Objective To analyze factors associated with long-term survival of acute leukemia(AL). Methods Clinical data is analyzed in 27 leukemia cases who had at least 5 years free survival (EFS). Combined intensive chemotherapy was administered under the principle of individualization to induce remission.Regular consolidation treatment after remission was strictly continued.Long-term follow up Was kept on,with the therapeutic regimen modified accordingly.Results Complete remission(CR) was achieved in 112 of 143(78.3%)AL patients and 27(18.9%)of them had survived more than 5 years.Conclusion The long-term survival of AL patients is related to the type of AL,leukemia cell burden,extramedullary leukemia, individual treatment,time required to achieve CR,continuous intensive chemotherapy and the regular postremission treatment.

OBJECTIVE To investigate the nosocomial infection and risk factors of extended spectrum beta-lactamases (ESBLs),and the concomitant infection with other bacteria and double infection in patients of malignant hematopathy.METHODS Forty six malignant hematopathy patients with nosocomial infection by ESBLs positive bacteria were studied retrospectively.RESULTS ESBLs positive bacteria of nosocomial infection in patients of malignant hematopathy were Escherichia coli and Klebsiella.67.4% Were pulmonary infection and 30.4% with septicemia.Major risk factors were the usage of the third generation cephalosporin,the usage of chemotherapy and adrenal cortical hormone,and agranulocytosis.41.3% Cases had infection with other bacteria and 13.0% cases had double infection at the same time.All cases were sensitive to carbopenems,35.7% cases were sensitive to amikacin.CONCLUSIONS The prognosis of patients with nosocomial infection by ESBLs positive bacteria is bad.It is important to select appropriate chemotherapy,measure granulocyte amount in time,control the use of third generation cephalosporin and intensify support therapy.

OBJECTIVE To investigate the effect of recombinant human granulocyte colony-stimulating factor(rhG-CSF) combined with antifungal drugs in the treatment of malignant hematologial diseases with fungus infection.METHODS Malignant hematologial patients with fungus infection were randomized to receive fluconazole with or without rhG-CSF.(RESULTS) The response rate in patients who received fluconazole combined with rhG-CSF was 89.1% and in(control) patients was 62.8%(P

Objective To investigate clinical significance of transforming growth factor-beta 1 ( TGF-β1 ) in patients with chronic idiopathic thrombocytopenic purpura(CITP). Methods The serum level of TGF-β1 in 38 pa-tients with initial CITP were detected using enzyme-linked immunosorbent assay(ELISA). Results The serum level of TGF-β1 in initial patients with CITP was significantly higher than that of the controls [( 132.57±5.17) μg/L vs ( 76.81±4.42) μ/L] ( P <0.01 ). The serum level of TGF-β1 in those having good response after therapy was sig-nificantly lower than before treatment[(81.26±3.78)μg/L] (P <0.01 ). There was no difference in TGF-β1 be-tween nonremission [(123.49 ± 4.31 ) μg/L] and initial patients (P > 0.05 ). There was negative correlation between TGF-β1 and platelet count(r = -0. 342 ,P < 0.05 ) ,there was positive correlation between TGF-β1 and megakaryo-cyte count (r = 0.409, P < 0.01 ). Conclusions TGF-β1 partakes in the pathogenesis of CITP, the determination of which in patients with CITP is useful to judge the state of illness, which can be regarded as an assistant index of cur-ative effect.

Background: Chronic exposure to elevated levels of saturated fatty acids results in pancreatic β-cell senescence. However, targets and effective agents for preventing stearic acid-induced β-cell senescence are still lacking. Although melatonin administration can protect β-cells against lipotoxicity through anti-senescence processes, the precise underlying mechanisms still need to be explored. Therefore, we investigated the anti-senescence effect of melatonin on stearic acid-treated mouse β-cells and elucidated the possible role of microRNAs in this process. Methods: β-Cell senescence was identified by measuring the expression of senescence-related genes and senescence-associated β-galactosidase staining. Gain- and loss-of-function approaches were used to investigate the involvement of microRNAs in stearic acid-evoked β-cell senescence and dysfunction. Bioinformatics analyses and luciferase reporter activity assays were applied to predict the direct targets of microRNAs. Results: Long-term exposure to a high concentration of stearic acid-induced senescence and upregulated miR-146a-5p and miR- 8114 expression in both mouse islets and β-TC6 cell lines. Melatonin effectively suppressed this process and reduced the levels of these two miRNAs. A remarkable reversibility of stearic acid-induced β-cell senescence and dysfunction was observed after silencing miR-146a-5p and miR-8114. Moreover, V-maf musculoaponeurotic fibrosarcoma oncogene homolog A (Mafa) was verified as a direct target of miR-146a-5p and miR-8114. Melatonin also significantly ameliorated senescence and dysfunction in miR-146a-5pand miR-8114-transfected β-cells. Conclusion These data demonstrate that melatonin protects against stearic acid-induced β-cell senescence by inhibiting miR-146a- 5p and miR-8114 and upregulating Mafa expression. This not only provides novel targets for preventing stearic acid-induced β-cell dysfunction, but also points to melatonin as a promising drug to combat type 2 diabetes progression.