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Background: Schizophrenia is a complex neuropsychiatric disorder whose pathophysiology may involve oxidative stress-induced neuronal damage and inflammation. We conducted a cross-species study to elucidate oxidative stress dysregulation in schizophrenia. Methods: We measured peripheral oxidative stress biomarkers (malondialdehyde [MDA], nitric oxide [NO], reduced glutathione [GSH], superoxide dismutase [SOD], catalase [CAT], advanced protein oxidation products [APOP]), and C-reactive protein (CRP) in antipsychotic-naïve schizophrenia patients and matched controls. We also assayed liver enzymes (ALP, ALT, AST) as indicators of systemic metabolic stress. In parallel, we re-analyzed published single-cell RNA-sequencing data from a Setd1a^+/–^ mouse model of schizophrenia, focusing on prefrontal cortex (PFC) cell types and oxidative stress-related gene expression. Results: Patients with schizophrenia showed markedly elevated MDA and NO (indicators of lipid and nitrosative stress) and significantly reduced antioxidant defenses (GSH, SOD, CAT) versus controls (p < 0.01 for all comparisons). Notably, urban patients exhibited higher oxidative stress biomarker levels than rural patients, implicating environmental contributions. Liver function tests revealed increased ALT, AST, and ALP in schizophrenia, suggesting hepatic/metabolic dysregulation. Single-cell analysis confirmed dysregulated redox pathways in the schizophrenia model; PFC neurons from Setd1a^+/–^ mice displayed significantly lower expression of key antioxidant genes (e.g., Gpx4, Nfe2l2) compared to wild-type, indicating impaired glutathione metabolism. Conclusions: Our integrative data identify convergent oxidative stress imbalances in schizophrenia across species. These findings advance a mechanistic understanding of schizophrenia as a disorder of redox dysregulation and inflammation. They also have translational implications as augmenting antioxidant defenses (for example, with N-acetylcysteine or vitamins C/E) could mitigate oxidative injury and neuroinflammation in schizophrenia, representing a promising adjunct to antipsychotic therapy.

Diabetes mellitus, a chronic metabolic disorder characterized by hyperglycemia, presents a formidable global health challenge with its associated complications. Adiponectin, an adipocyte-derived hormone, has emerged as a significant player in glucose metabolism and insulin sensitivity. Beyond its metabolic effects, adiponectin exerts anti-inflammatory, anti-oxidative, and vasoprotective properties, making it an appealing therapeutic target for mitigating diabetic complications. The molecular mechanisms by which adiponectin impacts critical pathways implicated in diabetic nephropathy, retinopathy, neuropathy, and cardiovascular problems are thoroughly examined in this study. In addition, we explore possible treatment options for increasing adiponectin levels or improving its downstream signaling. The multifaceted protective roles of adiponectin in diabetic complications suggest its potential as a novel therapeutic avenue. However, further translational studies and clinical trials are warranted to fully harness the therapeutic potential of adiponectin in the management of diabetic complications. This review highlights adiponectin as a promising target for the treatment of diverse diabetic complications and encourages continued research in this pivotal area of diabetes therapeutics.

Erectile dysfunction (ED) is a pathophysiological condition in which the patients cannot achieve an erection during sexual activity, and it is often overlooked yet prevalent among diabetic men, globally affecting approximately 35–75% of diabetic individuals. The precise mechanisms through which diabetes contributes to ED remain elusive, but the existing literature suggests the potential involvement of nerve and vascular damage that affects the penile supply. In the present review, we reanalyze the existing human single-cell transcriptomic data from patients having diabetes mellitus-associated ED with normal erections. The analysis validates the expression of genes associated with antioxidative pathways, growth factors, adipokines, angiogenesis, vascular functions, penile erection, sexual function, and inflammation in diverse cell types from healthy individuals and those with ED. Our transcriptomic analysis reveals alterations in the expression of adiponectin receptors in the pathogenesis of ED compared to their counterparts in healthy subjects. This comprehensive review sheds light on the molecular underpinnings of ED in the context of diabetes, providing an in-depth understanding of the biological and cellular alterations involved and paving the way for possible targeted therapeutic discoveries in the field of diabetes-associated male infertility.

Diabetic polyneuropathy (DPN) is the most frequent, although neglected, complication of long-term diabetes. Nearly 30% of hospitalized and 20% of community-dwelling patients with diabetes suffer from DPN; the incidence rate is approximately 2% annually. To date, there has been no curable therapy for DPN. Under these circumstances, cell therapy may be a vital candidate for the treatment of DPN. The epidemiology, classification, and treatment options for DPN are disclosed in the current review. Cell-based therapies using bone marrow-derived cells, embryonic stem cells, pluripotent stem cells, endothelial progenitor cells, mesenchymal stem cells, or dental pulp stem cells are our primary concern, which may be a useful treatment option to ease or to stop the progression of DPN. The importance of cryotherapies for treating DPN has been observed in several studies. These findings may help for the future researchers to establish more focused, accurate, effective, alternative, and safe therapy to reduce DPN. Cell-based therapy might be a permanent solution in the treatment and management of diabetes-induced neuropathy.

Background Gestational diabetes mellitus (GDM) is quite prevalent in low- and middle-income countries, and has been proposed to increase the risk of depression. There is only a prior study assessing antenatal depression among the subjects with GDM in the Bangladesh, which leads this study to be investigated. Objective To determine the prevalence of depressive symptoms and potential associations among pregnant women diagnosed with GDM. Methods A cross-sectional study was carried out among 105 pregnant women diagnosed with GDM over the period of January to December 2017 in 4- hospitals located in two different cities (Dhaka and Barisal). A semi-structured questionnaire was developed consisting of items related to socio-demographics, reproductive health history, diabetes, anthropometrics, and depression. Results Mild to severe antenatal depression was present in 36.2% of the subjects (i.e., 14.3%, 19% and 2.9% for mild, moderate and severe depression, respectively). None of the socio-demographic factors were associated with depression, but the history of reproductive health-related issues (i.e., abortion, neonatal death) and uncontrolled glycemic status were associated with the increased risk of depressive disorders. Conclusions GDM is associated with a high prevalence of depressive symptoms, which is enhanced by poor diabetes control. Thus, in women presenting with GDM, screening for depression should be pursued and treated as needed. Plain English Summary Pregnancy is a highly stressful period in a woman's life that can also be associated with mental health problems such as depression. Depression is reported in about 16% of pregnant women whereas and such prevalence can double in LMICs (e.g., Bangladesh). In addition, gestational diabetes mellitus (GDM) has emerged as a common condition affecting approximately 10% of all pregnancies. GDM has also been associated with adverse mental health outcomes, particularly depression. GDM women with antenatal depression are not only at increased risk of poorer quality of life, but are also at increased risk of adverse pregnancy and fetal outcomes, particularly in LMIC. This study investigates the prevalence of depressive symptoms among Bangladeshi pregnant women diagnosed with GDM. It is found that depression was detectable in 36.2% subjects. In addition, a history of reproductive health-related issues (i.e., abortion, neonatal death) and uncontrolled glycemic status were associated with increased risk of depressive disorders. Considering the negative effects of both GDM and depression on pregnancy-related outcomes, early screening of these conditions should be pursued, preferably once every trimester over the duration of the pregnancy.

Although diabetic polyneuropathy (DPN) is a frequent diabetic complication, no effective therapeutic approach has been established. Glucagon is a crucial hormone for glucose homeostasis but has pleiotropic effects, including neuroprotective effects in the central nervous system. However, the importance of glucagon in the peripheral nervous system (PNS) has not been clarified. Here, we hypothesized that glucagon might have a neuroprotective function in the PNS. The immortalized rat dorsal root ganglion (DRG) neuronal cell line 50B11 was treated with methylglyoxal (MG) to mimic an in vitro DPN model. The cells were cultured with or without glucagon or MG. Neurotoxicity, survival, apoptosis, neurite projection, cyclic adenosine monophosphate (cAMP), and protein kinase A (PKA) were examined. Glucagon had no cytotoxicity and rescued the cells from neurotoxicity. Cell survival was increased by glucagon. The ratio of apoptotic cells, which was increased by MG, was reduced by glucagon. Neurite outgrowth was accelerated in glucagon-treated cells. Cyclic AMP and PKA accumulated in the cells after glucagon stimulation. In conclusion, glucagon protected the DRG neuronal cells from MG-induced cellular stress. The cAMP/PKA pathway may have significant roles in those protective effects of glucagon. Glucagon may be a potential target for the treatment of DPN.

The COVID-19 pandemic caused by the SARS-CoV-2 virus has led to significant global health implications. Although the respiratory manifestations of COVID-19 are widely recognized, emerging evidence suggests that the disease may also significantly affect the gut microbiota, the intricate community of bacteria that lives within the gastrointestinal system. This extensive article intends to investigate the impact of COVID-19 on the gut microbiota, examining the underlying mechanisms, clinical implications, and potential therapeutic interventions. Understanding the complex interactions between COVID-19 and the gut microbiota will help us to gain valuable insights into the broader consequences of this viral infection on human health.

Background and Aims Despite evidence that COVID‐19 vaccination can strengthen mental health, there is limited evidence about this in Bangladesh. Thus, this comparative study assessed the prevalence and factors associated with mental health problems between vaccine receivers and nonreceivers. Methods Using a snowball sampling technique, a web‐based cross‐sectional study was conducted among a total of 459 participants. The survey questionnaire included sociodemographic information, the Patient Health Questionnaire (PHQ—9), the Generalized Anxiety Disorder (GAD—7), and the Trauma Screening Questionnaire (TSQ—10). Results The study found that mental health problems were nonsignificantly prevalent in the vaccine nonreceivers than those who received it (i.e., 24.79% vs. 20.60% for depression, 21.20% vs. 16.60% for anxiety, and 15.30% vs. 12.60% for posttraumatic stress disorder). Female gender, chronic condition, smoking status, and alcohol consumption were the risk factors for mental health problems. Conclusion This study's findings suggest that the COVID‐19 vaccination necessarily improves mental health outcomes. However, the study had limitations in terms of its design and sampling technique, and further research is needed to establish a cause‐effect relationship between vaccination and mental health problems.

Objective. Diabetic polyneuropathy (DPN) is one of the most prevalent diabetic complications. We previously demonstrated that exendin-4 (Ex4), a glucagon-like peptide-1 receptor agonist (GLP-1RA), has beneficial effects in animal models of DPN. We hypothesized that GLP-1 signaling would protect neurons of the peripheral nervous system from oxidative insult in DPN. Here, the therapeutic potential of GLP-1RAs on DPN was investigated in depth using the cellular oxidative insult model applied to the dorsal root ganglion (DRG) neuronal cell line. Research Design and Methods. Immortalized DRG neuronal 50B11 cells were cultured with and without hydrogen peroxide in the presence or absence of Ex4 or GLP-1(7-37). Cytotoxicity and viability were determined using a lactate dehydrogenase assay and MTS (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium inner salt), respectively. Antioxidant enzyme activity was evaluated using a superoxide dismutase assay. Alteration of neuronal characteristics of 50B11 cells induced by GLP-1RAs was evaluated with immunocytochemistry utilizing antibodies for transient receptor potential vanilloid subfamily member 1, substance P, and calcitonin gene-related peptide. Cell proliferation and apoptosis were also examined by ethynyl deoxyuridine incorporation assay and APOPercentage dye, respectively. The neurite projection ratio induced by treatment with GLP-1RAs was counted. Intracellular activation of adenylate cyclase/cyclic adenosine monophosphate (cAMP) signaling was also quantified after treatment with GLP-1RAs. Results. Neither Ex4 nor GLP-1(7-37) demonstrated cytotoxicity in the cells. An MTS assay revealed that GLP-1RAs amended impaired cell viability induced by oxidative insult in 50B11 cells. GLP-1RAs activated superoxide dismutase. GLP-1RAs induced no alteration of the distribution pattern in neuronal markers. Ex4 rescued the cells from oxidative insult-induced apoptosis. GLP-1RAs suppressed proliferation and promoted neurite projections. No GLP-1RAs induced an accumulation of cAMP. Conclusions. Our findings indicate that GLP-1RAs have neuroprotective potential which is achieved by their direct actions on DRG neurons. Beneficial effects of GLP-1RAs on DPN could be related to these direct actions on DRG neurons.

The recently developed Fear of COVID-19 Scale (FCV-19S) is a seven-item uni-dimensional scale that assesses the severity of fears of COVID-19. Given the rapid increase of COVID-19 cases in Bangladesh, we aimed to translate and validate the FCV-19S in Bangla. The forward-backward translation method was used to translate the English version of the questionnaire into Bangla. The reliability and validity properties of the Bangla FCV-19S were rigorously psychometrically evaluated (utilizing both confirmatory factor analysis and Rasch analysis) in relation to socio-demographic variables, national lockdown variables, and response to the Bangla Health Patient Questionnaire. The sample comprised 8550 Bangladeshi participants. The Cronbach α value for the Bangla FCV-19S was 0.871 indicating very good internal reliability. The results of the confirmatory factor analysis showed that the uni-dimensional factor structure of the FCV-19S fitted well with the data. The FCV-19S was significantly correlated with the nine-item Bangla Patient Health Questionnaire (PHQ-90) ( r  = 0.406, p  < 0.001). FCV-19S scores were significantly associated with higher worries concerning lockdown. Measurement invariance of the FCV-19S showed no differences with respect to age or gender. The Bangla version of FCV-19S is a valid and reliable tool with robust psychometric properties which will be useful for researchers carrying out studies among the Bangla speaking population in assessing the psychological impact of fear from COVID-19 infection during this pandemic.