Faberterkildsen2490

Acute myocardial infarction (AMI) seriously threatens human life. In this study we aimed to systemically analyze the function of key gene modules in human platelets in AMI. We used weighted gene co-expression network analysis (WGCNA) to construct a co-expression module, and analyzed the relationship between potential modules and clinical characteristics based on platelet RNA-seq RPKM count reads of 16 ST-segment elevation myocardial infarction (STEMI) patients and 16 non-STEMI (NSTEMI) patients provided by the GEO database. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were performed with the DAVID tool. MG132 Hub genes were calculated by the Cytohubba package. A total of 3653 genes was selected to construct the co-expression modules. A significant correlation between BMI and the module with color of sky-blue in STEMI. In NSTEMI, there was a significant correlation between the sky blue module and CAD, the Salmon module and HT, and the Cyan module and HT. In STEMI, the Hub genes were mainly enriched in functions related to cell membrane signal transduction including Aqp1, Armcx1, Gsta4, Hist3h2a and Il17re. In NSTEMI, the Hub genes are related mainly to energy metabolism in the sky-blue module including Olr1, Nap1l3, Gfer, Dohh, Crispld1 and Ccdc8b; they are mainly related to extracellular space and calcium binding in the Cyan module, including Clec12b, Chd4, Asgr1, Armcx4, Chid1 and Alkbh7. The hub genes in the Salmon module include Ell3, Aldh1b1, Cavin4, Cabp4, Eif1ay and Dus3l. Our results provide a framework for co-expression gene modules in STEMI and NSTEMI patients, and identify key targets as biomarkers for patients with different subtypes of AMI.Prostate cancer is one of the most frequently diagnosed malignancies in developed countries and approximately 248,530 new cases of prostate cancer are likely to be diagnosed in the United States in 2021. During the late 1990s and 2000s, the prostate cancer-related death rate has decreased by 4% per year on average because of advancements in prostate-specific antigen (PSA) testing. However, the non-specificity of PSA to distinguish between benign and malignant forms of cancer is a major concern in the management of prostate cancer. Despite other risk factors in the pathogenesis of prostate cancer, recent advancement in molecular genetics suggests that genetic heredity plays a crucial role in prostate carcinogenesis. Approximately, 60% of heritability and more than 100 well-recognized single-nucleotide-polymorphisms (SNPs) have been found to be associated with prostate cancer and constitute a major risk factor in the development of prostate cancer. Recent findings revealed that a low to moderate effect on the progression of prostate cancer of individual SNPs was observed compared to a strong progressive effect when SNPs were in combination. Here, in this review, we made an attempt to critically analyze the role of SNPs and associated genes in the development of prostate cancer and their implications in diagnostics and therapeutics. A better understanding of the role of SNPs in prostate cancer susceptibility may improve risk prediction, enhance fine-mapping, and furnish new insights into the underlying pathophysiology of prostate cancer.Internal hernias are a rare condition and sometimes life-threatening, and they need an emergency exploratory laparotomy. Appendicectomy for chronic appendicitis is controversial. Without timely treatment, chronic appendicitis may develop into a ruptured appendix and an infection that spreads to other parts of the body, and other serious complications. Here we report the case of 48-year-old female who had intestinal ischemia secondary to internal hernia caused by the appendix adhering to the right ovary. Her medical history indicated a chronic, right lower abdominal pain for three years.

This study aimed to investigate the effects and mechanisms of deoxyschizandrin (DSD) on treatment of ulcerative colitis (UC).

The models of mice with UC were established through dextran sulfate sodium (DSS) administration, and the successful models were treated with DSD. The therapeutic effects of DSD on UC mice were evaluated and its behind mechanisms were analyzed.

After DSS induction, the mice showed increased body weight and colon length, worse disease activity index (DAI) and body inflammation, oxidative stress injury and increased apoptosis of colonic epithelial cells, which were remarkably relieved after DSD intervention. Besides, the levels of TLR4, MyD88 and NF-κB in the colon tissues were elevated in UC mouse models, while DSD treatment reduced the levels of these markers.

DSD can alleviate the symptoms of mice with DSS-induced UC via inhibiting body inflammation, improving oxidative stress and reducing the apoptosis of colonic epithelial cells, which may be attributed to DSD inhibition of the TLR4/NF-κB signaling pathway.

DSD can alleviate the symptoms of mice with DSS-induced UC via inhibiting body inflammation, improving oxidative stress and reducing the apoptosis of colonic epithelial cells, which may be attributed to DSD inhibition of the TLR4/NF-κB signaling pathway.

To study the effect of hip replacement surgery on the clinical treatment efficacy, VAS score and Harris hip score of patients with necrosis of the femoral head (NFH). A total of 86 patients with NFH who were treated in our hospital from January 2016 to January 2019 were selected as the research subjects, and were divided into the control group (n = 43, conventional artificial hip replacement) and the observation group (n = 43, modified version of artificial hip replacement) according to a random number table method. The treatment efficacy, pain, hip function, motor function and adverse reactions of the two groups were compared.

The effective rate of the observation group was 93.02%, which was higher than 79.07% of the control group (P<0.05). There was no difference in VAS scores of the two groups before treatment (P>0.05); after treatment, VAS scores were reduced, and the observation group was lower than the control group (P<0.05). There was no difference in Harris hip scores between the two groups before treatment; after treatment, the Harris hip joint scores were elevated, and the observation group was higher than the control group (P<0.