Background: Sow endometritis is a common disease in pig breeding farms after artificial insemination, which leads to gray-green vaginal secretions and decreased conception rates. It is important to perform an etiologic diagnosis for effective treatments and control of diseases. The aim of this study was to carry out a pathogenic detection in five specimens of vaginal secretions collected from sick pigs with endometritis, implement identification of the pathogens by phenotypic detection and 16 s rDNA sequence and phylogeny analysis, and determinate antibiotic susceptibility of the isolates. Results: A Streptococcus strain was isolated and identified from all of the five specimens. The isolate was positive for Voges-Proskauer (V-P) and for the hydrolysis of arginine, esculin and myelin-associated glycoprotein (MAG). Acid formation was observed for sorbitol, mushroom sugar, sucrose, and glucose. The 16S rDNA sequence of the isolate possessed 99.93% similarity to that of Streptococcus porcinus. The phylogenetic analysis of 16S rDNA sequence showed that the isolate belonged to the same clade as the S. porcinus strains from humans, pigs, and other animals. The isolate exhibited multi-drug resistance to aminoglycosides, quinolones, macrolides and tetracyclines except being sensitive to some βlactams such as penicillin G, cephalothin, cefazolin, cephradine and cefuroxime. Conclusions: A S. porcinus isolate with multi-drug resistance was identified from vaginal secretions of sows with endometritis in one pig breeding farm, which suggests that the sow endometritis was caused by S. porcinus infection during artificial insemination. This study indicates that sensitive antibiotics such as penicillin G or some cephalosporins could be used for treatment of the diseases. In addition, the study hints that bacterial multi-drug resistance is a tough problem for disease treatment in pig farms.

Background Alterations in the cell metabolism, such as enhanced aerobic glycolysis, have been identified as a prominent hallmark of cancer cells. 3-Bromopyruvate (3-BrPA) is a proverbial hexokinase (HK)-II inhibitor, which can inhibit cancer cell energy metabolism. Rapamycin is a new type macrocyclic lactone, which can inhibit the serine/threonine protein kinase mTOR. In order to comprehend the influence of 3-BrPA on autophagy activity in vitro, we conducted a series of experiments using different human neuroblastoma (NB) cell lines. Materials and Methods The human NB cell lines were exposed to 3-BrPA and/or rapamycin, and the proliferation activity of the cells was detected by Cell Counting Kit-8 (CCK-8) assay. The mRNA expression of the cells treated with 3-BrPA and/or rapamycin was analyzed by quantitative real-time polymerase chain reaction (QPCR) assay. The protein expression of the cells was analyzed by Western Blotting (WB) assay. The effects of 3-BrPA and/or rapamycin treatment on cell cycle and cell apoptosis were analyzed by flow cytometry assay. Meanwhile, the cellular glucose absorption rate, lactate secretion rate and ATP content were also analyzed through the relevant metabolic analysis kits. Results Our results showed that 3-BrPA can induce growth inhibition in a dose-dependent pattern by cell apoptosis. 3-BrPA combined with rapamycin played a synergistic suppression role in NB cells, affected the cell apoptosis, cell cycle and the metabolic pathway. Up-regulated LC3-II accumulation was conscious in NB cells incubated with 3-BrPA and rapamycin. Rapamycin individually discourages the mTOR signaling pathway, while combined with 3-BrPA can enhance this phenomenon and influence cell metabolism of the NB cells. Conclusion The results suggested that 3-BrPA combined with rapamycin could induce cell apoptosis in NB cells by inhibiting mTOR activity. In conclusion, our research proposed that the dual inhibitory effect of the mTOR signaling pathway and the glycolytic activity may indicate a valid therapeutic tactic for NB chemoprevention.

Background Prostate cancer (PCa) is among the most prevalent cancers in males with high biochemical recurrence risk. LINC00106 contributes to the carcinogenesis of Hepatocellular carcinoma (HCC). However, it is unclear how it affects PCa advancement. Here, we studied LINC00106’s effects on PCa cells’ ability to proliferate, invade, and metastasize. Methods The data of LINC00106 from The Cancer Genome Atlas (TCGA) in human PCa tissues were analyzed using TANRIC and survival analysis. In order to determine the expression levels of genes and proteins, we also performed reverse transcription-quantitative PCR and western blot analysis. The migration, invasion, colony formation, and proliferation (CCK-8) of PCa cells with LINC00106 knockdown were investigated. The impact of LINC00106 on cell proliferation and invasion was also analyzed in mice. LncRNA prediction software catRAPID omics v2.1 (catRAPID omics v2.0 (tartaglialab.com)) was used to predict proteins that might interact with LINC00106. The interactions were verified via RNA immunoprecipitation and RNA pull-down assays and finally, the interaction between LINC00106 and its target protein and the p53 signaling pathway was studied using a dual-luciferase reporter assay. Results In PCa, LINC00106 was over-expressed in comparison to normal tissues, and it was linked to an unfavorableprognosis. In vitro and in vivo analyses showed that downregulating LINC00106 decreased PCa cells’ability to proliferate and migrate. A common regulatory axis generated by LINC00106 and RPS19BP1 prevents p53 activity. Conclusion Our experimental data indicate that LINC00106 functions as an oncogene in the onset of PCa, and the LINC00106/RPS19BP1/P53 axis canserve as a novel therapeutic target for PCa treatment.