Background and AimA growing body of literature suggests the association between dementia risk and proton pump inhibitor (PPI) use. Therefore, we aimed to investigate the association between PPI use and dementia risk.MethodsAn extensive literature search was performed in PubMed, Embase, and Cochrane till March 31, 2019. All the studies (cohort and case–control) assessing the association between PPI use and dementia risk were eligible for inclusion. Articles were selected based on the screening of title and abstract, data were extracted, and risk of bias was assessed using Newcastle–Ottawa scale. The primary outcome was pooled risk of dementia among PPI user as compared with non‐PPI user. Secondary outcomes include dementia risk based on subgroups. Statistical analysis was performed using review manager software.ResultsTwelve studies (eight cohort and four case–control) were found to be eligible for inclusion. Majority of the studies were of high quality. Dementia was diagnosed based on International Classification of Diseases 9/10 codes in majority of the included studies. PPI use was not associated with the dementia risk, with a pooled relative risk (RR) of 1.05 (95% confidence interval [CI]: 0.96–1.15), P = 0.31. Subgroup analysis based on study design (cohort: P = 0.14; case–control: P = 0.14), sex (RR 1.25 [95% CI: 0.97–1.60], P = 0.08), histamine 2 receptor antagonist blockers (P = 0.93), and Alzheimer's disease (RR 1.00 [95% CI: 0.91–1.09], P = 0.93) revealed no significant association between PPI use and dementia risk.ConclusionWe found no significant association between PPI use and the risk of dementia or Alzheimer's disease.

Peutz-Jeghers syndrome (PJS) is a well-described inherited syndrome, characterized by the development of gastrointestinal polyps, and characteristic mucocutaneous freckling. PJS, an autosomal prevailing disease due to genetic mutation on chromosome 19p, manifested by restricted mucocutaneous melanosis in association with gastrointestinal (GI) polyposis. The gene for PJS has recently been shown to be a serine/threonine kinase, known as LKB1 or STK11, which maps to chromosome subband 19p13.3. This gene has a putative coding region of 1302 bp, divided into nine exons, and acts as a tumour suppressor in the hamartomatous polyps of PJS patients and in the other neoplasms which develop in PJS patients. It is probable that these neoplasms develop from hamartomas, but remains possible that the LKB1 or STK11 locus plays a role in a different genetic pathway of tumour growth in the cancers of PJS patients. This article has focused on role of LKB1 or STK11 gene expression in PJS and related cancers.

The well‐known condition of heart failure is a clinical syndrome that results when the myocardium's ability to pump enough blood to meet the body's metabolic needs is impaired. Most of the cardiac activity is maintained by adrenoceptors, are categorized into two main α and β and three distinct subtypes of β receptor: β1‐, β2‐, and β3‐adrenoceptors. The β adrenoreceptor is the main regulatory macro proteins, predominantly available on heart and responsible for down regulatory cardiac signaling. Moreover, the pathological involvement of Angiotensin‐converting enzyme 1 (ACE1)/angiotensin II (Ang II)/angiotensin II type 1 (AT1) axis and beneficial ACE2/Ang (1‐7)/Mas receptor axis also shows protective role via Gi βγ, during heart failure these receptors get desensitized or internalized due to increase in the activity of G‐protein‐coupled receptor kinase 2 (GRK2) and GRK5, responsible for phosphorylation of G‐protein‐mediated down regulatory signaling. Here, we investigate the various clinical and preclinical data that exhibit the molecular mechanism of upset level of GRK change the cardiac activity during failing heart.

Purpose We carried out a meta-analytic synthesis to evaluate the association between diabetes mellitus (DM) and related clinical outcomes, co-morbidities, their risk factors and resource utilization in patients with COVID-19. Methods The MEDLINE and Web of Science databases were reviewed for identification of eligible studies. Meta-analysis was carried out using Review Manager 5.3. The random- effects model was used to compute the pooled estimates of odds ratio (OR)/mean difference and 95% confidence interval (CI). Results A total of 14 studies including 3,644 individuals without DM and 1,428 with DM were included in the meta-analysis. Cardiovascular diseases (CVDs) [OR 2.91, 95% CI 2.34, 3.63], hypertension [OR 2.19, 95% CI 1.39, 3.46], acute kidney injury (AKI) [OR 3.59, 95% CI 1.46, 8.84], cerebrovascular disease [OR 2.09, 95% CI 1.22, 3.61], and acute respiratory distress syndrome (ARDS) [OR 3.40, 95% CI 2.09, 5.55] were significantly associated with DM in COVID-19 patients compared with non-DM patients (p < 0.05 for all instances). Mortality was significantly higher among COVID-19 patients with DM [OR 2.46, 95% CI 1.68, 3.58]. Intensive Care Unit (ICU) admission and use of mechanical ventilation were significantly associated with COVID-19 patients with DM [OR 2.79, 95% CI 1.79, 4.34], and [OR 3.33, 95% CI 2.05, 5.42], respectively. No significant difference was observed in the length of stay (LOS) and hospitalization. Conclusions This meta-analysis shows that CVDs, hypertension, AKI, cerebrovascular disease, and ARDS are significantly higher among DM patients with COVID-19 compared with non-DM patients. Mortality, ICU admission and the use of mechanical ventilation were significantly associated with COVID-19 patients with DM. Further long-term, multinational and large sample size clinical studies are warranted to justify the current findings.

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