The association between ulcerative colitis and COVID-19 severity: a systematic review and meta-analysis systematic review.

PURPOSE: After the COVID-19 pandemic, many challenges arose regarding the impact of this disease on people with ulcerative colitis. The aims of this study were to estimate the prevalence, severity, and death consequences of COVID-19 in patients with ulcerative colitis using a systematic review and meta-analysis. METHODS: This study was conducted using a systematic review and meta-analysis method in the field of prevalence, severity, and clinical consequences of COVID-19 in people with ulcerative colitis worldwide. The search was conducted in international scientific databases, such as Web of Science, PubMed, Scopus, Cochrane Library, and Google Scholar, from the beginning of 2020 to October 2023. The quality of the eligible studies was assessed using the Strobe and Newcastle Ottawa checklists. The data were analyzed using a fixed-effects model in the meta-analysis. Subgroup analysis and meta-regression were performed using STATA version 17. RESULTS: Nineteen studies with a sample size of 224,520 patients were included in this meta-analysis. The results showed that, in COVID-19 patients with ulcerative colitis, the prevalence of hospitalization, death, COVID-19 severity, and mortality rate in severe patients was 54% (95% CI, 27-80%), 10% (95% CI, 4-16%), 20% (95% CI, 8-34%), 63% (95% CI, 46-80%), respectively. In comparison with the general population, the odds ratio (OR) of hospitalization in patients due to COVID-19 was OR = 1.28 (95% CI, 1.19-1.38, P < 0.001), and the chance of severe COVID-19 was OR = 1.30 (95% CI, 1.22-1.53, P < 0.001). CONCLUSION: The probability of contracting the severe type of COVID-19 and hospitalization in patients with ulcerative colitis was higher than in the general population.

Identification and Verification of Potential Hub Genes in Amphetamine-Type Stimulant (ATS) and Opioid Dependence by Bioinformatic Analysis.

Objective: Amphetamine-type stimulant (ATS) and opioid dependencies are chronic inflammatory diseases with similar symptoms and common genomics. However, their coexpressive genes have not been thoroughly investigated. We aimed to identify and verify the coexpressive hub genes and pathway involved in the pathogenesis of ATS and opioid dependencies. Methods: The microarray of ATS- and opioid-treatment mouse models was obtained from the Gene Expression Omnibus database. GEO2R and Venn diagram were performed to identify differentially expressed genes (DEGs) and coexpressive DEGs (CDEGs). Functional annotation and protein-protein interaction network detected the potential functions. The hub genes were screened using the CytoHubba and MCODE plugin with different algorithms, and further validated by receiver operating characteristic analysis in the GSE15774 database. We also validated the hub genes mRNA levels in BV2 cells using qPCR. Result: Forty-four CDEGs were identified between ATS and opioid databases, which were prominently enriched in the PI3K/Akt signaling pathway. The top 10 hub genes were mainly enriched in apoptotic process (CD44, Dusp1, Sgk1, and Hspa1b), neuron differentiation, migration, and proliferation (Nr4a2 and Ddit4), response to external stimulation (Fos and Cdkn1a), and transcriptional regulation (Nr4a2 and Npas4). Receiver operating characteristic (ROC) analysis found that six hub genes (Fos, Dusp1, Sgk1, Ddit4, Cdkn1a, and Nr4a2) have an area under the curve (AUC) of more than 0.70 in GSE15774. The mRNA levels of Fos, Dusp1, Sgk1, Ddit4, Cdkn1a, PI3K, and Akt in BV2 cells and GSE15774 with METH and heroin treatments were higher than those of controls. However, the Nr4a2 mRNA levels increased in BV2 cells and decreased in the bioinformatic analysis. Conclusions: The identification of hub genes was associated with ATS and opioid dependencies, which were involved in apoptosis, neuron differentiation, migration, and proliferation. The PI3K/Akt signaling pathway might play a critical role in the pathogenesis of substance dependence.

ERCC1 polymorphism and its expression associated with ischemic stroke in Chinese population.

Background: Excision repair cross-complementing group 1 (ERCC1) was considered a potential candidate gene for ischemic stroke, and its polymorphisms might be associated with the susceptibility to ischemic stroke. Methods: A total of 513 patients with ischemic stroke and 550 control subjects were recruited. The expression levels of ERCC1 messenger RNA (mRNA) in peripheral blood mononuclear cells and its protein in plasma were detected by quantitative real-time PCR (qPCR) and enzyme-linked immunosorbent assay (ELISA), respectively. Rs3212986 polymorphism of ERCC1 was detected by PCR-restriction fragment length polymorphism (RFLP-PCR) and was confirmed by sequencing. The association between the ERCC1 rs3212986 polymorphism or its expression and ischemic stroke was further analyzed. Results: The ERCC1 mRNA level in patients with ischemic stroke was lower than that in the control group (P < 0.05). However, the ERCC1 protein level in patients with ischemic stroke was higher than that in the control group (P < 0.05). The A allele of rs3212986 was associated with increased ischemic stroke risk (OR = 1.287, 95% CI = 1.076-1.540, P = 0.006). The association between rs3212986 polymorphism and ischemic stroke susceptibility was found in both recessive (OR = 2.638, 95% CI = 1.744-3.989, P < 0.001) and additive models (OR = 1.309, 95% CI = 1.028-1.667, P = 0.031), respectively. Similar results were obtained in the recessive model (OR = 2.015, 95% CI = 1.087-3.704, P = 0.026) after adjusting for demographic information and other variables. Additionally, the level of ERCC1 mRNA in the CC/CA genotype was higher than that in the AA genotype (P < 0.05). Conclusion: It was suggested that the ERCC1 rs3212986 polymorphism was associated with ischemic stroke susceptibility in a Chinese Han population and that an A allele of rs3212986 was related to increased ischemic stroke risk. The altered ERCC1 expression level caused by the rs3212986 polymorphism might participate in the pathophysiological process of ischemic stroke.

Study on Risk Factors for Death from Cardiomyopathy and Effectiveness of Health Information Management.

Objective: To explore risk factors for death from cardiomyopathy and the effectiveness of health information management (HIM). Methods: A total of 80 patients with cardiomyopathy admitted in ICU of our hospital (January 2016-January 2020) were selected as study subjects, and the clinical data of the patients were retrospectively analyzed. The patients were divided into the survival group (n = 72) and the death group (n = 14) according to the treatment outcome. Then, according to the management mode, the survival group was further equally divided into the conventional group and the HIM group to investigate the influence of risk factors on prognosis of patients with cardiomyopathy and the effectiveness of HIM. Results: No significant difference was found in baseline body mass, myocardial enzymes, troponin, infection factors, history of heart disease, and gender between the survival group and the death group (P > 0.05). Compared with the survival group, the patients of the death group were older (P < 0.05), LVEF of the death group was obviously lower (P < 0.05), and the scores of APACHE II and SOFA of the death group were obviously higher (P < 0.05). Further logistic regression analysis of the univariate factors influencing the risk of death from cardiomyopathy led to the conclusion that LVEF was an independent risk factor for death in patients with cardiomyopathy. LVEF below 24.69% examined by echocardiography had a high predictive value, with a sensitivity of 98.6% and a specificity of 78.6%. No obvious difference was found in general data between the conventional group and the HIM group (P > 0.05). Compared with the conventional group, the disease remission rate, complication rate, awareness rate of health knowledge, ICU length of stay, and scores of self-management efficacy of the HIM group were obviously better (P < 0.05). No significant difference was found in 5-year mean survival rate between the conventional group and the HIM group (P > 0.05). Conclusion: Older age, lower LVEF, and higher scores of APACHE II and SOFA are all risk factors for death from cardiomyopathy. Lower LVEF is an independent risk factor, and LVEF below 24.69% is an important indicator of increased risk of death. Moreover, HIM can effectively improve short-term treatment efficacy but has little effect on the long-term survival rate.

Anti-Arrhythmic Effects of Linalool via Cx43 Expression in a Rat Model of Myocardial Infarction.

BACKGROUND: Lavender is a traditional therapy for different heart symptoms including palpitation, which comprises an important symptom of cardiac arrhythmias. This experiment was designed to evaluate the antiarrhythmic effects of linalool using an experimental model of arrhythmia following myocardial infarction in rats. The underlying electrophysiological mechanism through cardiac connexin 43 (Cx43) expression was also investigated. METHODS: Fifty male Sprague-Dawley rats were divided into five equal groups. The first group was considered as the normal control group; MI was induced by ligation of the left anterior descending artery (LAD) in the second group. The other three groups received metoprolol (100 mg/kg/day) or linalool (50 or 100 mg/kg/day) for seven days before LAD ligation. The arrhythmia score, isolated myocyte resting potential, histological changes, and cardiac Cx43 expression levels were evaluated. RESULTS: In the MI group, there was a significant increase in the arrhythmia score but a marked decrease in resting membrane potential relative to the control; these changes were prevented by the administration of metoprolol or linalool. The histological changes were also minimized in the groups treated with these substances compared to the untreated MI group. The western blot and real-time PCR results showed that the protein expression of Cx43 in the infarct zone of the rat hearts was significantly higher in the MI groups receiving metoprolol or linalool compared with the untreated MI group. CONCLUSION: Linalool was shown to be able to dose-dependently decrease the incidence of arrhythmias in a rat model of myocardial infarction. We propose that the key mechanism behind this antiarrhythmic effect is probably the prevention of decreased Cx43 expression following MI.