Many genes are regulated by androgen and its receptor (AR), but the direct target genes of AR, especially those involved in spermatogenesis and male infertility, remain unclear. Here, we identified ubiquitin-conjugating enzyme E2B (Ube2b) as a critical target gene of AR. The expression of UBE2B was decreased in the testes of Sertoli cell AR knockout (S-AR(-/y)) mice analyzed by quantitative RT-PCR (qRT-PCR) and immunofluorescence. The upregulation of Ube2b gene by testosterone was further demonstrated by Western blot and qRT-PCR in TM4 cells, a mouse Sertoli cell line. Moreover, luciferase assay, electrophoretic mobility shift assay, and chromatin immunoprecipitation assay validated that the ligand-bound AR activated Ube2b transcription via direct binding to the androgen-responsive element of the Ube2b promoter. In vitro analyses showed that testosterone increased UBE2B expression and activated H2A ubiquitylation, while downregulation of UBE2B blocked the testosterone-induced H2A ubiquitylation. The ubiquitylation of H2A was markedly decreased in the testes of S-AR(-/y) mice by immunohistochemistry. Digital gene expression analysis showed that 113 genes were significantly downregulated and 71 were upregulated by UBE2B in TM4 cells. These results suggest that Ube2b, as a direct AR transcriptional target in Sertoli cells, mediates the function of AR in spermatogenesis by promoting H2A ubiquitylation.

The aim of the present study was to investigate the effects of Toll-like receptor (TLR) 9 and CpG oligodeoxynucleotide (CpG-ODN)1826 on sodium taurocholate-induced acute pancreatitis (AP) rats at different time points. Pathological examination indicated that the severity of pancreatic tissue damage following AP increased with time. Additionally, TLR9 protein levels were upregulated after AP, and were higher at 6 h compared with at 3 h. Subsequently, the TLR9 protein levels were downregulated at 12 h, but remained higher than the control group. In rats subjected to AP, tumor necrosis factor (TNF-α protein expression levels and serum amylase (AMS) in the serum were increased until 12 h. The expression level of TNF-α protein in the AP 12 h group was higher than that in the AP 3 and 6 h groups. In addition, following CpG-ODN1826 administration, the morphology of pancreatic tissue appeared worse compared with that in the AP only groups. Furthermore, CpG-ODN1826 administration induced an increase in TLR9 expression levels compared with the AP alone group at 0, 3, 6 and 12 h. TNF-α in the CpG + AP 12 h group was upregulated compared with that in the CpG + AP 3 and 6 h groups; however, no change was observed between 3 and 6 h. Thus, these data indicate that CpG-ODN1826 aggravates sodium taurocholate-induced pancreas damage in rats.

Background Giant hiatal hernia is defined as those with more than 30% of the stomach herniating into the chest cavity. The transabdominal laparoscopic approach is the well-established repair form for giant hiatal hernia. To our best knowledge, reports on post-operative gastric outlet obstruction of giant hiatal hernia repair have been scanty up till now. Case presentation A 45-year-old female patient was referred to the Emergency Department of our hospital with a chief complaint of acute right epigastric pain for 2 days. Physical examination revealed mild tenderness in the right epigastrium, without rebound tenderness or guarding. The abdominal computed tomography scan revealed a large low-density gastric artifact in the lower mediastinum—giant hiatal hernia. The barium swallow esophagogram and gastroscopy also confirmed the presence of a giant hiatal hernia. A transabdominal laparoscopic operation for reduction of the hernia contents and repair of the hiatal defect was performed. Her right epigastric pain alleviated obviously on the first postoperative day. On post-operative day five, however, she was presented with nausea and vomiting independent of meals. The nasogastric tube was inserted and kept in the stomach for 7 days. After removing the nasogastric tube, severe nausea and vomiting of the patient occurred again. Barium swallow revealed gastroptosis and enfoldment in the duodenal bulb, which indicated the presence of gastric outlet obstruction. Gastrojejunostomy was performed for her to relieve the gastric outlet obstruction. The patient was discharged on the tenth day after the second operation without any discomfort. During the regular follow-up period, she felt well and was satisfied with her status. Conclusions Facing the giant hiatal hernia repair, the reduction of the hernia contents and repair of the hiatal defect being well operated on are insufficient, and we must watch out the anatomical variation, like the deviation of partial intra-abdominal organs from their normal positions, as well as paying attention to the protection of abdominal vagal nerve during the operation. Post-operative gastric outlet obstruction of giant hiatal hernia repair is rare, while gastrojejunostomy can successfully relieve the gastric outlet obstruction.