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The community-friendly program " Online mobile payment of medical insurance" , launched by Guangzhou Municipal Medical Insurance Bureau, poses new challenges to hospital medical insurance management and information intelligence. To this end, the Second Affiliated Hospital of Guangzhou Medical University staged from January 2017 to March 2019 kept upgrading its IT system and built an intelligent monitoring system for medical insurance. These efforts prepared adequately for the medical insurance mobile payment, and explored a mode of medical insurance management, evolving from extensive management to standard and fine management.
ABSTRACT
The community-friendly program " Online mobile payment of medical insurance " , launched by Guangzhou Municipal Medical Insurance Bureau, poses new challenges to hospital medical insurance management and information intelligence. To this end, the Second Affiliated Hospital of Guangzhou Medical University staged from January 2017 to March 2019 kept upgrading its IT system and built an intelligent monitoring system for medical insurance. These efforts prepared adequately for the medical insurance mobile payment, and explored a mode of medical insurance management, evolving from extensive management to standard and fine management.
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Objective To investigate the role of Calcineurin binding protein 1(Cabin1)in renal tubular epithelial cells(RTECs)injury. Methods The male Sprague-Dawley rats were randomly divided into Sham-oper-ated and 5/6 nephrectomized group. Nephrectomized rats were further divided into two groups ,which were 4 and 8 weeks after operation,including 6 rats in each group. Rats were sacrificed at 4 or 8 weeks after nephrectomy,then control or remnant kidneys were harvested. 2μm sections of kidney tissues were collected and stained with Masson's trichrome and were graded for tubulointerstitial lesion score (TILS). RTECs mitochondrial morphology changes were detected by electron microscope. Western blot was applied to detect Cabin1 protein level in the renal tissue. Results At 8 weeks after the operation,plenty of RTECs fell off from the basement membrane,accompanied with interstitial fibrosis and the infiltration of inflammatory cells. Moreover ,TILS were significantly increased in rats at 8 weeks after operation while compared to sham-operated rats(7.16 ± 0.52 vs. 0.00 ± 0.00,P<0.05). RTECs mi-tochondria begun to swell at 4 weeks after 5/6 nephrectomy,while the disruption of cristae could be found in rats at 8 weeks. Cabin1 protein expression apparently increased in the remnant kidney. Cabin1 protein obviously increased in rats at 8 weeks after the surgery compared to sham-operated rats(0.97 ± 0.09 vs. 0.22 ± 0.07,P<0.05)and rats at 4 weeks after nephrectomy(0.97 ± 0.09 vs. 0.45 ± 0.03,P<0.05). Conclusions Cabin1 is overexpressed during RTECs injury in 5/6 nephrectomized rats. It can be a crucial factor regulating the damage of RTECs.
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Objective To investigate the role of Calcineurin binding protein 1(Cabin1)in renal tubular epithelial cells(RTECs)injury. Methods The male Sprague-Dawley rats were randomly divided into Sham-oper-ated and 5/6 nephrectomized group. Nephrectomized rats were further divided into two groups ,which were 4 and 8 weeks after operation,including 6 rats in each group. Rats were sacrificed at 4 or 8 weeks after nephrectomy,then control or remnant kidneys were harvested. 2μm sections of kidney tissues were collected and stained with Masson's trichrome and were graded for tubulointerstitial lesion score (TILS). RTECs mitochondrial morphology changes were detected by electron microscope. Western blot was applied to detect Cabin1 protein level in the renal tissue. Results At 8 weeks after the operation,plenty of RTECs fell off from the basement membrane,accompanied with interstitial fibrosis and the infiltration of inflammatory cells. Moreover ,TILS were significantly increased in rats at 8 weeks after operation while compared to sham-operated rats(7.16 ± 0.52 vs. 0.00 ± 0.00,P<0.05). RTECs mi-tochondria begun to swell at 4 weeks after 5/6 nephrectomy,while the disruption of cristae could be found in rats at 8 weeks. Cabin1 protein expression apparently increased in the remnant kidney. Cabin1 protein obviously increased in rats at 8 weeks after the surgery compared to sham-operated rats(0.97 ± 0.09 vs. 0.22 ± 0.07,P<0.05)and rats at 4 weeks after nephrectomy(0.97 ± 0.09 vs. 0.45 ± 0.03,P<0.05). Conclusions Cabin1 is overexpressed during RTECs injury in 5/6 nephrectomized rats. It can be a crucial factor regulating the damage of RTECs.
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Objective To investigate the function and molecular mechanism of tacrolimus in podocyte injury and restoration.Methods Cultured podocytes were stimulated by Angiotensin Ⅱ (Ang Ⅱ) or Ang Ⅱ plus tacrolimus.Cells were collected at different time points (0 h,12 h and 24 h).The distribution of F-actin was observed after immunofluorescence staining,and the protein expression of nephrin and podocin were detected by Western Blot (WB).Results In normal control podocytes,F-actin was arranged in cytoplasm powerfully.Ang Ⅱ induced the disruption and discontinuity of F-actin.Tacrolimus inhibited the effect of Ang Ⅱ,stabilized the regular arrangement the F-actin.Compared to normal cells,the protein expression of nephrin in Ang Ⅱ group significantly decreased at 24 h after stimulation (0.76 ± 0.32 in AngⅡ group vs.1.18 ± 0.40 in normal group,P ＜ 0.05).And tacrolimus stabilized the expression of nephrin protein (1.00 ± 0.19 in treatment group vs.0.76 ± 0.32 in Ang Ⅱ group,P ＜ 0.05).Ang Ⅱ and tacrolimus did not affect the expression of podocin protein.Conclusion Tacrolimus inhibits podocyte injury induced by Ang Ⅱ,stabilizes the regular arrangement of cytoskeleton and protein expression of nephrin.
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Objective To investigate the relationship between fetuin A and left ventricular function and their influences on residual renal function(RRF) in peritoneal dialysis patients.Method Eighty patients recently initiating peritoneal dialysis were enrolled into this study and were divided into high fetuin A group and low fetuin A group accordin to the value of serum fetuin A concentration.Hemoglobin,high sensitive C reactive protein(hsCRP),calcium,phosphorus,albumin,lipoproteins and left ventricular myocardial performance index(LV-MPI) were examined.All these patients were followed up for 12 months,to discover the parameters' differences between two groups and to investigate the association between fetuin A and left ventricular function and RRF.Results At the beginning of the study,there was no difference of hsCRP,calcium,phosphorus,albumin,lipoproteins and LV-MPI,estimated glomerular filtration rate (eGFR) between two groups;After 12 months follow-up,MPI was obviously shorter (P ＜ 0.05) and RRF was obviously higher (P ＜ 0.05) in high fetuin A group than thosein low fetuin A group.Compared with the beginning of the study,LV-MPI was significantly increased and eGFR was significantly decreased after 12 months follow-up (both P ＜ 0.05) in low fetuin A group,but no obviously change of LV-MPI or eGFR was found in high fetuin A group after followup.Pearson correlation analysis discovered an obvious negative correlation between fetuin A and MPI (r=-0.680,P ＜ 0.01).Multiple regression analysis indicated that eGFR had positive correlation with fetuin A (B=0.058,t=3.679,P＜ 0.01) and negative correlations with MPI (B=-0.511,t=-2.903,P=0.007),age(B=-0.144,t=-4.013,P＜0.01).Diabetes was risk factor to loss of RRF (B=-2.031,t=-2.759,P ＜ 0.05).Conclusion Fetuin A has very close relationship with left ventricular function.Decreased serum fetuin A level and decreased left ventricular function are risk factors to the loss of the RRF in ERSD patients.
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<p><b>OBJECTIVE</b>To investigate the association of fetuin-A with residual renal function and carotid artery calcification in patients with chronic kidney disease (CKD).</p><p><b>METHODS</b>Blood examples were collected form 60 CKD patients in stages CKD3 to CKD5 (20 patients per stage) for measurement of serum fetuin-A, albumin, calcium, phosphorus and parathyroid hormone, cholesterol, triglycercide, low-density lipoprotein, and high-density lipoprotein. MDRD equation was used to calculate the estimated glomerular filtration rate (eGFR), and ELISA was used to detect serum fetuin-A. Color Doppler ultrasound was performed to measure carotid intima-media thickness (CIMT).</p><p><b>RESULTS</b>As the eGFR decreased, serum fetuin-A significantly decreased in CKD5 stage compared with that in CKD4 stage (P<0.05); compared with that in CKD3 stage, serum fetuin-A level was significantly lowered in CKD4 stage (P<0.05). Linear regression analysis suggested a significant positive correlation between fetuin-A and eGFR. The rate of carotid artery calcification was the highest in CKD5 stage. Rank correlation analysis showed a negative correlation between fetuin-A and cIMT, and logistic regression analysis identified decreased serum Fetuin-A as a risk factor of carotid artery calcification.</p><p><b>CONCLUSION</b>Serum fetuin-A decreases following the decrease in eGFR, and decreased serum Fetuin-A level is a risk factor of carotid artery calcification in CKD patients.</p>
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Calcinosis , Carotid Artery Diseases , Carotid Intima-Media Thickness , Glomerular Filtration Rate , Renal Insufficiency, Chronic , Blood , Risk Factors , alpha-2-HS-Glycoprotein , MetabolismABSTRACT
Objective To investigate the association of vascular calcification,fetuin A and Creaction protein (CRP),and explore the influence on cardiovascular events.Methods Sixty peritoneal dialysis (PD) patients were enrolled in this study.Carotid intima-media thickness (cIMT),fetuin A and CRP,along with the other serum related parameters were detected to find out their influence on vascular calcification in PD patients.The relationship between cIMT,fetuin A,CPR and cardiovascular events was analyzed in PD patients with 18 months followed-up.Results Of the 60 PD patients,carotid intima-media thickness (cIMT) was increased in 38 patients(63.3％).Compared with the non-increased cIMT patients,serum fetuin A concentration was significantly decreased(P ＜ 0.05),CRP(P＜0.01) and calcium × phosphate products(P＜0.05) were significantly increased in the highincreased cIMT group.Compared with the low-increased cIMT patients,fetuin A concentration was obviously lower(P ＜ 0.05) and calcium×phosphate products were obviously higher(P ＜ 0.05) in the highincreased cIMT group.Linear regression analysis discovered an obvious negative correlation between CRP and fetuin A(R2 =0.629,F=47.522,P ＜ 0.01),as well as fetuin A and calcium×phosphate products (R2=0.299,F=11.948,P=0.002).Multiple regression analysis indicated that fetuin A was independently negatively correlated with cIMT(B=-0.019,t =-6.042,P ＜ 0.01).At 18 months,there were 36 newly-happened cardiovascular events and among which 6 cases died.Logistic regression analysis found that increased cIMT was risk factor to cardiovascular events in PD patients(OR=3.691,95％CI 1.467-9.258,P=0.006).Conclusion Decreased fetuin A and increased calcium×phosphate products deteriorate carotid calcification in PD patients.Micro-inflammation of PD patients represented by high CRP levels may increase calcium×phosphate products by depressing the fetuin A level,and in the end will stimulate carotid calcification.Increased cIMT is a risk factor for cardiovascular events.