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Resident standardization training is an essential way in cultivating medical professionals. It is important for subject development and talent reserve. For cultivating high-quality resident physicians with comprehensive theory, independent clinical thinking, great practical ability, and innovative scientific idea, it recourses to both optimizing training scheme and evaluation system with highly specialization and comprehensive quality. In this study, the authors proposed incorporate training patterns includingoptimiz-ing design, innovating training, and standardized assessment based on their recent experience on resident standardization training.
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Objective To observe the effects of uric acid (UA) on mitochondrial oxidative damage and apoptosis in renal tubular epithelial cells (HK-2),and investigate the possible mechanism.Methods HK-2 cells were exposed to UA (480 μmol/L,720 μmol/L) for different time (0 h,24 h,48 h)in vitro.The mitochondrial ROS production was detected by MitoSOX staining.The mitochondrial membrane potential was measured by JC-1 staining.The expressions of prohibitin and AIF were examined by Western blotting and irnmunofluorescence cytochemistry.The cell apoptosis was measured by Annexin V-FITC/PI staining.Results The mitochondrial ROS production in HK-2 cells exposed to 480 μ mol/L UA was increased than that of control group at 24 h (P ＜ 0.05),and increased gradually with UA concentration and incubation time increasing,while the mitochondrial membrane potential was reduced at the same time.There were no significant changes in AIF expression and apoptosis rate of HK -2 cells exposed to 480 μmol/L UA for 24 h compared with that of control group (P ＞ 0.05),while both of them were up-regulated when HK-2 cells were exposed to 480 μmol/L UA for 48 h and 720 μmol/L JA for 24 h and 48 h (P ＜ 0.05).The prohibitin expression in HK-2 cells exposed to 480 μmol/L UA was reduced than that of control group at 24 h (P ＜ 0.05),and down-regulated gradually with UA concentration and incubation time increasing.Conclusion Uric acid can induce the mitochondrial ROS production increased,the mitochondrial membrane potential reduced,the prohibitin expression down-regulated and the mitochondrial apoptosis pathway activated in HK-2 cells.
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Objective To investigate the effect of benazepril on intergrin-linked kinase (ILK) and α-smooth muscle actin (α-SMA) expression in glomerular mesangial cells induced by high-glucose.Methods The mesangial cells from SD rat (HBZY-1) were cultured conventionally and randomly divided into four groups:normal glucose (D-glucose 5.5 mmol/L,group NG),mannitol-treated group (mannitol 20 mmol/L,group MG),high glucose (D-glucose 30 mmol/L,group HG),Benazepril-treated high glucose group (D-glucose 30 mmol/L + Benazepril 10 μmol/L,group ACEI).Cells from NG,MG,HG,ACEI gronps were harvested after 3,6,12,24,48 and 72 hours of treatment respectively.The mRNA expressions of ILK and α-SMA were detected by RT-PCR.The protein levels of ILK and α-SMA were detected by Western blotting and immunofluorescence.Results The expressions of ILK mRNA and protein in HG group were significantly increased compared with those in NG group (all P ＜ 0.05).The increased expressions of ILK and α-SMA in HG group were time-dependent and the expression reached the peak at 48 h (ILK,P ＜ 0.05) or 72 h (α-SMA,P ＜ 0.01).The expressions of ILK and α-SMA in ACEI group were lower than those in HG group (all P ＜ 0.01),but failed to rescue to the same level as those in NG.There was no significant differences of ILK expressions between MG group and NG group at the same time point (P ＞ 0.05).The expressions of α-SMA mRNA and protein in MG were higher than that in NG (P ＜ 0.05),which suggest that high osmotic pressure could cause the increasing of α-SMA.Conclusions Benazepril can decrease the expressions of ILK and α-SMA to inhibit the process of fibrosis in DN and mediate the phenotypic transformation of glomerular mesangial cells.The phenotypic transformation of glomerular mesangial cells in glucose may also depend on high osmotic pressure in DN.
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objective To observe the effects of megsin gene transfection on glomerular mesangial cells(GMCs)and the expression of platelet-derived growth factor-BB(PDGF-BB),phosphorylated extracellular signal-regulated protein kinase(pERK1/2),transforming growth factor β1 (TGF-β1)and type Ⅳ collagen under high concentration of glucose,and to investigate the impact of megsin gene transfection on the extracellular signal-regulated protein kinase (ERK)siginal pathway. Methods Cultured mesangial cells were divided into seven groups:low glucose group (group A,5.5 mmol/L),high glucose group(group B,30 mmol/L),high glucose plus empty vector group (group C), high glucose plus megsin expression plasmid group (group D), high glucose plus megsin expression plasmids plus U0126 group (group E), high glucose plus megsin siRNA expression plasmids group (group F) and low glucose plus mannitol (24.5 mmol/L,group G). The expressions of megsin, PDGF-BB, pERK1/2, TGF-β1, as well as type Ⅳ collagen in GMCs of each group were detected by Western blotting, after being cultured for 12, 24 and 48 hours respectively. The concentration of type Ⅳ collagen in cell supernatant was measured by radioimmunochemistry. Results Compared with group A, the expression of megsin was increased in GMCs under high glucose medium, with an increase of PDGF-BB, pERK1/2, TGF-β1 in GMCs and type Ⅳ collagen in the supernatants (P＜0.05, respectively). The expression of above indices was in time-dependant manner. The over expression of megsin in exposure to high up-regulated the expression of PDGF-BB, pERK1/2, TGF-β1 and type Ⅳ collagen(P＜0.05, respectively). Compared with group D, the application of U0126 (pERK1/2 inhibitor) had no significant effect on the expression of megsin and PDGF-BB(P＞0.05, respectively). However, the expression of pERK 1/2,TGF-β1 and type Ⅳ collagen were obviously decreased (P＜0.05, respectively). Dowa-regulated expression of megsin by siRNA transfection decreased the expression of PDGF-BB, pERK1/2, TGFβ1 and type Ⅳ collagen(all P＜0.05). Conclusions The expression of megsin and PDGF-BB in GMCs with transfected megsin gene in high glucose medium is increased, possibly in a way of activating ERK signal pathway to some extent that boosts both the expression of TGF-β1 and the production of type Ⅳ collagen. The transfection of megsin siRNA inhibits the expression of obove indices, which probably contributes to the development of diabetic nephropathy.
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Objective To evaluate the efficacy of nuvastatin on the high level of serum lipoprotein(a) [Lp(a)] and itsclinical significance in patients with type 2 diabetic nephropathy. Methods In this study, 104 patients with microalbu-winuric type 2 diebetic h?phropathy) were divided into two groups randomly: the flu vastatin. group (zomg per day P.O. )and the control group. The efficacy at 6 weeks' beatment was evaluated. The serum Lp(a) concentration and the activityof tissue-type plasminogen activator(tPA ) and plasminogen activator inhibitor(PAI) were measured by enzyme-linkedimmunosorbent assay and chromogenic substances assay respechtively in all of the patients. Results At the beginning. ser-um Lp(a ) level and PAI activity along with a low tPA activity were abnormally high in every patient. In addition, the levelof Ccr was unconventionally high. After 6 weeks,the level of serum Lp(a) and the activity of PAI and tPA were cowectedsignilicanily in the teated group compared with the other group(P
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w-3 polyunsaturated fatty acids, particularly docosahexaenoic acid (DHA) , are essential components for the development of human brain. A fish oil product enriched with DHA (51. 65%) was used to conduct a preliminary memory study with rats employing the active avoidance test. Three doses of DHA, 1. 0 g/kg, 200 mg/kg and 40 mg/kg, were administered orally to the rats twice daily for 20 days. The results showed that there was a positive correlation between the effects on memory ability and DHA adiministration, and the effects were dose responsive. The results also showed that DHA, at 200 mg/kg, could antagonize dysmnesia caused by scopolamine and had hypermnesia effect.
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AIM To study effects of desulfated and poly sulfated heparin derivatives on rat mast cell (MC) degranulation. METHODS Different methods were used to prepare different sulfated heparin derivatives: 2 O desulfated heparin (2DeSH),N desulfated reacetylated heparin (NDeSAcH),6 O desulfated heparin (6DeSH),poly sulfated heparin (PSH). Passive MC degranulation induced by ovalbumin in rats to was employed observe the effects of different sulfated derivatives on rats MC degranulation. RESULTS All the sample groups were found of obvious inhibition of MC degranulation( P