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Objective Both QBC Star and Sysmex XP-100 hematology analyzers are convenient to carry,which can be used nor-mally under the condition of the field(emergency).This study would compare their test results and operating performance,so to provide guidance for rational use of the instruments.Methods 100 fresh blood samples of 100 health soldiers anti-coagulated by EDTA-K2 were detected by QBC Star and Sysmex XP-100 haematology analyzers respectively,the results of two analyzers were comparatively analyzed and their test time and operating convenience were analyzed.Results There was no significant difference in the results of hemoglobin concentration (HGB),hematocrit (HCT)tested by the two methods (P >0.05).There were significant difference of the mean corpuscular hemoglobin concentration (MCHC),the sum of lymphocyte percent and middle type cells (LYM%+MID%),neutrophil percentage(NEUT%),white blood cell count(WBC),platelet count(PLT)tested by the two meth-ods(P <0.05).The values of MCHC and LYM%+MID% tested by the QBC Star were significantly lower than that detected by Sysmex XP-100(P <0.05),while the rest indicators tested by the former were higher than that of the latter.It took about 5 minutes to complete a blood sample analysis with QBC Star,while about 1 min was needed for Sysmex XP-100.Conclusion The test results of QBC Star and Sysmex XP-100 hematology analyzers couldn′t exchanged except for that of HCT and HGB.Under the condition of field(emergency),QBC Star hematology analyzer is suitable for individual medical examination,and Sysmex XP-100 hematology an-alyzer can be used for the batch medical examination.
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Objective To investigate the influence of CD4+CD25+ regulatory T cells (Tregs) on the disease progression in MRL/lps mice. Methods Tregs were separated by using magnetic beads from splenic cells of MRL/lps mice and BALB/c mice, and concentrated. Twenty-four MRLAps mice were equally divided into 3 groups, test group 1 injected with Tregs from MRL/lps mice, test group 2 injected with Tregs from BALB/c mice, and control group injected with physiological sodium chloride solution. Three weeks later, the levels of urine protein as well as serum anti-dsDNA antibody were determined; subsequently, the mice were sacrificed followed by histopathological and immunopathological examination of renal tissue. Results A significant decline was observed in the test group 1 compared with the test group 2 and control group in the urine protein score (10.63 ± 4.17 vs. 20.00 ± 5.35 and 18.75 ± 8.34, both P 0.05). There was no statistical difference between the test group 2 and control group in terms of any of the above parameters (all P > 0.05). Conclusions Injection of Tregs from homologous mice could significantly down-regulate proteinuria degree, serum anti-dsDNA antibody level, glomerular sclerosis index and IgG immune complex level in renal tissue, and thereby decelerate the progression of renal impairment in MRL/lps mice.
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Objective To explore how the antibody of glucocorticoid-induced tumor necrosis factor receptor (GITR) exerts inhibitory effect on the L615 leukemia cells by strengthening the activation of the NK cells. Methods The 24 established L615 leukemia mice were equally and randomly divided into 4 experimental groups according to different drugs given intraperitoneally, groupⅠ (normal saline), Ⅱ (GITR), Ⅲ (cyclophosphamide), and Ⅳ (GITR +cyclophosphamide).Then the NK cells were extracted from the spleen of mice as effective cells, and L615 leukemia cells served as the target cells. The changes of the NK cells’killing activation was observed in vivo. The mRNA levels of 3 proteins tightly related to the NK cells’activation Perforin, IFN-? and Fas mRNAs were detected with RT-PCR. Results The GITR-antibody enhanced the killing activity of the NK cells obviously, with the expressions of the 3 proteins increasing obviously. Conclusion By regulation of the Treg cells, the GITR-antibody can inhibit the L615 leukemia cells through enhancing the NK cells' killing activity.
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Objective To investigate the effect and the mechanism of the GITR-antibody(glucocorticoid-induced tumor necrosis factor receptor-ligand antibody) on the mouse leukemia model induced by L615.Methods The mouse leukemia models induced by L615 cells were divided into 4 groups: negative controls(peritoneal injection of normal saline,0.2 ml/d),GITR group(GITR,100,infused through caudal vein 2 d before leukemic lymphocytes inoculation,again at dose of 50 ?g/each mouse after inoculation),Cyclophosphamide group(200 mg?kg~(-1)?d~(-1),intraperitoneal injection from the 3~(rd) day after inoculation for 3 d),GITR+ Cyclophosphamide group(100 mg?kg~(-1)?d~(-1) Cyclophosphamide instead).The survival time,leukocyte counting in the peripheal blood,liver and spleen index were calculated and the pathological examination of liver,spleen were performed.Results GITR-ligand could prolong the survival time of mouse leukemia model,lead the necrosis and apoptosis of leukemic cells in bone marrow,decrease the liver and spleen index,decrease and relieve the leukocyte increase of peripheal blood and the irregular swelling of liver and spleen.Conclusion Through immunoregulation,GITR-antibody can inhibit the L615 leukemic cells effectively,therefore inhibit the progress of leukemia to some extent.
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Objective:To investigate the changes of postburn activity on murine splenic T lymphocyte phosphoinositide-specific PLC signal pathway, and look for the relationship between the postburn and T cell function suppression, IL-2 and IL-10 secretion.Methods:The experimental model was 18% TSBA (total body surface area) fullthickness scalded mice by vapor. The activities of G-protein, PTK (membrane, cytoplasmic) PKC (membrane, plasmic),PI-PLC and cytoplasmic free calcium concentration were detected at different postburn periods, moreover T lymphocyte proliferating function, IL-2 and IL-10 secretion were examined.Results:Compared with control group, membrane GTPase and plasmic PI-PLC enzyme were suppressed after scalded, calcium concentration lowered down significantly, the activities of PTK and PKC were complex, membrane PKC activity elevated after decreasing, those of plasmic PKC were just on the contrary, and the total activity of membrane and plasmic PKC was not stable; Membrane PTK activity decreased in the postburn early stage, then increasing.T cells proliferating function and IL-2 production marginally reduced, and the depressed levels of IL-2 production and T cells proliferating activity were positive parallel with the activities of G-protein and Ca ++. Cytoplasmic PKC activity lowered down after elevating, which was just negative linearly correlated with IL-10 secretion.Conclusion:Inhibition of G-protein ?PTK and Ca ++ activities in phosphoinositide-specific PLC signal pathway was the main reason which resulted in the decrease of IL-2 secretion, suppressed T cell proliferation and the dual-directional changes in IL-10 secretion.