Objective To explore the improvement effect and possible mechanism of Toll like receptor 4(TLR-4) inhibitors on lipopolysaccharide(LPS) induced myocardial injury in septic cardiomyopathy(SIC) mice. Methods The experiment will be conducted at the Animal Experiment Center of Wuhan University of Science and Technology from March to June 2023. Nine SPF grade male C57BL/6 mice were randomly divided into a control group, SIC group, and TLR4 inhibitor intervention group(intervention group) using a random number table method, with three mice in each group. The SIC group was injected intraperitoneally with LPS(15 mg/kg) to construct a SIC mouse model. The intervention group received pre-treatment with TLR4 inhibitors at a rate of 0.3 mg·kg-1·h-1 via the tail vein 1 hour before constructing the SIC mouse model. The control group was intraperitoneally injected with physiological saline(15 mg/kg). After 24 hours of modeling, the mice were euthanized and their hearts were collected. Hematoxylin eosin(HE) staining was used to observe the pathological changes in the myocardial tissue of the mice. Enzyme linked immunosorbent assay(ELISA) was used to determine serum troponin(cTnI), creatine kinase isoenzyme(CK-MB), plasma brain natriuretic peptide(BNP), and tumor necrosis factor α(TNF-α), Interleukin-6 and IL-1 βin each group of mice. Detection protein expression status of TLR4 and NF κ B by Western Blot. Results The myocardial cell structure in the control group was normal; The arrangement of myocardial fibers in the SIC group was disordered, with some myocardial cells showing edema and obvious inflammatory cell infiltration in the interstitium; The intervention group had relatively intact tissue morphology and structure, with regular arrangement of myocardial fibers and scattered inflammatory cell infiltration in the interstitium. Mouse myocardial injury markers cTnI, CK-MB, BNP: SIC group>intervention group>control group(F=437.637, 631.009, 378.443, P<0.001); inflammatory="" factor="" il-1="" il-6="" expression:="" sic="" group="">intervention group>control group(F=546.621, 329.266, 665.091, all P<0.001); tlr4="" protein="" expression="" level:="" sic="" group="">control group>intervention group(F=388.491, P<0.001), b="" protein="" expression="" level:="" sic="" group="">intervention group>control group(F=77.421, P<0.001). Further correlation analysis revealed the inflammatory factor TNF-α, IL-1β, IL-6 levels and TLR4, NF-κB were positively correlated(r=0.990, 0.988, 0.994, 0.976, 0.981, 0.971, all P<0.001).Conclusion TLR4 inhibitors can downregulate TLR4/NF-κ The B signaling pathway reduces inflammatory response in septic cardiomyopathy mice and improves myocardial injury in SIC mice.

报道1例肾盂输尿管连接处腺性输尿管炎患者的临床资料，并进行文献复习。

Report of a patient with idiopathic hypoparathyroidism cardiomyopathy and review of the literature.

Early repolarization has long been considered as a benign ECG and has a high incidence in general population. In recent years, it has been found that early repolarization/early repolarization syndrome is a genetic-related disease that can manifest as syncope or even sudden cardiac death at the first presentation, which seriously threatens the life and health of the patients. Therefore, it is imminent to strengthen the understanding of early repolarization syndrome. However, it is not completely clear whether the cellular mechanism of early repolarization syndrome is repolarization or depolarization, genetic background, and how to identify high-risk early repolarization. Therefore, the article systematically reviewed the latest research progress on early repolarization and early repolarization syndrome.

Long non-coding RNA(lncRNA) is a kind of RNA molecule with transcript length greater than 200 nt, which does not code for protein. Its role in the development of tumor has been widely studied. LncRNA Linc00467 is a newly discovered lncRNA, and it has been confirmed that it has abnormal expression in liver cancer, stomach cancer, lung cancer, colorectal cancer and other tumors. It can regulate the malignant process of tumor cells and affect the survival and prognosis of patients. It is an oncogene related to many malignant tumors. Combined with the existing reports, the author reviewed the research progress of the role and mechanism of Linc00467 in malignant tumors, in order to provide help for the more comprehensive research of Linc00467.