Objective To explore the endoplasmic reticulum stress (ERS) apoptosis pathway in unilateral ureteral obstruction (UUO) mechanism of renal interstitial fibrosis in rats.Methods The rats were randomly divided into con-trol group and model group,UUO group line ligation of the left ureter,three days 3,7 and 14 days HE and Masson staining were used to observe the renal pathological changes;Take blood retinal venous plexus,separat and determina-tion of serum blood urea nitrogen and creatinine;Western blot was used to find protein 78 (GRP78) glucose regula-tion,endoplasmic reticulum source sex transcription factor (CHOP) and apoptosis related proteins cysteine aspartic acid proteinase 3(caspase-3) and caspase-12 protein expression. Results Compared with control group,the visible UUO model group 1) expansion of renal tubule and renal interstitial fibrosis degree with the extension of ureteral ob-struction time and progressive increase;2) GRP78,CHOP,caspase-3 and caspase-12 protein expression in postoper-ative 3 d have to rise,as the obstruction prolonged,the protein expression more significantly(P<0.01).Conclusions Endoplasmic reticulum stress related trademark protein in UUO rat renal interstitial fibrosis is the increase in expres-sion may promote the early renal interstitial fibrosis and continuous progress.

Objective To explore the endoplasmic reticulum stress (ERS) apoptosis pathway in unilateral ureteral obstruction (UUO) mechanism of renal interstitial fibrosis in rats.Methods The rats were randomly divided into con-trol group and model group,UUO group line ligation of the left ureter,three days 3,7 and 14 days HE and Masson staining were used to observe the renal pathological changes;Take blood retinal venous plexus,separat and determina-tion of serum blood urea nitrogen and creatinine;Western blot was used to find protein 78 (GRP78) glucose regula-tion,endoplasmic reticulum source sex transcription factor (CHOP) and apoptosis related proteins cysteine aspartic acid proteinase 3(caspase-3) and caspase-12 protein expression. Results Compared with control group,the visible UUO model group 1) expansion of renal tubule and renal interstitial fibrosis degree with the extension of ureteral ob-struction time and progressive increase;2) GRP78,CHOP,caspase-3 and caspase-12 protein expression in postoper-ative 3 d have to rise,as the obstruction prolonged,the protein expression more significantly(P<0.01).Conclusions Endoplasmic reticulum stress related trademark protein in UUO rat renal interstitial fibrosis is the increase in expres-sion may promote the early renal interstitial fibrosis and continuous progress.

Objective To evaluate the CT findings of pancreatic carcinoid tumors.Methods The CT imaging data of five patients with pancreatic carcinoid tumors confirmed by pathology were retrospectively analyzed.Results The tumors ranged in maximum diameter from 2.0 to 11.0 cm with a mean of 6.4 cm. On unenhanced CT,the tumors were slightly hypodense relative to the pancreatic parenchyma,homogenous in 2 cases,and heterogenous in 3 cases.One tumor showed calcification.After contrast material injection, the solid component of the tumor showed marked heterogenous enhancement on the arterial phase scanning in 3 cases,and mild heterogenous enhancement in 2 cases.The degree of tumor enhancement was less intense than the surrounding pancreatic parenchyma due to necrosis of various degree,which led to the cystic appearance of the tumor in 1 ease.On the portal phase scanning,all tumors showed marked enhancement similar to that of the pancreatic parenchyma.On the delayed phase scanning,the degree of enhancement was more intense than the surrounding pancreatic parenchyma in 1 case.Liver metastases with retroperitoneal lymphadenopathy and peripancreatic vessels invasion were seen in 1 case.No dilatation of the biliary tract or pancreatic duct was present.Conclusion The CT features of pancreatic carcinoid tumors included infrequent dilatation of the biliary tract or pancreatic duct and unusual vascular involvement,calcification within the mass,marked enhancement similar to that of the surrounding pancreatic parenchyma during the portal phase scanning and more intense during the delayed phase scanning.

Aneurysm, False/complications* ; Atrial Appendage ; Fistula/complications* ; Heart Aneurysm/complications* ; Humans ; Mitral Valve

Objective To discover critical genes contributing to the stemness and maintenance of spermatogonial stem cells (SSCs) and provide new insights into the function of the leucine-rich repeat (LRR) family member Lrrc34 (leucine-rich repeat-containing 34) in SSCs from mice. Methods Bioinformatic methods, including differentially expressed gene (DEG), gene ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, were used to uncover latent pluripotency-related genes. Reverse transcription-polymerase chain reaction (RT-PCR) and immunofluorescence analyses were utilized to verify the mRNA and protein expression levels, respectively. RNA interference of Lrrc34 using siRNA was performed to detect its transient impact on SSCs. Results Eight DEGs between ID4-EGFP⁺ (G) and ID4-EGFP⁺/TSPAN8^High (TH), eight DEGs between G and ID4-EGFP⁺/TSPAN8^Low (TL) and eleven DEGs between TH and TL were discovered, and eleven protein-protein interaction (PPI) modules were found to be significant in the PPI network of DEGs. One of the DEGs, Lrrc34, was selected as a potential pluripotency-related gene due to its differential expression among ID4-EGFP⁺ spermatogonia subsets and its interaction with fibroblast growth factor 2 in the fifth module. Immunofluorescence experiments exhibited specific expression of Lrrc34 in a subpopulation of undifferentiated spermatogonia marked by LIN28A, and RT-PCR experiments confirmed the high expression of Lrrc34 in SSCs from P7 and adult mice. The transient knockdown of Lrrc34 in SSCs resulted in reduced colony sizes and significant changes in the transcriptome and apoptotic pathways. Conclusion Lrrc34 is highly expressed in mouse SSCs and is required for SSC proliferation in vitro through effects on transcriptome and signaling transduction pathways.
Animals ; Apoptosis/genetics* ; Cell Proliferation/genetics* ; Cells, Cultured ; Gene Expression Profiling/methods* ; Gene Ontology ; Gene Regulatory Networks ; Humans ; Male ; Mice, Inbred C57BL ; Mice, Transgenic ; RNA Interference ; Repressor Proteins/metabolism* ; Signal Transduction/genetics* ; Stem Cells/metabolism*