Population-based differences in immune system response contribute to an increased risk of schizophrenia in African migrants?

2018 ◽  
Vol 29 (3) ◽  
pp. 347-353 ◽  
Author(s):  
Milica J. Nesic ◽  
Nadja P. Maric
Keyword(s):  
Immune System ◽  
African Descent ◽  
African Ancestry ◽  
Population Based ◽  
European Ancestry ◽  
System Response ◽  
Increased Risk ◽  
Inflammatory Phenotype ◽  
Research Population ◽  
The One

AbstractAmong the highest incidences of schizophrenia is the one documented in second-generation migrants of African descent in the Western countries. Interestingly, people of African and European ancestry demonstrate significant genetic-based differences in immune system regulation and response. As a result, the pro-inflammatory phenotype is more pronounced in people of African descent than it is in Europeans. At the same time, the role of the immune system in the etiology of schizophrenia is gaining increased recognition. Here, we propose that the population-specific genetic variation within the immune system interacts with unfavourable environments to contribute to a higher risk of schizophrenia in people of African ancestry. Our hypothesis is supported by recent findings from two separate fields of research−population genetics and psychoneuroimmunology. Moreover, we highlight the need to include African populations in genetic studies of schizophrenia.

Abstract 66: Causal Associations Between Genetically-determined Smoking and Risk of Subarachnoid Hemorrhage

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Julian N Acosta ◽  
Cameron Both ◽  
Stacy Brown ◽  
Audrey Leasure ◽  
Kevin N Vanent ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Smoking Behavior ◽  
Population Based ◽  
European Ancestry ◽  
Ratio Method ◽  
Polygenic Risk Score ◽  
Primary Analysis ◽  
Increased Risk ◽  
Secondary Analyses ◽  
Genetically Determined

Introduction: Animal and observational studies indicate that smoking is a risk factor for aneurysm formation and rupture, leading to subarachnoid hemorrhage (SAH). However, a definitive causal relationship between smoking and SAH has not been established. We leveraged the causal properties of mutation-disease associations to test the hypothesis that smoking is causally linked to SAH. Methods: We conducted a one-sample Mendelian Randomization (MR) study within the UK Biobank, a prospective, population-based observational study. We restricted the analysis to study participants with genetically-confirmed European ancestry. SAH cases were ascertained using previously validated codes. As the instrument, we built a polygenic risk score (PRS) using independent (R2<0.1) genetic variants known to be associated (p<5x10-8) with smoking. For the primary MR analysis, we implemented the ratio method using the estimates obtained from testing the PRS for association with risk of SAH and smoking. In secondary analyses, we implemented the inverse-variance weighted (IVW) and weighted median (WM) methods. Pleiotropy was assessed via the MR-Egger approach. Results: We included a total of 408,622 individuals in this study (mean age 57 [SD 8], female sex 220,944 [54%]). Of these, 132,568 (32%) ever smoked regularly and 904 (0.22%) had an SAH. Each additional standard deviation of the smoking PRS was associated with a 9% increased risk of SAH (OR 1.09, 95%CI 1.03-1.17; p=0.006) and 21% increased risk of smoking (OR 1.21, 95%CI 1.2-1.21; p=1x10-16). In the primary analysis, genetically-determined smoking was associated with a 63% increase in risk of SAH (OR 1.63, 95%CI 1.15-2.30; p=0.006). Secondary analyses using the IVW method (OR 1.57, 95%CI 1.13-2.17; p=0.007) and the WM method (OR 1.74, 95%CI 1.06-2.86; p=0.028) yielded comparable results. There was no significant pleiotropy (MR-Egger intercept p=0.38). Conclusion: Genetically-determined smoking is strongly associated with the risk of SAH. These findings provide evidence for a causal link between smoking and the occurrence of this often-debilitating condition. Interventions aimed at reducing smoking behavior could offer significant benefits, especially to those at high risk of SAH.

Genetic and treatment risks for diabetes mellitus (DM) in survivors of childhood cancer: A report from the Childhood Cancer Survivor Study (CCSS) and St. Jude Lifetime (SJLIFE) cohorts.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. 10014-10014
Author(s):  
Melissa A. Richard ◽  
Sogol Mostoufi-Moab ◽  
Nisha Rathore ◽  
Austin L. Brown ◽  
Stephen J. Chanock ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cancer Survivors ◽  
Cancer Treatment ◽  
Childhood Cancer ◽  
Regulatory Region ◽  
Childhood Cancer Survivors ◽  
Population Based ◽  
European Ancestry ◽  
Radiation Group ◽  
Increased Risk

10014 Background: Childhood cancer survivors face increased risk for DM, a polygenic trait also attributable to cancer treatment exposures, particularly abdominal radiation. We aimed to characterize the role of genetic and treatment risk factors for DM among two large cohorts of childhood cancer survivors. Methods: We performed a nested case-control genome-wide association study for DM managed with oral medications in the original CCSS cohort (diagnosed 1970-1986). Logistic regression was conducted in the total sample (N = 5083) and stratified by 1) European ancestry (EA) and 2) abdominal radiation. Replication of suggestive variants (P < 1×10-7) using Fisher’s exact test was performed in independent cohorts: i) CCSS expansion diagnosed 1987-1999 (N = 2588) and ii) SJLIFE diagnosed 1962-2012 (N = 2182). To evaluate the effect of cancer treatment on the background genetic predisposition to DM, we estimated standardized effect sizes (Z’) among EA survivors in each abdominal radiation group for 398 index variants from the largest population-based EA DM study. Radiation group Z’ estimates were compared using linear regression. Results: In the original CCSS cohort we identified nine variants associated with DM and provide further support for four linked variants in the ERCC6L2 locus. Among all survivors, the rs55849673-A allele was associated with increased odds for DM among survivors in the original CCSS cohort (minor allele frequency [MAF]-cases = 0.055; MAF-controls = 0.024; adjusted odds ratio [aOR] = 2.9, 95% CI: 2.0-4.2, P = 3.7×10-8). Allele frequencies were consistent in the CCSS expansion (MAF-cases = 0.075; MAF-controls = 0.028; P = 0.07) and SJLIFE (MAF-cases = 0.036; MAF-controls = 0.027; P = 0.5). Additionally, rs55849673-A estimates were consistent among EA survivors and stronger among survivors not treated with abdominal radiation (MAF-cases = 0.052; MAF-controls = 0.021; aOR = 3.6, P = 1.6×10-6). Notably, in the CCSS expansion all rs55849673-A EA carriers who developed DM did not receive abdominal radiation (MAF-cases = 0.1; MAF-controls = 0.026; P = 0.04). More broadly, the Z’ of population-based DM index variants were 78% lower in survivors treated with abdominal radiation than survivors not treated with abdominal radiation (beta = 0.22; P = 0.01), indicating the background genetic risk for DM may be altered by treatment. Conclusions: We provide evidence for a novel locus of DM in childhood cancer survivors. This locus is a regulatory region associated with expression of ERCC6L2, a gene implicated in an East Asian population-based DM study. Taken together, our findings support the overwhelming effect of abdominal radiation on DM risk in childhood cancer survivors, relative to other risk factors, and provide insight on a genetic locus that may be useful for DM risk prediction in the context of cancer treatment.

scholarly journals SURVIVAL ADVANTAGE OF APOE2

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S621-S621
Author(s):  
Sudha Seshadri
Keyword(s):  
Lower Risk ◽  
Large Population ◽  
Population Based ◽  
European Ancestry ◽  
Aggregated Data ◽  
Risk Of Death ◽  
Apoe Ε4 ◽  
Increased Risk ◽  
Ε4 Allele

Abstract Apolipoprotein E is a glycoprotein mediator and regulator of lipid transport and uptake. The APOE-ε4 allele has been associated with higher risk of Alzheimer’s disease and of mortality, but the effect of the less prevalent APOE-ε2 on survival remains elusive. We aggregated data of 38,537 individuals of European ancestry (mean age 65.5 years; 55.6% women) from six large population-based cohorts to determine the association of APOE-ε2, with survival in the general population. During a mean follow-up of 11.7 years, 17,021 individuals died. Compared with homozygous APOE-ε3 carriers, APOE-ε2 carriers were at lower risk of death (hazard ratio,95% confidence interval: 0.94,0.90-0.99; P=1.1*10-2), whereas APOE-ε4 carriers were at increased risk (HR 1.17,1.12-1.21; P=2.8*10-16). Risk was lowest for homozygous APOE-ε2 (HR 0.89,0.74-1.08), and highest for homozygous APOE-ε4 (HR 1.52,1.37-1.70). Results did not differ by sex. The association was unaltered after adjustment for baseline LDL or cardiovascular disease. Larger, multiethnic collaborations are ongoing.

scholarly journals Two genetic variants explain the association of European ancestry with multiple sclerosis risk in African-Americans

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Nathan Nakatsuka ◽  
Nick Patterson ◽  
Nikolaos A. Patsopoulos ◽  
Nicolas Altemose ◽  
Arti Tandon ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
African American ◽  
African Americans ◽  
Odds Ratio ◽  
African Ancestry ◽  
Epidemiological Studies ◽  
Chromosome 1 ◽  
European Ancestry ◽  
Increased Risk ◽  
West Africans

Abstract Epidemiological studies have suggested differences in the rate of multiple sclerosis (MS) in individuals of European ancestry compared to African ancestry, motivating genetic scans to identify variants that could contribute to such patterns. In a whole-genome scan in 899 African-American cases and 1155 African-American controls, we confirm that African-Americans who inherit segments of the genome of European ancestry at a chromosome 1 locus are at increased risk for MS [logarithm of odds (LOD) = 9.8], although the signal weakens when adding an additional 406 cases, reflecting heterogeneity in the two sets of cases [logarithm of odds (LOD) = 2.7]. The association in the 899 individuals can be fully explained by two variants previously associated with MS in European ancestry individuals. These variants tag a MS susceptibility haplotype associated with decreased CD58 gene expression (odds ratio of 1.37; frequency of 84% in Europeans and 22% in West Africans for the tagging variant) as well as another haplotype near the FCRL3 gene (odds ratio of 1.07; frequency of 49% in Europeans and 8% in West Africans). Controlling for all other genetic and environmental factors, the two variants predict a 1.44-fold higher rate of MS in European-Americans compared to African-Americans.

scholarly journals Lynch Syndrome–Associated Variants and Cancer Rates in an Ancestrally Diverse Biobank

2020 ◽  
pp. 1429-1444
Author(s):  
Rachel E. Rosenblum ◽  
Celina Ang ◽  
Sabrina A. Suckiel ◽  
Emily R. Soper ◽  
Meenakshi R. Sigireddi ◽  
...  
Keyword(s):  
New York ◽  
New York City ◽  
Lynch Syndrome ◽  
York City ◽  
Sequence Data ◽  
African Ancestry ◽  
European Ancestry ◽  
Electronic Health Record Data ◽  
Increased Risk ◽  
Cancer Rates

PURPOSE Limited data are available on the prevalence and clinical impact of Lynch syndrome (LS)–associated genomic variants in non-European ancestry populations. We identified and characterized individuals harboring LS-associated variants in the ancestrally diverse Bio Me Biobank in New York City. PATIENTS AND METHODS Exome sequence data from 30,223 adult Bio Me participants were evaluated for pathogenic, likely pathogenic, and predicted loss-of-function variants in MLH1, MSH2, MSH6, and PMS2. Survey and electronic health record data from variant-positive individuals were reviewed for personal and family cancer histories. RESULTS We identified 70 individuals (0.2%) harboring LS-associated variants in MLH1 (n = 12; 17%), MSH2 (n = 13; 19%), MSH6 (n = 16; 23%), and PMS2 (n = 29; 41%). The overall prevalence was 1 in 432, with higher prevalence among individuals of self-reported African ancestry (1 in 299) than among Hispanic/Latinx (1 in 654) or European (1 in 518) ancestries. Thirteen variant-positive individuals (19%) had a personal history, and 19 (27%) had a family history of an LS-related cancer. LS-related cancer rates were highest in individuals with MSH6 variants (31%) and lowest in those with PMS2 variants (7%). LS-associated variants were associated with increased risk of colorectal (odds ratio [OR], 5.0; P = .02) and endometrial (OR, 30.1; P = 8.5 × 10−9) cancers in Bio Me. Only 2 variant-positive individuals (3%) had a documented diagnosis of LS. CONCLUSION We found a higher prevalence of LS-associated variants among individuals of African ancestry in New York City. Although cancer risk is significantly increased among variant-positive individuals, the majority do not harbor a clinical diagnosis of LS, suggesting underrecognition of this disease.

scholarly journals Differences in stillbirth and infant mortality by maternal country of birth and descent in Denmark

2019 ◽  
Vol 29 (Supplement_4) ◽  
Author(s):  
T Damsted Rasmussen ◽  
S F Villadsen ◽  
S Smith Jervelund ◽  
A M Nybo Andersen
Keyword(s):  
Infant Mortality ◽  
Infant Death ◽  
Minority Groups ◽  
Immigrant Women ◽  
Population Based ◽  
Host Population ◽  
International Studies ◽  
Country Of Birth ◽  
Increased Risk ◽  
The One

Abstract International studies have reported inequalities in stillbirth and infant death among ethnic minority groups compared to the host population. The same tendencies have been reported in Denmark. We investigated differences in the risk of stillbirth and infant death among offspring of immigrants and descendants in Denmark, compared to the risk among women of Danish origin. The population-based register study included all live births and stillbirths with gestational age ≥ 22 weeks delivered by women of Danish origin, immigrant women and descendants in Denmark in the period 2005-2016. The study population was restricted to deliveries by women of Danish origin and country groups of immigrants and descendants with more than 2000 deliveries during the study period (n = 792 705). Logistic regression analysis adjusted for year of birth was used to estimate odds ratios (OR) with 95 % confidence intervals (CI) of the association between maternal country of birth and country of descent and respectively stillbirth and infant mortality. Immigrant mothers from Turkey, Iraq, Somalia, Pakistan, Afghanistan, Syria and Iran had a statistically significant elevated OR of stillbirth compared to women of Danish origin; adjusted OR`s ranging 1.45-2.93. Danish-born women with respectively Turkish (OR 1.44, 95 % CI 1.00-2.07) and Pakistani descent (OR 2.32, 95 % CI 1.50-3.60) had an increased risk of stillbirth similar to the one among immigrant women with the same origin. For infant death, we found increased O&Racute;s among immigrant women from Turkey (OR 1.76, 95 % CI 1.28-2.40), Somalia (OR 1.84, 95 % CI 1.31-2.58), Lebanon (OR 1.63, 95 % CI 1.03-2.60) and Pakistan (OR 2.85, 95 % CI 2.05-3.96). Only women of Pakistani descent (2.22, 95 % CI 1.28-3.86) had a statistically significant increased risk of infant death. These findings show substantial differences in stillbirth and infant death according to maternal country of birth and descent in Denmark during the first decades of the 21st century.

Nicotine metabolism predicted by CYP2A6 genotypes in relation to smoking cessation: A systematic review

2021 ◽  
Author(s):  
Stephanie K Jones ◽  
Bethany J Wolf ◽  
Brett Froeliger ◽  
Kristin Wallace ◽  
Matthew J Carpenter ◽  
...  
Keyword(s):  
Smoking Cessation ◽  
African Ancestry ◽  
Population Based ◽  
European Ancestry ◽  
Nicotine Metabolism ◽  
Quit Smoking ◽  
End Of Treatment ◽  
Major Interest ◽  
Normal Metabolism ◽  
Asian People

Abstract Introduction Identifying genetic factors associated with smoking cessation could inform precision cessation interventions. Of major interest is genetic variation in nicotine metabolism, largely predicted by CYP2A6 variations. Methods We conducted a systematic literature review to summarize the population-based evidence of the association between CYP2A6 and smoking cessation. In the 12 studies meeting the inclusion criteria, the known functional metabolic effect of CYP2A6 variants was used to classify nicotine metabolism as normal (&gt;75% metabolic activity), intermediate (50.1 - 75% activity), slow (25 - 50% activity), and poor (&lt;25% activity). Summary odds ratios of smoking cessation were calculated across metabolic groups, stratified by ancestry and whether participants received pharmacotherapy or placebo/no treatment. Results Among untreated people of European ancestry (n = 4 studies), those with CYP2A6 reduced metabolism were more likely to quit smoking than those with normal metabolism [Summary OR = 2.05, 95% CI 1.23 – 3.42] and the likelihood of cessation increased as nicotine metabolism decreased. Nicotine replacement therapy attenuated the association at end-of-treatment, while bupropion modified the association such that intermediate/slow metabolizers were less likely to quit than normal metabolizers [Summary OR = 0.86, 95% CI 0.79 – 0.94]. Among untreated Asian people (n = 3 studies), results differed compared to those with European ancestry: those with slow metabolism were less likely to have quit smoking than normal metabolizers [Summary OR = 0.52, 95% CI 0.38 – 0.71]. Evidence for people of African ancestry (n = 1 study) suggested the CYP2A6 association with cessation may differ compared to those of European ancestry. Implications Most studies included in this review were of European ancestry populations; these showed slower nicotine metabolism was associated with increased likelihood of smoking cessation in a dose-related manner. Pharmacotherapy appeared to attenuate or modify this association among people of European ancestry, but it is unclear whether the change in the association remains consistent after treatment ceases. This finding has implications for precision medicine cessation interventions. Based on only a few studies of people of Asian or African ancestry, the association between CYP2A6 variants and cessation may differ from that observed among those of European ancestry, but more evidence is needed.

scholarly journals Prevalence of IGFBP3, NOS3 and TCF7L2 Polymorphisms and Their Association With Hypertension: A Population-Based Study With Brazilian Women of African Descent

2020 ◽  
Author(s):  
Abel Lira ◽  
Nancy Vasconcelos ◽  
Tamara Santos ◽  
Luisa Duarte ◽  
Monica Assunção ◽  
...  
Keyword(s):  
African Descent ◽  
African Ancestry ◽  
Prevalence Ratio ◽  
Population Based ◽  
Cross Sectional Study ◽  
Allelic Discrimination ◽  
Cross Sectional ◽  
Selection Of Variables ◽  
Women Of African Descent ◽  
Measure Of Association

Abstract Background: African ancestry seems to be a risk factor for hypertension; however, few genetic studies have addressed this issue. This study aimed to investigate the prevalence of polymorphisms NOS3; rs1799983, IGFBP3; rs11977526 and TCF7L2; rs7903146 in Brazilian women of African descent and their association with hypertension.Methods: This is a cross-sectional study with a sample of 1021 women (19–59 years old) from the quilombola communities of Alagoas (Brazil). Demographic, socioeconomic, lifestyle, anthropometric, biochemical, and blood pressure data were collected. DNA was extracted from mucosa epithelial cells of the participants’ cheek. Genotyping was performed by PCR allelic discrimination. Prevalence ratio (PR) was the measure of association, calculated by Poisson regression, with a hierarchical selection of variables.Results: The prevalences of the less frequent genotypes were 26.5% TT genotype of NOS3; rs1799983, 16.7% AA genotype of IGFBP3; rs11977526, and 18.3% TT genotype of TCF7L2; rs7903146. For these conditions, the prevalence of hypertension and PR (adjusted) relatively to the ancestral genotype were, respectively: 52.0% vs 24.5% (PR=1.54; p<0.001), 62.0% vs 24.1% (PR=1.59; p<0.001), and 38.9% vs 27.9% (PR=0.86; p=0.166). Associations with hypertension were statistically significant, except for the TCF7L2; rs7903146 polymorphism, after adjusted analysis. Conclusions: Brazilian Afro-descendant women with the TT genotype for the NOS3 gene and the AA genotype for the IGFBP3 gene are more susceptible to hypertension. The understanding of underlying mechanisms involving the pathogenesis of hypertension can motivate research for the development of new therapeutic targets related to nitric oxide metabolism and the management of oxidative stress.

Abstract MP67: Fatty Acid Desaturase Gene-induced Omega-3 Deficiency In Amerindian-Ancestry Hispanic Populations

Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Sarah Blomquist ◽  
Dawn Coletta ◽  
Lawrence J Mandarino ◽  
Brian Hallmark ◽  
Chaojie Yang ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Disease Risk ◽  
African Ancestry ◽  
Strong Association ◽  
Fatty Acid Desaturase ◽  
European Ancestry ◽  
Increased Risk ◽  
Hispanic Populations ◽  
Pufa Biosynthesis

Hispanic populations in the US have increased risk of obesity, elevated circulating triglycerides, nonalcoholic fatty liver disease, and diabetes. Our previous studies suggest that ancestry-related differences in the frequency of variants in the fatty acid desaturase ( FADS) gene cluster in the context of the modern Western diet can lead to inadequate circulating and tissues levels of n-3 long-chain (LC-; ≥ 20 carbons) polyunsaturated fatty acids (PUFA); these deficiencies in turn have the capacity to increase metabolic disease risk. Specifically, we and others have demonstrated Amerindian (AI)-Ancestry populations have high frequencies of FADS gene variants that may lead to less efficient n-3 LC-PUFA biosynthesis. To test this hypothesis, concentrations of fatty acids, including LC-PUFAs in plasma phospholipids were analyzed in 1,102 Hispanic American participants from Multi-Ethnic Study of Atherosclerosis (MESA) cohort, which represent six Hispanic subgroups based on self-reported region of origin: Central America, South America, Mexico, Cuba, Dominican Republic, and Puerto Rico. These data revealed a striking inverse relationship between genome-wide AI-ancestry and levels of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Additional analyses revealed that the genotype at FADS SNP rs174537, for which the frequency of the T allele increases with AI-ancestry, could primarily explain the associations. There also was a strong association between the number of T alleles (additive model) at rs174537 and circulating triglycerides (18.5 mg/dL per T allele; P =2.0 x 10 -5 ) as well as an important marker of vascular inflammation sICAM-1 (β=12.7 ng/mL, P =0.02). We also genotyped the FADS SNP, rs174537, in a separate adult Arizona Hispanic cohort (Arizona Insulin Resistance [AIR] registry) and compared the FADS genotypic frequencies with other racial/ethnic groups. Importantly, the TT genotype associated with limited LC-PUFA biosynthesis ranges from <1% in African-Ancestry populations to 40.2% in AI-Ancestry Hispanics in the AIR Registry, with ~11 % in European-Ancestry populations. These data demonstrate that high AI-ancestry populations have a dramatically higher frequency of the TT genotype versus African and European populations. Importantly similar to MESA, there also was a significant association between the number of T alleles and plasma triglycerides (p = 0.0036; GG = 125±8.18 mg/dl, GT = 135±5.63 mg/dl, TT = 143±5.58 mg/dl) again suggesting the AI-associated TT genotype places this population at higher risk of hypertriglyceridemia. Together, these data reveal that FADS gene*dietary PUFA interactions give rise to n-3 LC-PUFA deficiencies and may enhance metabolic and inflammatory diseases in a large proportion of individuals in AI-Ancestry Hispanic populations.

scholarly journals A Dynamic Simulation of the Immune System Response to Inhibit And Eliminate Abnormal Cells

Symmetry ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 572 ◽  
Author(s):  
S. A. Alharbi ◽  
A. S. Rambely
Keyword(s):  
Immune System ◽  
Point Of View ◽  
System Response ◽  
Recovery Stage ◽  
Food Pyramid ◽  
Increased Risk ◽  
Abnormal Cells ◽  
Unhealthy Diet ◽  
Risk Of Cancer ◽  
The Relationship

Diet has long been considered a risk factor related to an increased risk of cancer. This challenges us to understand the relationship between the immune system and diet when abnormal cells appear in a tissue. In this paper, we propose and analyze a model from the point of view of a person who follows a healthy diet, i.e., one correlated to the food pyramid, and a person who follows an unhealthy diet. Normal cells and immune cells are used in the design of the model, which aims to describe how the immune system functions when abnormal cells appear in a tissue. The results show that the immune system is able to inhibit and eliminate abnormal cells through the three following stages: the response stage, the interaction stage, and the recovery stage. Specifically, the failure of the immune system to accomplish the interaction stage occurs when a person follows an unhealthy diet. According to the analysis and simulation of our model, we can deduce that dietary pattern has a significant impact on the functioning of the immune system.

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