1016/S1474-4422(24)00141-8>10.1016/S1474-4422(24)00141-8</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760090</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Fergus Rugg-Gunn</dc:creator>
<dc:creator>David Hunt</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>The Lancet. Neurology</dc:source>
<dc:title>The prescription of valproate: risk of harm</dc:title>
<dc:identifier>pmid:38760090</dc:identifier>
<dc:identifier>doi:10.1016/S1474-4422(24)00141-8</dc:identifier>
</item>
<item>
<title>The prescription of valproate: risk of harm</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760089/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>No abstract</description>
<content:encoded><![CDATA[<div>Lancet Neurol. 2024 Jun;23(6):557. doi: 10.1016/S1474-4422(24)00142-X.NO ABSTRACTPMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760089/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760089</a> | DOI:<a href=https://doi.org/10.1016/S1474-4422(24)00142-X>10.1016/S1474-4422(24)00142-X</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760089</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Alison Cave</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>The Lancet. Neurology</dc:source>
<dc:title>The prescription of valproate: risk of harm</dc:title>
<dc:identifier>pmid:38760089</dc:identifier>
<dc:identifier>doi:10.1016/S1474-4422(24)00142-X</dc:identifier>
</item>
<item>
<title>Two peptides LLRLTDL and GYALPCDCL inhibit foam cell formation through activating PPAR-γ/LXR-α signaling pathway in oxLDL-treated RAW264.7 macrophages</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760074/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>Foam cell formation plays a pivotal role in atherosclerosis-associated cardiovascular diseases. Bioactive peptides generated from marine sources have been found to provide multifunctional health advantages. In the present study, we investigated the anti-atherosclerotic effects of LLRLTDL (Bu1) and GYALPCDCL (Bu2) peptides, isolated from ark shell protein hydrolysates by assessing their inhibitory effect on oxidized LDL (oxLDL)-induced foam cell formation. The two peptides showed a promising...</description>
<content:encoded><![CDATA[<div>Biofactors. 2024 May 17. doi: 10.1002/biof.2075. Online ahead of print.ABSTRACTFoam cell formation plays a pivotal role in atherosclerosis-associated cardiovascular diseases. Bioactive peptides generated from marine sources have been found to provide multifunctional health advantages. In the present study, we investigated the anti-atherosclerotic effects of LLRLTDL (Bu1) and GYALPCDCL (Bu2) peptides, isolated from ark shell protein hydrolysates by assessing their inhibitory effect on oxidized LDL (oxLDL)-induced foam cell formation. The two peptides showed a promising anti-atherosclerotic effect by inhibiting foam cell formation, which was evidenced by inhibiting lipid accumulation in oxLDL-treated RAW264.7 macrophages and oxLDL-treated primary human aortic smooth muscle cells (HASMC). Two peptides effectively reduced total cholesterol, free cholesterol, cholesterol ester, and triglyceride levels by upregulating cholesterol efflux and downregulating cholesterol influx. Expression of cholesterol influx-related proteins such as SR-A1 and CD36 were reduced, whereas cholesterol efflux-related proteins such as ATP-binding cassette transporter ABCA-1 and ABCG-1 were highly expressed. In addition, Bu1 and Bu2 peptides increased PPAR-γ and LXR-α expression. However, PPAR-γ siRNA transfection reversed the foam cell formation inhibitory activity of Bu1 and Bu2 peptides. Furthermore, the synergistic effect of Bu1 and Bu2 peptides on foam cell formation inhibition was observed with PPAR-γ agonist thiazolidinediones, indicating that PPAR-γ signaling pathway plays a key role in foam cell formation of macrophages. Beyond their impact on foam cell formation, Bu1 and Bu2 peptides demonstrated anti-inflammatory potential by inhibiting the generation of pro-inflammatory cytokines and nitric oxide and NF-κB nuclear activation. Taken together, these results suggest that Bu1 and Bu2 peptides may be useful for atherosclerosis and associated anti-inflammatory therapies.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760074/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760074</a> | DOI:<a href=https://doi.org/10.1002/biof.2075>10.1002/biof.2075</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760074</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Chathuri Kaushalya Marasinghe</dc:creator>
<dc:creator>Soon-Do Yoon</dc:creator>
<dc:creator>Jae-Young Je</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>BioFactors (Oxford, England)</dc:source>
<dc:title>Two peptides LLRLTDL and GYALPCDCL inhibit foam cell formation through activating PPAR-γ/LXR-α signaling pathway in oxLDL-treated RAW264.7 macrophages</dc:title>
<dc:identifier>pmid:38760074</dc:identifier>
<dc:identifier>doi:10.1002/biof.2075</dc:identifier>
</item>
<item>
<title>Fluorescent Probe as Dual-Organelle Localizer Through Differential Proton Gradients Between Lipid Droplets and Mitochondria</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38760019/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>Dual-organelle molecular localizers represent powerful new tools allowing the exploration of interorganelle physical contacts and subcellular chemical communication. Here, we describe new dynamic molecular probes to localize mitochondria and lipid droplets taking advantage of the differential proton gradients present in these organelles as well as the activity of mitochondrial esterase. We unveil their potential utility when organelle retention mechanisms and proton gradients are synchronized,...</description>
<content:encoded><![CDATA[<div>Anal Chem. 2024 May 17. doi: 10.1021/acs.analchem.4c01703. Online ahead of print.ABSTRACTDual-organelle molecular localizers represent powerful new tools allowing the exploration of interorganelle physical contacts and subcellular chemical communication. Here, we describe new dynamic molecular probes to localize mitochondria and lipid droplets taking advantage of the differential proton gradients present in these organelles as well as the activity of mitochondrial esterase. We unveil their potential utility when organelle retention mechanisms and proton gradients are synchronized, an insight that has not been documented previously. Our discoveries indicate that dual-organelle probes serve as a valuable multiplexing assay during starvation-induced autophagy. The pioneering molecular mechanism they employ opens doors to avoid using labile esters such as acetoxymethyl derivatives which are not optimal in imaging microscopy assays.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38760019/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38760019</a> | DOI:<a href=https://doi.org/10.1021/acs.analchem.4c01703>10.1021/acs.analchem.4c01703</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38760019</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Cinthia Hernández-Juárez</dc:creator>
<dc:creator>Martha Calahorra</dc:creator>
<dc:creator>Antonio Peña</dc:creator>
<dc:creator>Arturo Jiménez-Sánchez</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Analytical chemistry</dc:source>
<dc:title>Fluorescent Probe as Dual-Organelle Localizer Through Differential Proton Gradients Between Lipid Droplets and Mitochondria</dc:title>
<dc:identifier>pmid:38760019</dc:identifier>
<dc:identifier>doi:10.1021/acs.analchem.4c01703</dc:identifier>
</item>
<item>
<title>HDL and plaque regression in a multiphase model of early atherosclerosis</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38759951/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>Atherosclerosis is a chronic disease of the arteries characterised by the accumulation of lipids and lipid-engorged cells in the artery wall. Early plaque growth is aggravated by the deposition of low density lipoproteins (LDL) in the wall and the subsequent immune response. High density lipoproteins (HDL) counterbalance the effects of LDL by accepting cholesterol from macrophages and removing it from the plaque. In this paper, we develop a free boundary multiphase model to investigate the...</description>
<content:encoded><![CDATA[<div>Math Biosci. 2024 May 15:109208. doi: 10.1016/j.mbs.2024.109208. Online ahead of print.ABSTRACTAtherosclerosis is a chronic disease of the arteries characterised by the accumulation of lipids and lipid-engorged cells in the artery wall. Early plaque growth is aggravated by the deposition of low density lipoproteins (LDL) in the wall and the subsequent immune response. High density lipoproteins (HDL) counterbalance the effects of LDL by accepting cholesterol from macrophages and removing it from the plaque. In this paper, we develop a free boundary multiphase model to investigate the effects of LDL and HDL on early plaque development. We examine how the rates of LDL and HDL deposition affect cholesterol accumulation in macrophages, and how this impacts cell death rates and emigration. We identify a region of LDL-HDL parameter space where plaque growth stabilises for low LDL and high HDL influxes, due to macrophage emigration and HDL clearance that counterbalances the influx of new cells and cholesterol. We explore how the efferocytic uptake of dead cells and the recruitment of new macrophages affect plaque development for a range of LDL and HDL influxes. Finally, we consider how changes in the LDL-HDL profile can change the course of plaque development. We show that changes towards lower LDL and higher HDL can slow plaque growth and even induce regression. We find that these changes have less effect on larger, more established plaques, and that temporary changes will only slow plaque growth in the short term.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38759951/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38759951</a> | DOI:<a href=https://doi.org/10.1016/j.mbs.2024.109208>10.1016/j.mbs.2024.109208</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38759951</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Ishraq U Ahmed</dc:creator>
<dc:creator>Mary R Myerscough</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Mathematical biosciences</dc:source>
<dc:title>HDL and plaque regression in a multiphase model of early atherosclerosis</dc:title>
<dc:identifier>pmid:38759951</dc:identifier>
<dc:identifier>doi:10.1016/j.mbs.2024.109208</dc:identifier>
</item>
<item>
<title>Elucidation of molecular mechanisms by which amyloid β1-42 fibrils exert cell toxicity</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38759921/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>Abrupt aggregation of amyloid β(1-42) (Aβ(1-42)) peptide in the frontal lobe is the expected underlying cause of Alzheimer's disease (AD). β-Sheet-rich oligomers and fibrils formed by Aβ(1-42) exert high cell toxicity. A growing body of evidence indicates that lipids can uniquely alter the secondary structure and toxicity of Aβ(1-42) aggregates. At the same time, underlying molecular mechanisms that determine this difference in toxicity of amyloid aggregates remain unclear. Using a set of...</description>
<content:encoded><![CDATA[<div>Biochim Biophys Acta Mol Cell Biol Lipids. 2024 May 15:159510. doi: 10.1016/j.bbalip.2024.159510. Online ahead of print.ABSTRACTAbrupt aggregation of amyloid β1-42 (Aβ1-42) peptide in the frontal lobe is the expected underlying cause of Alzheimer's disease (AD). β-Sheet-rich oligomers and fibrils formed by Aβ1-42 exert high cell toxicity. A growing body of evidence indicates that lipids can uniquely alter the secondary structure and toxicity of Aβ1-42 aggregates. At the same time, underlying molecular mechanisms that determine this difference in toxicity of amyloid aggregates remain unclear. Using a set of molecular and biophysical assays to determine the molecular mechanism by which Aβ1-42 aggregates formed in the presence of cholesterol, cardiolipin, and phosphatidylcholine exert cell toxicity. Our findings demonstrate that rat neuronal cells exposed to Aβ1-42 fibrils formed in the presence of lipids with different chemical structure exert drastically different magnitude and dynamic of unfolded protein response (UPR) in the endoplasmic reticulum (ER) and mitochondria (MT). We found that the opposite dynamics of UPR in MT and ER in the cells exposed to Aβ1-42: cardiolipin fibrils and Aβ1-42 aggregates formed in a lipid-free environment. We also found that Aβ1-42: phosphatidylcholine fibrils upregulated ER UPR simultaneously downregulating the UPR response of MT, whereas Aβ1-42: cholesterol fibrils suppressed the UPR response of ER and upregulated UPR response of MT. We also observed progressively increasing ROS production that damages mitochondrial membranes and other cell organelles, ultimately leading to cell death.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38759921/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38759921</a> | DOI:<a href=https://doi.org/10.1016/j.bbalip.2024.159510>10.1016/j.bbalip.2024.159510</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38759921</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Kiryl Zhaliazka</dc:creator>
<dc:creator>Dmitry Kurouski</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Biochimica et biophysica acta. Molecular and cell biology of lipids</dc:source>
<dc:title>Elucidation of molecular mechanisms by which amyloid β1-42 fibrils exert cell toxicity</dc:title>
<dc:identifier>pmid:38759921</dc:identifier>
<dc:identifier>doi:10.1016/j.bbalip.2024.159510</dc:identifier>
</item>
<item>
<title>Effects of low protein feed on hepato-intestinal health and muscle quality of grass carp (Ctenopharyngodon idellus)</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38759883/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>In this study, grass carp (33.28 ± 0.05 g) were fed three diets for 8 weeks: control (crude protein [CP] 30%, crude lipid [CL] 6%), low protein (LP; CP16%, CL6%), and low protein with high-fat (LPHF; CP16%, CL10%). The final body weight decreased in the LP and LPHF groups compared to the Control (P < 0.05). Liver triglycerides, total cholesterol, and nonesterified fatty acids were higher in the LP group than the Control, whereas these indexes in the LPHF group were higher than those in the LP...</description>
<content:encoded><![CDATA[<div>Comp Biochem Physiol B Biochem Mol Biol. 2024 May 15:110989. doi: 10.1016/j.cbpb.2024.110989. Online ahead of print.ABSTRACTIn this study, grass carp (33.28 ± 0.05 g) were fed three diets for 8 weeks: control (crude protein [CP] 30%, crude lipid [CL] 6%), low protein (LP; CP16%, CL6%), and low protein with high-fat (LPHF; CP16%, CL10%). The final body weight decreased in the LP and LPHF groups compared to the Control (P < 0.05). Liver triglycerides, total cholesterol, and nonesterified fatty acids were higher in the LP group than the Control, whereas these indexes in the LPHF group were higher than those in the LP group (P < 0.05). The LP group had intestinal barrier damage, while the LPHF group had a slight recovery. TNF-α, IL-8, and IL-1β content were lower in the LP group than in the Control (P < 0.05), and even higher in the LPHF group (P < 0.05). The expressions of endoplasmic reticulum stress-related genes Activating transcription factor 6 (ATF-6) and Glucose-regulated protein (GRP78) were higher in the LPHF group against the LP group (P < 0.05). The IL-1β and TNF-α content negatively correlated with intestinal Actinomycetes and Mycobacterium abundance (P < 0.05). The muscle fiber diameter was smaller in both the LP and LPHF groups than the control (P < 0.05), with the LP group showing metabolites related to protein digestion and absorption, and LPHF group exhibiting metabolites related to taste transmission. The results demonstrate reducing dietary protein affects growth, causing liver lipid accumulation, reduced enteritis response, and increased muscle tightness, while increasing fat content accelerates fat accumulation and inflammation.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38759883/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38759883</a> | DOI:<a href=https://doi.org/10.1016/j.cbpb.2024.110989>10.1016/j.cbpb.2024.110989</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38759883</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Mengmeng Ji</dc:creator>
<dc:creator>Binbin Wang</dc:creator>
<dc:creator>Jun Xie</dc:creator>
<dc:creator>Guangjun Wang</dc:creator>
<dc:creator>Ermeng Yu</dc:creator>
<dc:creator>Peng Jiang</dc:creator>
<dc:creator>Ronghua Lu</dc:creator>
<dc:creator>Jingjing Tian</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Comparative biochemistry and physiology. Part B, Biochemistry & molecular biology</dc:source>
<dc:title>Effects of low protein feed on hepato-intestinal health and muscle quality of grass carp (Ctenopharyngodon idellus)</dc:title>
<dc:identifier>pmid:38759883</dc:identifier>
<dc:identifier>doi:10.1016/j.cbpb.2024.110989</dc:identifier>
</item>
<item>
<title>All we need to know about lipoprotein(a)</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38759878/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>Lipoprotein(a) [Lp(a)], a genetically determined macromolecular complex, is independently and causally associated with atherosclerotic cardiovascular disease (ASCVD) and calcific aortic stenosis via proposed proinflammatory, prothrombotic, and proatherogenic mechanisms. While Lp(a) measurement standardization issues are being resolved, several guidelines now support testing Lp(a) at least once in each adult's lifetime for ASCVD risk prediction which can foster implementation of more aggressive...</description>
<content:encoded><![CDATA[<div>Prog Cardiovasc Dis. 2024 May 15:S0033-0620(24)00075-6. doi: 10.1016/j.pcad.2024.05.007. Online ahead of print.ABSTRACTLipoprotein(a) [Lp(a)], a genetically determined macromolecular complex, is independently and causally associated with atherosclerotic cardiovascular disease (ASCVD) and calcific aortic stenosis via proposed proinflammatory, prothrombotic, and proatherogenic mechanisms. While Lp(a) measurement standardization issues are being resolved, several guidelines now support testing Lp(a) at least once in each adult's lifetime for ASCVD risk prediction which can foster implementation of more aggressive primary prevention therapies. Currently, there are several emerging targeted Lp(a) lowering therapies in active clinical investigation for safety and cardiovascular benefit among both primary and secondary prevention populations. First degree relatives of patients with high Lp(a) should be encouraged to undergo cascade screening. Primary prevention patients with high Lp(a) should consider obtaining a coronary calcium score for further risk estimation and to guide further ASCVD risk factor management including consideration of low dose aspirin therapy. Secondary prevention patients with high Lp(a) levels should consider adding PCSK9 inhibition to statin therapy.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38759878/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38759878</a> | DOI:<a href=https://doi.org/10.1016/j.pcad.2024.05.007>10.1016/j.pcad.2024.05.007</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38759878</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Courtney Bess</dc:creator>
<dc:creator>Anurag Mehta</dc:creator>
<dc:creator>Parag Joshi</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Progress in cardiovascular diseases</dc:source>
<dc:title>All we need to know about lipoprotein(a)</dc:title>
<dc:identifier>pmid:38759878</dc:identifier>
<dc:identifier>doi:10.1016/j.pcad.2024.05.007</dc:identifier>
</item>
<item>
<title>Chlorpyrifos-induced suppression of the antioxidative defense system leads to cytotoxicity and genotoxicity in macrophages</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38759849/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>Chlorpyrifos, widely used for pest control, is known to have various harmful effects, although its toxic effects in macrophages and the mechanisms underlying its toxicity remain unclear. The present study investigated the toxic effects of chlorypyrifos in a macrophage cell line. Here, we found that chlorpyrifos induced cytotoxicity and genotoxicity in RAW264.7 macrophages. Moreover, chlorpyrifos induced intracellular ROS production, subsequently leading to lipid peroxidation. Chlorpyrifos...</description>
<content:encoded><![CDATA[<div>Environ Toxicol Pharmacol. 2024 May 15:104468. doi: 10.1016/j.etap.2024.104468. Online ahead of print.ABSTRACTChlorpyrifos, widely used for pest control, is known to have various harmful effects, although its toxic effects in macrophages and the mechanisms underlying its toxicity remain unclear. The present study investigated the toxic effects of chlorypyrifos in a macrophage cell line. Here, we found that chlorpyrifos induced cytotoxicity and genotoxicity in RAW264.7 macrophages. Moreover, chlorpyrifos induced intracellular ROS production, subsequently leading to lipid peroxidation. Chlorpyrifos reduced the activation of antioxidative enzymes including superoxide dismutase, catalase, and glutathione peroxidase. Chlorpyrifos upregulated HO-1 expression and activated the Keap1-Nrf2 pathway, as indicated by enhanced Nrf2 phosphorylation and Keap1 degradation. Chlorpyrifos exerted effects on the following in a dose-dependent manner: cytotoxicity, genotoxicity, lipid peroxidation, intracellular ROS production, antioxidative enzyme activity reduction, HO-1 expression, Nrf2 phosphorylation, and Keap1 degradation. Notably, N-acetyl-L-cysteine successfully inhibited chlorpyrifos-induced intracellular ROS generation, cytotoxicity, and genotoxicity. Thus, chlorpyrifos may induce cytotoxicity and genotoxicity by promoting intracellular ROS production and suppressing the antioxidative defense system activation in macrophages.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38759849/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38759849</a> | DOI:<a href=https://doi.org/10.1016/j.etap.2024.104468>10.1016/j.etap.2024.104468</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38759849</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Yin-Che Lu</dc:creator>
<dc:creator>Chen-Yu Chiang</dc:creator>
<dc:creator>Shih-Pin Chen</dc:creator>
<dc:creator>Yu-Wei Hsu</dc:creator>
<dc:creator>Wen-Ying Chen</dc:creator>
<dc:creator>Chun-Jung Chen</dc:creator>
<dc:creator>Yu-Hsiang Kuan</dc:creator>
<dc:creator>Sheng-Wen Wu</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Environmental toxicology and pharmacology</dc:source>
<dc:title>Chlorpyrifos-induced suppression of the antioxidative defense system leads to cytotoxicity and genotoxicity in macrophages</dc:title>
<dc:identifier>pmid:38759849</dc:identifier>
<dc:identifier>doi:10.1016/j.etap.2024.104468</dc:identifier>
</item>
<item>
<title>Associations of Abnormal Maternal Glucose Regulation in Pregnancy with Offspring Adiposity, Insulin Resistance, and Adipokine Markers during Childhood and Adolescence</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38759779/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>CONCLUSION: Exposure to GDM is associated with higher adiposity, insulin resistance, and altered adipokines in mid-adolescence. Our findings suggest that the peri-pubertal period could be a key time for the emergence of prenatally programmed metabolic abnormalities.</description>
<content:encoded><![CDATA[<div>J Pediatr. 2024 May 15:114100. doi: 10.1016/j.jpeds.2024.114100. Online ahead of print.ABSTRACTOBJECTIVE: To examine the associations of abnormal maternal glucose regulation in pregnancy with offspring adiposity, insulin resistance, adipokine, and inflammatory markers during childhood and adolescence.STUDY DESIGN: Project Viva is a prospective pre-birth cohort (n = 2,128 live births) initiated from 1999 through 2002 in Eastern Massachusetts, US. During the second trimester of pregnancy, clinicians used two-step oral glucose challenge testing to screen for gestational diabetes mellitus (GDM). In the offspring, we measured anthropometry, insulin resistance, adipokines, lipids, and inflammatory markers in mid-childhood (n=1107), early adolescence (n=1027), and mid-adolescence (n=693). We used multivariable linear regression models and generalized estimating equations adjusted for child age and sex, and for maternal age, race/ethnicity, education, parity, and smoking during pregnancy; we further adjusted for pre-pregnancy body mass index (BMI).RESULTS: At mid-adolescence (17.1 [0.8] years old), offspring of mothers with GDM (n=27) had a higher BMI z-score (β; 95%Cl; 0.41 SD; 0.00, 0.82), sum of skinfolds (8.15 mm; 2.48, 13.82), homeostatic model assessment for insulin resistance (HOMA-IR, 0.81 units; 0.13, 1.50), leptin z-score (0.40 SD; 0.01, 0.78), and leptin/adiponectin ratio z-score (0.51 SD; CI 0.09, 0.93) compared with offspring of mothers with normoglycemia (multivariable-adjusted models). The associations with BMI, (HOMA-IR), and adiponectin seemed stronger in mid-adolescence compared with earlier time points. The associations were attenuated towards the null after adjustment for maternal pre-pregnancy BMI.CONCLUSION: Exposure to GDM is associated with higher adiposity, insulin resistance, and altered adipokines in mid-adolescence. Our findings suggest that the peri-pubertal period could be a key time for the emergence of prenatally programmed metabolic abnormalities.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38759779/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38759779</a> | DOI:<a href=https://doi.org/10.1016/j.jpeds.2024.114100>10.1016/j.jpeds.2024.114100</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38759779</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Sarah Cho</dc:creator>
<dc:creator>Sheryl L Rifas-Shiman</dc:creator>
<dc:creator>Soren Harnois-Leblanc</dc:creator>
<dc:creator>Izzuddin M Aris</dc:creator>
<dc:creator>Emily Oken</dc:creator>
<dc:creator>Marie-France Hivert</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>The Journal of pediatrics</dc:source>
<dc:title>Associations of Abnormal Maternal Glucose Regulation in Pregnancy with Offspring Adiposity, Insulin Resistance, and Adipokine Markers during Childhood and Adolescence</dc:title>
<dc:identifier>pmid:38759779</dc:identifier>
<dc:identifier>doi:10.1016/j.jpeds.2024.114100</dc:identifier>
</item>
<item>
<title>Cardiovascular outcomes in patients with homozygous familial hypercholesterolaemia on lipoprotein apheresis initiated during childhood: long-term follow-up of an international cohort from two registries</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38759658/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>BACKGROUND: Homozygous familial hypercholesterolaemia (HoFH) is a rare genetic disease characterised by extremely high plasma LDL cholesterol from birth, causing atherosclerotic cardiovascular disease at a young age. Lipoprotein apheresis in combination with lipid-lowering drugs effectively reduce LDL cholesterol, but long-term health outcomes of such treatment are unknown. We aimed to investigate the long-term cardiovascular outcomes associated with lipoprotein apheresis initiated in childhood...</description>
<content:encoded><![CDATA[<div>Lancet Child Adolesc Health. 2024 May 14:S2352-4642(24)00073-7. doi: 10.1016/S2352-4642(24)00073-7. Online ahead of print.ABSTRACTBACKGROUND: Homozygous familial hypercholesterolaemia (HoFH) is a rare genetic disease characterised by extremely high plasma LDL cholesterol from birth, causing atherosclerotic cardiovascular disease at a young age. Lipoprotein apheresis in combination with lipid-lowering drugs effectively reduce LDL cholesterol, but long-term health outcomes of such treatment are unknown. We aimed to investigate the long-term cardiovascular outcomes associated with lipoprotein apheresis initiated in childhood or adolescence.METHODS: In this cohort study, data were drawn from the HoFH International Clinical Collaboration (HICC) and the international registry for Children with Homozygous Hypercholesterolemia on Lipoprotein Apheresis (CHAIN). An overall cohort included patients diagnosed with HoFH aged 0-18 years who were alive and in follow-up between Jan 1, 2010, and Nov 8, 2021, and whose high plasma LDL cholesterol concentrations made them eligible for lipoprotein apheresis. To compare cardiovascular outcomes, patients who initiated lipoprotein apheresis in childhood (lipoprotein apheresis group) and patients who only received lipid-lowering drugs (pharmacotherapy-only group) were matched by sex and untreated plasma LDL cholesterol concentrations. The primary outcome was a composite of cardiovascular death, myocardial infarction, ischaemic stroke, percutaneous coronary intervention, coronary artery bypass grafting, aortic valve replacement, peripheral artery disease, carotid endarterectomy, angina pectoris, and supra-aortic or aortic stenosis (collectively referred to as atherosclerotic cardiovascular disease), for which survival analyses were performed in the matched cohort. Cox regression analyses were used to compare disease-free survival between cohorts and to calculate hazard ratio (HR) and 95% CI adjusted for sex, age at diagnosis, untreated plasma LDL cholesterol concentration, and number of lipid-lowering therapies other than lipoprotein apheresis.FINDINGS: The overall cohort included 404 patients with a median age at diagnosis of 6·0 years (IQR 3·0-9·5) and median untreated plasma LDL cholesterol of 17·8 mmol/L (14·7-20·8). The matched cohorts included 250 patients (125 patients per group), with a median untreated LDL cholesterol of 17·2 mmol/L (14·8-19·7). Mean reduction in plasma LDL cholesterol concentrations between baseline and final follow-up was greater in the lipoprotein apheresis group (-55% [95% CI -60 to -51] vs -31% [-36 to -25]; p<0·0001). Patients in the lipoprotein apheresis group had longer atherosclerotic cardiovascular disease-free survival (adjusted HR 0·52 [95% CI 0·32-0·85]) and longer cardiovascular death-free survival (0·0301 [0·0021-0·4295]). Cardiovascular death was more common in the pharmacotherapy-only group than in the lipoprotein apheresis group (ten [8%] vs one [1%]; p=0·010), whereas median age at coronary artery bypass grafting was lower in the lipoprotein apheresis group than in the pharmacotherapy-only group (15·0 years [IQR 12·0-24·0] vs 30·5 years [19·0-33·8]; p=0·037).INTERPRETATION: Among patients with HoFH, lipoprotein apheresis initiated during childhood and adolescence is associated with reduced long-term risk of atherosclerotic cardiovascular disease and death, and clear benefits of early initiation of high-frequency treatment on reducing plasma cholesterol were found. Consensus recommendations are now needed to guide more widespread and timely use of lipoprotein apheresis for children with HoFH, and research is required to further optimise treatment and ensure benefits of early and aggressive treatment delivery are balanced against effects on quality of life.FUNDING: Amsterdam University Medical Centers, Location Academic Medical Center; Perelman School of Medicine at the University of Pennsylvania; European Atherosclerosis Society; and the US National Heart, Lung, and Blood Institute, National Institutes of Health.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38759658/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38759658</a> | DOI:<a href=https://doi.org/10.1016/S2352-4642(24)00073-7>10.1016/S2352-4642(24)00073-7</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38759658</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>M Doortje Reijman</dc:creator>
<dc:creator>Tycho R Tromp</dc:creator>
<dc:creator>Barbara A Hutten</dc:creator>
<dc:creator>G Kees Hovingh</dc:creator>
<dc:creator>Dirk J Blom</dc:creator>
<dc:creator>Alberico L Catapano</dc:creator>
<dc:creator>Marina Cuchel</dc:creator>
<dc:creator>Eldad J Dann</dc:creator>
<dc:creator>Antonio Gallo</dc:creator>
<dc:creator>Lisa C Hudgins</dc:creator>
<dc:creator>Frederick J Raal</dc:creator>
<dc:creator>Kausik K Ray</dc:creator>
<dc:creator>Fouzia Sadiq</dc:creator>
<dc:creator>Handrean Soran</dc:creator>
<dc:creator>Jaap W Groothoff</dc:creator>
<dc:creator>Albert Wiegman</dc:creator>
<dc:creator>D Meeike Kusters</dc:creator>
<dc:creator>Homozygous Familial Hypercholesterolaemia International Clinical Collaborators (HICC)</dc:creator>
<dc:creator>Children with Homozygous Hypercholesterolemia on Lipoprotein Apheresis: an International Registry (CHAIN) consortia</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>The Lancet. Child & adolescent health</dc:source>
<dc:title>Cardiovascular outcomes in patients with homozygous familial hypercholesterolaemia on lipoprotein apheresis initiated during childhood: long-term follow-up of an international cohort from two registries</dc:title>
<dc:identifier>pmid:38759658</dc:identifier>
<dc:identifier>doi:10.1016/S2352-4642(24)00073-7</dc:identifier>
</item>
<item>
<title>Unraveling ETC complex I function in ferroptosis reveals a potential ferroptosis-inducing therapeutic strategy for LKB1-deficient cancers</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38759628/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>The role of the mitochondrial electron transport chain (ETC) in regulating ferroptosis is not fully elucidated. Here, we reveal that pharmacological inhibition of the ETC complex I reduces ubiquinol levels while decreasing ATP levels and activating AMP-activated protein kinase (AMPK), the two effects known for their roles in promoting and suppressing ferroptosis, respectively. Consequently, the impact of complex I inhibitors on ferroptosis induced by glutathione peroxidase 4 (GPX4) inhibition is...</description>
<content:encoded><![CDATA[<div>Mol Cell. 2024 May 16;84(10):1964-1979.e6. doi: 10.1016/j.molcel.2024.04.009.ABSTRACTThe role of the mitochondrial electron transport chain (ETC) in regulating ferroptosis is not fully elucidated. Here, we reveal that pharmacological inhibition of the ETC complex I reduces ubiquinol levels while decreasing ATP levels and activating AMP-activated protein kinase (AMPK), the two effects known for their roles in promoting and suppressing ferroptosis, respectively. Consequently, the impact of complex I inhibitors on ferroptosis induced by glutathione peroxidase 4 (GPX4) inhibition is limited. The pharmacological inhibition of complex I in LKB1-AMPK-inactivated cells, or genetic ablation of complex I (which does not trigger apparent AMPK activation), abrogates the AMPK-mediated ferroptosis-suppressive effect and sensitizes cancer cells to GPX4-inactivation-induced ferroptosis. Furthermore, complex I inhibition synergizes with radiotherapy (RT) to selectively suppress the growth of LKB1-deficient tumors by inducing ferroptosis in mouse models. Our data demonstrate a multifaceted role of complex I in regulating ferroptosis and propose a ferroptosis-inducing therapeutic strategy for LKB1-deficient cancers.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38759628/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38759628</a> | DOI:<a href=https://doi.org/10.1016/j.molcel.2024.04.009>10.1016/j.molcel.2024.04.009</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38759628</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Chao Mao</dc:creator>
<dc:creator>Guang Lei</dc:creator>
<dc:creator>Amber Horbath</dc:creator>
<dc:creator>Min Wang</dc:creator>
<dc:creator>Zhengze Lu</dc:creator>
<dc:creator>Yuelong Yan</dc:creator>
<dc:creator>Xiaoguang Liu</dc:creator>
<dc:creator>Lavanya Kondiparthi</dc:creator>
<dc:creator>Xiong Chen</dc:creator>
<dc:creator>Jun Cheng</dc:creator>
<dc:creator>Qidong Li</dc:creator>
<dc:creator>Zhihao Xu</dc:creator>
<dc:creator>Li Zhuang</dc:creator>
<dc:creator>Bingliang Fang</dc:creator>
<dc:creator>Joseph R Marszalek</dc:creator>
<dc:creator>Masha V Poyurovsky</dc:creator>
<dc:creator>Kellen Olszewski</dc:creator>
<dc:creator>Boyi Gan</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Molecular cell</dc:source>
<dc:title>Unraveling ETC complex I function in ferroptosis reveals a potential ferroptosis-inducing therapeutic strategy for LKB1-deficient cancers</dc:title>
<dc:identifier>pmid:38759628</dc:identifier>
<dc:identifier>doi:10.1016/j.molcel.2024.04.009</dc:identifier>
</item>
<item>
<title>Transient hydroxycholesterol treatment restrains TCR signaling to promote long-term immunity</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38759618/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>T cell receptor (TCR) plays a fundamental role in adaptive immunity, and TCR-T cell therapy holds great promise for treating solid tumors and other diseases. However, there is a noticeable absence of chemical tools tuning TCR activity. In our study, we screened natural sterols for their regulatory effects on T cell function and identified 7-alpha-hydroxycholesterol (7a-HC) as a potent inhibitor of TCR signaling. Mechanistically, 7a-HC promoted membrane binding of CD3ε cytoplasmic domain, a...</description>
<content:encoded><![CDATA[<div>Cell Chem Biol. 2024 May 16;31(5):920-931.e6. doi: 10.1016/j.chembiol.2024.04.005.ABSTRACTT cell receptor (TCR) plays a fundamental role in adaptive immunity, and TCR-T cell therapy holds great promise for treating solid tumors and other diseases. However, there is a noticeable absence of chemical tools tuning TCR activity. In our study, we screened natural sterols for their regulatory effects on T cell function and identified 7-alpha-hydroxycholesterol (7a-HC) as a potent inhibitor of TCR signaling. Mechanistically, 7a-HC promoted membrane binding of CD3ε cytoplasmic domain, a crucial signaling component of the TCR-CD3 complex, through alterations in membrane physicochemical properties. Enhanced CD3ε membrane binding impeded the condensation between CD3ε and the key kinase Lck, thereby inhibiting Lck-mediated TCR phosphorylation. Transient treatments of TCR-T cells with 7a-HC resulted in reduced signaling strength, increased memory cell populations, and superior long-term antitumor functions. This study unveils a chemical regulation of TCR signaling, which can be exploited to enhance the long-term efficacy of TCR-T cell therapy.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38759618/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38759618</a> | DOI:<a href=https://doi.org/10.1016/j.chembiol.2024.04.005>10.1016/j.chembiol.2024.04.005</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38759618</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Zhengxu Ren</dc:creator>
<dc:creator>Kun Wang</dc:creator>
<dc:creator>Yong Zhang</dc:creator>
<dc:creator>Hui Chen</dc:creator>
<dc:creator>Yiming Zhu</dc:creator>
<dc:creator>Hua Li</dc:creator>
<dc:creator>Jizhong Lou</dc:creator>
<dc:creator>Haopeng Wang</dc:creator>
<dc:creator>Chenqi Xu</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Cell chemical biology</dc:source>
<dc:title>Transient hydroxycholesterol treatment restrains TCR signaling to promote long-term immunity</dc:title>
<dc:identifier>pmid:38759618</dc:identifier>
<dc:identifier>doi:10.1016/j.chembiol.2024.04.005</dc:identifier>
</item>
<item>
<title>Glucagon-like peptide-1 analog liraglutide reduces fat deposition in chicken adipocytes</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38759567/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>Previously, we reported that glucagon-like peptide-1 (GLP-1) and its analog liraglutide could inhibit fat de novo synthesis in the liver and reduce abdominal fat accumulation in broiler chickens. Nevertheless, the impact of GLP-1 on adipocyte fat deposition remains enigmatic. This study aimed to investigate the effects of GLP-1, via its analog liraglutide, on chicken chicken adipocytes in vitro. Chemical assays, quantitative real-time polymerase chain reaction (qRT-PCR), and western blot were...</description>
<content:encoded><![CDATA[<div>Poult Sci. 2024 Apr 12;103(7):103766. doi: 10.1016/j.psj.2024.103766. Online ahead of print.ABSTRACTPreviously, we reported that glucagon-like peptide-1 (GLP-1) and its analog liraglutide could inhibit fat de novo synthesis in the liver and reduce abdominal fat accumulation in broiler chickens. Nevertheless, the impact of GLP-1 on adipocyte fat deposition remains enigmatic. This study aimed to investigate the effects of GLP-1, via its analog liraglutide, on chicken chicken adipocytes in vitro. Chemical assays, quantitative real-time polymerase chain reaction (qRT-PCR), and western blot were employed to assess the proliferation, differentiation, and fat deposition of chicken adipocytes. Our findings indicated that liraglutide significantly suppressed cell proliferation and promoted preadipocyte differentiation in comparison to the control group. This was evidenced by elevated triglyceride (TG) content and upregulated mRNA expression of lipogenesis-related enzymes, such as acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), as well as regulators including peroxisome proliferator-activated receptor γ (PPARγ), sterol regulatory element binding protein-1 (SREBP1) and CCAAT/enhancer binding protein α (CEBPα). In mature adipocytes, liraglutide attenuated fat deposition by inhibiting fat de novo synthesis, evidenced by decreased mRNA expression of ACC, FAS, PPARγ, C/EBPα, and SREBP1, and concurrent upregulation of phosphorylated AMP-activated protein kinase (p-AMPK) and phosphorylated ACC (p-ACC). This resulted in reduced accumulation of lipid droplets and TG content in mature adipocytes. Collectively, our findings indicate that liraglutide suppresses the proliferation of preadipocytes, enhances their differentiation, and concurrently inhibits de novo lipogenesis in mature adipocytes. This observation offers profound insights into the mechanisms that underlie liraglutide's anti-adipogenic effects, which could have significant implications for the treatment of obesity in broiler chickens.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38759567/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38759567</a> | DOI:<a href=https://doi.org/10.1016/j.psj.2024.103766>10.1016/j.psj.2024.103766</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38759567</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Jianmei Zhang</dc:creator>
<dc:creator>Guangcheng Yang</dc:creator>
<dc:creator>Jingbo Liu</dc:creator>
<dc:creator>Zhenxian Lin</dc:creator>
<dc:creator>Jie Zhang</dc:creator>
<dc:creator>Jin Zhao</dc:creator>
<dc:creator>Guozheng Sun</dc:creator>
<dc:creator>Hai Lin</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Poultry science</dc:source>
<dc:title>Glucagon-like peptide-1 analog liraglutide reduces fat deposition in chicken adipocytes</dc:title>
<dc:identifier>pmid:38759567</dc:identifier>
<dc:identifier>doi:10.1016/j.psj.2024.103766</dc:identifier>
</item>
<item>
<title>Letter to the editor: Comment on "The effect of dairy products on liver fat and metabolic risk markers in males with abdominal obesity - A four-arm randomized controlled trial"</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38759492/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>No abstract</description>
<content:encoded><![CDATA[<div>Clin Nutr. 2024 May 6;43(6):1595-1596. doi: 10.1016/j.clnu.2024.05.012. Online ahead of print.NO ABSTRACTPMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38759492/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38759492</a> | DOI:<a href=https://doi.org/10.1016/j.clnu.2024.05.012>10.1016/j.clnu.2024.05.012</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38759492</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Luping Quan</dc:creator>
<dc:creator>Chao Ding</dc:creator>
<dc:creator>Yumeng Jin</dc:creator>
<dc:creator>Yaping Li</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Clinical nutrition (Edinburgh, Scotland)</dc:source>
<dc:title>Letter to the editor: Comment on "The effect of dairy products on liver fat and metabolic risk markers in males with abdominal obesity - A four-arm randomized controlled trial"</dc:title>
<dc:identifier>pmid:38759492</dc:identifier>
<dc:identifier>doi:10.1016/j.clnu.2024.05.012</dc:identifier>
</item>
<item>
<title>Accumulation of persistent organic pollutants in the kidneys of pet cats (Felis silvestris catus) and the potential implications for their health</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38759481/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>Persistent organic pollutants (POPs), such as polychlorinated diphenyls (PCBs) and brominated diphenyl ethers (PBDEs), are ubiquitous in the pet cat's living environment and are ingested through dietary intake and environmental exposure such as house dust. Cats are known to be susceptible to chronic kidney disease (CKD) and exposure to POPs may be associated with CKD. However, no studies have been conducted on the renal accumulation and health effects of POPs in cats. The objective of this study...</description>
<content:encoded><![CDATA[<div>Sci Total Environ. 2024 May 16;933:173212. doi: 10.1016/j.scitotenv.2024.173212. Online ahead of print.ABSTRACTPersistent organic pollutants (POPs), such as polychlorinated diphenyls (PCBs) and brominated diphenyl ethers (PBDEs), are ubiquitous in the pet cat's living environment and are ingested through dietary intake and environmental exposure such as house dust. Cats are known to be susceptible to chronic kidney disease (CKD) and exposure to POPs may be associated with CKD. However, no studies have been conducted on the renal accumulation and health effects of POPs in cats. The objective of this study was to elucidate the accumulation of PCBs, PBDEs, and organochlorine pesticides (OCPs) in the kidneys of domestic cats and discuss their potential impact on feline health. We report here that cats specifically accumulate POPs in their kidneys. Tissue samples were collected from the kidneys, livers, and muscles of cats and the concentrations of POPs in these tissues were analyzed in this study. The results showed that these compounds accumulated significantly higher in the kidney compared to other tissues. In addition, the ability to accumulate in the kidney was higher in cats than in other animals, suggesting that cats have a unique pattern of POPs accumulation in their kidneys, which is thought to occur because cats store a significant number of lipid droplets in the proximal tubules of the kidneys. This unique feature suggests that lipophilic POPs may accumulate in these lipid droplets during the excretory process. Accumulation of certain POPs in the kidneys causes necrosis and sloughing of renal tubular epithelial cells, which may be associated with CKD, a common disease in cats. This study provides valuable insight into understanding the renal accumulation and risk of POPs in cats and provides essential knowledge for developing strategies to protect the health and welfare of domestic cats.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38759481/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38759481</a> | DOI:<a href=https://doi.org/10.1016/j.scitotenv.2024.173212>10.1016/j.scitotenv.2024.173212</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38759481</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Kei Nomiyama</dc:creator>
<dc:creator>Rina Sato</dc:creator>
<dc:creator>Fuka Sato</dc:creator>
<dc:creator>Akifumi Eguchi</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>The Science of the total environment</dc:source>
<dc:title>Accumulation of persistent organic pollutants in the kidneys of pet cats (Felis silvestris catus) and the potential implications for their health</dc:title>
<dc:identifier>pmid:38759481</dc:identifier>
<dc:identifier>doi:10.1016/j.scitotenv.2024.173212</dc:identifier>
</item>
<item>
<title>Elucidating the modulatory role of dietary hydroxyproline on the integrity and functional performance of the intestinal barrier in early-weaned piglets: A comprehensive analysis of its interplay with the gut microbiota and metabolites</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38759371/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>Piglets receive far less hydroxyproline (Hyp) from a diet after weaning than they obtained from sow's milk prior to weaning, suggesting that Hyp may play a protective role in preserving intestinal mucosal homeostasis. This study aimed to evaluate the effect of Hyp on intestinal barrier function and its associated gut microbiota and metabolites in early-weaned piglets. Eighty weaned piglets were divided into four groups and fed diets containing different Hyp levels (0 %, 0.5 %, 1 %, or 2 %) for...</description>
<content:encoded><![CDATA[<div>Int Immunopharmacol. 2024 May 16;134:112268. doi: 10.1016/j.intimp.2024.112268. Online ahead of print.ABSTRACTPiglets receive far less hydroxyproline (Hyp) from a diet after weaning than they obtained from sow's milk prior to weaning, suggesting that Hyp may play a protective role in preserving intestinal mucosal homeostasis. This study aimed to evaluate the effect of Hyp on intestinal barrier function and its associated gut microbiota and metabolites in early-weaned piglets. Eighty weaned piglets were divided into four groups and fed diets containing different Hyp levels (0 %, 0.5 %, 1 %, or 2 %) for 21 days. Samples, including intestinal contents, tissues, and blood, were collected on day 7 for analysis of microbial composition, intestinal barrier function, and metabolites. We demonstrated that dietary supplementation with 2 % Hyp improved the feed conversion ratio and reduced the incidence of diarrhea in early-weaned piglets compared to the control group. Concurrently, Hyp enhanced intestinal barrier function by facilitating tight junction protein (zonula occludens (ZO)-1 and occludin) expression and mucin production in the jejunal, ileal, and colonic mucosas. It also improved mucosal immunity (by increasing the amount of secretory IgA (sIgA) and the ratio of CD4+/CD8+ T lymphocytes and decreasing NF-κB phosphorylation) and increased antioxidant capacity (by raising total antioxidant capacity (T-AOC) and glutathione levels) in the intestinal mucosa. In addition, Hyp supplementation resulted in an increase in the levels of glycine, glutathione, and glycine-conjugated bile acids, while decreasing the concentrations of cortisol and methionine sulfoxide in plasma. Intriguingly, piglets fed diet containing Hyp exhibited a remarkable increase in the abundance of probiotic Enterococcus faecium within their colonic contents. This elevation occurred alongside an attenuation of pro-inflammatory responses and an enhancement in intestinal barrier integrity. Further, these changes were accompanied by a rise in anti-inflammatory metabolites, specifically glycochenodeoxycholic acid and guanosine, along with a suppression of pro-inflammatory lipid peroxidation products, including (12Z)-9,10-dihydroxyoctadec-12-enoic acid (9,10-DHOME) and 13-L-hydroperoxylinoleic acid (13(S)-HPODE). In summary, Hyp holds the capacity to enhance the intestinal barrier function in weaned piglets; this effect is correlated with changes in the gut microbiota and metabolites. Our findings provide novel insights into the role of Hyp in maintaining gut homeostasis, highlighting its potential as a dietary supplement for promoting intestinal health in early-weaned piglets.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38759371/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38759371</a> | DOI:<a href=https://doi.org/10.1016/j.intimp.2024.112268>10.1016/j.intimp.2024.112268</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38759371</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Zhining Tang</dc:creator>
<dc:creator>Yang Yang</dc:creator>
<dc:creator>Mingrui Yang</dc:creator>
<dc:creator>Da Jiang</dc:creator>
<dc:creator>Yao Ge</dc:creator>
<dc:creator>Xinyu Zhang</dc:creator>
<dc:creator>Haozhen Liu</dc:creator>
<dc:creator>Qingyao Fu</dc:creator>
<dc:creator>Xiyuan Liu</dc:creator>
<dc:creator>Ying Yang</dc:creator>
<dc:creator>Zhenlong Wu</dc:creator>
<dc:creator>Yun Ji</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>International immunopharmacology</dc:source>
<dc:title>Elucidating the modulatory role of dietary hydroxyproline on the integrity and functional performance of the intestinal barrier in early-weaned piglets: A comprehensive analysis of its interplay with the gut microbiota and metabolites</dc:title>
<dc:identifier>pmid:38759371</dc:identifier>
<dc:identifier>doi:10.1016/j.intimp.2024.112268</dc:identifier>
</item>
<item>
<title>Effect of residual feed intake on meat quality in fattening Charolais bulls fed two contrasting diets</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38759326/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>The selection of more efficient animals for breeding is of both economic and environmental interest to the industry. The aim of this study was to evaluate the influence of the animals' residual feed intake (RFI) ranking in interaction with the type of diet on the meat quality of Charolais beef cattle. Indeed, several biological mechanisms are associated with RFI, especially when animals are fed high starch-diets. It is therefore possible that quality parameters may show greater changes due to...</description>
<content:encoded><![CDATA[<div>Meat Sci. 2024 May 8;214:109536. doi: 10.1016/j.meatsci.2024.109536. Online ahead of print.ABSTRACTThe selection of more efficient animals for breeding is of both economic and environmental interest to the industry. The aim of this study was to evaluate the influence of the animals' residual feed intake (RFI) ranking in interaction with the type of diet on the meat quality of Charolais beef cattle. Indeed, several biological mechanisms are associated with RFI, especially when animals are fed high starch-diets. It is therefore possible that quality parameters may show greater changes due to RFI in the context of high starch diets compared to high forage diets. An 84-day feed efficiency trial followed immediately by a second 112-day feed efficiency trial was conducted with a total of 100 animals fed either maize- or grass-diets for 196-days. At the end of the 84-day period, the 32 most divergent RFI animals (16 extreme RFI animals per diet, 8 RFI+ and 8 RFI-) were identified. They were slaughtered after 112-days of finishing. The Longissimus thoracis was characterised in terms of nutritional and sensory quality. RFI had no effect on lab colour, muscle shear force, total fat, fatty acid ratios and most of the total fatty acid content (especially n-3) irrespective of the diet. However, more efficient animals (RFI-) showed higher CLA contents compared to less efficient animals (RFI+) regardless of the diet and also a lower n6/n3 ratio only in animals fed the maize diets. Diet also had a significant effect on lipid and FA content as well as on FA composition.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38759326/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38759326</a> | DOI:<a href=https://doi.org/10.1016/j.meatsci.2024.109536>10.1016/j.meatsci.2024.109536</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38759326</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>M P Ellies-Oury</dc:creator>
<dc:creator>K Insausti</dc:creator>
<dc:creator>S Papillon</dc:creator>
<dc:creator>J Albechaalany</dc:creator>
<dc:creator>G Cantalapiedra-Hijar</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Meat science</dc:source>
<dc:title>Effect of residual feed intake on meat quality in fattening Charolais bulls fed two contrasting diets</dc:title>
<dc:identifier>pmid:38759326</dc:identifier>
<dc:identifier>doi:10.1016/j.meatsci.2024.109536</dc:identifier>
</item>
<item>
<title>Multi-omics analysis of kidney, bone and bone marrow explored potential mechanisms of Erzhi Wan against osteoporosis with kidney-Yin deficiency</title>
<link>https://pubmed.ncbi.nlm.nih.gov/38759323/?utm_source=Feedvalidator&utm_medium=rss&utm_campaign=None&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&fc=None&ff=20240518072257&v=2.18.0.post9+e462414</link>
<description>Osteoporosis (OP) is a metabolic bone disease that can lead to major health challenges. The theory of Traditional Chinese medicine believes that kidney-Yin deficiency (KYD) is the main cause of postmenopausal osteoporosis. This study was aimed to investigate the effect of EZW on anti-osteoporosis with KYD, and explore potential mechanisms from the perspective of the kidney, bone and bone marrow through analysis of metabolomics and proteomics. The model of OP with KYD was established by rats...</description>
<content:encoded><![CDATA[<div>J Pharm Biomed Anal. 2024 May 14;246:116211. doi: 10.1016/j.jpba.2024.116211. Online ahead of print.ABSTRACTOsteoporosis (OP) is a metabolic bone disease that can lead to major health challenges. The theory of Traditional Chinese medicine believes that kidney-Yin deficiency (KYD) is the main cause of postmenopausal osteoporosis. This study was aimed to investigate the effect of EZW on anti-osteoporosis with KYD, and explore potential mechanisms from the perspective of the kidney, bone and bone marrow through analysis of metabolomics and proteomics. The model of OP with KYD was established by rats treated with bilateral ovariectomy (OVX), and then given intragastric administration of thyroid and reserpine to induce. Micro-CT was applied to determine the microstructures of bone. Serum levels associated with bone turnover markers and kidney-Yin deficiency were detected by enzyme-linked immunosorbent (ELISA) assay. The differential metabolites in the kidney, bone and bone marrow were analyzed by metabolomics. The differentially expressed proteins in these three tissues were detected via proteomics. The findings suggested that EZW could alleviate a variety of metabolites and proteins among the kidney, bone and bone marrow, primarily in amino acid metabolism, carbohydrate metabolism, nucleotide metabolism and lipid metabolism, thus leading to improvements of OP with KYD, which provided theoretical basis for clinical treatment of EZW on OP with KYD.PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38759323/?utm_source=Feedvalidator&utm_medium=rss&utm_content=0lFT7HlkDPhpSC3O4zXvjmq-zDArwBcCTeWrUvID7QU&ff=20240518072257&v=2.18.0.post9+e462414">38759323</a> | DOI:<a href=https://doi.org/10.1016/j.jpba.2024.116211>10.1016/j.jpba.2024.116211</a></div>]]></content:encoded>
<guid isPermaLink="false">pubmed:38759323</guid>
<pubDate>Fri, 17 May 2024 06:00:00 -0400</pubDate>
<dc:creator>Guanxiong Shang</dc:creator>
<dc:creator>Xiaoqi Zhou</dc:creator>
<dc:creator>Jiu Yin</dc:creator>
<dc:creator>Xuan Niu</dc:creator>
<dc:creator>Yan Zhao</dc:creator>
<dc:creator>Xin Li</dc:creator>
<dc:creator>Qingheng Tong</dc:creator>
<dc:creator>Beihua Bao</dc:creator>
<dc:creator>Yudan Cao</dc:creator>
<dc:creator>Fangfang Cheng</dc:creator>
<dc:creator>Zhipeng Li</dc:creator>
<dc:creator>Weifeng Yao</dc:creator>
<dc:date>2024-05-17</dc:date>
<dc:source>Journal of pharmaceutical and biomedical analysis</dc:source>
<dc:title>Multi-omics analysis of kidney, bone and bone marrow explored potential mechanisms of Erzhi Wan against osteoporosis with kidney-Yin deficiency</dc:title>
<dc:identifier>pmid:38759323</dc:identifier>
<dc:identifier>doi:10.1016/j.jpba.2024.116211</dc:identifier>
</item>
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