Objective To raise the etiological diagnostic rate of renal colic in remission period with intravenous urography.Methods High-dense intravenous urography with TV monitoring (HIVP-TV) was employed to detect the 48 cases,including 37 cases in remission and 11 cases in attack periods.Results There were signfiicantly differences in imaging time of obstractive sites of injured kidney and ureter between both remission and attack periods(P

Aim To investigate the expression of G protein-coupled receptor TGR5 and its effects on FN and TGF-β1 expression cultured under high glucose condition in rat glomerular mesangial cells , and then to explore the role of TGR5 in diabetic nephropathy. Methods INT-777 and TGR5 plasmid were used to activate TGR5 under high glucose(HG,30 mmol·L - 1 glucose ) condition, and anti-TGR5 small interfering RNA(TGR5 siRNA) was used to knock down TGR5. The protein expression of FN and TGF-β1 in rat me-sangial cells was detected by Western blot. Results TGR5 could be detected in rat glomerular mesangial cells. Both FN and TGF-β1 protein levels could be in-creased by high glucose compared with control group(P < 0. 05),and be inhibited by activiation of TGR5(P <0. 05). On the other hand,knockdown of TGR5 could increase FN and TGF-β1 protein to abnormal levels(P< 0. 01,P < 0. 05). Conclusion TGR5 suppresses HG-induced FN and TGF-β1 expression in rat glomer-ular mesangial cells,suggesting a protective role in the process of diabetic nephropathy.

Objectives To investigate the effects of seasonal changes on peritoneal dialysis associated peritonitis (PDAP) in patients on peritoneal dialysis (PD),and to provide evidence for clinical prevention and treatment of PDAP.Methods All episodes of PD-related peritonitis during clinic follow-up in maintenance PD patients from Jan 1st,2007 to Dec 31st,2015 in Peking University People's Hospital were reviewed.The incidence of peritonitis,laboratory indexes,pathogens and clinical outcomes in different seasons were recorded and analyzed.One-way ANOVA and chi square test were employed to compare the incidence of PDAP and related data in different seasons,and Pearson correlation was used to analyze correlations between PDAP rate and monthly mean temperature and mean humidity.Results During nine years,a total of 119 PD patients occurred 190 times of peritonitis during home PD.The PDAP rate in summer was the highest,0.21 episodes/year,followed by spring (0.16 episodes/year) and autumn (0.16 episodes/risk year),but there was no significant difference among peritonitis rates in four seasons.There were significant positive correlation between monthly mean temperature,monthly mean humidity and the peritonitis rate (mean temperature:r=0.828,P ＜ 0.01;mean humidity r=0.657,P ＜ 0.05).(2) As for bacteria,in Summer the PDAP rate caused by Staphylococcus aureus and Coagulase negative staphylococcus (CoNS),and Gram-negative bacteria was higher than that in other seasons,but there was no statistical difference.There were significant positive correlation between monthly mean temperature,mean humidity and the rate of CoNS peritonitis (mean temperature:r=0.704,P ＜ 0.05;mean humidity:r=0.607,P ＜ 0.05).(3) There were no statistical difference among results of PD related peritonitis in different seasons about general situation,clinical manifestation,causes of peritonitis and laboratory index before peritonitis episodes.PD procedure-related problems were the main cause of peritonitis in summer and autumn.(4) The cure rate of all peritonitis was 90％.The highest cure rate was in autumn and winter,while the lowest cure rate was in summer,but no statistical difference.Among the peritonitis episodes with treatment failure,52.6％ occurred in summer.Conclusions There is some correlation between the rate of PDAP and seasons.Higher temperature and higher humidity were significantly correlated with higher peritonitis rate,especially the rate of CoNS peritonitis.The prognosis of PDAP in summer was relatively poor,with higher proportion of hospitalization and lower cure rate.

Autophagy is a highly conserved catabolic process that degrades cytosolic proteins and organelles via formation of autophagosomes that fuse with lysosomes to form autolysosomes, whereby autophagic cargos are degraded. Numerous studies have demonstrated that autophagy plays a critical role in the regulation of liver physiology and homeostasis, and impaired autophagy leads to the pathogenesis of various liver diseases such as viral hepatitis, alcohol associated liver diseases (AALD), non-alcoholic fatty liver diseases (NAFLD), and liver cancer. Recent evidence indicates that autophagy may play a dual role in liver cancer: inhibiting early tumor initiation while promoting progression and malignancy of already formed liver tumors. In this review, we summarized the progress of current understanding of how hepatic viral infection, alcohol consumption and diet-induced fatty liver diseases impair hepatic autophagy. We also discussed how impaired autophagy promotes liver tumorigenesis, and paradoxically how autophagy is required to promote the malignancy and progression of liver cancer. Understanding the molecular mechanisms underlying how autophagy differentially affects liver cancer development and progression may help to design better therapeutic strategies for prevention and treatment of liver cancer.

Objective To explore the clinical efficacy of endovenous laser ablation (EVLA) of great saphenous vein combined with foam sclerotherapy in the treatment of variceal ulcer of lower extremities (VULE).Methods Data of 19 patients (20 affected limbs) with VULE were analyzed retrospectively.EVLA combined with foam sclerotherapy was performed,and the clinical effect was observed.Results The treatment was successfully performed in 19 patients (20 affected limbs).Diameters of the ulcer was (2.30 ± 1.61) cm before operation and (0.90± 0.32) cm 2 weeks after operation,respectively (t=10.53,P＜0.01),and the ulcers healed from 7 days to 3 months after the surgery in 20 patients without recurrence.Conclusion EVLA of great saphenous vein combined with foam sclerotherapy has good clinical efficacy.

Macroautophagy (referred to as autophagy hereafter) is a major intracellular lysosomal degradation pathway that is responsible for the degradation of misfolded/damaged proteins and organelles. Previous studies showed that autophagy protects against acetaminophen (APAP)-induced injury (AILI) via selective removal of damaged mitochondria and APAP protein adducts. The lysosome is a critical organelle sitting at the end stage of autophagy for autophagic degradation via fusion with autophagosomes. In the present study, we showed that transcription factor EB (TFEB), a master transcription factor for lysosomal biogenesis, was impaired by APAP resulting in decreased lysosomal biogenesis in mouse livers. Genetic loss-of and gain-of function of hepatic TFEB exacerbated or protected against AILI, respectively. Mechanistically, overexpression of TFEB increased clearance of APAP protein adducts and mitochondria biogenesis as well as SQSTM1/p62-dependent non-canonical nuclear factor erythroid 2-related factor 2 (NRF2) activation to protect against AILI. We also performed an unbiased cell-based imaging high-throughput chemical screening on TFEB and identified a group of TFEB agonists. Among these agonists, salinomycin, an anticoccidial and antibacterial agent, activated TFEB and protected against AILI in mice. In conclusion, genetic and pharmacological activating TFEB may be a promising approach for protecting against AILI.