The relationship between prognosis and temporal muscle thickness in 102 patients with glioblastoma.

Temporal muscle thickness measured on 3D MRI has recently been linked to prognosis in glioblastoma patients and may serve as an independent prognostic indicator. This single-center study looked at temporal muscle thickness and prognosis in patients with primary glioblastoma. Overall survival was the major study outcome. For a retrospective analysis from 2010 to 2020, clinical data from 102 patients with glioblastoma at the Department of Oncology Radiotherapy of the First Affiliated Hospital of Dalian Medical University were gathered. Fifty-five cases from 2016 to 2020 contained glioblastoma molecular typing data, of which 45 were IDH wild-type glioblastomas and were analysed separately. TMT was measured on enhanced T1-weighted magnetic resonance images in patients with newly diagnosed glioblastoma.Overall patient survival (OS) was calculated by the Kaplan-Meier method and survival curves were plotted using the log-rank-sum test to determine differences between groups, and multifactorial analyses were performed using a Cox proportional-risk model.The median TMT for 102 patients was 6.775 mm (range: 4.95-10.45 mm). Patients were grouped according to median TMT, and the median overall survival (23.0 months) was significantly longer in the TMT > median group than in the TMT median group (P 0.001; Log-rank test). Analysing 45 patients with IDH wild type alone, the median overall survival (12 months) of patients in the TMT > median group was significantly longer than that of patients in the TMT ≤ median group (8 months) (P < 0.001; Log-rank test).TMT can serve as an independent prognostic factor for glioblastoma.

Advances in Biomarkers for Detecting Early Cancer Treatment-Related Cardiac Dysfunction.

With the gradual prolongation of the overall survival of cancer patients, the cardiovascular toxicity associated with oncology drug therapy and radiotherapy has attracted increasing attention. At present, the main methods to identify early cancer treatment-related cardiac dysfunction (CTRCD) include imaging examination and blood biomarkers. In this review, we will summarize the research progress of subclinical CTRCD-related blood biomarkers in detail. At present, common tumor therapies that cause CTRCD include: (1) Chemotherapy-The CTRCD induced by chemotherapy drugs represented by anthracycline showed a dose-dependent characteristic and most of the myocardial damage is irreversible. (2) Targeted therapy-Cardiovascular injury caused by molecular-targeted therapy drugs such as trastuzumab can be partially or completely alleviated via timely intervention. (3) Immunotherapy-Patients developed severe left ventricular dysfunction who received immune checkpoint inhibitors have been reported. (4) Radiotherapy-CTRCD induced by radiotherapy has been shown to be significantly associated with cardiac radiation dose and radiation volume. Numerous reports have shown that elevated troponin and B-type natriuretic peptide after cancer treatment are significantly associated with heart failure and asymptomatic left ventricular dysfunction. In recent years, a few emerging subclinical CTRCD potential biomarkers have attracted attention. C-reactive protein and ST2 have been shown to be associated with CTRCD after chemotherapy and radiation. Galectin-3, myeloperoxidas, placental growth factor, growth differentiation factor 15 and microRNAs have potential value in predicting CTRCD. In this review, we will summarize CTRCD caused by various tumor therapies from the perspective of cardio-oncology, and focus on the latest research progress of subclinical CTRCD biomarkers.

Investigation on Risk Stratification and the Prognostic Value of hs-TnT Combined with MMP-2 in Patients with Acute Coronary Syndrome.

OBJECTIVE: The aim of this study was at investigating the risk stratification and prognostic value of hypersensitive troponin T (hs-TnT) combined with matrix metalloproteinase 2 (MMP-2) in patients with acute coronary syndrome (ACS). METHODS: 80 patients with coronary syndrome admitted to our hospital from January 2019 to January 2020 and 40 healthy people (control group) in the same period were selected. According to different types of diseases, the patients were divided into an acute group (n = 40) and stable group (n = 40). Besides, they all were monitored by the hs-TnT value, serum MMP-2, and coronary angiography at admission and the comparative analysis was carried out. The patients in both groups were followed up for 30 days, and the incidence of adverse cardiovascular events in the patients during this period was recorded. RESULTS: Compared with those in the control group, the MMP-2 and hs-TnT levels in the acute group and the stable group were significantly higher and the MMP-2 and hs-TnT levels in the acute group were significantly higher than those in the stable group, with statistically significant differences (P < 0.05). The 30-day follow-up results showed that the incidence of adverse cardiovascular events in the acute group was significantly higher than that in the stable group, with statistically significant differences (P < 0.05). The hs-TnT and MMP-2 levels in the acute myocardial infarction (AMI) group were significantly higher than those in the unstable angina pectoris (UAP) group, with statistically significant differences (P < 0.01). The hs-TnT and MMP-2 levels in the non-single-vessel group were significantly higher than those in the single-vessel group, with statistically significant differences (P < 0.01). CONCLUSION: The hs-TnT and MMP-2 high expression levels are closely associated with myocardial injury, and they can effectively predict the severity of patients' disease. In addition, the hs-TnT and MMP-2 elevated levels can be considered as an important index to judge the short-term treatment efficacy and the risk stratification of early ACS, playing an important role in clinical treatment and rehabilitation in the later stage.

Effects of GST null genotypes on individual susceptibility to atherosclerotic cardiovascular diseases: a meta-analysis.

Some genetic association studies tried to investigate potential associations between glutathione S-transferase (GST) null genotypes and atherosclerotic cardiovascular diseases (ASCVD). However, the results of these studies were not consistent. Thus, we performed the present meta-analysis to explore associations between GST null genotypes and ASCVD in a larger pooled population. Systematic literature research was performed in PubMed, Web of Science, and Embase to identify eligible studies. We calculated odds ratios (ORs) and 95% confidence intervals (CIs) to estimate the strength of associations. Totally 47 studies were included for analyses. Pooled analyses suggested that GSTM1 (p = .007, OR = 1.29, 95%CI 1.07-1.56) and GSTP1 (p = .01, OR = 1.28, 95%CI 1.06-1.55) null genotypes were significantly associated with individual susceptibility to ASCVD in overall population. Further subgroup analyses revealed similar positive results for GSTM1 null genotype in South Asians and patients with coronary artery disease (CAD). No other significant results were observed for GST null genotypes in overall and subgroup analyses. In conclusion, our meta-analysis suggested that GSTM1 and GSTP1 null genotypes could impact individual susceptibility to ASCVD. These results suggested that these variations could be used to identify individuals at higher susceptibility to ASCVD.

NF2 Inhibits Proliferation and Cancer Stemness in Breast Cancer.

BACKGROUND: Previous studies have shown that NF2 plays a key role in tumorigenesis. NF2 has been illustrated to be downregulated in several types of human cancer. However, the role of NF2 in breast cancer remains unclear. METHODS: We used UALCAN and KM-plotter database to study NF2 expression in human breast cancer and corresponding normal tissues and analyzed its relationship with clinicopathological parameters. We investigated the role of NF2 in breast cancer cells behavior by inhibiting its expression in MDA-MB-231 and MCF-7 cells. RESULTS: In this study, we found that NF2 was downregulated in breast cancer tissues compared to the adjacent normal tissues. We found that the low expression of NF2 was related with the tumor stage. NF2 overexpression inhibited the cell colon formation and stemness. CONCLUSION: Our results indicate a role of NF2 in the progression of breast cancer.

Identification of an Integrase That Responsible for Precise Integration and Excision of Riemerella anatipestifer Genomic Island.

Riemerella anatipestifer is a Gram-negative, pathogenic bacterium, which is harmful to poultry. However, the genomic islands (GIs) in R. anatipestifer are not well-studied. In this study, a 10K genomic island was predicted by the bioinformatics analysis of R. anatipestifer ATCC 11845, which is widely found in other R. anatipestifer genomes. We had first reported the genomic island integration and excision function in R. anatipestifer. We successfully constructed the integration plasmid by using the integrase and 53 bp attP elements. The 10K GI was found integrated at the 53 bp attB located in the Arg-tRNA of the R. anatipestifer RA-YM chromosome. We identified an integrase that helped in the precise integration and excision in R. anatipestifer and elucidated the molecular mechanism of the 10K genomic island integration and excision. Furthermore, we provided a new method for the gene expression and construction of complementary strain.

Transmissible Gastroenteritis Virus Infection Up-Regulates FcRn Expression via Nucleocapsid Protein and Secretion of TGF-ß in Porcine Intestinal Epithelial Cells.

Transmissible gastroenteritis virus (TGEV) is a porcine intestinal coronavirus that causes fatal severe watery diarrhea in piglets. The neonatal Fc receptor (FcRn) is the only IgG transport receptor, its expression on mucosal surfaces is triggered upon viral stimulation, which significantly enhances mucosal immunity. We utilized TGEV as a model pathogen to explore the role of FcRn in resisting viral invasion in overall intestinal mucosal immunity. TGEV induced FcRn expression by activating NF-κB signaling in porcine small intestinal epithelial (IPEC-J2) cells, however, the underlying mechanisms are unclear. First, using small interfering RNAs, we found that TGEV up-regulated FcRn expression via TLR3, TLR9 and RIG-I. Moreover, TGEV induced IL-1ß, IL-6, IL-8, TGF-ß, and TNF-α production. TGF-ß-stimulated IPEC-J2 cells highly up-regulated FcRn expression, while treatment with a JNK-specific inhibitor down-regulated the expression. TGEV nucleocapsid (N) protein also enhanced FcRn promoter activity via the NF-κB signaling pathway and its central region (aa 128-252) was essential for FcRn activation. Additionally, N protein-mediated FcRn up-regulation promotes IgG transcytosis. Thus, TGEV N protein and TGF-ß up-regulated FcRn expression, further clarifying the molecular mechanism of up-regulation of FcRn expression by TGEV.