Objective To study the detection method of insulin resistance in congestive heart failure.Methods Levels of fasting plasma insulin and glucose were determined in 41 patients of CHF and 26 normal controls through radioimmunoassay.The application value of the inverse of the product of fasting plasma glucose and insulin (IAI) and the ratio of fasting plasma glucose and fasting insulin (FPG/FINS) were compared.Results IAI levels in patients with CHF were significantly lower than those of the control group(P

Objective To investigate the clinical manifestations,laboratory findings and renal patho logic changes,as well as their relationships in patients with lupus nephritis (LN).Methods According to the latest classification criteria of lupus nephritis,the clinical manifestations,laboratory findings and renal patho logic changes and their relationships of 281 cases of biopsy proven LN were retrospectively analyzed.Results Totally 281 cases of LN patients were enrolled in total.The ratio of male to female was 1∶9.7.Proteinuria ac companied with hematuria (35.2%) and nephrotie syndrome (33.8%) were the main clinical manifestations. The most common renal pathological change was type Ⅳ LN (35.9%) and type Ⅲ,Ⅳ and Ⅴ accounting for 89.0% totally.The main pathologic changes of nephrotic syndrome were type Ⅳ and Ⅴ,while those who ac companied with renal dysfunction were mainly type Ⅵ and Ⅳ.Most simple hematuria cases showed mild renal injury.However,type Ⅳ and Ⅴ accounted for 40.4% in the 47 cases of LN whose 24 hours urine protein＜ 1.0 g and with normal renal function.Most severe proteinuria was found in Type Ⅴ and higher serum creatinine and anti-dsDNA antibody level were found in type Ⅵ and Ⅳ.The lowest lever of serum complement 3 (C3) was found in type Ⅳ.The amount of 24 hours urine protein showed negative correlation with semm C3 but positive correlation with serum creatinine.Serum C3 demonstrated negative relationship with serum creatinine and anti-dsDNA antibody,while serum creatinine was positively related to anti-dsDNA antibody level. Conclusion The major renal pathological lesions of LN are type Ⅲ,Ⅳ and Ⅴ.There are associations be tween clinical and pathological changes,but axe not always consistent.Proteinuria,low serum C3 and high an ti-dsDNA antibody level may provide clue to severe and active LN.Renal biopsy is important in the diagnosis and progression evaluation of LN.

Objective To test the hypothesis that p53 gene therapy combined with endostatin can enhance tumor response to radiation therapy of RM-1 mouse xenograft prostate cancer and to investigate its mechanism. Methods A mouse prostate cancer model was established. Then mice with xenograft tumor were randomly divided into group A (control), B (radiation), C (radiation and rAdp53), D (radiation and rh-endostatin) and E (radiation and rAdp53 and rh-endostatin). On day 1, rAdp53 was injected intra-tumorously with 1 × 1010 vp per animal to group C and E. From day 1 to 14, rh-endostatin was given 15 mg/kg intraperitoneally daily to group D and E. On day 4 single fraction of 15 Gy was given to tumors in groups B, C, D and E. Normal saline was injected intra-tumorously or intraperitoneaUy accordingly as control. No treatment was done to group A. Tumor volume was measured daily. Samples were collected on Days 5, 10 and 15. Ki67, CD31, p53 and VEGF were detected by means of immunohistochemistry. Results (1) Radiation alone, radiation combined with intra-tumorous injection of Adp53 and/or intraperitoneal injection of rh-endostatin resulted in tumor growth arrest of RM-1 cells in vivo (P = 0.000). Radiation combined with both rAdp53 and rh-endostatin was the most effective treatment (P < 0.05). (2) All the four treatment groups had a decreased expression of mutant type P53 (P = 0.000). The expression of Ki67 in groups B and C were equal (P 0.05) and increasing (P = 0.000), respectively. Group D had a up-down-up curve (P < 0.05), but group E had a up-down one. On day 5 the expresion of VEGF in group E was the lowest (P < 0.05). An increased expression of MVD compared with the control was shown, and MVD in groups C, D and E were always higher than that in the control (P < 0.05). Conclusions The limitation of radiotherapy could be overcome by combination with beth p53 gene therapy and endostatin on the growth of mouse prostate cancer cell. Radiation, rAdp53 and endostatin have their own role but they can be interacted with each other.