pH值对IFN-α2b、rIL-2、ADM合用维拉帕米对人肝癌细胞杀伤作用的影响

目的　观察培养液在 pH值为 6 .8、7.3、7.6条件下rIL - 2、IFN -α2b、ADM及合用维拉帕米对人肝癌细胞 74 0 4杀伤作用的影响。方法　MTT法于 96孔培养板上进行杀伤实验 ,测定培养液pH值分别为 6 .8、7.3、7.6状态下 ,rIL - 2、IFN -α2b、ADM、及与维拉帕米联合杀伤人肝癌细胞 70 4 0的差异。结果　pH值为 7.6状态下rIL - 2、IFN -α2b、ADM及合用维拉帕米杀伤效果最佳。pH值为 6 .8、7.3、7.6时 ,IFN -α2b都能增加ADM抗肿瘤作用 ,但pH值为 7.6时 ,IFN -α2b +ADM杀伤效果最佳。结论　在偏硷性环境下 ,rIL - 2、IFN -α2b、ADM及合用维拉帕米对肿瘤细胞杀伤效果最佳     

pH指示剂吸收度比值法测定盐酸乙胺丁醇的含量

本文报道pH指示剂吸收度比值法测定盐酸乙胺丁醇的含量。该法采用指示剂为0.05%茜素黄R,测定波长374nm和500nm;标准液为0.1mol/L NaOH;仪器为WFZ-800D_2型分光光度计。测得三批盐酸乙胺丁醇的含量分别为99.5±0.04%,99.4±0.05%和99.6±0.03%.同时与药典法比较,结果一致。     

霍乱毒素B亚单位基因的克隆和表达

用DNA重组技术构建CT-B表达性质粒pXB1及进一步修饰的pXB2,使CT-B基因在大肠杆菌中得到较高水平的表达(280～350ng/ml),且有71.5％分泌率。表达动力学研究阐明,克隆子培养24h产物收率较高。一定浓度的Mg~(2+)、L-组氨酸和天冬酰胺能刺激CT-B的表达。GM1-ELISA、CHO细胞测毒结合间接免疫荧光检测和家兔肠段结扎试验证实,表达的CT-B能与游离的或活细胞膜上的GM1受体结合,但无细胞和肠段毒性。这种细胞测毒结合免疫荧光序贯试验,为客观证实CT-B的生物学活性开拓了新途径。     

幽门螺杆菌重组粘附素rHpaA生物学活性及免疫原性的体外评价

目的：体外评价幽门螺杆菌（Hp)重组粘附素rHpaA的生物学活性及免疫原性,探讨其在Hp疫苗应用中的可行性。方法：流式细胞术和光镜定量计数法检测rHpaA及其抗体对Hp与胃上皮细胞粘附的影响;ELISA法测定Hp感染者血清中抗HpaA抗体,^3H-TDR掺入法测定人外周血淋巴细胞（PBL）对rHpaA的增殖反应,评价rHpaA对体液和细胞免疫的细胞;流式细胞术检测rHpaA对T辅助细胞（Th）表型的选择作用,探讨rHpaA可能的免疫机制。结果rHpaA和抗rHpaA抗血清均能部分阻断Hp与胃上皮细胞系的粘附;ELISA法能检测出Hp阳性患者血清中存在抗HpaA抗体,检测出率与Hp超声破碎抗原（HpSON)包被下的检出率相近（50%vs54%,P＞0．05）;不论培养基中是否加入IL－2,rHpaA均可刺激Hp PBL的增殖（P＜0．05）;Hp阳性或阴性PBL细胞与rHpaA孵育后均能显著提高IL－4阳性T细胞比例（P＜0．05）。结论HpaA是具有免疫原性的Hp菌体成分,且能选择性增加Th2细胞比例,有望成为Hp疫苗研制中一种有效的新抗原。     

猫胃粘膜螺旋菌的调查与鉴定

本研究应用多种分子生物学和病理学技术,对18只猫胃粘膜的螺旋样细菌进行了调查和鉴定。15/18的猫胃粘膜组织尿素酶阳性,5只猫胃培养出弯曲样和HP样细菌,后者及8/11只猫胃粘膜DNA与螺杆菌属细菌特异寡核苷酸探针发生阳性杂交。且该株细菌与及7/11的猫胃粘膜组织DNA应用幽门螺杆菌特异PCR引物扩增阳性.涂片及组织切片W-S银染发现三种类型的螺旋样菌:幽门螺杆菌样细菌;人胃螺旋菌样细菌及弯曲菌样细菌。PCR对照研究发现切片发现的HP样菌即为HP,而GH-LOs也为螺杆菌属细菌。提示猫也是幽门螺杆菌的动物宿主,其与人类HP感染之间的关系尚待进一步阐明。     

氢氯噻嗪分别与氯沙坦或卡托普利联合应用的降压疗效和安全性的比较观察

目的:比较联合应用氯沙坦和氢氯噻嗪与卡托普利和氢氯噻嗪治疗高血压的疗效和安全性。方法:72例新诊断或经2周洗脱期后基线平均舒张压为95～115mmHg,平均收缩压<180mmHg的高血压病患者,随机分成A、B两组各36例。A组每天服用氯沙坦50mg和氢氯噻嗪12.5mg,B组每天服用卡托普利50mg和氢氯噻嗪25mg。用药后每周测血压,以基线值与第4周末血压的平均变化作为疗效指标,并记录药物不良反应,结合实验室检查结果作安全性评估。结果:两治疗组第4周平均舒张压及平均收缩压降低无显著差异(P>0.10)。但与药物相关的不良反应A组显著低于B组(8.4％对16.7％)。结论:联合应用氯沙坦和氢氯噻嗪与卡托普利和氢氯噻嗪降压疗效相似,但前者的安全性和耐受性较好。     

淋巴滤泡形成与幽门螺杆菌致病——313例青年志愿者病理研究报告

作者调查了313例青年志愿者胃内HP感染状态与胃粘膜淋巴滤泡形成的关系。通过内镜普查,细菌和病理学诊断发现螺杆菌感染率为58.5％(183/313),淋巴滤泡形成率为28.4％(52/183),通过研究HP的感染量与淋巴滤泡大小证实了二者的正相关关系,并发现淋巴滤泡形成与内镜诊断无关,结合国外的报道提出了淋巴滤泡形成可能是HP感染致胃MALT发生过程中的一个重要步骤。     

Effects of the volume conductor on the apparent orientation of a known cardiac dipole

The surface electrocardiogram (EKG) is dependent on two major factors: the cardiac generator and the volume conductor. This investigation assessed the effects of the volume conductor in man on the apparent orientation of a simulated cardiac dipole. The apparent orientation of the dipole was calculated from measured surface potentials from about 60 locations on the body of five patients with implanted cardiac pacemakers. The real orientation of the dipole (an implanted pacemaker) was determined radiographically. The effects of both inhomogeneity and boundary characteristics of the volume conductor on the apparent orientation of the dipole were assessed using a new inverse algorithm. The difference between the orientation of the real and the calculated dipoles averaged 30 degrees (range 15 degrees--40 degrees) when the torso was assumed to be an infinite-homogeneous volume conductor. When the configuration of the torso was accounted for, however, the difference between the orientation of the real and calculated dipoles was reduced to 9 degrees (range 5 degrees--13 degrees). Thus, by taking into account the geometry of the torso and neglecting the inhomogeneities in the volume conductor, it is possible to calculate the orientation of a dipole in the cardiac region with an accuracy of about 9 degrees. It is reasonable to assume that the orientation of real activation wave fronts from localized areas of the heart could be calculated with a similar degree of accuracy.     

γ-Aminobutyric Acid Regulates Both the Survival and Replication of Human β-Cells

γ-Aminobutyric acid (GABA) has been shown to inhibit apoptosis of rodent β-cells in vitro. In this study, we show that activation of GABA_A receptors (GABA_A-Rs) or GABA_B-Rs significantly inhibits oxidative stress–related β-cell apoptosis and preserves pancreatic β-cells in streptozotocin-rendered hyperglycemic mice. Moreover, treatment with GABA, or a GABA_A-R– or GABA_B-R–specific agonist, inhibited human β-cell apoptosis following islet transplantation into NOD/scid mice. Accordingly, activation of GABA_A-Rs and/or GABA_B-Rs may be a useful adjunct therapy for human islet transplantation. GABA-R agonists also promoted β-cell replication in hyperglycemic mice. While a number of agents can promote rodent β-cell replication, most fail to provide similar activities with human β-cells. In this study, we show that GABA administration promotes β-cell replication and functional recovery in human islets following implantation into NOD/scid mice. Human β-cell replication was induced by both GABA_A-R and GABA_B-R activation. Hence, GABA regulates both the survival and replication of human β-cells. These actions, together with the anti-inflammatory properties of GABA, suggest that modulation of peripheral GABA-Rs may represent a promising new therapeutic strategy for improving β-cell survival following human islet transplantation and increasing β-cells in patients with diabetes.A central focus of research in the type 1 diabetes (T1D) field is to develop ways to safely improve β-cell survival and function and promote their replication. The addition of γ-aminobutyric acid (GABA) or the GABA_B receptor (GABA_B-R)–specific agonist baclofen to culture media has been shown to inhibit β-cell apoptosis in cultured rodent cell lines and islets (1,2). It remains to be determined whether GABA treatment can inhibit mouse β-cell apoptosis in vivo or, more importantly, whether it can protect human β-cells from stress-induced apoptosis. If GABA can inhibit human β-cell apoptosis, elucidating whether this effect is mediated through the G-protein–coupled GABA_B-Rs, and/or the chloride channel GABA_A-Rs will enable more specific drug targeting.GABA can promote neurogenesis and neuronal proliferation and is a neuronal survival factor (3–8). GABA has also been shown to promote rodent β-cell replication (1,2). Those studies, however, differentially pointed to GABA_A-Rs or GABA_B-Rs as modulators of GABA’s effects, making it important to clarify whether one or both types of GABA receptors modulate rodent β-cell replication. While a number of mitogens and growth factors can promote rodent β-cell replication, most fail to promote human β-cell replication (reviewed in refs. 9,10). Therefore, a key question is whether GABA can promote human β-cell replication. Even a small amount of GABA-induced human β-cell replication may be clinically useful by lowering insulin requirements and reducing the risk for long-term complications in T1D patients (11).