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Rodent studies suggest muscle fibre type-specific insulin response in the recovery from exercise. The current study investigates muscle fibre type-specific insulin action in the recovery from exercise in healthy subjects. In type I and type II muscle fibres, key proteins in glucose metabolism are similarly regulated by insulin during recovery from exercise. Our findings imply that both type I and type II muscle fibres contribute to the phenomenon of increased insulin sensitivity in the recovery from a single bout of exercise in humans.

Human skeletal muscle consists of slow-twitch (type I) and fast-twitch (type II) muscle fibres. Muscle insulin action, regulating glucose uptake and metabolism, is improved following a single exercise bout. Rodent studies suggest that this phenomenon is confined to specific muscle fibre types. Whether this phenomenon is also confined to specific fibre types in humans has not been described. To investigate this, nine healthy men underwent a euglycaemic hyperinsulinaemic clamof glycogen synthase was also similar in the two fibre types. Thus, insulin-induced regulation of key proteins important for transport and intracellular flux of glucose towards glycogen storage in the recovery from exercise, does not differ between fibre types. In conclusion, the insulin-sensitizing effect of a single bout of exercise includes both type I and type II fibres in human skeletal muscle. This may be an important observation for future pharmacological strategies targeting muscle insulin sensitivity in humans.Hepatocellular carcinoma (HCC), a primary liver tumor, is the third leading cause of cancer-related mortality worldwide. The proteasome system is overactivated in the majority of tumors, including HCC. However, targeting the proteasome system in HCC is not as effective as in other types of cancer. Therefore, a new target of HCC therapy needs to be identified, and the potential mechanism must be studied. Using the The Cancer Gene Genome Atlas and GEO datasets, the present investigation demonstrated for the first time that ADRM1 is overexpressed in HCC, and the high level of its expression predicts poor overall survival in HCC patients. The high expression of ADRM1 in HCC was verified using tumor tissue arrays. By comparing paired tumor and nontumor tissues, it was shown that the majority of HCC patients (76.25%) exhibited higher ADRM1 expression in the tumor than in normal tissues. in vitro experiments demonstrated that targeting ADRM1 with shRNAs significantly suppressed the proliferation of HCC cells. RA190, a specific inhibitor of ADRM1, suppressed cell proliferation and colony formation by HCC cells in a concentration-dependent manner. The study of the mechanism of the effects of RA190 revealed that targeting ADRM1 blocked the G2/M transition in the cell cycle and induced apoptosis of HCC cells. Together, the obtained results indicate that ADRM1 is a promising target for HCC therapy and suggest that ADRM1 inhibitors, such as RA190, have the potential for clinical application in the treatment of HCC.

To determine the factors for failure of endoscopic ureteric stenting in patients with malignant ureteric obstruction.

We performed a search strategy in the Medical Literature Analysis and Retrieval System Online (MEDLINE), the Excerpta Medica dataBASE (EMBASE), the Literatura Latino-Americana e do Caribe em Ciências da Saúde database (LILACS), and the Cochrane Central Register of Controlled Trials (CENTRAL) databases. We included patients with malignant ureteric obstruction, who had a JJ catheter insertion. The studies reported the percentage of failure and risk factors, e.g. bladder invasion or deformity of the trigone, hydronephrosis, renal failure, previous radiotherapy, age, obstruction aetiology, and patient's health status. We performed a meta-analysis using R software ('meta' and 'metafor' libraries).

We included nine studies that met the inclusion criteria, with 761 patients and an average age of 60.5years. The studies assessed the time to failure during the first 30days. Rapamycin molecular weight The reported failure rate was 32% (95% confidence interval [CI] 21-45%; I

= 88%). Regarding risk factors for failure, bladder invasion or deformity of the trigone had a hazard ratio (HR) of 4.8 (95% CI 1.28-8.5; I

= 97.4%); severe hydronephrosis had a HR of 3.92 (95% CI 0.32-7.52; I

= 93.9%); and age <65years had a HR of 0.93 (95% CI 0.8-0.9; I

= 0%).

We found a high probability of failure for endoscopic urinary decompression in patients with malignant ureteric obstruction. Factors such as bladder invasion or deformity of the trigone and age >65years had an increased risk of failure.

65 years had an increased risk of failure.Acute myocardium infarction (AMI) is one of the main causes of cardiovascular death, and timely intervention and diagnosis are essential. Owing to the irreversible apoptosis and death of myocardial cells, which ultimately causes heart failure, the problem of myocardial repair after myocardial infarction needs to be urgently addressed. Exosomes can act as messengers between cells, delivering large amounts of proteins, RNA, and lipids to receptor cells, and regulating target cell functions. Studies have shown that exosomes can repair infarcted myocardium. We aimed to investigate the relationship between long non-coding RNA NEAT1 in serum exosomes of patients and AMI and its underlying mechanism. Subjects were divided into control, UA, and STEMI groups. RNA was extracted from the serum exosomes, and the expressions of lncRNA NEAT1 and miR-204 were detected by qRT-PCR. MMP-9 was detected by western blot, Spearman test was used to analyze the correlation among the three. Logistic regression and Receiver-operating characteristic curve (ROC) were used to evaluate the prediction of acute myocardial infarction. The expressions of NEAT1 and MMP-9 in serum exosomes of patients with acute ST-segment elevation myocardial infarction were up-regulated and positively correlated, miR-204 expression was down-regulated, there were no correlations between miR-204 with NEAT1, or MMP-9. Exosomal NEAT1, miR-204, and MMP-9 displayed potent biomarkers for diagnosis of acute ST-segment elevation myocardial infarction.

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