Objective To evaluate the role of albumin and the involvement of mitogenactivated protein kinases(MAPKs) in rat tubular cells apoptosis. Methods Rat tubular cells (NRK-52E) were incubated with various concentrations (10, 20, 30 mg/ml) of delipidated, endotoxin-free bovine serum albumin(BSA) for 6, 12, 18 and 24 h, respectively. The process of apoptosis was evaluated by fluorescence microscope, transmission electron microscope, scanning electron microscope, confocal laser scanning microscope (CLSM) and flow cytometry. To assess the roles of p38, and the activities of JNK and ERK in albumin-induced apoptosis, SB202190 (20 ?mol/L, p38 inhibitor), SP600125 (10 ?mol/L, JNK inhibitor) or PD98059 (20?mol/L, ERK inhibitor) were added to the NRK-52E cells separately in the presence of albumin for 24 hours. Activities of p38, JNK and ERK were assessed by Western blot analyses. Results The albumin induced tubular cell apoptosis in a doseand time-dependent manner. Albumin stimulated the expression of p38 and JNK, whereas it inhibited the expression of ERK. SB202190 and SP600125 ameliorated tubular cells apoptosis but PD980S9 treatment enhanced their apoptosis. Conclusions Albumin induces tabular cell apoptosis in a time- and dose-dependent manner in vitro, transducted through activation of p38 and JNK, and inhibition of ERK.

Objective: To evaluate the role of the MAPK subtypes (p38MAPK, ERK and JNK) in ANG Ⅱ induced apoptosis of cultured human podocytes. Methods: The cultured podocytes were incubated in media containing either vehicle, SB202190(5 ?mol/L, an inhibitor of p38MAPK), PD98059 (1 ?mol/L, an inhibitor of ERK), SP600125 (5 ?mol/L, an inhibitor of JNK), ANG Ⅱ (10 -8 mol/L) with or without SB202190、PD98059 and SP600125 for 18 hours; the cells were assayed for apoptosis by morphologic staining with H 33342 and propidium iodide and DNA fragmentation assays; the cell proteins were probed for phosphorylated MAPKs to determine the activation of specific MAPK subtypes. Results: ANG Ⅱ promoted podocyte apoptosis in a time and dose dependent manner; ANG Ⅱ stimulated p38MAPK, but inhibited JNK; SB202190 inhibited both ANG Ⅱ induced podocyte apoptosis and p38MAPK phosphorylation; Inhibition of ERK by PD98059 had no effect on ANG Ⅱ induced cell apoptosis. Conclusion: ANG Ⅱ induced apoptosis through stimulation of p38MAPK and inhibition of JNK in human podocytes.

Objective:To build the model of the gene FKBP38 (FK506 binding protein 38) conditional knock out in liver.Methods:Transgenic mouse whose FKBP38 gene was flanked with loxP was constructed by embryo microinjection.The FKBP38 gene was deleted by breeding mice harboring two loxP sites in FKBP38 (FKBP38fl/fl) with the mice bearing the expression ofCre recombinase mice driven by an album promoter.Afterward,the genotype of FKBP38 conditional knockout mice was analyzed.Results:①Relative hepatic FKBP38 mRNA levels showed significant difference between FKBP38 conditional knockout mice (FKBP38-/-) and wild type(P＜ 0.001).②Relative hepatic FKBP38 protein expression levels of FKBP38 conditional knockout mice (FKBP38-/-) were significantly different with wild type(P＜0.001).③Relative phosphorylation of hepatic p70 S6K and 4E-BP-1 protein of FKBP38 conditional knockout mice (FKBP38-/-) showed no significant difference,with slight decrease in phosphorylation of 4E-BP-1,compared with wild type.④No significant difference in expression of hepatic Bcl-2 between FKBP38-/-and wild type.Conclusions:The mouse model of the gene FKBP38 (FK506 binding protein 38) conditional knock out in liver is successfully built.

Objective:To analyze the detection rate of hyperuricemia (HUA) and the distribution of serum uric acid (SUA) levels by multiple correlation analysis in middle-aged and elderly population receiving health examination.Methods:In this cross-sectional study, the study object were 25 587 middle-aged and elderly people who receiving health examination in Nanfang Hospital from January to December in 2014. According to the latest diagnostic criteria, the population was divided into HUA and non-HUA groups. Furthermore, the subjects were divided into 4 groups with the level of SUA (Q 1: SUA<313 μmol/L, Q 2:313 μmol/L≤SUA<375 μmol/L, Q 3:375 μmol/L≤SUA<440 μmol/L, Q 4: SUA≥440 μmol/L). According to the data types, two independent sample t test, Mann-Whitney U test, Chi-square test and multiple correspondence analysis were used for statistical analysis. Results:The mean age of the study subjects was (54.78±8.80) years with 16 570 males (64.8%) and 9 017 females (35.2%). The overall detection rate of HUA was 31.5%, and it was higher in men (43.1%) than in women (10.1%). The body mass index(BMI), systolic blood pressure, diastolic blood pressure, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), triglyceride (TG) and fasting blood glucose (FBG) in the HUA group were all higher than those in the non-HUA group (all P<0.001); and high-density lipoprotein cholesterol (HDL-C) was lower than that in the non-HUA group( P<0.001). In multiple correspondence analysis, Cronbach′s α coefficients of the first dimension and the second dimension was 0.608 and 0.237, respectively. Further analysis was performed stratified by gender, it indicated that 45-<55 years old male and overweight were closely associated with the Q 3 group, fatty liver and hyperlipidemia were closely associated with Q 4 group; the 55-<65 years old female, hyperlipidemia, fatty liver and obesity were closely associated with the Q 3 group, while hyperglycemia and hypertension were closely associated with the Q 4 group. Conclusion:The detection rate of HUA in middle-aged and elderly population receiving health examination was high, and the detection rate of HUA in male was higher than that in female. SUA levels are higher in middle-aged and elderly men who have fatty liver and hyperlipidemia. While SUA levels are higher in middle-aged and elderly women who have hyperglycemia and hypertension.

Median arcuate ligament syndrome(MALS)is compression of the celiac trunk by the median arcuate ligament.Median arcuate ligament release is the corner stone for the surgical treatment of MALS.Open surgery,laparoscopic surgery,and robot-assisted surgery have been developed,among which laparoscopic surgery has been proposed as the preferred approach in view of its minimal trauma and short hospital stay.Auxiliary celiac plexus neurolysis could further alleviate the patient's discomfort.Moreover,vascular reconstitution is of vital importance in the case of persistent stenosis in the celiac artery despite of median arcuate ligament decompression.Vascular reconstruction has satisfactory long-term patency rate,while endovascular treatment is less invasive.This article aims to summarize the consensuses and advances and shed light on the surgical treatment of MALS.
Celiac Artery/surgery* ; Constriction, Pathologic/surgery* ; Decompression, Surgical ; Humans ; Laparoscopy ; Ligaments/surgery* ; Median Arcuate Ligament Syndrome/surgery*

Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with unclear etiology and limited treatment options. The median survival time for IPF patients is approximately 2-3 years and there is no effective intervention to treat IPF other than lung transplantation. As important components of lung tissue, endothelial cells (ECs) are associated with pulmonary diseases. However, the role of endothelial dysfunction in pulmonary fibrosis (PF) is incompletely understood. Sphingosine-1-phosphate receptor 1 (S1PR1) is a G protein-coupled receptor highly expressed in lung ECs. Its expression is markedly reduced in patients with IPF. Herein, we generated an endothelial-conditional S1pr1 knockout mouse model which exhibited inflammation and fibrosis with or without bleomycin (BLM) challenge. Selective activation of S1PR1 with an S1PR1 agonist, IMMH002, exerted a potent therapeutic effect in mice with bleomycin-induced fibrosis by protecting the integrity of the endothelial barrier. These results suggest that S1PR1 might be a promising drug target for IPF therapy.