Biomedical subjects

Li Jin

Publications and source records attributed to Li Jin.

At least 19 recordsLinked to original sources

PubMed2026

Meta-ERS: an exposome-based risk score using non-genetic factors to guide osteoporosis prevention.

BACKGROUND: Osteoporosis is influenced by both genetic and environmental factors, yet the relative contribution of the exposome remains unclear. This study aimed to systematically identify non-genetic exposures related to osteoporosis and develop an exposome risk score (ERS) to evaluate individual osteoporosis susceptibility. METHODS: We conducted an exposome-wide analysis of 477,792 UK Biobank participants to identify key exposures associated with osteoporosis. The selected exposures were combined into a weighted Meta-ERS and validated in the Scotland/Wales cohort. The Meta-ERS was further compared with polygenic risk scores (PRS) and linked to plasma proteomics to explore underlying biological pathways. RESULTS: We identified 41 independent non-genetic exposures spanning socioeconomic status, mental health, sleep, diet, smoking, physical activity, environment, and marital status, with socioeconomic status and mental health emerging as the most significant drivers. Based on the identified exposures, we constructed eight domain-specific exposure risk scores and integrated them into a weighted Meta-ERS. The Meta-ERS (R2 = 5.1%; Proportion of Chi-Square = 14.3%) demonstrated an ability to explain osteoporosis variation that was on par with polygenic risk scores (R2 = 4.8%; Proportion of Chi-Square = 12.0%). Importantly, modifying unfavorable exposures mitigated the negative effect of PRS on osteoporosis, particularly among high PRS individuals (1.5- to 1.8-fold greater absolute risk reduction than in those with low PRS). Proteomic analyses further revealed potential mechanisms through which the exposome influences osteoporosis, including hormonal regulation, inflammation, ossification, muscle development, lipid metabolism, and accelerated bone aging. Among these, growth/differentiation factor 15 was identified as a key mediator protein, with a mediation proportion of 13.13%-36.52%. CONCLUSIONS: The Meta-ERS facilitates the quantification of individual osteoporosis risk and identifies modifiable exposures for targeted prevention. Its application can enable personalized risk stratification and guide lifestyle or environmental interventions.

Aged↗

PubMed2026

Proteomics-driven discovery of intervention windows and risk subtypes in osteoporosis: A prospective cohort study.

Given the limited feasibility of population-wide bone mineral density screening and the infrequency of long-term monitoring in healthy individuals, identifying the window for early intervention and the populations to be prioritized for screening is critical. This study aimed to identify intervention windows for osteoporosis and to determine potential high-risk subtypes within the healthy population. Based on proteomic data from 41,408 healthy adults, we conducted the DE-SWAN method to identify change peaks in plasma protein during the pre-diagnostic osteoporosis phase, and employed finite Gaussian mixture model-based clustering to delineate high-risk subtypes of osteoporosis. We identified 122 protein biomarkers significantly associated with osteoporosis risk throughout the follow-up period. Importantly, we identified two critical peaks occurring approximately 10 and 6 years before diagnosis, with the former enriched in immune-related pathways and the latter prominently involving responses to retinoic acid and glucocorticoids. Furthermore, one high-risk subtype for osteoporosis was identified in both males and females, termed the Frailty and Obesity Subtype. This subtype is characterized by a high degree of frailty and obesity, accompanied by a significantly elevated risk of both osteoporosis and fractures. Finally, we developed a predictive model comprising 10 proteins for identifying high-risk subtypes of osteoporosis, which demonstrated better performance than the traditional risk factor model (AUC: 0.743 vs. 0.680). Our findings demonstrate that proteomic profiling can reveal early molecular changes and identify high-risk subtypes years before clinical onset, providing a foundation for screening and precision prevention of osteoporosis.

Proteomics↗

PubMed2007

Evidence for linkage of red blood cell size and count: genome-wide scans in the Framingham Heart Study.

Red blood cell (RBC) count and size are major criteria for evaluating anemia and related hematology disease diagnoses. While environmental factors influence RBC count (RBCC) and size, mean corpuscular volume (MCV), and mean corpuscular hemoglobin (MCH), studies have indicated that each of these measures has a substantial genetic component. So far, no linkage analysis or genome scan has been reported. We carried out 10 cM genome-wide scans on RBCC, MCV, and MCH in a community-based Caucasian cohort, the Framingham Heart Study, using 325 pedigrees with 1,144 individuals genotyped and phenotyped. Using variance-component linkage methods, heritabilities were estimated as 56, 52, and 52% after covariate adjusted for RBCC, MCV, and MCH, respectively. For RBCC, we found a maximum LOD score of 3.2 on chromosome 19, 24 cM (7.0 Mbp). Near this region, there lie a few important candidate genes, including erythropoietin receptor and erythroid Krüppel-like factor. For linkage analyses for MCV and MCH, there were coinciding maximized LOD scores on chromosome 11, 9 cM (5.2 Mbp) with values of 3.8 and 3.6, respectively. Under the peak resides the hemoglobin beta cluster - several beta-like genes, which are important candidates for RBC size. In subsequent analyses, we excluded individuals with low MCV to assess the possible influence of beta-thalassemia carriers, and there continued to be evidence for linkage in the same region on chromosome 11p15 (LOD scores of 2.6 and 2.7 for MCV and MCH, respectively). For MCV, we also identified a new region on chromosome 6q24 with a LOD score of 2.9. These findings suggest that further studies are warranted to identify potential causal genetic variants for RBC size and count and related erythrocyte indices.

Adolescent↗

PubMed2006

Effect of mu-opioid receptor gene polymorphisms on heroin-induced subjective responses in a Chinese population.

BACKGROUND: Genetic factors that influence subjective responses to drug use (such as euphoria) contribute to the risk of addiction. mu-opioid receptor is the molecular target of heroin mediating its effects in both pain relief and euphoria. METHODS: To evaluate the association of mu-opioid receptor gene (OPRM1) variants with heroin-induced positive responses on first use, we studied 336 Chinese Han heroin addicts recruited in Shanghai and divided heroin addicts into two groups (positive vs. negative) according to the self-reporting feeling on first use. Association analyses with the genotypes and alleles in nine tagging single nucleotide polymorphisms (tSNPs) in OPRM1 with subjective responses were performed. Similar analysis with haplotypes of these tSNPs was also performed. RESULTS: Allele frequencies of three tSNPs were significantly different between the positive and negative groups. They were rs696522 (odds ratio [OR] = 3.06, p = .0013), rs1381376 (OR = 3.16, p = .0008), and rs3778151 (OR = 3.12, p = .0004). Such association remains after adjustment for demographic covariates and for multiple testing. The subjects with heroin-induced positive responses on first use consumed more drugs than the negative group (Mann-Whitney U = 224.0, Wilcoxon W = 16334.0, p <or= .0001). CONCLUSIONS: Self-reported positive responses on first use of heroin were found to be associated with OPRM1. The findings suggest that heroin-induced positive responses are likely associated with more heroin consumption.

Adult↗

PubMed2006

Test for interaction between two unlinked loci.

Despite the growing consensus on the importance of testing gene-gene interactions in genetic studies of complex diseases, the effect of gene-gene interactions has often been defined as a deviance from genetic additive effects, which is essentially treated as a residual term in genetic analysis and leads to low power in detecting the presence of interacting effects. To what extent the definition of gene-gene interaction at population level reflects the genes' biochemical or physiological interaction remains a mystery. In this article, we introduce a novel definition and a new measure of gene-gene interaction between two unlinked loci (or genes). We developed a general theory for studying linkage disequilibrium (LD) patterns in disease population under two-locus disease models. The properties of using the LD measure in a disease population as a function of the measure of gene-gene interaction between two unlinked loci were also investigated. We examined how interaction between two loci creates LD in a disease population and showed that the mathematical formulation of the new definition for gene-gene interaction between two loci was similar to that of the LD between two loci. This finding motived us to develop an LD-based statistic to detect gene-gene interaction between two unlinked loci. The null distribution and type I error rates of the LD-based statistic for testing gene-gene interaction were validated using extensive simulation studies. We found that the new test statistic was more powerful than the traditional logistic regression under three two-locus disease models and demonstrated that the power of the test statistic depends on the measure of gene-gene interaction. We also investigated the impact of using tagging SNPs for testing interaction on the power to detect interaction between two unlinked loci. Finally, to evaluate the performance of our new method, we applied the LD-based statistic to two published data sets. Our results showed that the P values of the LD-based statistic were smaller than those obtained by other approaches, including logistic regression models.

Alleles↗

PubMed2006

A shared Y-chromosomal heritage between Muslims and Hindus in India.

Arab forces conquered the Indus Delta region in 711 AD: and, although a Muslim state was established there, their influence was barely felt in the rest of South Asia at that time. By the end of the tenth century, Central Asian Muslims moved into India from the northwest and expanded throughout the subcontinent. Muslim communities are now the largest minority religion in India, comprising more than 138 million people in a predominantly Hindu population of over one billion. It is unclear whether the Muslim expansion in India was a purely cultural phenomenon or had a genetic impact on the local population. To address this question from a male perspective, we typed eight microsatellite loci and 16 binary markers from the Y chromosome in 246 Muslims from Andhra Pradesh, and compared them to published data on 4,204 males from East Asia, Central Asia, other parts of India, Sri Lanka, Pakistan, Iran, the Middle East, Turkey, Egypt and Morocco. We find that the Muslim populations in general are genetically closer to their non-Muslim geographical neighbors than to other Muslims in India, and that there is a highly significant correlation between genetics and geography (but not religion). Our findings indicate that, despite the documented practice of marriage between Muslim men and Hindu women, Islamization in India did not involve large-scale replacement of Hindu Y chromosomes. The Muslim expansion in India was predominantly a cultural change and was not accompanied by significant gene flow, as seen in other places, such as China and Central Asia.

Arabs↗

PubMed2006

Poly(gamma,L-glutamic acid)-cisplatin conjugate effectively inhibits human breast tumor xenografted in nude mice.

An easily administered cis-dichlorodiammineplatinum (II) (CDDP) formulation with less toxicity and greater antitumor effect would be extremely valuable. We describe PGA-CDDP, a water-soluble CDDP derivative. The hydrolyzed gamma-PGA has a molecular weight between 45 and 60 kDa, and is a water-soluble, biodegradable, and nontoxic polymer produced by microbial fermentation. CDDP can be released from the resulting conjugate in PBS: there was initially a burst release during the first 6h, followed by sustained release. In vitro, PGA-CDDP was less potent than free CDDP at inhibiting cell growth in the Bcap-37 cell line. PGA-CDDP was given as 3 doses at an equivalent CDDP dose of 4 or 12 mg/kg with 2-day intervals between injections to Bcap-37-grafted mice. This treatment showed stronger antitumor activity and was less toxic than CDDP in vivo. Antitumor activity assays demonstrated that the PGA-CDDP conjugate treatment had significantly higher antitumor activity than control PBS treatment (P<0.01). PGA-CDDP also increased the survival of mice bearing Bcap-37 cells with reference to PBS treatment or free CDDP treatment. Furthermore, mice treated with PGA-CDDP (4 mg/kg, administered on day 0 and 5) showed no body weight loss (P>0.05 with respect to PBS treatment), whereas free CDDP treatment at the same dose caused a body weight loss of 20-30% (P<0.001). These findings suggest that PGA produced by microbial fermentation may be used as an effective drug carrier for CDDP and that PGA-CDDP may have potential applications in the treatment of human breast cancer.

Animals↗

PubMed2006

Nonlinear tests for genomewide association studies.

As millions of single-nucleotide polymorphisms (SNPs) have been identified and high-throughput genotyping technologies have been rapidly developed, large-scale genomewide association studies are soon within reach. However, since a genomewide association study involves a large number of SNPs it is therefore nearly impossible to ensure a genomewide significance level of 0.05 using the available statistics, although the multiple-test problems can be alleviated, but not sufficiently, by the use of tagging SNPs. One strategy to circumvent the multiple-test problem associated with genome-wide association tests is to develop novel test statistics with high power. In this report, we introduce several nonlinear tests, which are based on nonlinear transformation of allele or haplotype frequencies. We investigate the power of the nonlinear test statistics and demonstrate that under certain conditions, some nonlinear test statistics have much higher power than the standard chi2-test statistic. Type I error rates of the nonlinear tests are validated using simulation studies. We also show that a class of similarity measure-based test statistics is based on the quadratic function of allele or haplotype frequencies, and thus they belong to nonlinear tests. To evaluate their performance, the nonlinear test statistics are also applied to three real data sets. Our study shows that nonlinear test statistics have great potential in association studies of complex diseases.

Acyltransferases↗

PubMed2006

Transposon-free insertions for insect genetic engineering.

Methods involving the release of transgenic insects in the field hold great promise for controlling vector-borne diseases and agricultural pests. Insect transformation depends on nonautonomous transposable elements as gene vectors. The resulting insertions are stable in the absence of suitable transposase, however, such absence cannot always be guaranteed. We describe a method for post-integration elimination of all transposon sequences in the pest insect Medfly, Ceratitis capitata. The resulting insertions lack transposon sequences and are therefore impervious to transposase activity.

Animals↗

PubMed2006

Variants in the HEPSIN gene are associated with prostate cancer in men of European origin.

There is considerable evidence that genetic factors are involved in prostate cancer susceptibility. We have studied the association of 11 single nucleotide polymorphisms (SNPs) in the HEPSIN gene (HPN) with prostate cancer in men of European ancestry. HPN is a likely candidate in prostate cancer susceptibility, as it encodes a transmembrane cell surface serum protease, which is overexpressed in prostate cancer; HPN is also located on 19q11-q13.2, where linkage is found with prostate cancer susceptibility. In this case-control association study (590 men with histologically verified prostate cancer and 576 unrelated controls, all of European descent), we find significant allele frequency differences between cases and controls at five SNPs that are located contiguously within the gene. A major 11-locus haplotype is significantly associated, which provides further support that HPN is a potentially important candidate gene involved in prostate cancer susceptibility. Association of one of the SNPs with Gleason score is also suggestive of a plausible role of HPN in tumor aggressiveness.

Case-Control Studies↗

PubMed2006

Dopamine D4 receptor polymorphism modulates cue-elicited heroin craving in Chinese.

RATIONALE: Subjective craving, which contributes to the continuation of drug use in active abuser and the occurrence of relapse in detoxified abusers, is considered to be a central phenomenon in addiction. Dopamine pathway has been implicated in the mechanism underlying the cue-elicited craving for a variety of addictive substances. OBJECTIVES: The objective of this study was to test the hypothesis that heroin addicts carrying D4 dopamine receptor gene (DRD4) variable number tandem repeat (VNTR) long type allele would have higher craving after exposure to a heroin-related cue. MATERIALS AND METHODS: Craving was induced by a series of exposure to neutral and heroin-related cue and were assessed in a cohort of Chinese heroin abusers (n=420) recruited from the Voluntary Drug Dependence Treatment Center at Shanghai. RESULTS: Significantly stronger cue-elicited heroin craving was found in individuals carrying DRD4 VNTR long type allele than the non-carriers (F=31.040, p<0.001). As for baseline craving and mean change in craving responding to neutral stimuli, no significance was found (1.06+/-0.34 vs 1.07+/-0.36, F=0.067, p=0.797 and 0.42+/-0.34 vs 0.45+/-0.37, F=0.277, p=0.599, respectively). CONCLUSIONS: The results of our study suggest that DRD4 VNTR polymorphism contributes to cue-elicited craving in heroin dependence, indicating DRD4 VNTR represents one of potential genetic risk factors for cue-induced craving.

Adolescent↗

PubMed2006

The effect of dopamine D2, D5 receptor and transporter (SLC6A3) polymorphisms on the cue-elicited heroin craving in Chinese.

Heroin dependence is resulted from the interaction between multiple genetic and environmental factors. Subjective craving is considered to be a central phenomenon, which contributes to the continuation of drug use in active abuser and the occurrence of relapse in detoxified abusers. Dopamine pathway has been implicated in the cue-elicited craving for a variety of addictive substances. The objective of this study was to test the hypothesis that heroin addicts carrying specific variants in dopamine-related genes would have higher levels of craving following exposure to a heroin-related cue. Craving induced by a series of exposure to heroin-related cue was assessed in a cohort of Chinese heroin abuser (n = 420) recruited from natural abstinence center at Shanghai. Significantly stronger cue-elicited heroin craving was found in individuals carrying D2 dopamine receptor gene (DRD2) TaqI RFLP A1 allele than the non-carriers (P < 0.001). Furthermore, we did not observed significant association of cue-elicited craving with the nine-repeat allelic variants in dopamine transporter gene (DAT) SLC6A3 and with the dinucleotide repeat polymorphism (DRP) 148bp allele in D5 dopamine receptor gene (DRD5). The results of our study suggest that human dopamine pathway be involved in cue-induced heroin craving, and indicate a potential genetic risk factor for persistent heroin behavior and relapse.

Adolescent↗

PubMed2006

Complete sequence data support lack of balancing selection on PRNP in a natural Chinese population.

The M129V mutation in the human prion protein gene (PRNP) is the primary site linked to susceptibility to prion diseases in humans. The heterozygous state of this allele has been proven to be more resistant to prion-related diseases such as Creutzfeldt-Jakob disease. Based on a study of the common genetic variations, it has been proposed that balancing selection has played a critical role in shaping the distribution of 129V in worldwide populations. Kreitman and Di-Rienzo [Kreitman and Di-Rienzo (2004)Trend Genet 20:300-304] challenged this hypothesis by pointing out that the exclusion of polymorphisms with low frequency may introduce an ascertainment bias and, in turn, lead to a wrong conclusion. By studying sequence variations in samples from the Human Genome Diversity Project, Soldevila et al. [Soldevila et al. (2005) Trends Genet 21:389-391] showed that this ascertainment bias does exist. We argue that the evidence presented by Soldevila et al. may be compromised by the samples tested since they were selected from a population that may be substructured. In this study, we re-evaluated the hypothesis of balancing selection in a natural Chinese population using a much longer segment encompassing the entire genomic region of the PRNP gene (15 kb). We showed that the pattern of genetic variation in PRNP is not consistent with the presence of balancing selection in this gene.

Asian People↗

PubMed2006

Polymorphisms in DNA damage binding protein 2 (DDB2) and susceptibility of primary lung cancer in the Chinese: a case-control study.

DNA damage binding protein 2 (DDB2) is one of the major DNA repair proteins involved in the nucleotide excision repair (NER) pathway. Mutations in the DDB2 gene can cause a repair-deficiency syndrome xeroderma pigmentosum group E. Because tobacco carcinogens can cause DNA damage that is repaired by NER and suboptimal NER capacity is reported to be associated with lung cancer risk, we hypothesized that common variants in the DDB2 gene are associated with lung cancer risk. To test this hypothesis, we conducted a case-control study of 1010 patients with incident lung cancer and 1011 cancer-free controls and genotyped two DDB2 single nucleotide polymorphisms (SNPs) (rs830083 and rs3781620) that are in linkage disequilibrium with other untyped SNPs. We found that compared with the rs830083CC, subjects carrying the heterozygous rs830083CG genotype had a significantly 1.31-fold increased risk of lung cancer [95% confidence interval (CI) 1.08-1.60] and those carrying the homozygous rs830083GG genotype had a non-significantly 1.22-fold elevated risk (95% CI 0.89-1.67). In addition, effects of the combined rs830083CG/GG variant genotypes were more evident in young subjects, heavy smokers and subjects with a positive family history of cancer. These findings indicate, for the first time, that the DDB2 rs830083 polymorphism may contribute to the etiology of lung cancer. Further functional studies on this SNP and/or related variants are warranted to elucidate the underlying molecular mechanisms of the association.

Aged↗

PubMed2006

[An unusual recombination event occurring between HLA-B and -Cw loci within a Chinese Han family].

OBJECTIVE: To investigate the recombination event occurring between HLA-B and -Cw loci discovered in a family of Chinese Han nationality with an acute myeloid leukemia (AML) patient. METHODS: Peripheral blood samples were collected from a Chinese man with M5 type AML, aged 39, and his healthy wife and daughter, all of Han nationality. HLA class I (-A, -B, and -Cw) and II (-DRB1 and -DQB1) alleles were typed by both low and high resolution PCR with sequence specific primers (PCR-SSP) and sequence-based typing (SBT). Then the recombination sites were analyzed by family study. RESULTS: The 2 haplotypes of the patient, his daughter, and his wife were A*2402101-Cw*030401/0402-B*1301-DRB1*0406-DQR1*030302/0303 and A*02011-Cw*150201/0202-B*4002-DRB1*1405-DQB1*05031, A*02011-Cw*150201/0202-B*1301-DRB1*0406-DQB1*030302/0303 and A*2406-Cw*0602-B*1302_DRB1*070101/0102-DQB1*0202, and A*330301/0302-Cw*030201/0202-B*58-1-DRB1*17-DQB1*0202 and A*2406-Cw*0602-B*1302-DRB1*070101/0102-B*5801-DRB1*0202 respectively. Family study demonstrated that A*02011-Cw*150201/0202 recombination and B*1301-DRB1*030302/0303 recombination carried by the daughter came from the 2 isolated chromosomes of her father, indicating that the recombination event occurred between HLA-B and -Cw loci during meiosis of the father and resulted in a new HLA haplotype that was inherited by the daughter. CONCLUSION: An unusual HLA-B/Cw recombination event occurring between HLA-B and -Cw loci has been found in a Han family, which helps further study the mechanisms of HLA recombination.

Adult↗

PubMed2006

A novel SNP at exon 17 of INSR is associated with decreased insulin sensitivity in Chinese women with PCOS.

To investigate the association of single-nucleotide polymorphisms (SNPs) in exon 17 of the insulin receptor (INSR) gene with insulin resistance and INSR beta-subunit expression in polycystic ovary syndrome (PCOS) patients, a case-control study was carried out in an academic endocrinology clinic of China. One hundred and nine Chinese patients with PCOS and 107 healthy Chinese women as control were recruited. Their leukocytes and red blood cells were separated from blood samples, for SNP analysis with single-stranded conformation polymorphism and for the INSR beta-subunit expression detection by western blot analysis, respectively. A novel T/C SNP at codon Cys1008 (position 3128 of NM_000208) of INSR was found in two allele genotypes, i.e. the homozygous CC and the heterozygous TC. A higher frequency of the mutant homozygous CC was observed in the PCOS women with PCOS than that in the controls (21.1 versus 5.6%, P < 0.01). In contrast with the women with wild-type genotype, a significantly lower insulin sensitivity index in the women with each of the two mutant genotypes was revealed (CC: 0.335 +/- 0.026/TC: 0.346 +/- 0.027 versus TT: 0.367 +/- 0.029, P < 0.05). No relationship was found between the novel SNP and the INSR beta-subunit expression. We concluded that the novel T/C SNP at codon Cys1008 of INSR is associated with decreased insulin sensitivity in Chinese women with PCOS and that the association is not by the change of synthesis or secretion of INSR beta-subunit, but most possibly by the effects of this novel SNP on the function of INSR beta-subunit.

Adult↗

PubMed2006

Mitochondrial aldehyde dehydrogenase-2 (ALDH2) Glu504Lys polymorphism contributes to the variation in efficacy of sublingual nitroglycerin.

Glyceryl trinitrate (GTN), also known as nitroglycerin, has been used to treat angina and heart failure for more than 130 years. Recently, it was shown that mitochondrial aldehyde dehydrogenase-2 (ALDH2) is responsible for formation of NO, the metabolite needed for GTN efficacy. In the present study, we show that the common G-to-A polymorphism in exon 12 of ALDH2--resulting in a Glu504Lys replacement that virtually eliminates ALDH2 activity in both heterozygotes and homozygotes--is associated with a lack of efficacy of sublingual GTN in Chinese subjects. We also show that the catalytic efficiency (Vmax/Km) of GTN metabolism of the Glu504 protein is approximately 10-fold higher than that of the Lys504 enzyme. We conclude that the presence of the Lys504 allele contributes in large part to the lack of an efficacious clinical response to nitroglycerin; we recommend that this genetic factor be considered when administering nitroglycerin to patients, especially Asians, 30-50% of whom possess the inactive ALDH2*2 mutant allele.

Administration, Sublingual↗

PubMed2006

Linkage disequilibrium sharing and haplotype-tagged SNP portability between populations.

The discovery of the block-like structure of linkage disequilibrium (LD) in human populations holds the promise of delineating the etiology of common diseases. However, understanding the magnitude, mechanism, and utility of between-population LD sharing is critical for future genome-wide association studies. In this study, substantial LD sharing between six non-African populations was observed, although much less between African-American and non-African, based on 20,000 SNPs of chromosome 21. We also demonstrated the respective roles of recombination and demographic events in shaping LD sharing. Furthermore, we showed that the haplotype-tagged SNPs chosen from one population are portable to the others in East Asia. Therefore, we concluded that the magnitude of LD sharing between human populations justifies the use of representative populations for selecting haplotype-tagged SNPs in genome-wide association studies of complex diseases.

Africa↗