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Purpose To investigate the role of S3I-201 on tubular interstitial lesion in lupus nephritis.Methods MRt/MpJ mice were designated as the control group.MRL/lpr nice were randomly divided into LN group,S3I-201 group and DMSO group.The serum and 24 h-urine were collected to detect the serum creatinine,blood urea nitrogen and urine protein.Immunohistochemistry was used to detect the expression of FN.Western blotting analysis was used to determine the expression of E-cadherin,α-SMA,MCP-1,ICAM1,STAT3 and p-STAT3.Results Compared with the expression level in control group,the protein level of α-SMA,MCP-1,ICAM1 and FN were increased in renal tissue of MRL/lpr mice,while the expression of E-cadherin was markedly decreased.And the STAT3 was activated in renal tissue of MRL/lpr mice.The administration of S3I-201 could inhibite the activation of STAT3 and ameliorate the expression of E-cadherin,α-SMA,MCP-1,ICAM-1 and FN.Conclusion S3I-201 can relieve the tubular interstitial leison,which maybe concerned with the phosphorylation of STAT3.
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Objective To analyze the impac factors of serum N?terminal pro?brain natriuretic peptide (NT?proBNP) in patients with renal failure in non?dialysis phase, and to determine the cut?off point of as a diagnostic values in these patients with heart failure (HF). Methods Cross?sectional study was applied. Clinical data of 145 patients (37 cases of CKD4, 89 cases of CKD5, and 19 cases of acute renal injury (AKI) with renal failure in non?dialysis phase were collected. Comparison between groups and lineal regression analysis were utilized to investigate the impact factors of NT?proBNP, and the receiver operating characteristic curve (ROC curve) to select a better cut?off point of diagnosis in these patients with HF. Results (1) Compared with patients without HF, patients with HF had significantly higher edema, cardiac troponin I, serum phosphorus concentration, and left atrial diameter (LA), while ALB and left ventricular ejection fraction (LVEF) were decreased (P0.05). (4) The best cut?off point of NT?proBNP predicting HF in patients with renal failure in non?dialysis phase was 3805 ng/L, AUC=0.848, 95%CI 0.786?0.910. Sensitivity was 82.4%, specificity 74.5%, positive predictive value 62.1%, negative predictive value 87.3%, positive likelihood ratio 3.2, negative likelihood ratio 0.24. Conclusions The level of NT?proBNP>20 000 ng/L is mainly found in end?stage renal disease patients with HF. HF is a main factor for the increase of NT?proBNP in patients with renal failure in non?dialysis phase. High phosphorus viremia, anemia, and hypoalbuminemia are closely related to NT?proBNP. Therefore NT?proBNP predicting HF should take into account the effects of these confounding factors in these patients.
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Purpose To investigate the role of SOCS3 on diabetic renal injury. Methods Male CD-1 mice were randomly divided into four groups:control group, diabetic group, empty plasmid vector transfection group and SOCS3 plasmid transfection group. The diabet-ic mice were induced by intraperitoneal injection of STZ at a dose of 150 mg/kg body weight. The mice of transfection group were re-ceived an injection of SOCS3 plasmid or empty vector at every 7 days thereafter. Specimens were collected at 12 week after STZ injec-tion. The morphological changes of tubular epithelial cells were observed by transmission electron microscope. RT-PCR and immuno-histochemistry were used to determine the mRNA and protein expression of CK18 and α-SMA. Western blotting analysis was used to determine the protein expression of SOCS3, p-STAT3, CK18 and α-SMA. Results SOCS3 overexpression in kidney down-regulated the levels of p-STAT3 andα-SMA but up-regulated the expression of CK18. Conclusion Overexpression of SOCS3 can ameliorate the tubular epithelial-mesenchymal transdifferentiation of diabetic mice via inhibiting the phosphorylation of STAT3.
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Purpose To investigate the role of PTEN in podocyte injury in patients with diabetic nephropathy ( DN) . Methods Uri-nary samples from 30 patients with DN and 10 healthy volunteers were collected to detect the level of PCX by ELISA. Renal biopsies were reviewed to observe the morphological changes. All patients with DN were divided into three groups by glomerular lesion. The ex-pression of p-Akt and PTEN in glomeruli was detected by immunohistochemistry. Results The levels of PCX in the urine were signifi-cantly higher in patients with DN compared with those in healthy volunteers, and gradually increased along with glomerular lesion aggra-vating. The expression of p-Akt and PTEN increased in patients with DN compared with healthy volunteers. Although the expression of p-Akt and PTEN decreased with the aggravation of glomerular lesion, they were still higher than that in volunteers. There were obvious-ly positive correlation between the level of PCX and 24-h urinary protein and negative correlation between the level of PCX and the ex-pression level of p-Akt and PTEN. Conclusion PTEN down-regulation may be associated with podocyte injury in DN, which may be associated with the phosphorylation of Akt.
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OBJECTIVE To understand disinfection quality in newborn Spa room,to give prevention messures against nosocomial infection.METHODS The air,UV intensity,the object surface,staff′s hands,and the using of disinfectant were detected.RESULTS The total qualified rate was 98.61% and that of the object surface was 97.22%,of staff′s hands was 98.61%,of UV intensity and indoor air was 100% and of the using disinfectant was 97.22%.CONCLUSIONS Strengthening the disinfection,finding the weak timely and taking the effective measures can prevent the occurrence of hospital infection.
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Objective To investigate the effects of TNF-?,IL-12,IL-15 and underglycosylation IgA_1 in mesangial deposition in the clinicopathological study of IgA nephropathy(IgAN).Methods Seventy-four patients with IgAN were enrolled in the study,with 10 patients randomly selected after remission,10 MCD and 10 healthy volunteers as control groups.The levels of TNF-? in serum and urine were examined by radioimmunoassay,and the levels of IL-12 and IL-15 were examined by ELISA.Immunohistochemistry was used to detect the expression of TNF-? in renal tissue,and the directed immunofluorescence was used to detect the underglycosylation of IgA_1(UGIgA_1)in mesangial deposition.Results The levels of TNF-?,IL-12 and IL-15 in serum of patients with IgAN were higher than those of MCD group,healthy control group and remission group.Compared with the negative group,33 patients with UGIgA_1 positive in renal tissues had lower levels of TNF-? in serum,longer course and less class of renal tissue injury.The positive areas of TNF-? in renal tissue and levels of TNF-? in serum were positively correlated with urinary protein(r=0.249,0.702,P=0.000).There was negative correlation between the levels of TNF-? in serum and Ccr(r=-0.231,P=0.048).The levels of IL-15 was positively correlated with the course of disease(r=0.266,P=0.022) and negatively with Scr(r=-0.320,P=0.005).Conclusions The TNF-?,IL-12 and IL-15 are all involved in the onset of proteinuria in IgAN patients,and IL-15 acts as a factor against renal injury.The patients with UGIgA_1 positive in mesangial have longer course and less pathological changes damaged than those of the UGIgA_1 negative patients.The TNF-? may serve as an important factor in the aggravation of IgAN.
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Objective To investigate the clinicopathological relation between the TNF-? and IgA nephropathy. Methods TNF-? levels in serum, urine and renal tissues of 50 patients with IgA nephropathy were measured, and 10 patients with minimal change nephrotic syndrome(MCNS) and 10 healthy subjects served as negative control group. Results The serum and urine levels of TNF-? in the patients with IgA nephropathy were significantly higher than those in the patients with MCNS and healthy subjects, and had a significant positive correlation with the degree of proteinuria and renal demage. TNF-? expression was mainly localized in the cytoplasm of the proximal renal tubular epithelial cells, and the interstitium with more monocyte-macrophages infiltration. Conclusion TNF-? took part in the onset of hematuria and proteinuria, was correlated with the degree of renal damage, and played an important role in the aggravation of IgA nephropathy.