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Objective:To investigate the diagnostic value of urinary nuclear matrix protein 22 (NMP22) combined with bladder tumor antigen (BTA) detection for bladder cancer, in order to provide a laboratory basis for early screening of bladder cancer.Methods:The clinicopathological data of 315 suspected bladder cancer patients in Baoji Central Hospital in Shaanxi Province from August 2018 to July 2019 were retrospectively analyzed. Among the patients, 248 patients with bladder cancer and 67 patients with urological benign disease were diagnosed by surgical pathology or cystoscope biopsy, and 100 healthy people that took the normal physical examination in the same period were selected as healthy control group. The levels of urinary NMP22 and BTA were detected by enzyme-linked immunosorbent assay (ELISA).Results:The expression levels of urinary NMP22 in the bladder cancer group, urological benign disease group and healthy control group were (28.4±8.8) ng/ml, (12.7±3.0) ng/ml and (4.3±1.5) ng/ml, and the difference was statistically significant ( F = 26.41, P < 0.05); BTA expression levels were (25.1±8.1) ng/ml, (10.4±2.9) ng/ml and (6.4±2.4) ng/ml, and the difference was statistically significant ( F = 23.62, P < 0.05). The differences in the expression levels of urinary NMP22 and BTA in bladder cancer patients with different TNM stages and pathological grades were statistically significant (all P < 0.05). The area under the receiver operating characteristic curve, sensitivity, and negative predictive value of the combined detection of urinary NMP22 and BTA were 0.895, 96.98%, and 61.11%, respectively, which were higher than the single detection, and the differences were statistically significant (all P < 0.05). The cut-off values of urinary NMP22 and BTA for diagnosis of bladder cancer were 32.42 ng/ml and 29.13 ng/ml, respectively. Conclusions:The combined detection of urinary NMP22 and BTA has a high clinical value for the diagnosis of bladder cancer. The detection has the advantages of simple, rapid, non-invasive, and mass screening, which is worthy of clinical promotion.
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Objective To investigate the effects of different doses of 1 ,25(OH)2D3 on rat Thy‐1 nephritis mesangial cell ap‐optosis .Methods 120 clean SD rats were divided into the blank control group(group A) and the experimental group .The experi‐mental group was re‐divided into the nephritis group(group B) ,0 .25μg 1 ,25(OH)2D3 intervention group(group C) and 0 .50μg 1 , 25(OH)2D3 group(group D) ,30 cases in each group .The group C and D were performed the medication intervention after success‐fully constructing the model .6 rats were randomly killed in each group on 1 ,3 ,7 ,14 ,21 d after intervention .The renal tissues were taken for determining the renal pathological injury classification after hematoxylin and eosin staining and PAS staining .The expres‐sion of Caspase‐3 in the renal tissues was detected by the immunohistochemistry method ,and the glomerular cell apoptosis was de‐tected by TUNEL .Results The immunohistochemistry results showed that compared with the group A ,the Caspase‐3 expression in the group B was increased (P 0 .05);the Caspase‐3 expression in the group D was highest ,but the difference was not statistically significant compared with the group C .The TUNEL results showed that compared with the group A ,the apoptotic glomerular cells in the group B were increase obviously (P0 .05) .Conclusion 1 ,25(OH)2D3 has the effect for inducing glomerular mesangial cell apoptosis in rat , which participates in the regulation of Caspase‐3 ,induces glomerular mesangial cell apoptosis ,promotes the recovery of nephritis and could delay the progression of renal disease .
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Objective To study the expressions of Ki67 and mTOR in Thy-1 nephritis model of rat who were given 1,25-dihydroxyvitamin D3[1,25(OH)2D3] and to explore its mechanism. Methods Healthy male SD rats (n=90) were random?ly divided into three groups: control group, model group, 1,25(OH)2D3 treatment group (n=30 in each group). Model group and 1,25(OH)2D3 treatment group were intravenously injected with anti-Thy1 monoclonal antibody once via tail vein while the control group were administrated with same volume of normal saline through the same route. 1,25(OH)2D3 were adminis?trated at 0.5μg per day intra-gastrically for consecutive 21 days in 1,25(OH)2D3 treatment group while equal volume of pea?nut oil were given in control group and model group. Six rats were randomly selected from each group and sacrificed at the 1st , 3rd , 7th , 14th and 21st after drug intervention. Twenty four hour urine sample were collected in each rat just before it was culled to detect 24-hour urinary protein excretion. Renal tissue samples were harvested and stained with hematoxylin&eo?sin (H&E) and PAS to determine the renal pathological variation and the expressions of mTOR and Ki67 were assessed by immunohistochemistry. Results Urine protein begin to be detected at the first day after model was established, peaked at the 3rd days then started dropping until the 14th day when urine sample turned to normal. Urine protein levels were lower in 1, 25(OH)2D3 treatment group at the 1st,3rd,7th day after model establishment than those in model group(P<0.05). Compared with model group, the pathological damage of renal tissue in 1,25(OH)2D3 treatment group were alleviated at the 3rd and 7th day after model establishment (P < 0.05). Expressions of Ki67 and mTOR in 1, 25(OH)2D3 treatment group were reduced compared with those in model group (P<0.05). Twenty four hour urinary protein and expressions of Ki67 and mTOR as well as renal pathological damage were all positively correlated with each other. Conclusion 1,25(OH)2D3 can inhibit the proliferation of glomerular mesangial cells in Thy-1 nephritis model of rat. And its therapeutic mechanism may be associated with down reg? ulating expressions of Ki67 and mTOR.