IntroductionThe significant increase in the rate of morbidity and mortality due to cardiovascular diseases has become a health challenge globally. Lack of enough knowledge on the underlying causes in Iran and taking the unique characteristics of the Shiraz metropolitan city (the capital city of Fars Province) into consideration prompted us to conduct the Shiraz Heart Study. The aim of this study is to determine the predisposing elements leading to coronary heart disease, cerebrovascular disease and peripheral arterial disease.Methods and analysisIn this population-based, prospective study, family physician clinics will become the executive arms. Participants aged 40–70 years old will be recruited to achieve a sample size of 10 000. Socioeconomicta and anthropometric indices supplemented by physical activity, nutritional and psychological questionnaires, as well as routine blood laboratory tests, medical history and electrocardiographic records, will be collected at enrolment in clinics. In addition, blood samples will be obtained to explore the possible role of genetics in outcome occurrence. Follow-up with blood sampling, completion of a lifestyle questionnaire and evaluation of clinical risk factors will be carried out five times in a 2-year interval for all participants. Advanced statistical methods such as mixed model and time-to-event models will be used for data analysis.Ethics and disseminationThis study is in accordance with the Helsinki Declaration and has been approved by the Research Ethics Committee of Shiraz University of Medical Sciences (No: 2017–358). Signing a written informed consent is the preliminary step. Participants are free to withdraw on their request at any time. Collected data are kept encrypted in a software with authorities’ access only. Findings of the study will be published at a national or international scale through peer-reviewed journals.

Although a large number of studies have shown the associations of high plasma lipid profile levels with cancer, few studies demonstrate the association between low serum cholesterol (<160 mg/dl) and risk for cancer mortality. The aim of this study was to determine the association of low serum cholesterol level as a risk factor for mortality in cancer. The prospective cohort studies were conducted on 19 of 52 cohort studies including 30 179 male and 26 005 female participants who were followed up for 9 years. Cox proportion hazard model was applied to analyze these data. The associations are presented as hazard ratios (HRs) with 95% confidence intervals (CI). The statistical package for the social sciences software was used for analysis. The multivariate analysis results showed risk associations with low serum cholesterol for the first decile among male participants (cancer: HR=1.52, 95% CI: 1.06-2.18; noncancer liver dysfunction: HR=10.73, 95% CI: 3.74-30.18) and female participants (cancer: HR=1.03, 95% CI: 0.52-2.05; noncancer liver dysfunction: HR=25.8, 95% CI: 3.09-217.70). Furthermore, in the second decile, this association among male patients (noncancer liver dysfunction: HR=3.73, 95% CI: 1.16-11.95) had a statistically significant result. For the remaining deciles in both sexes, cancer and noncancer liver dysfunction has some risk or protective association, although not significant. Findings of this study indicated an inverse association between low serum cholesterol and cancer and noncancer liver dysfunction mortality.

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CD4 + T-lymphocyte counts are used to assess CD4 + decline and the stage of human immunodeficiency virus (HIV) progression in HIV-infected patients. Clinical observation suggests that HIV progress more rapid in females than males. Of the original 5000 HIV-infected population of Western New York HIV/AIDS, Referral Center at Erie County Medical Center (ECMC), 1422 participated in the cohort study. We identified 333 HIV-infected patients with CD4 + T-cell-counts ≥ 500/µƖ, among them 178 met the inclusion criteria for the 10-year study. Females had higher mode (600 vs. 540) and mean (741.9 vs. 712.2) CD4 + counts than males at baseline. However, CD4 + declined faster among females in a shorter time than males (234.5 vs. 158.6, P < 0.004), with rapid HIV progression. Univariate analyses determined that females had a 40% higher risk for CD4 + decline than males. The bivariate analyses specified CD4 + decline remained greater in females than males. Multivariate analyses which employed Cox’s proportional Hazard-Model to adjust for numerous variables simultaneously identified women had almost twice the risk for CD4 + decline and rapid HIV progression than males (RR = 1.93; 95%CI 1.24, 2.99). Although the biological mechanism remains unknown, findings suggest gender differences in CD4 + decline, with a higher risk of rapid HIV progression and shorter longevity in females.