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Objective To analyze the clinical features and risk factors of urinary tract infection in patients with gestational diabetes mellitus ( GDM).Methods A total of 1 068 patients with GDM were enrolled from Nanshan People's Hospital between January and December 2014.The incidence of urinary tract infection, pathogens distribution and drug resistance rate were retrospectively analyzed.Multivariate Logistic regression was performed to analyze the risk factors of urinary tract infection in GDM patients . Results Among 1 068 patients with GDM, 130 (12.17%) were compliacated with urinary tract infection One hundred of forty-two strains of pathogens were detected in the middle urine culture sample from urinary tract infection patients, Escherichia coli (67.61%,96/142) and Klebsiella pneumonia (11.97%,17/142) were the most frequent strains.Escherichia coli has high resistance to semi-synthetic penicillins, quinolones and sulfonamides, and relatively low resistance rate to carbapenems , aminoglycoside antibiotics and nitrofurantoin.Klebsiella pneumoniae was completely resistant to ampicillin , while was completely sensitive to carbapenems, aminoglycoside antibiotics , piperacillin/tazobactam, aztreonam.Logistic regression analysis showed that glycated hemoglobin ＞6.5%(OR＝8.631, 95%CI 2.969-25.090, P＜0.01), fasting blood glucose＞5.3 mmol/L(OR＝3.116, 95%CI 2.040-4.761,P＜0.01), low density lipoprotein ＞2.6 mmol/L (OR＝1.649, 95%CI 1.083-2.511, P＜0.05), triglyceride＞1.7 mmol/L(OR＝2.986, 95%CI 1.256-7.112, P＜0.05), history of urinary tract infection (OR＝5.561,95%CI 1.315-23.519, P＜0.05) and history of maternity(OR＝1.631, 95%CI 1.018-2.614, P＜0.05) were the independent risk factors for urinary tract infection in GDM.Conclusion The incidence of urinary tract infection in patients with GDM is high.The control of blood glucose and blood lipids , enhanced health education for pregnant women with history of urinary tract infection and history of childbirth may reduce the occurrence of urinary tract infection in GDM patients.
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Objective To investigate the effect of different puncture methods on dialysis adequacy in maintenance hemodialysis patients. Methods One hundred and twenty patients receiving maintenance hemodialysis were divided into the observation group and the control group according to the sequence of receiving the hemodialysis with 60 cases in each group. Patients in the observation group were treated with increasing distance arteriovenous fistula of more than 10 cm , while patients in the control group received normal dialysis care without changing the way of puncture. The difference of dialysis adequacy before and after intervention were compared between the two groups. Result The dialysis adequacy after intervention in the observation group was improved significantly compared with the control group (P<0.05). Conclusion The dialysis adequacy in patients with maintenance dialysis can be improved by increasing the puncture distance of internal arteriovenous fistula.
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Objective To investigate the expression of p38 mitogen actirated protein kinase (p38MAPK) in renal fibrosis in diabetic mice. Methods Male homozygous C57 BL/6 mice were divided at random into control group intraperitoneally(i. p.) injected with citrate buffer and diabetes group received 5 consecutive daily intraperitoneal inserum glucose level exceeding 16.7 mmol/L. Mice were killed at 0,4weeks ,8weeks, 12weeks and 16weeks respectively after STZ injected. The kidney tissues were obtained from diabetic and control mice. Serum glucose, extracellular matrix,and 24 h urinary albumin excretion rate(UAE)and the serum creatinine(Scr) were measured. The kidney tissue was used for histological and morphometric studies of glomerular matrix expansion (PAS), and the expression of phosphorylated p38MAPK and TGFβ1 were measured by immunohisteehemical staining. p38MAPK and TGFβ1mRNA were analyzed by reverse transeriptase-PCR. Results The serum level of glucose in diabetic mice increased significantly. Scr and 24 h UAE, and glomerular matrix expansion in diabetic mice were obviously higher than that in control mice. Phosphorylated p38MAPK and TGFβ1 levels were obviously increased in the kidney of diabetic mice compared with those in control mice(P ＜0. 01) ;TGFβ1 expression was positively related to the expression of phosphorylated p38MAPK. Conclusion The overexpression of phosphorylated p38MAPK in kidney shoud play an important role in the development of renal fibrosis associated with diabetic nephropathy in mice.
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Objective To investigate the expression and activation of Smad2/3 in renal fibrosis associated with diabetic model in mice.Methods Male homozygous C57BL/6 mice were divided at random into control group intraperitoneally (ip)injected with citrate buffer and diabetes group received 5 consecutive daily intraperitoneal injections of streptozoto- cin(STZ 50 mg/kg?d).All mice were followed up for 16 weeks.Diabetes was confirmed by serum glucose levels ex- ceeding 16.7 mmol/L.Mice were killed at 0,4,8,12 and 16week respectively after STZ injected.The kidney tissue was used for histological and morphometric studies,and the expression of TGF-?,phosphorylated Smad2/3 and ?- SMA by immunohistochemical staining.Results TGF-?,phosphorylated Smad2/3 and ?-SMA levels were obvious- ly increased in the diabetic kidney compared with those in control mice,phosphorylated Smad 2/3 was positively related to the expression of ?-SMA in the diabetic kidney.Conclusion The overexpression and activation of Smad 2/3 in dia- betic kidney may play an important role in renal fibrosis.
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AIM: The aim of this study was to reveal the regulatory role of glutathione (GSH) in the transcriptional activity of activating transcription factor-2 (c-Jun/ATF-2) and nuclear factor-?B (NF-?B) of macrophages induced by angiotensin Ⅱ(AngⅡ). METHODS: Macrophage intracellular GSH was determined by fluorophotometry, and buthionine-[S,R]-sulfoximine(BSO)was used for depletion of intracellular GSH. The phosphorylation of c-Jun/ATF-2 and expression of NF-?B p65 were determined by immunoblot, and the activity of NF-?B was determined by electrophoresis mobility shift assay (EMSA). The c-Jun/ATF-2 was also determined by Immunohistochemical staining. RESULTS: The GSH content in the macrophage was decreased in cells that were lipid-peroxidized with AngⅡ (1.0 (?mol/L)) for 30 min and 60 min, respectively, followed by an adaptive GSH increase in the presence of AngⅡ (1.0 (?mol/L)) for longer time. In parallel, exposure to AngⅡfor 60 min also decreased macrophage GSH content in a dose-dependent manner. The GSH of RAW 264.7 cells were depleted by BSO, a specific inhibitor of GSH synthesis, and incubation for 18 h with 0.5 mmol/L BSO was sufficient for complete depletion of intracellular GSH. The phosphorylation of c-Jun/ATF-2 could be induced by the AngⅡ (1.0 (?mol/L)), whereas it did not occur in glutathione-depleted RAW 264.7 macrophages. The activation of NF-?B could also be induced by the AngⅡ (1.0 (?mol/L)), but it did not occur in glutathione-depleted RAW 264.7 macrophages. CONCLUSION: These data provide evidences that the intracellular glutathione redox may participate in the regulation of transcription activity of c-Jun/ATF-2 and NF-?B in macrophages. [
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AIM: To investigate the functional role of TGF-?_1 signal protein Smad2/3 in tubulointerstitial fibrosis associated with unilateral ureteral obstruction in rats. METHODS: The unilateral ureteral obstruction (UUO) model was induced by the ligation of left ureter. Rats were sacrificed at 1, 3, 7, 14, 21, and 28 days after UUO was initiated. TGF?_1 protein, phosphorylated Smad2/3 and interstitial ?-smooth muscle actin (?-SMA) expression were assayed by immunohistochemical staining. TGF-?_1 mRNA in the obstructed kidney was analyzed with in situ hybridration. HE and Masson staining were used for histological and morphometric studies of the pathological change in obstructed kidney. RESULTS: The results showed that upregulation of TGF-?_1 in tubulointerstitium of both cortex and medulla at day 3 (a 3.1 fold increase vs control, P
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AIM: To investigate the effects of advanced glycation end products on activation of Smad signaling pathway and collagenⅠ synthesis in proximal tubular epithelial cells.METHODS: Advanced glycation end products(AGE-BSA) were prepared by incubation of bovine serum albumin(BSA) with D-glucose.Normal rat proximal tubular epithelial(NRK52E) cells were cultured in RPMI-1640 medium with AGE-BSA.Phosphorylation and nuclear translocation of Smad2/3 were examined by immunocytochemistry.Levels of TGF-?_1 in supernatant of cell culture were measured by enzyme-linked immunosorbent assay(ELISA).Expression of TGF-?_1,Smad2,Smad3 and Smad7 mRNA were detected by RT-PCR.Expression of ?-SMA,E-cadherin and collagenⅠproteins were detected by Western blotting.RESULTS: AGE-BSA induced Smad2/3 phosphorylation and nuclear translocation,two peaks occured at 30 min(68% vs 16%,P
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AIM:To investigate the expression and probable role of extracellular signal-regulated protein kinase(ERK1/2)in renal fibrosis associated with diabetic in mice.METHODS:Male homozygous C57BL/6 mice were divided at random into control group(intraperitoneally injected with citrate buffer)and diabetes group(received 5 consecutive daily intraperitoneal injections of streptozotocin at dose of 50 mg?kg-1?d-1).All mice were followed up for 16 weeks.Diabetes was confirmed by serum glucose levels exceeding 16.7 mmol/L.Mice were killed at 0,4,8,12 and 16 weeks respectively after streptozotocin injection.The kidney tissues were obtained from diabetic and control mice.Serum glucose,kidney weight/body weight(KW/BW),24 h albumin excretion rate(UAE)and the serum creatinine(Scr)were measured.The kidney tissue was used for histological and morphometric studies of glomerular size,glomerular matrix expansion(PAS),and the expression of TGF-?1,phosphorylated ERK1/2 and collagen Ⅲ by immunohistochemical staining.RESULTS:The serum level of glucose in streptozotocin-induced diabetic mice increased significantly.The kidney weight/body weight ratio,glomerular volume and glomerular matrix expansion in diabetic mice were obviously higher than those in control mice.Serum creatinine and 24 h albumin excretion rate in diabetic mice increased significantly compared with control mice.TGF-?1,phosphorylated ERK1/2 and collagen Ⅲ levels were obviously increased in the kidney of diabetic mice compared with those in control mice(P
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Objective To investigate the function role and mechanism of p38 mitogen-activated protein kinase(p38MAPK) in up-regulating osteopontin mRNA expression in rat glomerular mesangial cells induced by interleukin-1?.Methods Activation of p38MAPK was detected with Western blotting,The effect of p38MAPK specific blockade SB203580 on the expression of osteoponlin mRNA in rat mesangial cells induced by interleukin-1? was measured with RT-PCR. Results interleukin-1? could activate p38MAPK in time- and dosage-dependent manner,and up-regulate osteopontin mRNA expression in rat glomerular mesangial cells. SB203580 obviously inhibited the up-regulation of osteopontin mRNA induced by interleukin-1? in dosage dependent manner. Conclusion p38MAPK may play an important role in the up-regulation of osteopontin in rat glomerular mesangial cells induced by interleukin-1?.
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AIM: To observe the expression of fractalkine, and its receptor, CX3CR1, in renal tissues of patients with diffuse proliferative lupus glomerulonephritis (WHO class IV), minimal glomerular abnormalities, and normal kidney. Meanwhile, the correlation among the expression of fractalkine, CX3CR1 and CD68-positive macrophages was investigated, and the role of fractalkine and CX3CR1 in the pathogenesis of lupus nephritis was discussed. METHODS: The expressions of fractalkine, CX3CR1 and CD68 were detected immunohistochemically in kidney tissue sections obtained from twenty-one patients with WHO class IV lupus nephritis, eighteen cases with minimal glomerular abnormalities, and eight normal kidneys which were no abnormality under light microscope. RESULTS: (1) Fractalkine was generally indistinguishable in tissue sections from normal kidney and minimal glomerular abnormalities. CX3CR1-positive cells and CD68-positive macrophages were sparsely detected in the glomeruli and in the cortical interstitium. (2) There were considerable CX3CR1-positive cells and macrophages in both the glomeruli and the interstitium in sections from class IV lupus nephritis. The number of CX3CR1-positive cells significantly correlated with the number of macrophages in the glomeruli and in the interstitium respectively (r=0.956, P
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AIM: To investigate the expression and functional role of p38MAPK in the kidney after unilateral ureteral obstruction in rats. METHODS: Unilateral ureteral obstruction (UUO) models were induced by ligating the left ureter. Rats were sacrificed at 1 h, 3 h, 6 h, 12 h, 1, 3, 5, 7, 14, 21, and 28 days after UUO was initiated. p38MAPK activity was assayed by immunohistochemical staining and specific substrate phosphorylation with immunoprecipitation and Western blotting. TGF? mRNA and protein expression were analyzed with in situ hybridization and immunohistochemical stainning. RESULTS: A basic p38MAPK activity was detectable in the normal kidney(0.22?0.06). p38MAPK pathway was rapidly activated at 1 hour(0.45?0.14 vs control, P
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AIM: To detect the expression of connective tissue growth factor (CTGF), transforming growth factor-?_1 (TGF-?_1) and ?-smooth muscle actin (?-SMA) in rat unilateral ureteral obstructive (UUO) nephropathy animal model, and to observe the kinetic changes at different stages of firosis. METHODS: Male SD rats were subjected to either left ureteral ligation or sham operation, then killed at 3, 7, 14, 21 or 28 days after UUO or sham operation (n=6 at each time point). HE, Masson or PAS staining were applied to the renal tissue sections. The extent of tubulointerstitial injury was determined by Banff classification. RESULTS: The extent of tubulinterstitial fibrosis became serious with the time of obstruction. Tubules were mostly atropic and replaced by proliferative fibrous tissue at day 28. The expression of CTGF and ?-SMA were consistent with the damage of tubulointerstitial. The positive correlation among CTGF or ?-SMA and the tubulointerstitial injury scores were significant. The expression of TGF-?_1 came to peak at day 7 to 14, and gradually decreased at day 21 and 28. CONCLUSION: These results indicate that the expression of CTGF may be upregulated by TGF-? in UUO rats, and CTGF may be involved in tubulointerstitial fibrosis through the development of myofibroblasts.