Objective To assess the significance of insulin tolerance test(ITT) in clinical diagnosis of adult growth hormone deficiency(GHD).Methods Eighty-two patients with an established diagnosis of adult GHD [53males,29 females,mean age (30.9 ± 12.3) years (18-65 years)] were reviewed retrospectively for evaluating the GH response to ITT in the General Hospital of the People' s Liberation Army.Control data for peak GH after ITT were obtained in 15 healthy subjects [9 males,6 females,mean age (26.7 ± 5.6) years (22-41 years)].Receiver operating characteristic (ROC) curve analysis and the area under the curve (AUC) were used to evaluate the diagnostic cut-off point of peak GH and GH increment response to ITT.Results (1) Mean peak GH response to ITT was significantly higher in 15 controls compared with 82 patients (the median 14 μg/L vs 0.62 μg/L,P =0.001).The cut-off point of the peak GH(chemiluminescent immunoassay,CLIA) response to ITT in adult GHD was 4.935 μg/L (AUC 0.993).(2) Mean GH increment was significantly higher in 15 controls compared with 82 patients (the median 13.17 μg/L vs 0.19 ug/L,P＜0.001).The cut-off point of the GH increment was 4.088 μg/L(AUC 0.937),with a 91.5％ sensitivity and 100％ specificity.(3) The peak GH showed even higher diagnostic value than the GH increment after ITT.(4)The above mentioned cut-off points (peak GH less than 4.935 μg/L and 5 μg/L) had a coincidence with a 95.1％ sensitivity and 100％ specificity,respectively.Conclusion The current guidelines for the diagnosis of adult GHD based on the optimal cut-off point of the peak GH(CLIA) response to ITT less than 5 μg/L turned to be of reliable diagnostic value in our country.

OBJECTIVE：To investigate the synergistic effect and deficiencies between centralized drug quantity purchase policy and medical insurance reimbursement system ，and to provide feasible suggestion to further improve its synergistic effect. METHODS：The literature analysis method and policy evaluation method were adopted to expounds the direct and indirect synergistic effect between the current centralized drug quantity purchase policy and medical insurance reimbursement system in China，and analyze the existing problems so as to put forward the feasible suggestions. RESULTS & CONCLUSIONS ：The centralized drug quantity purchase policy had a direct impact on the payment mode of medical insurance reimbursement system in technical level ，performance evaluation in effect level and process control in management level. The indirect synergy included ： centralized drug quantity purchase policy could promote the adjustment of drug supply security system to adapt to the reform of medical insurance payment ；it could adjust the pharmaceutical market ，and affect the reform of medical insurance reimbursement system. The disadvantages were as follows ：the varieties of selected drugs was still narrow ，and there was room for further improvement in purchasing scope and medical insurance fee reduction ；“one-size-fits-all”payment standard for unselected drug might weaken pharmaceutical companies ’enthusiasm for generic drug research and development. Therefore ，the next step is to significantly expand the variety and scope of procurement ，and appropriately liberalize the medical insurance payment restrictions for drugs with fewer varieties ；coordinate medical insurance reimbursement policies and procurement programs ，and improve the rationality and perfection of medical insurance payment ；guide the medical institutions to change the concept from “price-based medical treatment ”to“value-based medical treatment ”，take into account the interests of all parties in the market ，so as to form a comprehensive coordination adjustment mechanism of drug price and medical insurance reimbursement system.

BACKGROUNDBone marrow hematopoietic function suppression is one of the most common side effects of chemotherapy. After chemotherapy, the bone marrow structure gets destroyed and the cells died, which might cause the hematopoietic function suppression. Heme oxygenase-1 (HO-1) is a key enzyme of antioxidative metabolism that associates with cell proliferation and resistance to apoptosis. The aim of this study was to restore or resist the bone marrow from the damage of chemotherapy by the HO-1 expression of mouse mesenchymal stem cells (mMSCs) homing to the mice which had the chemotherapy-induced bone marrow suppression.

METHODSOne hundred and sixty female Balb/c mice (6-8-weeks old) were randomly divided into four groups. Each group was performed in 40 mice. The control group was intraperitoneally injected for 5 days and tail intravenously injected on the 6th day with normal saline. The chemotherapy-induced bone marrow suppression was established by intraperitoneally injecting cyclophosphamide (CTX) into the mice which performed as the chemotherapy group. The mMSCs were tail intravenously injected into 40 chemotherapically damaged mice which served as the mMSCs group. The difference between the HO-1 group and the mMSCs group was the injected cells. The HO-1 group was tail intravenously injected into the mMSCs that highly expressed HO-1 which was stimulated by hemin. The expression of HO-1 was analyzed by Western blotting and RT-PCR. Cell proliferation was measured using the 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay. Histopathologic examinations were performed 1 week after injection.

RESULTSCompared with the control group, the expression levels of HO-1 mRNA and protein were significantly higher in the HO-1 group (all P < 0.05), even obviously than the mMSCs group. CTX treatment induced apoptosis and inhibited proliferation. After injected, the white blood cell (WBC), red blood cell (RBC) and platelet (PLT) declined fast and down to the bottom at the 7th day. The bone marrow structure was destroyed incomplete. In vitro, the survival rate of cells in chemotherapy group was less than 50% after 24 hours. In contrast, mMSCs could do a favor to the cellular cleavage and proliferation. They slowed down the cell mortality and more than 50% cells survived after 24 hours. The effects of blocking apoptosis and bone marrow recovery could be more effective in the HO-1 group. In the HO-1 group, it had observed that the bone marrow structure became complete and the hemogram closed to normal at 7th day.

CONCLUSIONSHO-1 played an important role in promoting the recovery of CTX-induced hematopoietic damage. We suggest that HO-1 is able to restore the functions of chemotherapy-induced hematopoietic damage.

Animals ; Apoptosis ; drug effects ; Blood Platelets ; drug effects ; Blotting, Western ; Bone Marrow ; drug effects ; enzymology ; Cell Proliferation ; drug effects ; Cells, Cultured ; Cyclophosphamide ; toxicity ; Erythrocytes ; drug effects ; Female ; Heme Oxygenase-1 ; genetics ; metabolism ; Leukocytes ; drug effects ; Mesenchymal Stem Cell Transplantation ; Mesenchymal Stromal Cells ; enzymology ; physiology ; Mice ; Mice, Inbred BALB C ; Reverse Transcriptase Polymerase Chain Reaction