Lifestyle Genomics最新文献

{"title":"Inflammatory Proteins Mediate the Causal Association between Sleep Traits and Breast Cancer: A Mendelian Randomization Study.","authors":"Jiawei Zhou, Lijun Mao","doi":"10.1159/000550315","DOIUrl":"10.1159/000550315","url":null,"abstract":"<p><strong>Introduction: </strong>Breast cancer (BC) is the most frequent cancer in women, driven by a combination of genetic, environmental, and lifestyle factors. Whether modifiable sleep behaviors causally affect BC risk remains unclear. Aims of the study were to systematically assess the causal impact of sleep-related phenotypes on overall BC and its major subtypes using two-sample mendelian randomization (MR) and to determine whether inflammatory proteins mediate these relationships.</p><p><strong>Methods: </strong>Inverse variance weighted served as the main analysis, with sensitivity and reverse-MR analyses as supporting checks. Mediation was quantified with a two-step MR design.</p><p><strong>Results: </strong>Morning chronotype significantly reduced the risk of overall BC (OR = 0.936, 95% CI: 0.893-0.980) and luminal A subtype (OR = 0.944, 95% CI: 0.894-0.996). Short sleep duration was associated with decreased risk of overall BC (OR = 0.482, 95% CI: 0.284-0.818) and luminal A subtype (OR = 0.385, 95% CI: 0.194-0.766), whereas long sleep duration increased the risk of triple-negative BC (OR = 9.433, 95% CI: 2.419-36.775) and luminal A subtype (OR = 2.186, 95% CI: 1.111-4.302). Mediation analysis indicated that CXCL11 accounted for 22.4% of the total causal effect of short sleep duration on luminal A BC.</p><p><strong>Conclusion: </strong>Morning chronotype confers protection against BC, whereas prolonged sleep duration elevates the risk of triple-negative and luminal A BC. CXCL11 mediates part of the protective effect of short sleep on luminal A BC. These findings provide evidence-based support for BC prevention strategies focusing on sleep optimization.</p>","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":" ","pages":"63-75"},"PeriodicalIF":1.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12923251/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145966395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Current Evidence and Outlook Regarding the Combined Effects of Fructose Consumption, Obesity Status, and Genetic Variation on C-reactive Protein.","authors":"Tamara K Reed","doi":"10.1159/000547980","DOIUrl":"https://doi.org/10.1159/000547980","url":null,"abstract":"","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":" ","pages":"1-9"},"PeriodicalIF":1.4,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144873822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Linking dietary creatine to DNA methylation-based predictors of mortality in individuals aged 50 and above.","authors":"Sergej M Ostojic, Ivana Kavecan","doi":"10.1159/000547260","DOIUrl":"10.1159/000547260","url":null,"abstract":"<p><strong>Background: </strong>Creatine is a conditionally essential nutrient integral to cellular energy homeostasis, with emerging evidence suggesting its potential role in modulating biological aging. However, associations between dietary creatine intake and epigenetic biomarkers of mortality remain unexplored.</p><p><strong>Objective: </strong>This study investigates the relationship between dietary creatine intake and DNA methylation-derived mortality indices in U.S. adults aged 50 years and older.</p><p><strong>Methods: </strong>Data from the NHANES 1999-2002 cycles were analyzed, including dietary creatine intake estimated from 24-hour recall interviews and DNA methylation profiles measured using the Illumina EPIC array. Epigenetic mortality predictors GrimAgeMort and GrimAge2Mort were examined in relation to creatine intake.</p><p><strong>Results: </strong>Among 4,983 participants (mean age 67.6 ± 10.7 years), a significant inverse correlation was observed between dietary creatine and both GrimAgeMort (r = -0.041, P = 0.045) and GrimAge2Mort (r = -0.047, P = 0.019), indicating that higher creatine consumption was associated with lower epigenetic mortality risk scores. These associations persisted as statistically significant after adjustment for demographic variables and pertinent dietary factors.</p><p><strong>Conclusions: </strong>Higher dietary creatine intake is linked to reduced biological age acceleration and mortality risk as estimated by epigenetic biomarkers. These findings highlight creatine's potential as a modifiable dietary factor promoting healthy aging and longevity. Further research is warranted to elucidate underlying mechanisms.</p>","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":" ","pages":"1-8"},"PeriodicalIF":1.4,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12503492/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144637452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Precision nutrition and nutriomics in the machine learning era.","authors":"Omar Ramos-Lopez, Begoña de Cuevillas, Maria P Portillo, J Alfredo Martinez","doi":"10.1159/000546650","DOIUrl":"https://doi.org/10.1159/000546650","url":null,"abstract":"","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":" ","pages":"1-10"},"PeriodicalIF":2.0,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234479","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nicotine Metabolism-Related Genetic Polymorphisms Associated with Smoking Cessation in Korean Men: A Candidate Gene Association Study in a Korean Cohort.","authors":"Jae-Min Park, Ja-Eun Choi, Ji-Won Lee, Kyung-Won Hong","doi":"10.1159/000543543","DOIUrl":"10.1159/000543543","url":null,"abstract":"<p><strong>Introduction: </strong>Smoking cessation is influenced by genetic and environmental factors, particularly genetic polymorphisms influencing nicotine metabolism. This study investigated the association between specific nicotine metabolism-related genetic variants and smoking cessation among Korean men.</p><p><strong>Methods: </strong>A candidate gene association study was performed targeting single nucleotide polymorphisms (SNPs) within nicotine metabolism-related genes. Participants were categorized as never, former, or current smokers. A Genetic Risk Score (GRS) was computed using significant SNPs to evaluate cumulative genetic influence.</p><p><strong>Results: </strong>Six SNPs showed significant association with smoking cessation in a Korean cohort. A higher GRS was associated with increased odds of current smoking compared to former smoking (OR = 1.18, 95% CI: 1.12-1.25, p < 0.001).</p><p><strong>Conclusion: </strong>This study indicates a substantial genetic component in smoking cessation, highlighting the importance of population-specific approaches, and may aid personalized smoking cessation strategies based on genetic predisposition among Koreans.</p>","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":" ","pages":"20-26"},"PeriodicalIF":2.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11844709/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142979027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Experimental Environment Is a Determinant of Gene Methylation and One-Carbon Metabolism in Obese Adult Mice.","authors":"Zeyu Yang, Ruslan Kubant, Eva Kranenburg, Clara E Cho, G Harvey Anderson","doi":"10.1159/000546727","DOIUrl":"10.1159/000546727","url":null,"abstract":"<p><strong>Background: </strong>Diet-induced obesity (DIO) leads to insulin resistance (IR) and alters gene expression through epigenetic mechanisms, including DNA methylation. Here, we aimed to investigate whether experimental environment is an important variable in determining DNA methylation and one-carbon metabolism in DIO mice fed a multi-vitamin-mineral mixture (MVM).</p><p><strong>Methods: </strong>Three experiments with identical design were conducted in three independent animal facilities (i.e., experimental environments or locations). In each location, 12-week-old male C57BL/6J mice were randomly assigned to two dietary groups: high-fat (HF) and HF-MVM for an average of 10 weeks. Global and gene-specific methylation of adipose function related genes in epididymal white adipose tissue (eWAT), and insulin signaling genes in the liver were analyzed using bisulfite pyrosequencing. Hepatic 1-C metabolites were measured and the ratio of S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH) was used as an indicator of methylation potential.</p><p><strong>Results: </strong>Experimental location affected global methylation patterns in the eWAT, but not in the liver. At the gene-specific level, experimental location, MVM, and their interaction altered the methylation of genes related to adipose function (Srebf1, Acaca, Fasn, Pparg, and Rbp4) in the eWAT and insulin signaling (Pi3kr1 and Akt1) in the liver (p < 0.05). The SAM/SAH ratio was correlated with gene-specific methylation at some CpG sites of Srebf1, Pi3kr1, Acaca, Fasn, Pparg, Rbp4, and Akt1) genes (p < 0.05).</p><p><strong>Conclusion: </strong>The experimental environment is a significant determinant of the effects of micronutrient supplement on 1-C metabolism and the methylation of genes associated with IR in tissues of DIO adult male mice.</p>","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":" ","pages":"116-130"},"PeriodicalIF":1.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12503451/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144506073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Machine Learning-Based Prediction of Gout Using Polygenic Risk Scores and Clinical Variables: A Korean Cohort Study.","authors":"Do-Hyeon Kwak, Hyunjung Kim, Hee-Won Park, Sun Shim Choi, Ki Won Moon","doi":"10.1159/000548169","DOIUrl":"10.1159/000548169","url":null,"abstract":"<p><strong>Introduction: </strong>The prevalence of gout, a chronic metabolic disease, has recently increased. Polygenic risk scores (PRSs) represent a useful tool for predicting patient outcomes of this condition. However, the clinical utility of PRS in disease prediction remains controversial.</p><p><strong>Methods: </strong>Using data from the Korean Genome and Epidemiology Study, machine learning (ML) models were developed to predict gout based on PRS and clinical variables such as uric acid, lifestyle habits, and metabolic syndrome (MetS) profiles. Five supervised learning algorithms were applied: logistic regression (a traditional statistical model often used in ML contexts), random forest (RF), decision tree, extreme gradient boosting, and light gradient boosting.</p><p><strong>Results: </strong>Among the models, the RF model incorporating PRS, age, sex, MetS, and uric acid levels achieved the highest area under the curve (0.7204, 95% CI = 0.7124-0.7284). Feature importance analysis highlighted uric acid levels as the most important predictor of gout, followed by PRS and age. Although PRS enhanced the predictive power of the ML models, its effect was modest, suggesting that traditional risk factors remain important for gout prediction.</p><p><strong>Conclusion: </strong>This study demonstrated that integrating genetic data with clinical variables improves gout prediction. Further research is necessary to optimize the utility of PRS in diverse populations.</p>","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":" ","pages":"142-151"},"PeriodicalIF":1.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145149789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring Differentially Methylated Genes among Preterm Birth and Full-Term Birth.","authors":"Aleem Razzaq, Razan ElKahlout, Gheyath K Nasrallah, Faisal E Ibrahim, Muthanna Samara, Hatem Zayed, Palli Valapila Abdulrouf, Rana Al-Jurf, Ahmed Najjar, Thomas Farrell, M Walid Qoronfleh, Hilal Al Rifai, Nader Al-Dewik","doi":"10.1159/000543372","DOIUrl":"10.1159/000543372","url":null,"abstract":"<p><strong>Introduction: </strong>Preterm birth (PTB) is a major contributor to neonatal morbidity and mortality. DNA methylation plays a critical role in fetal development and may serve as an epigenetic biomarker for PTB. However, few epigenetic studies have investigated PTB-specific DNA methylation changes. This study aimed to identify epigenetic differences between PTB and term birth (TB) infants.</p><p><strong>Methods: </strong>A total of 218 cord blood samples from three independent PTB studies were analyzed to identify epigenetic differences between PTB and TB infants. Differential methylation analysis was conducted while adjusting for key covariates, including gestational age, sex, and disease status. Differentially methylated regions (DMRs) (genes and promoters) and differentially methylated sites (DMSs) (CpG sites) were assessed for significant methylation differences between the two groups.</p><p><strong>Results: </strong>In PTB infants, several genes, including RNASE3, HGF, CLEC5A, LIPN, NXF1, and CCDC12 showed significant hypermethylation (p < 0.05), while the MUC20 and IFNL4 genes showed significant hypomethylation (p < 0.05). The eForge analysis revealed that hypermethylated (p < 0.05) CpG sites were significantly enriched in different fetal tissues such as the small and large intestines, adrenal gland, fetal heart, lungs, and kidney, whereas hypomethylated CpGs showed no significant enrichment. Gene ontology analysis indicated that differentially methylated genes were primarily involved in immune response regulation. Notably, S100A9 and S100A8 genes, which play crucial roles in neonatal immune function and sepsis risk, were hypermethylated (p < 0.05) in PTB infants.</p><p><strong>Conclusion: </strong>This study identified PTB-associated DNA methylation changes in immune-related genes, suggesting their potential epigenetic biomarkers for PTB. These findings enhance our understanding of PTB pathogenesis and may contribute to the development of novel diagnostic and therapeutic strategies.</p>","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":" ","pages":"76-89"},"PeriodicalIF":2.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12097759/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142922039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CC Genotype at TCF7L2 Diabetes Risk Locus rs7903146 Directs a Coordinated Fatty Acid Response to a Mediterranean Diet Intervention: A Randomized Controlled Trial.","authors":"Laurence D Parnell, Chao-Qiang Lai, Christina Holzapfel, Jacob J Christensen, José M Ordovás","doi":"10.1159/000542468","DOIUrl":"10.1159/000542468","url":null,"abstract":"<p><strong>Introduction: </strong>Previous studies identified genetic links between the TCF7L2 C/T variant rs7903146, type 2 diabetes (T2D), and obesity. We wished to deepen our understanding of how specific diets interact with this variant to affect blood metabolites, an aspect not previously investigated. Hence, we conducted a controlled study where individuals with different genotypes followed a Mediterranean (Med) or low-fat (LF) diet for 1 week.</p><p><strong>Methods: </strong>Participants were recruited from the Boston, MA (USA) area. Anthropometric and clinical measures were taken. Genotypes at rs7903146 were ascertained, with homozygous carriers of the more common and protective CC or risk TT genotype invited to participate. Participants followed both diets (LF or Med) for 1 week with ∼10 days' washout between diets. Blood samples taken at the beginning and end of each diet period underwent metabolomics analysis using nuclear magnetic resonance spectroscopy. We evaluated how the diet affected different metabolites based on genetic profile.</p><p><strong>Results: </strong>The cohort of 35 persons was 43% female, aged 18-70 y, with BMI between 26.4 and 33.9 kg/m2. Focusing on fatty acids (FAs) and other lipid metabolic factors (n = 23), we observed a greater number and stronger correlations among these factors in the CC genotype-Med diet group than in the other three genotype-diet combinations. An aggregate of 11 factors, each negatively correlating with delta-saturated fatty acids (SFA), showed a significant genotype-Med diet interaction on delta-SFA in CC individuals on the Med diet (p = 0.0046). A similar genotype-Med diet interaction was observed for delta-monounsaturated fatty acids (p = 0.0078). These interactions were not statistically significant at the end of the LF intervention.</p><p><strong>Conclusion: </strong>Our findings suggest that the Med diet has a stronger influence on regulating lipid factors in individuals with the CC genotype at the TCF7L2 variant rs7903146. This diet-genotype interaction may have significant implications for understanding the inter-individual variation of metabolic response on specific dietary regimens.</p>","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":" ","pages":"36-51"},"PeriodicalIF":2.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Uncoupling Proteins Variants Are Linked to Hypercholesterolemia and Abdominal Obesity in Metabolically Unhealthy Women.","authors":"Erika Sierra-Ruelas, Nathaly Torres-Castillo, Barbara Vizmanos, Wendy Campos Pérez, Erika Martínez-López","doi":"10.1159/000543484","DOIUrl":"10.1159/000543484","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;It has been reported that even with the same body mass index (BMI); there are subjects with metabolically healthy (MH) or unhealthy (MUH) phenotype. The main determinants of the unhealthy phenotype are the type and distribution of fat, ectopic fat accumulation, genetics, and lifestyle factors. Uncoupling proteins (UCPs) disengage mitochondrial respiration from ATP synthesis and result in heat production, which in turn is related to energy expenditure and, thus, to fat mass accumulation. The association of the UCP1 3826A/G (rs1800592), UCP2 Ala55Val (rs660339), and UCP3 55C/T (rs1800849) variants with metabolic variables was evaluated according to metabolic phenotype in Mexican women.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Women aged 18-65 years classified as normal weight (NW) or excessive weight (EW) according to their BMI (from 18.5 to &lt;25 kg/m2 for NW, and from 25 to &lt;40 kg/m2 for EW), were included. Participants were classified into two metabolic phenotypes: MH or MUH, respectively, based on ATP-III criteria and the homeostasis model assessment of insulin resistance (HOMA-IR). The genetic variants were determined by allelic discrimination using TaqMan® probes.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;In participants with the UCP1 3826A/G variant, an increased risk of hypercholesterolemia was observed in those with the NW-MUH phenotype (OR = 5.09, 95% CI = 1.03-25.12, p = 0.017). The UCP2 Ala55Val variant in EW-MUH subjects was associated with higher abdominal obesity risk (OR = 3.23, 95% CI = 1.21-8.60, p = 0.019), while no associations were found with the UCP3 55C/T variant.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;UCP1 and UCP2 variants are related with hypercholesterolemia and visceral fat accumulation in women with MUH phenotype.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;It has been reported that even with the same body mass index (BMI); there are subjects with metabolically healthy (MH) or unhealthy (MUH) phenotype. The main determinants of the unhealthy phenotype are the type and distribution of fat, ectopic fat accumulation, genetics, and lifestyle factors. Uncoupling proteins (UCPs) disengage mitochondrial respiration from ATP synthesis and result in heat production, which in turn is related to energy expenditure and, thus, to fat mass accumulation. The association of the UCP1 3826A/G (rs1800592), UCP2 Ala55Val (rs660339), and UCP3 55C/T (rs1800849) variants with metabolic variables was evaluated according to metabolic phenotype in Mexican women.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Women aged 18-65 years classified as normal weight (NW) or excessive weight (EW) according to their BMI (from 18.5 to &lt;25 kg/m2 for NW, and from 25 to &lt;40 kg/m2 for EW), were included. Participants were classified into two metabolic phenotypes: MH or MUH, respectively, based on ATP-III criteria and the homeostasis model assessment of insulin resistance (HOMA-IR). The genetic variants were determined by allelic discrimination using TaqMan® probes.&lt;/p&gt;&lt;p&gt;&lt;","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":" ","pages":"27-35"},"PeriodicalIF":1.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11838145/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143007863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}