重庆市新生儿高胆红素血症患儿G6PD基因突变类型及临床特点

目的研究重庆市新生儿黄疸儿G6PD三种常见基因突变与其临床表现特点之间的关系。初步估计其基因突变频率并探讨其临床意义和遗传学特征。方法应用突变特异性扩增系统(ARMS)法,检测54例重庆市新生儿黄疸儿的G6PD基因突变类型。结果检出G1388A突变39例(72%),G1376T突变8例(15%),未定型者7例(13%)。未检出G95A。结论本研究首次对重庆市新生儿黄疸儿进行G1388A、G1376T和A95G突变检测。提示G1388A和G1376T为重庆市新生儿黄疸儿G6PD缺乏症基因突变的主要类型。ARMS法是一种简便、快速、经济的检测G6PD已知基因突变的方法。本研究发现这两种突变类型仅见于中国人和华裔人群,具有遗传学及临床意义。     

硬膜外腔阻滞对胸部手术应激反应的影响

目的 观察硬膜外腔阻滞对胸部手术应激激素和细胞因子的影响。方法20例食管癌手术病人,随机分为两组,每组10例,即全麻复令硬膜外腔阻滞(GEA)组和全麻(GA)组,分别测定麻醉诱导前、手术2h、手术4h、术毕、术后1d及术后3d的血浆去甲肾上腺素、肾上腺素、血清促肾上腺皮质激素(ACTH)、皮质醇、C-反应蛋白、IL-6及IL-10的水平。结果 血浆去甲肾上腺素和血清皮质醇GEA组术中术后无显著改变,但GA组术毕和术后1d显著升高(P<0.05),术后3d恢复至术前水平,组间比较前者有显著差异(P<0.05)。两组血浆肾上腺素、IL-10术中术后均无显著变化。两组血清ACTH、IL-6及CRP术中术后均显著升高(P<0.05),组间比较无显著差异。结论 硬膜外腔阻滞可以减轻胸部手术的应激反应。IL-6是较CRP更灵敏的反映组织损伤的炎性指标。     

IL-2诱导外周血单个核细胞对肿瘤细胞的杀伤效应

目的　了解白细胞介素 2 (IL 2 )诱导外周血单个核细胞 (PBMC)对肿瘤细胞的杀伤效应 ,探讨其作用机制。方法　IL 2 ( 10 5IU/L)体外诱导PBMC 5d ,并与Raji细胞株共同培养 ,采用MTT法测定不同时间诱导后的PBMC对Raji细胞的杀伤效应 ;采用BAS ELISA法检测杀伤活性最大时的IFN γ、TNF α、sFasL的表达 ,采用流式细胞仪检测诱导后PBMC的FasL、穿孔素、颗粒酶B的表达。结果　IL 2 ( 10 5IU/L)体外诱导PBMC 5d时 ,都能明显增强对Raji细胞的杀伤活性 ,而且在培养的第 4天杀伤活性最高 (P <0 0 5 ) ,诱导PBMC 4d后 ,FasL、穿孔素、颗粒酶B的表达与B组相比 ,明显增加 ,差异有显著性 (P <0 0 5 )。结论　IL 2 ( 10 5IU/L)体外诱导PBMC能明显增强对Raji细胞的杀伤活性 ,主要是通过诱导PBMC表达IFN γ、穿孔素、颗粒酶B和FasL的表达而发挥抗肿瘤细胞的作用     

Biocompatibility pattern of a bicarbonate/lactate-buffered peritoneal dialysis fluid in APD: a prospective, randomized study.

BACKGROUND: In chronic ambulatory peritoneal dialysis, bicarbonate-buffered fluids, with their neutral pH and less advanced glycosylation end-products (AGE) and glucose degradation products (GDP), have better biocompatibility than conventional peritoneal dialysis (PD) solutions. That difference may be more beneficial in automated peritoneal dialysis (APD), due to its more frequent exchanges and longer contact times with fresh dialysate. We performed a prospective, randomized study in APD patients to compare the biocompatibility of conventional and bicarbonate/lactate-buffered PD fluids. METHODS: We randomized 14 APD patients to have APD with either conventional or bicarbonate/lactate-based fluids. After 6 months, both groups changed to the other solution. The overall observation period was 12 months. After 1 and 5 months and again after 7 and 11 months, phagocytotic and respiratory burst capacities of effluent peritoneal macrophages were determined. Plasma interleukin (IL)-6 and C-reactive protein (CRP) as well as effluent IL-6, CRP, transforming growth factor (TGF)-beta 1, AGE and CA125 concentrations were measured. Inflow pain was quantified using a patient questionnaire. RESULTS: Respiratory burst capacity remained unchanged and phagocytotic activity increased significantly during APD (P<0.001) with the bicarbonate/lactate fluid. Effluent IL-6 release was significantly lower than with the lactate fluid (P<0.05). While in the effluent TGF-beta 1 was unaffected, AGE concentration was lower after bicarbonate/lactate treatment (P<0.05). Effluent CA125 concentration, an indicator of mesothelial cell integrity, was higher (P<0.05) in neutral effluents. Finally, patients' inflow pain diminished (P = 0.05) when using the neutral fluid. CONCLUSIONS: The use of a neutral PD fluid in APD improved patients' inflow pain as well as biocompatibility parameters reflecting enhanced phagocytotic activity of peritoneal macrophages, reduced constitutive inflammatory stimulation (IL-6), reduced AGE accumulation in the peritoneal cavity and better preservation of the mesothelial cell integrity. From the biocompatibility point of view, a neutral fluid with low GDP content can be recommended as the primary choice for APD.     

左旋精氨酸与维生素B6对低密度脂蛋白抑制兔胸主动脉内皮舒张功能的影响

目的观察正常人的低密度脂蛋白(native low density lipoprotein,nLDL),人工氧化的低密度脂蛋白(oxidized lowdensity lipoprotein,ox-LDL)及非胰岛素依赖型糖尿病(Non-insulin dependent diabetes mellitus,MDDM)患者的低密度脂蛋白(diabetic low density lipoprotein,dLDL)对兔胸主动脉环内皮的损伤作用及左旋精氨酸(L-arginine,L-Arg),维生素B6(pyridoxine,VB6)的拮抗效应.方法采用离体动脉环灌流的方法,观察兔胸主动脉环对乙酰胆碱(acetycholine,Ach),钙离子载体A23187的舒张反应.结果3种LDL均抑制动脉环对Ach及A23187的舒张,损伤强度为ox-LDL＞dLDL＞nLDL,并具有浓度依赖性;L-Arg、VB6能明显拮抗LDL的抑制作用,但并不能完全逆转.以SOD作为保护药对照,250 U/ml的浓度能够显著抑制dLDL对内皮的损伤.结论3种低密度脂蛋白主要可能通过降低NO生物活性损伤内皮,L-Arg、VB6具有内皮保护作用.     

The Van der Woude syndrome: a case report and review of the literature

The Van der Woude syndrome is a rare autosomal dominant developmental malformation usually associated with bilateral lower lip pits. These congenital lip pits appear clinically as a malformation in the vermilion border of the lip, with or without excretion. As a genetic defect has been identified as a microdeletion of chromosome bands 1q32-q41, genetic counselling of patients may be considered. A nonsense mutation in the interferon regulatory factor-6 (IRF-6) is discussed as a pathogenic relevant factor. Therapeutic intervention is generally not necessary, although surgical excision is especially indicated in patients with recurrent inflammation. Physicians should be aware of the Van der Woude syndrome because it has been reported to be associated with a variety of malformations or other congenital disorders.     

IL-2对垂体瘤细胞系RC-4B/C细胞分泌ACTH的影响

目的 :探讨白细胞介素 2 (IL 2 )对垂体瘤细胞系RC 4B/C细胞ACTH分泌的调控作用及其影响因素 .方法 :以放射免疫方法测定培养的垂体瘤细胞系RC 4B/C细胞的培养液中的ACTH浓度 .结果 :IL 2 (1× 10 4～ 5× 10 5U·L-1)促进RC 4B/C细胞分泌ACTH ;蛋白激酶A的抑制剂H 9(1μmol·L-1)和酪氨酸蛋白激酶的抑制剂tyrphostin2 3 (1μmol·L-1)均可显著性抑制IL 2的促ACTH分泌作用 .结论 :IL 2可促进RC 4B/C细胞分泌ACTH ,该作用与蛋白激酶A和酪氨酸蛋白激酶信号转导途径紧密相关     

Inflammatory biomarkers in blood of patients with acute brain ischemia

Although many failed surrogate markers are provided in the literature, inflammation may contribute to the outcome of ischemic stroke. In 50 consecutive patients with acute ischemic stroke, in the absence of symptoms and signs of concomitant infection, we evaluated a panel of biomarkers reported to be variably associated with brain ischemia, and correlate their serum level with the brain lesion volume and clinical outcome. Infarct size was calculated on computed tomography (CT) scans by means of the Cavalieri's method. Neurological impairment was scored by using the Glasgow Coma Scale, Glasgow Outcome Scale and National Institutes of Health (NIH) scales at stroke onset and 3-month follow-up. Some markers showed a direct significant correlation with both initial and final NIH scale and with infarct size, particularly tumor necrosis factor alpha (TNF-alpha) (P=0.002), intercellular adhesion molecule-1 (P<0.01) and matrix metalloproteinase-2/9 (P=0.001). In contrast to previous reports, interleukin-6 (IL-6) serum level showed a significant inverse correlation with both final neurological impairment and infarct size (P<0.001). This novel finding allows us suggesting that IL-6, in the context of a complex pro-inflammatory network occurring during stroke, is associated with neuroprotection rather than neurotoxicity in patients with ischemic brain injury.     

Fever and feeding in the rat: Actions of intrahypothalamic interleukin-6 compared to macrophage inflammatory protein-1β (MIP-1β)

The chemokines, macrophage inflammatory protein-1 (MIP-1) and its subunit MIP-1β, induce an intense fever in the rat when they are injected directly into the anterior hypothalamic, pre-optic area (AH/POA), a region containing thermosensitive neurons. The purpose of this study was to compare the central action on body temperature (T_b) of MIP-1β with that of interleukin-6 (IL-6), which also has been implicated in the cerebral mechanism underlying the pathogenesis of fever. Following the stereotaxic implantation in the AH/POA of guide cannulae for repeated micro-injections, radio transmitters which monitor T_b continuously were inserted intraperitoneally in each of 15 male Sprague-Dawley rats. Each micro-injection was made in a site in the AH/POA in a volume of 1.0 μl of pyrogen-free artificial CSF, recombinant murine MIP-1β, or recombinant human IL-6. MIP-1β in a dose of 25 pg evoked an intense fever characterized by a short latency, a mean maximum rise in T_b of 2.4 ± 0.21°C reached by 3.7 ± 0.42 hr, and a duration exceeding 6.5 hr. Injected into homologous sites in the AH/POA, IL-6 induced a dose dependent fever of similar latency and a mean maximal increase in T_b of 1.2 ± 0.25°C, 1.8 ± 0.15°C, and 2.1 ± 0.22°C and duration of 6.2 ± 1.28 hr, 6.7 ± 0.49 hr, and 6.8 ± 0.65 hr when given in doses of 25, 50, and 100 ng, respectively. These results show that MIP-1β and the highest dose of IL-6 induce a fever of comparable intensity, but MIP-1β exerts its action in a much lower concentration. Thus, the de novo synthesis and subsequent action of the MIP-1 family of cytokines on neurons of the AH/POA in response to a pyrogen challenge apparently play a functional role in the pathogenesis of fever. Further, the endogenous activity of IL-6 in the hypothalamus which is enhanced in response to a lipopolysaccharide also may reflect its essential part in the acute phase response to a bacterial challenge. Copyright © 1994 Wiley-Liss, Inc.