Prevalence of dysmenorrhea and associated risk factors among university students in Zimbabwe.

BACKGROUND: Dysmenorrhea is an often incapacitating condition that is characterized by painful menstruation and general body malaise. In Zimbabwe, this condition is understudied, and its associated risk factors are poorly understood. OBJECTIVES: To investigate the prevalence and associated risk factors of dysmenorrhea among female students at Midlands State University in Zimbabwe. DESIGN: This is a cross-sectional study that employed simple random sampling technique to obtain data from 382 students using pretested and self-administered questionnaires. METHODS: Data were analyzed using STATA version 16. Associations between dysmenorrhea, menstrual, sociodemographic, and lifestyle characteristics were measured using chi-square test and logistic regression model. RESULTS: The prevalence of dysmenorrhea was 75.9%, with 28.6% of sufferers describing their pain as severe. Dysmenorrhea significantly affected the school/daily activities of respondents (χ2 = 18.22, p < 0.001). Family history (χ2 = 4.28, p = 0.04), age of menarche (χ2 = 14.8, p < 0.001), regularity of menstrual cycle (χ2 = 18.1, p < 0.001), and parity (χ2 = 8.8, p = 0.03) were associated with the prevalence of dysmenorrhea. The risk of developing dysmenorrhea almost doubled with positive family history (prevalence odds ratio = 1.68 (95% confidence interval: 1.03 to 2.75, p = 0.040)); increased with decrease in age of menarche (prevalence odds ratio = 0.19 (95% confidence interval: 0.10 to 0.45, p < 0.001)) and decreased with increase in parity (prevalence odds ratio = 0.15 (95% confidence interval: 0.03 to 0.82, p = 0.029)). However, the risk was low among those with irregular menstrual cycles (prevalence odds ratio = 0.14 (95% confidence interval: 0.10 to 0.33, p < 0.001)). Physical exercise, smoking, alcohol, and coffee consumption were not associated with the prevalence of dysmenorrhea (p > 0.05). CONCLUSION: Dysmenorrhea is common among female students at Midlands State University, and it significantly affects their academic activities. Family history, regular menstrual cycle, nulliparity, and lower age of menarche were risk factors. More awareness is recommended including studies on impact and management strategies.

The potential of Artemisia species for use as broad-spectrum agents in the management of metabolic syndrome: a review.

Although the prevalence of metabolic syndrome (MetS), a cluster of cardiometabolic risk factors that predispose to the development of type 2 diabetes mellitus and cardiovascular diseases, is increasing globally, there is no broad-spectrum agent for its holistic treatment. Natural plant-derived products with a wide spectrum of biological activities are currently being explored as alternatives in the management of diseases. Artemisia species are a heterozygous group of plants of the Compositae family that possess several health benefits. Here we highlight their antidiabetic, anti-obesity, anti-hyperlipidaemic, hepatoprotective and cardioprotective properties among others. These activities have been linked to the presence of phytochemicals that act on several molecular targets to exert their effects and the species of Artemisia are considered to be relatively safe. Artemisia species offer significant anti-MetS activity and thus are strong therapeutic candidates for the effective management of MetS.

HIV-Related Myocardial Fibrosis: Inflammatory Hypothesis and Crucial Role of Immune Cells Dysregulation.

Although the underlying mechanisms driving human immunodeficiency virus (HIV)-mediated cardiovascular diseases (CVD) onset and progression remain unclear, the role of chronic immune activation as a significant mediator is increasingly being highlighted. Chronic inflammation is a characteristic feature of CVD and considered a contributor to diastolic dysfunction, heart failure, and sudden cardiac death. This can trigger downstream effects that result in the increased release of pro-coagulant, pro-fibrotic, and pro-inflammatory cytokines. Subsequently, this can lead to an enhanced thrombotic state (by platelet activation), endothelial dysfunction, and myocardial fibrosis. Of note, recent studies have revealed that myocardial fibrosis is emerging as a mediator of HIV-related CVD. Together, such factors can eventually result in systolic and diastolic dysfunction, and an increased risk for CVD. In light of this, the current review article will focus on (a) the contributions of a chronic inflammatory state and persistent immune activation, and (b) the role of immune cells (mainly platelets) and cardiac fibrosis in terms of HIV-related CVD onset/progression. It is our opinion that such a focus may lead to the development of promising therapeutic targets for the treatment and management of CVD in HIV-positive patients.

The Role of Immunometabolism in HIV-1 Pathogenicity: Links to Immune Cell Responses.

With the successful roll-out of combination antiretroviral treatment, HIV is currently managed as a chronic illness. Of note, immune activation and chronic inflammation are hallmarks of HIV-1 infection that persists even though patients are receiving treatments. Despite strong evidence linking immune activation and low-grade inflammation to HIV-1 pathogenesis, the underlying mechanisms remain less well-understood. As intracellular metabolism is emerging as a crucial factor determining the fate and activity of immune cells, this review article focuses on how links between early immune responses and metabolic reprograming may contribute to HIV pathogenicity. Here, the collective data reveal that immunometabolism plays a key role in HIV-1 pathogenesis. For example, the shift from quiescent immune cells to its activation leads to perturbed metabolic circuits that are major drivers of immune cell dysfunction and an altered phenotype. These findings suggest that immunometabolic perturbations play a key role in the onset of non-AIDS-associated comorbidities and that they represent an attractive target to develop improved diagnostic tools and novel therapeutic strategies to help blunt HIV-1 pathogenesis.

Medicinal Plants, Phytochemicals, and Their Impacts on the Maturation of the Gastrointestinal Tract.

The gastrointestinal tract (GIT) is the first point of contact for ingested substances and thus represents a direct interface with the external environment. Apart from food processing, this interface plays a significant role in immunity and contributes to the wellbeing of individuals through the brain-gut-microbiota axis. The transition of life from the in utero environment, to suckling and subsequent weaning has to be matched by phased development and maturation of the GIT; from an amniotic fluid occupancy during gestation, to the milk in the suckling state and ultimately solid food ingestion at weaning. This phased maturation of the GIT can be affected by intrinsic and extrinsic factors, including diet. Despite the increasing dietary inclusion of medicinal plants and phytochemicals for health benefits, a dearth of studies addresses their impact on gut maturation. In this review we focus on some recent findings mainly on the positive impact of medicinal plants and phytochemicals in inducing precocious maturation of the GIT, not only in humans but in pertinent animals. We also discuss Paneth cells as mediators and potential markers of GIT maturation.

Administration of ursolic acid to new-born pups prevents dietary fructose-induced non-alcoholic fatty liver disease in Sprague Dawley rats.

Overconsumption of fructose time dependently induces the development of non-alcoholic fatty liver disease (NAFLD). We investigated whether ursolic acid (UA) intake by new-born rats would protect against fructose-induced NAFLD. One hundred and seven male and female Sprague Dawley rat pups were randomly grouped and gavaged (10 ml/kg body weight) with either 0.5% dimethylsulphoxide (vehicle control), 0.05% UA, 50% fructose mixed with UA (0.05%) or 50% fructose alone, from postnatal day 6 (P6) to P20. Post-weaning (P21-P69), the rats received normal rat chow (NRC) and water to drink. On P70, the rats in each group were continued on water or 20% fructose to drink, as a secondary high fructose diet during adulthood. After 8 weeks, body mass, food and fluid intake, circulating metabolites, visceral adiposity, surrogate markers of liver function and indices of NAFLD were determined. Food intake was reduced as a result of fructose feeding in both male and female rats (p < 0.0001). Fructose consumption in adulthood significantly increased fluid intake and visceral adiposity in female rats (p < 0.05) and had no apparent effects in male rats (p > 0.05). In both sexes of rats, fructose had no significant (p > 0.05) effects on body mass, circulating metabolites, total calorie intake and surrogate markers of hepatic function. Fructose consumption in both early life and adulthood in female rats promoted hepatic lipid accumulation (p < 0.001), hypertrophy, microvesicular and macrovesicular steatosis (p < 0.05). Early-life UA intake significantly (p < 0.001) reduced fructose-induced hepatic lipid accumulation in both male and female rats. Administration of UA during periods of developmental plasticity shows prophylactic potential against dietary fructose-induced NAFLD.