M. Abbasalizad Farhangi, M. Vajdi, L. Nikniaz, Zeinab Nikniaz
{"title":"Interaction between Vascular Endothelial Growth Factor-A (rs2010963) Gene Polymorphisms and Dietary Diversity Score on Cardiovascular Risk Factors in Patients with Metabolic Syndrome","authors":"M. Abbasalizad Farhangi, M. Vajdi, L. Nikniaz, Zeinab Nikniaz","doi":"10.1159/000503789","DOIUrl":"https://doi.org/10.1159/000503789","url":null,"abstract":"Background: The vascular endothelial growth factor-A (VEGFA) family of cytokines regulates proliferation, angiogenesis, and migration of endothelial cells, increases vascular permeability, and controls thrombogenicity. Recent studies have suggested that the VEGFA gene plays an important role in the pathogenesis of metabolic syndrome and its related disorders. Dietary diversity score (DDS) has also been shown to have potential favorable effects against features of metabolic syndrome. This study examined the interactions between +405 VEGFA C/G (rs2010963) polymorphism and DDS on the metabolic and biochemical profile of metabolic syndrome. Therefore, in the current study, we aimed to evaluate the interaction between DDS and VEGFA rs2010963 gene polymorphisms in modification of metabolic risk factors including serum lipids, blood pressure, serum adiponectin, and matrix metalloproteinase (MMP)-3 concentrations in patients with metabolic syndrome. Methods and Materials: In the current cross-sectional study, 254 patients with metabolic syndrome were recruited. Measurements of blood pressure, anthropometric parameters, and dietary intakes were performed and the DDS was calculated. Biochemical variables including serum adiponectin concentrations, lipid profile, serum glucose, and MMP-3 concentrations were measured by enzyme-linked immunosorbent assay method (ELISA) and enzymatic colorimetric methods. Determination of +405 C/G VEGFA gene polymorphisms was performed using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Results: Patients in the lowest DDS quartile had higher insulin and homeostatic model assessment of insulin resistance (HOMA-IR), while patients in the highest DDS quartile had higher quantitative insulin check index (QUICKI; p < 0.05). Higher serum triglyceride and systolic blood pressure (SBP) values and lower serum adiponectin concentrations were also observed in lower DDS quartiles (p < 0.05). Patients with the CC genotype in the VEGFA rs2010963 polymorphism had significantly higher body mass index (BMI), fasting blood glucose, aspartate aminotransferase (AST), and alanine aminotransferase (ALT; p < 0.05) compared to patients with the other 2 genotypes. In lower quartiles of DDS, 30% of patients with metabolic syndrome had the GG genotype, while 30.4 and 30.8% of patients with metabolic syndrome in higher DDS quartiles had GC and CC genotypes, respectively (p = 0.04). Conclusion: Our study found lower insulin resistance, serum triglyceride, and SBP and higher adiponectin concentrations among patients with metabolic syndrome in highest quartiles of DDS. Moreover, patients with the CC genotype were more likely to have higher BMI, fasting blood glucose, AST, and ALT. This significant interaction gives a possible evidence of a VEGFA-DDS association that may be relevant to metabolic syndrome. Further studies are warranted to clarify the underlying mechanisms of these interactions.","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":"13 1","pages":"1 - 10"},"PeriodicalIF":2.6,"publicationDate":"2019-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000503789","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47995457","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":"Nutrition Assessment and Intervention in a Pediatric Patient with Angelman Syndrome: A Case Presentation Highlighting Clinical Challenges and Evidence-Based Solutions","authors":"K. Fisher, J. Keng, J. Ziegler","doi":"10.1159/000504300","DOIUrl":"https://doi.org/10.1159/000504300","url":null,"abstract":"Background: Angelman syndrome (AS) is a rare disorder of genetic imprinting which results in intellectual and developmental disability. It meets criteria of a disorder of neurologic impairment. A deletion in the long arm of chromosome 15 (del 15q11.2–q13) is responsible for about 70% of cases of AS (deletion genotype). Summary: There is a paucity of evidence to allow algorithmic nutrition assessment and intervention in pediatric patients with AS. Therefore, our objective is to use a case presentation to provide an example of nutrition assessment and intervention in a pediatric patient with the deletion genotype of AS and then highlight common challenges to providing evidenced-based nutrition care. For the highlighted challenges, we suggest evidence-based solutions to provide a resource for clinicians who may encounter similar challenges in clinical practice. Key Messages: There are genotype-phenotype correlations in AS that can help guide clinicians regarding nutritionally relevant clinical characteristics and corresponding interventions that are patient specific. The deletion genotype in AS is associated with multiple characteristics that are relevant to nutrition care and may also be different and/or more severe than characteristics seen in other AS genetic mechanisms. There is also overlap in certain nutritionally relevant clinical characteristics between AS and other conditions, including Prader-Willi syndrome, autism spectrum disorders, and disorders of neurological impairment like cerebral palsy. Clinicians can utilize nutrition resources related to these conditions to expand the scope of relevant resources available.","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":"13 1","pages":"43 - 52"},"PeriodicalIF":2.6,"publicationDate":"2019-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000504300","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49014541","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}
Maximilien Franck, J. de Toro-Martín, F. Guénard, I. Rudkowska, S. Lemieux, B. Lamarche, P. Couture, M. Vohl
{"title":"Prevention of Potential Adverse Metabolic Effects of a Supplementation with Omega-3 Fatty Acids Using a Genetic Score Approach","authors":"Maximilien Franck, J. de Toro-Martín, F. Guénard, I. Rudkowska, S. Lemieux, B. Lamarche, P. Couture, M. Vohl","doi":"10.1159/000504022","DOIUrl":"https://doi.org/10.1159/000504022","url":null,"abstract":"Introduction: The consumption of long-chain omega-3 polyunsaturated fatty acids (n-3 PUFA) has been reported to have beneficial health effects, notably, by reducing plasma triglyceride levels. Nonetheless, a concomitant decrease in insulin sensitivity has also been observed, but is highly variable among subjects. Herein, we aimed to determine the importance of the genetic background in the interindividual variability of the insulin sensitivity response following an n-3 PUFA supplementation. Methods: A total of 210 participants completed a 6-week n-3 PUFA supplementation with 5 g/day of fish oil (providing 1.9–2.2 g of eicosapentaenoic acid + 1.1 g of docosahexaenoic acid). Insulin resistance was estimated by the homeostatic model assessment (HOMA-IR), and participants were further classified as high-risk or low-risk depending on their HOMA-IR change following the n-3 PUFA supplementation, as compared to pre-supplementation values. Genome-wide genotyping data were obtained for 138 participants using HumanOmni-5-Quad BeadChips containing 4,301,331 single nucleotide polymorphisms. A genome-wide association analysis (GWAS) was carried out between high-risk and low-risk participants. The population study was split into training (60%) and testing (40%) datasets to assess the predictive accuracy of a genetic risk score (GRS) constructed by summing the number of risk alleles. Results: Following the n-3 PUFA supplementation, 32 participants had increased HOMA-IR as compared to initial values and were classified as high risk (23.2%), whereas remaining subjects were classified as low risk (n = 106, 76.8%). A total of 8 loci had frequency differences between high-risk and low-risk participants at a suggestive GWAS association threshold (p value <1 × 10–5). After applying 10-fold cross validation, the GRS showed a significant association with the risk of increased HOMA-IR in the testing dataset (OR = 3.16 [95% CI, 1.85–7.14]), with a predictive accuracy of 0.85, and explained 40% of variation in HOMA-IR change. Conclusions: These results suggest that the genetic background has a relevant role in the interindividual variability observed in the insulin sensitivity response following an n-3 PUFA supplementation. Subjects being at risk of insulin sensitivity lowering following an n-3 PUFA supplementation may be identified using genetic-based precision nutrition approaches.","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":"13 1","pages":"32 - 42"},"PeriodicalIF":2.6,"publicationDate":"2019-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000504022","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43521115","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}
Bénédicte L. Tremblay, F. Guénard, B. Lamarche, L. Pérusse, M. Vohl
{"title":"Integrative Network Analysis of Multi-Omics Data in the Link between Plasma Carotenoid Concentrations and Lipid Profile","authors":"Bénédicte L. Tremblay, F. Guénard, B. Lamarche, L. Pérusse, M. Vohl","doi":"10.1159/000503828","DOIUrl":"https://doi.org/10.1159/000503828","url":null,"abstract":"Introduction: Carotenoids, which are a reliable biomarker of fruit and vegetable consumption, are positively associated with the lipid profile. Circulating carotenoid concentrations may interact with several omics profiles including genome, transcriptome, and epigenome. Few studies have used multi-omics approaches, and they rarely include environmental factors, such as diet. Objective: The objective of this observational study was to examine the potential role of multi-omics data in the interconnection between diet, represented by total carotenoids, and lipid profile using weighted gene correlation network analysis (WGCNA). Methods: Blood leukocyte DNA methylation levels of 472,245 CpG sites and whole blood gene expression levels of 18,160 transcripts were tested for associations with total carotenoid concentrations using regressions in 48 healthy subjects. WGCNA was used to identify co-omics modules and hub genes related to the lipid profile. Results: Among genes associated with total carotenoid concentrations, a total of 236 genes were identified at both DNA methylation and gene expression levels. Using WGCNA, six modules, consisting of groups of highly correlated genes represented by colors, were identified and linked to the lipid profile. Probes clustered in the turquoise and green modules correlated with plasma lipid concentrations. A total of 28 hub genes were identified. Conclusions: Genome-wide DNA methylation and gene expression levels were both associated with plasma total carotenoid concentrations. Several hub genes, mostly involved in lipid metabolism and inflammatory response with several genetic variants associated with plasma lipid concentrations, came out of the integrative analysis. This provides a comprehensive understanding of the interactive molecular system between carotenoids, omics, and plasma lipid profile.","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":"13 1","pages":"11 - 19"},"PeriodicalIF":2.6,"publicationDate":"2019-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000503828","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42598173","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":"Adiponectin Gene Variant rs266729 Interacts with Different Macronutrient Distribution of Two Different Hypocaloric Diets","authors":"D. D. de Luis, D. Primo, O. Izaola, R. Aller","doi":"10.1159/000503863","DOIUrl":"https://doi.org/10.1159/000503863","url":null,"abstract":"Background: The role of ADIPOQ gene variants in weight loss after different dietary fat amounts remains unclear. Objective: Our aim was to analyze the effects of ADIPOQ gene polymorphism rs266729 on metabolic changes after two different amounts of dietary fat in two hypocaloric diets. Design: A population of 283 obese patients was recruited in a randomized clinical trial with two diets: Diet HF (high-fat diet: 38% carbohydrates, 24% proteins, and 38% fats) versus Diet LF (low-fat diet: 53% carbohydrates, 20% proteins, and 27% fats). Before and after 3 months, an anthropometric evaluation, an assessment of nutritional intake, and a biochemical analysis were carried out. The variant of the ADIPOQgene was assessed by real-time PCR. Results: Weight loss was similar with both diets in both genotypes (CC vs. CG+GG). After dietary intervention with Diet HF, only subjects with CC genotype showed a significant improvement in insulin levels (–3.3 ± 0.6 vs. –1.8 ± 0.9 mU/L; p = 0.03) and the homeostasis model assessment for insulin resistance (HOMA-IR) (–1.3 ± 0.1 vs. –0.8 ± 0.2 units; p = 0.02). After Diet LF, subjects with CC genotype showed a significant improvement in total cholesterol levels (CC vs. CG+GG) (–15.3 ± 1.4 vs. –6.4 ± 1.3 mg/dL; p = 0.01), LDL cholesterol (–14.6 ± 1.8 vs. –6.4 ± 1.3 mg/dL; p = 0.01), insulin levels (–4.6 ± 1.0 vs. –1.6 ± 0.5 mU/L; p = 0.01), and HOMA-IR (–1.6 ± 0.1 vs. –1.0 ± 0.2 units; p = 0.02). Only subjects with CC genotype showed a significant increase of adiponectin levels after both diets (CC vs. CG+GG): Diet HF (10.6 ± 2.0 vs. 1.8 ± 1.0 ng/dL; p = 0.01) and Diet LF (16.1 ± 2.8 vs. 1.3 ± 1.0 ng/dL: p = 0.03). Conclusion: CC genotype of ADIPOQgene variantrs266729 was associated with a better metabolic response after both diets. Additionally, Diet LF produced a significant improvement in lipid profile in noncarriers of allele G.","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":"13 1","pages":"20 - 27"},"PeriodicalIF":2.6,"publicationDate":"2019-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000503863","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49384719","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":"Front & Back Matter","authors":"María Elizabeth Tejero Barrera","doi":"10.1159/000504004","DOIUrl":"https://doi.org/10.1159/000504004","url":null,"abstract":"","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":"1 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2019-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42772766","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}
E. Barrón-Cabrera, O. Ramos-López, Karina González-Becerra, J. Riezu-Boj, F. Milagro, E. Martínez-López, J. A. Martínez
{"title":"Epigenetic Modifications as Outcomes of Exercise Interventions Related to Specific Metabolic Alterations: A Systematic Review","authors":"E. Barrón-Cabrera, O. Ramos-López, Karina González-Becerra, J. Riezu-Boj, F. Milagro, E. Martínez-López, J. A. Martínez","doi":"10.1159/000503289","DOIUrl":"https://doi.org/10.1159/000503289","url":null,"abstract":"Background: Chronic diseases arise as a consequence of an unhealthy lifestyle primarily characterized by physical inactivity and unbalanced diets. Regular physical activity can improve health, and there is consistent evidence that these improvements may be the result of epigenetic modifications. Objective: To identify epigenetic modificationsas outcomes of exercise interventions related to specific metabolic alterations. Methods: The Preferred Reporting Items for Systematic Reviews and Meta-Analyses Protocols (PRISMA-P) methodology for manuscript research and preparation was followed using PubMed and EBSCO databases for literature review. Out of 2,638 articles identified, only 34 articles met the inclusion criteria. Results: The sections of the review were organized by metabolic alterations in which studies were grouped according to healthy, diseased, and trained individuals. Resistance exercise in humans induced epigenetic changes in pathways associated with energy metabolism and insulin sensitivity, contributing to healthy skeletal muscle. Endurance exercise also caused modifications in biomarkers associated to metabolic alterations through changes in DNA methylation and the expression of specific miRNAs. However, both resistance and endurance exercise are necessary to obtain a better physiological adaptation and a combination of both seems to be needed to properly tackle the increasing prevalence of non-communicable pathologies. Conclusion: Given the heterogeneity and complexity of the existing literature, it is currently not possible to propose a specific recommendation about the type, intensity, or duration of exercise that could be beneficial for different subsets of the population (healthy, diseased, and/or trained). Nevertheless, this review highlights the importance of exercise for health and shows the need to perform more research in this emerging area to identify epigenetic biomarkers that could serve as indicators of exercise adaptations.","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":"12 1","pages":"25 - 44"},"PeriodicalIF":2.6,"publicationDate":"2019-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000503289","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42980300","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}
C. Kuttner, R. Mancina, G. Wagenpfeil, F. Lammert, C. Stokes
{"title":"Four-Week Omega-3 Supplementation in Carriers of the Prosteatotic PNPLA3 p.I148M Genetic Variant: An Open-Label Study","authors":"C. Kuttner, R. Mancina, G. Wagenpfeil, F. Lammert, C. Stokes","doi":"10.1159/000502008","DOIUrl":"https://doi.org/10.1159/000502008","url":null,"abstract":"Background/Aims: The PNPLA3 loss-of-function variant p.I148M is a strong genetic determinant of nonalcoholic fatty liver disease. The PNPLA3 protein functions as an intracellular lipase in the liver, with a greater activity on unsaturated fatty acids. This study aimed to determine whether short-term supplementation with omega-3 fatty acids impacts hepatic steatosis differently in PNPLA3 p.148I wild-type individuals as compared to homozygous carriers of the PNPLA3 p.148M variant. Methods: Twenty subjects with hepatic steatosis (50% women, age 18–77 years) were included. Ten subjects homozygous for the PNPLA3 148M variant were matched to 10 wild-type individuals. The subjects received 4 g omega-3 fatty acids (1,840 mg eicosapentaenoic acid and 1,520 mg docosahexaenoic acid) a day for 4 weeks. Transient elastography with a controlled attenuation parameter (CAP) was used to quantify liver fat before and after the intervention. Body composition, fibrosis, liver function tests, serum free fatty acids (FFA) and glucose markers were compared. Results: Patients homozygous for the PNPLA3 p.148M variant (risk group) demonstrated no significant changes in CAP compared to baseline (284 ± 55 vs. 287 ± 65 dB/m) as did the control group (256 ± 56 vs. 262 ± 55 dB/m). While serum liver enzyme activities remained unchanged in both groups, the risk group displayed significantly (p = 0.02) lower baseline FFA concentrations (334.5 [range 281.0–431.0] vs. 564.5 [range 509.0–682.0] μmol/L), which markedly increased by 9.1% after the intervention. In contrast, FFA concentrations decreased significantly (p = 0.01) by 28.3% in the wild-type group. Conclusions: Short-term omega-3 fatty acid supplementation did not significantly alter hepatic steatosis. The nutrigenomic and metabolic effects of omega-3 fatty acids should be investigated further in carriers of the PNPLA3 148M risk variant.","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":"12 1","pages":"10 - 17"},"PeriodicalIF":2.6,"publicationDate":"2019-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000502008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42991143","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":"Front & Back Matter","authors":"B. Koletzko, R. Shamir, D. Turck, M. Phillip","doi":"10.1159/000502462","DOIUrl":"https://doi.org/10.1159/000502462","url":null,"abstract":"169 13th Congress of the International Society of Nutrigenetics/Nutrigenomics (ISNN) July 12–13, 2019, Cambridge, UK Guest Editors: Kohlmeier, M. (Kannapolis, NC, USA); Chirita, A. (Timisoara, Romania); Beckett, E. (New Lambton Heights, NSW, Australia); Angelino, D. (Parma, Italy); Del Rio, D. (Parma, Italy); Niculescu, M. (Hillsborough, NC, USA) 168 Erratum 194","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2019-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47535023","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":"Contents","authors":"Iwona Rudkowska, M. E. Tejero","doi":"10.1159/000502164","DOIUrl":"https://doi.org/10.1159/000502164","url":null,"abstract":"Selected Abstracts from the 19 3rd European Summer School on Nutrigenomics Jesi, June 25–29, 2018","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":"11 1","pages":"I - IV"},"PeriodicalIF":2.6,"publicationDate":"2019-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000502164","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47353448","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}