Transplantation of microencapsulated bovine chromaffin cells reduces lesion-induced rotational asymmetry in rats

Surrounding bovine chromaffin cells by a semipermeable membrane may protect the transplanted cells from a host immune response and shield them from the inflammatory process resulting from the surgical trauma. Encapsulation of the chromaffin cells was achieved by inter-facial adsorption of a polycation on a polyanionic colloid matrix in which the chromaffin cells were entrapped. Basal and potassium-evoked release of catecholamines from encapsulated bovine chromaffin cells was analyzed over a 4-week period in vitro. Norepinephrine and dopamine release remained constant over time whereas epinephrine release significantly decreased. The chromaffin cells also retained the capacity for depolarization-elicited catecholamine release 4 weeks following the encapsulation procedure. Morphological analysis revealed the presence of intact chromaffin cells with well-preserved secretory granules. Striatial implantation of chromaffin cell-loaded capsules significantly reduced apomorphine-induced rotation compared to empty polymer capsules in animals lesioned with 6-hydroxydopamne frr at least 4 weeks. Intact chromaffin cells expressing tyrosine hydroxylase and dopamine-β-hydroxylase were observed in all capsules implanted in the striatum for 4 weeks. The assessment of the clinical potential of transplanting encapsulated adrenal chromaffin cells of either allo- or xenogeneic origin for Parkinson's disease will require long-term behavioral studies. The present study suggests, however, that the polymer encapsulation procedure may offer an alternative to adrenal autografts as a source of dopaminergic tissue.     

Open, Double-Blind and Long-Term Study of Vigabatrin in Chronic Epilepsy

We performed an open, double-blind, and long-term study of vigabatrin (gamma-vinyl-GABA, GVG) in patients with treatment-resistant epilepsy who were receiving only one or at most two standard antiepileptic drugs (AEDs). The novel design included a parallel, double-blind, placebo-controlled phase that minimized the number of patients receiving placebo and allowed determination of the optimum dose of GVG for each patient before initiation of the double-blind phase. The study was divided into four phases. The first phase was a 6-week period of baseline observation. In the second phase, GVG was added openly to previous AEDs for 8 weeks. During the first 2 weeks of this phase, the dose of GVG was increased weekly and then, in the absence of adverse effects, was held constant for the next 6 weeks. At the end of this open phase, seizure frequency during the 6 weeks of constant treatment was compared with the baseline seizure frequency for each patient. Patients who experienced reduction greater than 50% in the frequency of any seizure type during the open phase were defined as responders. These responders were then entered into the third and double-blind phase, in which they were randomly allocated wither to continue active GVG treatment or placebo for 8 weeks. Thirty-three patients entered the study; 31 of 33 patients completed the initial open phase. Twenty patients achieved a reduction greater than or equal to 50% in the frequency of one or more seizure types and were eligible for the double-blind phase; 10 were randomized to continue GVG and 10 were randomized to placebo.(ABSTRACT TRUNCATED AT 250 WORDS)     

益肾调督针法对实验大鼠脑梗死恢复期TNF-α、IL-6和IL-8的影响

目的 观察益肾调督针法对脑梗死恢复期治疗及预防再梗的作用机制。方法 将实验大鼠随机分为对照组、模型组、益肾调督针法组、常规针法组和非穴针刺组各10例，用血栓栓塞法制备局灶性脑梗死模型，观察治疗前后大鼠神经功能改变，应用双抗体夹心ELISA法分别测定各组大鼠血清中TNF-α、IL-6和IL-8的含量。结果 治疗前后大鼠神经功能评分以益。肾调督针法组及常规针法组有效，差异具有显著性（P〈0．01）；模型组大鼠血清中TNF．仅、IL-6和IL．8含量较对照组明显升高（P〈0．01），施予针刺治疗后各针法组含量均有不同程度的下降。结论 益肾调督针法可以有效地抑制TNF-α、IL-6和IL-8的表达．从而在脑梗死恢复期治疗及预防再梗方面发挥作用。     

卡维地洛对不稳定型心绞痛患者血浆炎症因子的影响

目的观察卡维地洛对不稳定型心绞痛（UAP）患者高敏C反应蛋白（hs-CRP）、白介素-6（IL-6）及细胞间可溶性黏附分子1（sICAM-1）水平的影响。方法UAP患者62例采用完全随机化方法分成对照组（n=30）和治疗组（n=32）,在常规抗血小板、扩血管治疗基础上,对照组予美托洛尔（12.5mg,2次/d×3d）口服,治疗组服卡维地洛（6.25mg,2次/d×3d）,在治疗前后分别测定hs-CRP、IL-6、sICAM-1值。结果对照组和治疗组在治疗前hs-CRP、IL-6、sICAM-1均无显著性差异;用药后两组3指标均较用药前显著降低（P<0.05）;治疗组在用药后IL-6、sI-CAM-1显著低于对照组（P<0.05）。同时,用药后两组患者的心率、血压、心肌耗氧量均较用药前显著降低（P<0.05）,治疗组的心肌耗氧量显著低于对照组（P<0.05）。结论卡维地洛可显著降低UAP患者的炎症因子IL-6、sICMA-1水平。     

白介素-6、血管内皮生长因子、D-二聚体对CSDH的影响

目的探讨血肿局部炎症、假膜新血管生成、局部纤溶状况及其在CSDH发生、发展中的作用。进而探讨CSDH的发病机制，并为CSDH的治疗及预防复发提供理论依据。方法以78例CSDH患者作为病例组，20例健康人作为正常对照组。采用ELISA法测定患者血清及血肿液中VEGF及IL-6的含量。比较患者末梢静脉血及血肿液中四种因子的含量变化并与正常对照组比较。结果病例组血肿液FDP、d-dimer检测均为阳性，血液为阴性；正常对照组血液FDP、d-dimer检测均为阴性；病例组血清VEGF含量与正常对照组比较差异无统计学意义。血肿液中VEGF浓度高于血清中。病例组血清IL-6浓度与正常对照组差异无统计学意义，血肿液中IL-6浓度高于血清中。CSDH患者血肿液VEGF、IL-6水平没有相关性。结论CSDH患者血肿液局部纤溶亢进，局部VEGF分泌旺盛，新血管生成活跃，局部炎症活跃，可导致CSDH不断扩大而参与CSDH发病机制。抗炎治疗、抑制VEGF的生理作用、有选择的对病人施行促凝治疗，可成为部分CSDH病人保守治疗及预防复发的有效手段。     

白细胞介素-15对骨髓增生异常综合征骨髓造血干/祖细胞增殖的影响

目的：观察白细胞介素(IL-15)对体外培养的骨髓增生异常综合征(MDS)患者CD34^ 细胞增殖作用。方法：应用单克隆抗体免疫磁珠分离系统提取MDS患者CD34^ 细胞，以加IL-15组为实验组，不加IL-15组为对照组，进行液体和甲基纤维素半固体集落培养，计算培养后细胞数和CFU—E、BFU—E、CFU—GM、CFU—GEMM等集落数，并用MTT比色法检测IL-15对MDS患者CD34^ 细胞增殖的抑制作用，流式细胞术检测上述培养细胞周期的变异情况。结果：11例MDS对象平均CD34^ 细胞比例、回收率、纯度和富集倍数均达要求，MTT比色法检测IL-15对CD34^ 细胞的增殖作用呈最佳浓度效应，最佳浓度为20μg／L，细胞增殖抑制最低峰值时间为8d。用0μg／L IL-15(对照组)和20μg／L IL-15(实验组)作用MDS CD34^ 细胞，计数显示培养细胞最大增殖倍数和集落形成比率实验组均较对照组明显增加，IL-15作用后各细胞周期G1、S、G2期比例有明显改变，与对照组比较，差异有统计学意义。结论：IL-15对MDS CD34^ 细胞有促增殖效应，与其它造血生长因子具有协同作用，对MDS治疗可能有一定的应用前景。     

云南东川非铀矿山矿工血清IL-2、IL-6、TNF-α检测及其基因多态性的初步研究

目的 通过对云南非铀矿山矿工血清IL-2、IL-6和TNF-α浓度及基因多态性位点的检测,对氡致非铀矿山矿工机体生物效应进行初步探讨。方法 血清中IL-2、IL-6和TNF-α的浓度测定采用双抗夹心ABC-ELISA法。TNF-α(-308,G→A)检测基因型采用基因体外扩增限制性片段长度多态性分析方法,IL-2(-330, T→G)基因型检测采用PCR体外扩增后测序的方法。结果 矿工组与对照组比较,年龄(F＝1.07,P>0.05),工龄(F＝0.40,P>0.05),血清IL-2浓度(F＝0.71,P>0.05),血清IL-6浓度(F＝1.09,P>0.05),血清TNF-α浓度(F＝0.95,P>0.05),IL-2基因型频度(χ²=0.02,P>0.05)和TNF-α基因型频度(χ²=2.21,P>0.05),差异均无统计学意义。结论 云南东川非铀矿山矿工血清IL-2、IL-6和TNF-α平均浓度有下降的趋势, TNF-α(-308,A A)基因型频度有增高的趋势。     

Histopathological characterisation of effects of the mouse Pax6 missense mutation on eye development

Mutations in PAX6/Pax6 lead to a variety of ocular anomalies in humans and mice. The aim of the study was to characterise the ocular abnormalities caused by the missense Pax6^Leca4 mutation and compare them to published observations on Pax6 alleles that are functionally equivalent to Pax6⁻ null alleles (such as Pax6^Sey and Pax6^Sey-Neu) and human inherited eye diseases. Ocular features of homozygous Pax6^Leca4/Leca4 and heterozygous Pax6^Leca4/+ embryos at E12.5-E18.5, heterozygous Pax6^Leca4/+ young mice at P18 and heterozygous Pax6^Leca4/+ adults at 12 weeks were analysed histologically with their wild-type Pax6^+/+ littermates. Homozygous Pax6^Leca4/Leca4 fetuses died perinatally with no eyes although an optic cup rudiment with pigmented cells developed. Pax6^Leca4/+ mice were microphthalmic and a range of other severe ocular phenotypes affected both the anterior and the posterior segments. In contrast to Pax6^+/−, the Pax6^Leca4/+ eyes had no goblet cells in the corneal epithelium, the iris was not hypoplastic and there was no lens-corneal epithelial plug. However, microphthalmia was more severe, corneal vascularisation occurred earlier (during fetal stages), pigmented cells were present in the vitreous and corneal stroma and the ciliary body was malformed or abnormal. These results show that, although Pax6^Leca4/+ lacked some eye abnormalities commonly seen in Pax6^Sey/+ and Pax6^Sey-Neu/+ eyes, in most respects their eyes were more severely affected. These differences probably reflect both differences between the Pax6^Leca4 and the Pax6^Sey-Neu mutations and differences in modifier gene expression in different genetic backgrounds. The presence of pigmented cells in the cornea is a novel observation. Some Pax6^Leca4/+ ocular abnormalities were similar to those present in human Peters' anomaly and persistent hyperplastic primary vitreous (PHPV) so Pax6^Leca4/+ mice provide a useful model for some inherited eye diseases.     

Asymmetric dimethyl-arginine (ADMA) response to inflammation in acute infections.

BACKGROUND AND METHODS: The endogenous inhibitor of nitric oxide synthase (NOs) asymmetrical dimethyl-arginine (ADMA) has been implicated as a possible modulator of inducible NOs during acute inflammation. We examined the evolution in the plasma concentration of ADMA measured at the clinical outset of acute inflammation and after its resolution in a series of 17 patients with acute bacterial infections. RESULTS: During the acute phase of inflammation/infection, patients displayed very high levels of C-reactive protein (CRP), interleukin-6 (IL-6), procalcitonin and nitrotyrosine. Simultaneous plasma ADMA concentration was similar to that in healthy subjects while symmetric dimethyl-arginine (SDMA) levels were substantially increased and directly related with creatinine. When infection resolved, ADMA rose from 0.62 +/- 0.23 to 0.80 +/- 0.18 micromol/l (+29%, P = 0.01) while SDMA remained unmodified. ADMA changes were independent on concomitant risk factor changes and inversely related with baseline systolic and diastolic pressure. Changes in the ADMA/SDMA ratio were compatible with the hypothesis that inflammatory cytokines activate ADMA degradation. CONCLUSIONS: Resolution of acute inflammation is characterized by an increase in the plasma concentration of ADMA. The results imply that ADMA suppression may actually serve to stimulate NO synthesis or that in this situation plasma ADMA levels may not reflect the inhibitory potential of this methylarginine at the cellular level.     

BcL-2、Bax、CD44V6在乳腺癌表达及预后的研究

目的探讨影响乳腺癌患者预后的因素,协助临床制定手术方式及术后治疗方案。方法选择80例各型乳腺癌患者的标本,应用免疫组化SP方法,检测乳腺癌组织中癌基因BcL-2、Bax及黏附因子CD44V6的表达情况。结果乳腺癌中BcL-2、Bax及CD44V6的表达情况与肿瘤组织学分级、瘤体直径。有无转移及患者术后存活时间均有显著性相关(P<0.05或0.01)。结论BcL-2高表达、Bax低表达、CD44V6低表达的患者组织学分级好,肿瘤体积小,淋巴结转移少,术后存活时间长,这部分患者可做肿物扩大切除而保留乳房或即使已做乳房切除,术后也可减少放疗及化疗剂量。