ABSTRACT
Abstract Objective Menopause causes several changes in the body that may affect the response to COVID-19. We aimed to investigate the possible association between menopausal status and incidence and outcomes in COVID-19 patients. Methods Combinations of keywordsCOVID-19, menopause, and estrogen were used to search the PubMed, Embase, Web-of-Science, and Scopus databases for articles reporting the incidence and outcomes of COVID-19 (discharge, length-of-admission, intensive care, or mortality) in premenopausal women, available through December 29, 2022. Data from studies comparing the incidence of COVID-19 infection with the age-matched male population were pooled and meta-analyzed using a random-effects model. Results Overall, 1,564 studies were retrieved, of which 12 were finally included in the systematic review to compare disease outcomes, and 6 were meta-analyzed for the incidence of COVID-19 in premenopausal and postmenopausal women. All studies reported better COVID-19-associated outcomes in premenopausal women compared with postmenopausal women. After adjusting for confounding factors, three studies found better outcomes in postmenopausal women, and two found no association between menopausal status and COVID-19 outcomes. Our meta-analysis found a higher incidence of COVID-19 infection among premenopausal women than postmenopausal women, when compared with age-matched men (odds ratio = 1.270; 95% confidence interval: 1.086-1.486; p= 0.003). Conclusion The incidence of COVID-19 was significantly higher in premenopausal women than in postmenopausal women when compared with age-matched men. Although premenopausal women may have more favorable COVID-19-associated outcomes, the presumed preventive effect of estrogens on the incidence and related outcomes of COVID-19 in premenopausal women cannot be proven at present. Further longitudinal studies comparing pre- and post-menopausal women are required to provide further insight into this matter.
Resumo Objetivo A menopausa causa diversas alterações no corpo que podem afetar a resposta ao COVID-19. Nosso objetivo foi investigar a possível associação entre o status da menopausa e a incidência e os resultados em pacientes com COVID-19. Métodos Combinações de palavras-chave COVID-19, menopausa e estrogênio foram usadas para pesquisar os bancos de dados PubMed, Embase, Web-of-Science e Scopus para artigos relatando a incidência e os resultados do COVID-19 (alta, tempo de internação, tratamento intensivo cuidados ou mortalidade) em mulheres na pré-menopausa, disponível até 29 de dezembro de 2022. Dados de estudos comparando a incidência de infecção por COVID-19 com a população masculina da mesma idade foram agrupados e meta-analisados usando um modelo de efeitos aleatórios. Resultados No geral, 1.564 estudos foram recuperados, dos quais 12 foram finalmente incluídos na revisão sistemática para comparar os resultados da doença e 6 foram meta-analisados para a incidência de COVID-19 em mulheres na pré e pós-menopausa. Todos os estudos relataram melhores resultados associados ao COVID-19 em mulheres na pré-menopausa em comparação com mulheres na pós-menopausa. Após o ajuste para fatores de confusão, três estudos encontraram melhores resultados em mulheres na pós-menopausa e dois não encontraram associação entre o status da menopausa e os resultados do COVID-19. Nossa meta-análise encontrou uma maior incidência de infecção por COVID-19 entre mulheres na pré-menopausa do que mulheres na pós-menopausa, quando comparadas com homens da mesma idade (odds ratio = 1,270; intervalo de confiança de 95%: 1,086-1,486; p = 0,003). Conclusão A incidência de COVID-19 foi significativamente maior em mulheres na pré-menopausa do que em mulheres na pós-menopausa quando comparadas com homens da mesma idade. Embora as mulheres na pré-menopausa possam ter resultados mais favoráveis associados ao COVID-19, o efeito preventivo presumido dos estrogênios na incidência e nos resultados relacionados ao COVID-19 em mulheres na pré-menopausa não pode ser comprovado no momento. Mas estudos longitudinais comparando mulheres pré e pós-menopausa são necessários para fornecer mais informações sobre este assunto.
Subject(s)
Humans , Female , Middle Aged , Climacteric , Menopause , Estrogens , COVID-19ABSTRACT
Abstract Ginger is traditionally used as a sexual enhancer in folk medicine. Despite extensive studies on the effect of ginger on reproduction, the molecular mechanism of ginger prevention effect on ethanol-induced reproductive disorder is not fully understood. Twenty-four adult male ratswereallocated into control, ethanol (4 g/kg of body weight (BW)/day), ginger (250 mg/kg of BW/day) and ginger-ethanol group. Ginger and ethanol were administrated by gavage for 28 days. Testicular concentration of testosterone, TNF-α, and antioxidant enzymes activity and serum concentration of gonadotropins hormone and testosterone were measured. The gene expression of Nrf2 and NF-κB which regulate oxidative damage and inflammation, respectively, and StAR, P450scc and 17βHSD which are involved in testosterone synthesis were detected. Ethanol significantly decreased gonadotropin hormones, oxidative markers, expression of genes involved in testosterone synthesis and Nrf2, and in reverse significantly increased TNF-α, MDA and gene expression of NF-κB compared to control (p<0.05). While ginger could significantly improve all of the above factors compared to the ethanol group (p<0.05). These results were also supported by histological findings. It can be concluded that ginger prevents the ethanol-induced reproductive dysfunction by improving the gonadotropins, oxidative damage and inflammation and the genes involved in testosterone synthesis.
ABSTRACT
Introduction: Gastric cancer is responsible for a large number of death worldwide and its high death rate is associated with a lack of noninvasive tools in GC diagnosis. MicroRNAs (miRNAs), as gene regulators, were shown to dysregulate in different types of cancer. Moreover, it is proven that miRNAs are stable in serum/plasma, so they can be used as a potential noninvasive marker in GC diagnosis. The objective of this study is to investigate the plasma miRNA expression in GC samples compared to controls as a potential biomarker in cancer diagnosis. Materials and Methods: Expression levels of miR-21 and miR-222 were assessed using quantitative real-time polymerase chain reaction in plasma of 30 GC patients and 30 healthy controls. Diagnostic value of selected miRNAs was evaluated using receiver operating characteristic curve. Target prediction was done using bioinformatics tools to investigate the signaling pathways and function of the selected miRNAs. Results: Our results demonstrated that the expression levels of miR-21 and miR-222 were significantly higher in GC plasma than in the controls (P < 0.0001, P = 0.043). The sensitivity and specificity for miR-21 and in plasma were 86.7% and 72.2% and for miR-222 were 62.5% and 56.2%, respectively. Bioinformatics analysis revealed that most target genes of miR-21 and miR-222 are involved in cancer-related signaling pathway such as tumor initiation and progression. Conclusion: Our results indicated that miR-21 and miR-222 in plasma samples can be served as a potential noninvasive tool in GC detection. Furthermore, the miRNA target prediction manifested that miR-21 and miR-222 involve in key processes associated with GC initiation and development
ABSTRACT
Aims: Retinoblastoma is a childhood ocular tumor rapidly developing from the immature cells of the retina due to loss of functional retinoblastoma protein. Digoxin, a cardiac glycoside, has been reported to be effective in inducing apoptosis, cell cycle arrest, and cytotoxic effects on human cancers. In this regard, the present study aims to investigate whether digoxin could suppress retinoblastoma cancer through the regulation of transforming growth factor-β (TGF-β) signaling pathway. Methodology: The effects of digoxin on Y-79 cells, retinoblastoma cancer cell line, were investigated using MTT (3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyltetrazoli-umbromide) and BrdU (bromodeoxyuridine) assays to measure cellular cytotoxicity effects and cell apoptosis, respectively. Also, a qPCR assay was employed to analyze the mRNA expression levels of TGFβ signaling pathway including C-MYC, P21, P15, TGFβRI, TGFβRII, and SMAD2, 3, and 4 genes. Results: The results of the cell function assays revealed that digoxin inhibited the cell viability and proliferation of Y-79 cells. In addition, it was found that digoxin significantly suppressed C-MYC expression and enhanced the expression of P21, P15, SMAD2 and SMAD4 genes in a dose-and time-dependent manner. However, the obtained results could not detect any significant effect of digoxin on TGFβRI, TGFβRII and SMAD3 genes. Conclusion: Taken together, the findings of the present study suggest that digoxin could be a potential therapeutic agent in the treatment of retinoblastoma by regulating the cell cycle genes via a non-canonical TGF-β signaling pathway.