“医联卡-册”在区域医疗服务中的推广

区域医疗中自费患者的“一院一卡”、互不通用的现象,是阻碍区域医疗卫生信息共享的重要瓶颈之一。通过申康对“医联卡-册”的推行,方便了自费患者在医联联网的市级医院就医,提高了医院服务效率,促进了医疗信息共享。     

多台全自动血细胞分析仪检测结果的比对研究

目的 通过对多台不同型号全自动血细胞分析仪检测结果的比对分析,探讨其检测结果是否可达临床要求.方法 以参加卫生部血细胞分析室间质评的SYSMEX XT-1800i全自动血细胞分析仪作为标准机,其它四台仪器分别为BECKMAN Coulter LH785及LH750和SYSMEX XS-800i及XE-2100作为比对机.每天仅选用SYSMEX XT-1800i和BECKMAN Coulter LH785两台仪器的配套质控物进行室内质控的WBC,RBC,HGB,HCT及PLT值的检测,连续检测30天.同时用上述五台仪器对新鲜血液标本的WBC,RBC,HGB,HCT及PLT值进行检测,连续检测30天.结果 五台仪器检测结果经统计学分析,相关系数在0.94～0.99之间;F检验P值均＞0.05;检测结果偏倚值均在1/2美国CLIA'88能力验证分析质量要求范围内.结论同一实验室使用多台型号不同的血细胞分析仪时,选择性进行室内质量控制并结合新鲜血对仪器进行比对检测分析,能有效提高血细胞分析仪检测结果的可比性,这样不仅减少了质控物的用量,同时也可为临床提供准确一致的实验室检测结果.使临床对疾病的诊断和治疗监测有一个统一的判断标准.     

微量荧光法体外测定恶性疟原虫对4种常用抗疟药的敏感性

目的 验证微量荧光法(MFA)用于恶性疟原虫体外药物敏感性和抗疟药物筛选的适用性。方法 运用MFA测定氯喹、青蒿素、蒿甲醚和咯萘啶等4种常用抗疟药物对体外培养FCC1/HN株恶性疟原虫的敏感性,并对该方法所测得的量效曲线(dose-response curves)及50%有效抑制浓度(IC₅₀)与光学显微镜镜检法所得的结果进行比较。结果 MFA所测定的氯喹、青蒿素、蒿甲醚和咯萘啶的IC50分别为18.79、6.32、3.67和2.00 nmol/L,光学显微镜镜检法的结果分别为19.65、5.82、4.38和2.83nmol/L,两者差异均无统计学意义(P>0.05)。结论 用MFA体外测定恶性疟原虫对抗疟药的敏感性敏感、快速,可用于体外抗疟药物的敏感性测定及抗疟药物筛选。     

罗格列酮对免疫性肝纤维化大鼠肝组织IGF-1表达的影响

目的探讨免疫性肝纤维化大鼠肝组织中胰岛素样生长因子-1(IGF-1)的表达变化,并观察罗格列酮对其的影响。方法应用猪血清腹腔注射诱导大鼠肝纤维化模型,适时给予罗格列酮干预。采用ELISA法检测血清IGF-1水平和免疫组织化学法检测肝组织IGF-1的表达。结果与对照组相比,第4、6、8周模型组大鼠血清及肝组织IGF-1水平均显著升高(P<0.05);与模型组相比,8周罗格列酮组大鼠纤维化程度减轻(P<0.01),血清及肝组织IGF-1表达水平降低(P<0.01)。结论随肝纤维化进展,大鼠血清和肝组织IGF-1的表达均增强,罗格列酮可降低肝组织IGF-1的表达,因而能减轻大鼠肝纤维化。     

High levels of interleukin-6 are associated with low tumor burden and low growth fraction in multiple myeloma

Interleukin-6 (IL-6) is a multifunctional cytokine postulated to play a central role as a growth factor for multiple myeloma (MM). We evaluated the spontaneous secretion of IL-6 in supernatants of Ficoll-Hypaque-- enriched bone marrow (BM) cultures from 35 patients with MM. The levels of IL-6 were correlated with biological and clinical characteristics of the disease. High levels of IL-6 production defined a subgroup of patients with low tumor burden as determined by lower serum beta 2- microglobulin (B2M) (P = .02) and lower percentage of myeloma cells infiltrating the bone marrow (P = .003), higher synthetic rates of monoclonal protein (P = .006), and low proliferative compartments as measured by the percentage of Ki-67--positive myeloma cells. Patients with high proliferative fractions (Ki-67--positive myeloma cells > 20%) had significantly lower levels of IL-6 when compared with patients with low proliferative fractions (P = .005). Our findings do not support IL- 6 as a major growth factor for MM, but demonstrate an association of high levels of IL-6 secretion with low tumor cell burden and low proliferative fraction.     

Platelet-dependent primary hemostasis promotes selectin- and integrin- mediated neutrophil adhesion to damaged endothelium under flow conditions

Co-localization of blood platelets and granulocytes at sites of hemostasis and inflammation has triggered an intense interest in possible interactions between these cellular processes and induction of vessel wall injury. Leukocyte adhesion to endothelial cells decreases with increasing shear and is dependent on an initial rolling phase mediated by selectins. We hypothesized that flow-dependent platelet adhesion at an injured vessel wall will lead to P-selectin expression by platelets, thus mediating leukocyte co-localization. A perfusion chamber was used in which flowing whole blood induced platelet adhesion to a subendothelial matrix (ECM) of cultured human umbilical vein endothelial cells (HUVEC). We compared neutrophil (polymorphonuclear leukocyte [PMN]) interactions with HUVEC and their ECM with and without adhered platelets. PMNs adhered predominantly to ECM-adhered platelets and not to endothelial cells. ECM alone did not support PMN adhesion under flow conditions. PMN adhesion to unstimulated HUVEC was only substantial at low shear (up to 200 cells/mm2 at shear stress 80 mPa). In marked contrast, PMN adhesion to ECM-adhered platelets was dramatically increased, and adhesion was demonstrated at much higher shear stress (up to 640 mPa). Studies with specific antibodies showed that the platelet-dependent neutrophil adhesion was selectin-mediated. Inhibition of P-selectin caused a marked inhibition of adhesion at high shear stress, whereas the role of leukocyte L-selectin was less pronounced. beta2-Integrin-blocking antibodies inhibited static neutrophil adhesion. fMLP induced L-selectin shedding from leukocytes, resulting in decreased leukocyte adhesion. In conclusion, platelet- dependent hemostasis at the ECM appears to be a powerful intermediate in neutrophil-vessel wall interactions at shear stresses that normally do not allow neutrophil adhesion to intact endothelium.