Further investigation suggested that sophocarpine-induced autophagy was essential for this suppression of NLRP3 inflammasome activation, the inhibition of which reversed the protective effects of sophocarpine on CLP-induced liver injury. Collectively, results from the present study suggested a protective role for sophocarpine against septic liver injury, where sophocarpine may suppress NLRP3 inflammasome activation by autophagy-mediated degradation.The present study aimed to investigate the clinical effectiveness and safety of endovascular embolization for the treatment of pseudoaneurysm secondary to previous abdominal and pelvic surgery or radiological percutaneous abdominal procedure. A retrospective review was performed on all patients with abdominal and pelvic pseudoaneurysm confirmed by CT angiography or digital subtraction angiography and treated with endovascular embolization. Different techniques of embolization with coils were applied and the outcomes, including clinical effectiveness and safety, were assessed. A total of 31 patients with a total of 32 pseudoaneurysms were included in the present study. Of these pseudoaneurysms, 23 were from the main trunks and branches of the gastroduodenal artery, 5 were from the splenic artery, 2 were from the common hepatic artery, 1 was from the right hepatic artery and 1 was from the right internal iliac artery. There were no serious complications observed and there was no occurrence of re-bleeding following embolization. The embolization of the pseudoaneurysms was successful in all patients. In conclusion, endovascular embolization is a safe and effective method for the treatment of secondary iatrogenic pseudoaneurysm in the abdomen and pelvis.Prostate cancer (PCa), an epithelial malignancy that occurs in the prostate, is the second leading cause of cancer death worldwide. MicroRNAs (miRs/miRNAs) are reported to have important applications in the field of cancer diagnosis and treatment. The present study aimed to investigate the function of miRNA-122 in the chemoresistance of PCa cells and the underlying mechanism. Significantly decreased miR-122 and increased pyruvate kinase (PKM2) levels were observed in docetaxel-resistant PCa cells, and PKM2 was negatively correlated with miR-122. MiR-122 mimic transfection in docetaxel-resistant LNCaP cells significantly inhibited cell proliferation, promoted apoptosis and decreased glucose uptake and lactate production, which was counteracted by PKM2 overexpression.  https://www.selleckchem.com/products/l-arginine-l-glutamate.html  Inhibition of miR-122 in LNCaP cells had an opposite effect to miR-122 mimic transfection. In addition, miR-122 mimic transfection significantly increased the sensitivity of docetaxel-resistant LNCaP cells to docetaxel, while inhibition of miR-122 significantly decreased the sensitivity of LNCaP cells to docetaxel. Luciferase reporter assays showed that miR-122 regulated PKM2 expression by binding to the 3'-untranslated region of PKM2. The results suggest that upregulation of miR-122 could enhance docetaxel sensitivity, inhibit cell proliferation and promote apoptosis in PCa cells,possibly through the downregulation of its target protein PKM2.Diabetic retinopathy (DR) is a serious complication of diabetes and the most common metabolic disorder. Recently, long non-coding (lnc)RNAs have been identified as critical regulators of DR. Ribosomal protein SA pseudogene 52 (RPSAP52) is an oncogenic lncRNA expressed in pituitary tumors. The present study aimed to investigate the functions of RPSAP52 in DR. RPSAP52 levels in the plasma of diabetic patients with or without DR complication was detected. Luciferase reporter assays, RT-qPCR and western blotting were performed to detect the interaction between RPSAP52 and micro RNA (miR)-365. Moreover, expression vectors of RPSAP52 and Timp3, as well as miR-365 mimics were transfected into ARPE-19 cells exposed to high glucose and the apoptotic cells were detected. The results showed that RPSAP52 was downregulated in patients with DR compared with patients with diabetes without obvious complications. RPSAP52 directly interacted with miR-365, while overexpression of RPSAP52 and miR-365 did not affect the expression of one another. In addition, overexpression of RPSAP52 upregulated TIMP metallopeptidase inhibitor 3 (Timp3) in retinal pigment epithelial (RPE) cells. High glucose treatment led to downregulated RPSAP52 and Timp3, but upregulated miR-365 in RPE cells. Moreover, cell apoptosis analysis identified that overexpression of RPSAP52 and Timp3 led to a decreased apoptotic rate of RPE cells under high glucose treatment. Therefore, it was speculated that RPSAP52 may upregulate Timp3 by serving as the endogenous sponge of miR-365 in DR to suppress RPE cell apoptosis.In the present study, differences in the expression of target genes between chromatin immunoprecipitation sequencing (ChIP-seq) datasets of breast cancer MCF-7 cells treated with antibodies to E74-like factor 1 (ELF1) and cold-shock domain-containing E1 (CSDE1) were analyzed and gene regulatory networks were established. The datasets were downloaded from the Gene Expression Omnibus (GEO) database. ELF1-associated target genes and CSDE1-associated target genes were analyzed for functional prediction and protein-protein interaction (PPI) networks. The ELF1 ChIP-seq dataset contained 95 ELF1-associated target genes, while the CSDE1 ChIP-seq dataset contained 826 CSDE1-associated target genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated that the ELF1- and CSDE1-associated target genes had different potential functions and signaling pathways. The ELF1-associated target genes were mainly enriched in the GO terms of molecular transducer activity, catalytic activity, cellu which included mitochondrial ribosomal protein L4, NADH ubiquinone oxidoreductase subunit B7, small nuclear ribonucleoprotein polypeptide E, ribosomal protein S26 (RPS26), RPS11 and RPS6, in the MCF-7 cells. In breast cancer MCF-7 cells, the target genes and regulatory pathways of ELF1 and CSDE1 were different. Understanding these regulatory pathways may help to develop strategies for personalized breast cancer treatment.