There is a dearth of evidence synthesis on the prevalence of anxiety among university students even though the risk of psychological disorders among this population is quite high. We conducted a quantitative systematic review to estimate the global prevalence of anxiety among university students during the COVID-19 pandemic. A systematic search for cross-sectional studies on PubMed, Scopus, and PsycINFO, using PRISMA guidelines, was conducted from September 2020 to February 2021. A total of 36 studies were included, using a random-effects model to calculate the pooled proportion of anxiety. A meta-analysis of the prevalence estimate of anxiety yielded a summary prevalence of 41% (95% CI = 0.34–0.49), with statistically significant evidence of between-study heterogeneity (Q = 80801.97, I2 = 100%, p ≤ 0.0001). A subgroup analysis reported anxiety prevalence in Asia as 33% (95% CI:0.25–0.43), the prevalence of anxiety in Europe as 51% (95% CI: 0.44–0.59), and the highest prevalence of anxiety in the USA as 56% (95% CI: 0.44–0.67). A subgroup gender-based analysis reported the prevalence of anxiety in females as 43% (95% CI:0.29–0.58) compared to males with an anxiety prevalence of 39% (95% CI:0.29–0.50). University students seem to have a high prevalence of anxiety, indicating an increased mental health burden during this pandemic.

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As the leading cause of dementia worldwide, Alzheimer's disease has garnered intense academic and clinical interest. Yet, trials in search of a disease-modifying therapy have failed overwhelmingly. We suggest that, in part, this may be attributable to the influence of disruptive variables inherent to the framework of a clinical trial. Specifically, we observe that everyday factors such as diet, education, mental exertion, leisure participation, multilingualism, sleep, trauma, and physical activity, as well as clinical/study parameters including environment, family coaching, concurrent medications, and illnesses may serve as potent confounders, disruptors, or sources of bias to an otherwise significant drug-disease interaction. This perspective briefly summarizes the potential influence of these hidden variables on the outcomes of clinical trials and suggests strategies to abate their impact.

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In recent decades, clinical trials in Alzheimer’s disease (AD) have failed at an unprecedented rate. The etiology of AD has since come under renewed scrutiny, both to elucidate the underlying pathologies and to identify novel therapeutic strategies. Here, diet has emerged as a potential causative/protective agent. A variety of nutrients, including lipids, minerals, vitamins, antioxidants and sugars as well as broader dietary patterns and microbiotal interactions have demonstrated associations with AD. Although clinical trials have yet to definitively implicate any singular dietary element as therapeutic or causative, it is apparent that dietary preferences, likely in complex synergies, may influence the risk, onset and course of AD. This review catalogs the impact of major dietary elements on AD. It further examines an unexplored reciprocal association where AD may modulate diet, as well as how potential therapeutics may complicate these interactions. In doing so, we observe diet may have profound effects on the outcome of a clinical trial, either as a confounder of a drug/disease interaction or as a generally disruptive covariate. We therefore conclude that future clinical trials in AD should endeavor to control for diet, either in study design or subsequent analyses.

Background: Pantothenate, the fundamental precursor to coenzyme A, is required for optimal growth and virulence of microbial pathogens. It is synthesized by the enzyme-catalyzed condensation of β-alanine and pantoate, which has shown susceptibility to inhibition by analogs of its molecular constituents. Accordingly, analogs of β-alanine are gaining inquiry as potential antimicrobial chemotherapeutics. Methods: We synthesized and evaluated 35 derivatives of β-alanine, substituted at the α, β, amine, and carboxyl sites, derived from in silico, dynamic molecular modeling to be potential competitive inhibitors of pantothenate synthetase. Employing the Clinical Laboratory Standards M7-A6 broth microdilution method, we tested these for inhibition of growth in Escherichia coli, Staphylococcus aureus, and Pseudomonas aeruginosa. Results: All compounds proved entirely ineffective in all species tested, with no inhibition of growth being observed up to 200 µM/mL. Conclusions: Upon revision of the literature, we conclude that high enzyme selectivity or external salvage mechanisms may render this strategy futile against most bacteria.

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