地方性克汀病病区加碘盐11年后胎儿大脑M—胆碱受体的观察

报告１２例非克汀病病区人工引产胎儿和６例地方性克汀病病区加碘盐１１年后人工引产胎儿大脑Ｍ－胆碱受体的变化。结果显示，与非病区相比，病区胎儿大脑Ｍ－胆碱受体密度（Ｂｍａｘ）显著降低Ｐ（〈０．０５），而配基－受体解离常数（Ｋｄ）则明显升高（Ｐ〈０．０１）。表明病区补碘后胎儿发育过程中，大脑Ｍ－胆碱受体发育存在显著的迟滞现象，这可能是病区仍然有亚克汀病病例存在的分子基础。     

神经型地方性克汀病患者大脑神经细胞的定量组织学研究

本文应用快速 Golgi 镀银技术对6例典型神经型地克病人大脑运动皮质区及听皮质区的神经细胞及其突起进行了(?)量组织学研究;并与4例同龄正常人脑进行了对比。研究结果表明地克病人上述两个皮质区的锥体细胞及星形神经细胞胞体明显小于正常人;锥体细胞主干树突分支及基树突,尤其星形神经细胞周围树突的数量比正常人显著减少。此外,光镜下的形态学定性观察还发现地克病人的小脑皮质浦氏细胞顶树突分支较稀疏,未形成典型的茂密的树冠状。上述结果均说明地克病患者的神经细胞的生长发育受到明显障碍,从而为地克病的临床表现提供形态学证据。     

综合治疗地方性克汀病九个月后的智力变化观察

用恢智片等药物和智力训练相结合的方法治疗地方性克汀病患者18例。治疗前平均年龄为16.7岁,平均智龄为6.0岁。智龄落后于年龄10.7岁,治疗九个月后同体比较平均提高智龄2.5岁。治疗前平均智商为36.11,治疗后平均为51.41,治疗后智商水平较治疗前显著提高(P<0.001)。其中粘肿型平均增加20.6(P<0.001),混合型平均增加16.3(P<0.01),神经型平均增加5.5(P>0.05)。18例中10岁以下2例,治疗后全部达基本治愈,11～20岁14例治疗后5例达基本治愈(35.7％),21岁以上的2例,治疗后均未达基本治愈。治疗开始的年龄不同,其疗效有显著差异(P<0.05)。年龄愈小智力恢复愈好。     

Tan评分对急性大脑中动脉M1段闭塞患者溶栓效果的评估价值

目的 探讨Tan评分对急性大脑中动脉（AMCA）M1段闭塞患者溶栓效果的评估价值。方法 选取156例接受静脉溶栓治疗的AMCA M1段闭塞患者,根据脑梗死溶栓（TICI）血管灌注分级将患者分为未通组94例和再通组62例。比较两组基础资料和Tan评分,多因素Logistic回归分析AMCA M1段闭塞患者溶栓未通影响因素。受试者工作特征（ROC）曲线分析Tan评分预测AMCA M1段闭塞患者溶栓未通价值,比较不同Tan评分患者改良Rankin量表（mRS）分级。结果 未通组Tan评分<2分、高血压史、心房颤动史比例和入院时国立卫生研究院卒中量表（NIHSS）评分、空腹血糖（FPG）、低密度脂蛋白胆固醇（LDL-C）、尿酸（UA）、C反应蛋白（CRP）水平高于再通组,发病至入院时间长于再通组（P均<0.05）。多因素Logistic回归分析显示,高血压史（OR=4.318,95%CI:2.405～8.276）、发病至入院时间（OR=1.076,95%CI:1.025～1.128）、入院时NIHSS评分（OR=1.170,95%CI:1.081～1.395）为AMCA M1段闭塞...     

大脑中动脉M1段闭塞时MRA所见"大脑后动脉偏侧优势"对脑梗死范围和分布以及NIHSS评分的影响

目的 探讨大脑中动脉(middle cerebral artery,MCA)M1段闭塞患者磁共振血管造影(magnetic resonance angiography,MRA)所见"大脑后动脉偏侧优势(prominent laterality of the posterior cerebral artery,PLPCA)"与脑梗死范围和分布以及美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale,NIHSS)评分的关系.方法 50例MCA M1段闭塞所致急性肭梗死患者根据MRA表现分为PLPCA阳性组(24例)和PLPCA阴性组(26例),对两组患者NIHSS评分、脑梗死范围评分以及脑梗死在MCA各供血亚区的分布构成比进行比较.结果 PLPCA阳性组危险因素个数≥3的患者比例(9/24对18/26,P=0.046)、NIHSS评分(5.4±4.4对10.4±4.9,t=-3.690,P=0.001)和脑梗死范围评分(1.92±1.10对2.88±1.37,t=-2.745,P=0.008)均显著低于PLPCA阴性组.PLPCA阳性组脑梗死累及MCA中部分支供血区(6/24对19/26,P=0.002)和后部分支供血区(2/24对15/26,P＜0.001)的患者比例显著低于PLPCA阴性组,累及后部分水岭区的患者比例显著高于PLPCA阴性组(6/24对1/26,P=0.045),而发生MCA完全梗死的比例显著低于PLPCA阴性组(0/24对6/26,P=0.023).结论 MCAM1段闭塞时,如果MRA观察到PLPCA,预示梗死范围较小和NIHSS评分较低,梗死较少累及MCA中、后部分支供血区,而易出现后部分水岭梗死.     

于中晚孕期超声检查发现的胎儿变异大脑前动脉A1段血流速度变化观察

目的 基于中晚孕期超声检查结果观察胎儿变异大脑前动脉A1(ACA-A1)段的血流速度变化情况.方法 中晚期孕妇1116例,应用超声高清血流显像(HD-Flow)对胎儿ACA-A1段血管显示情况进行观察,依据胎儿ACA-A1段血管显示情况进行分组,对照组胎儿的双侧ACA-A1段血管能够清晰显示,单侧缺如组胎儿的一侧ACA...     

肾移植术后可溶性白介素－2受体的动态观察

多年来人们一直在寻找一种非创伤性检查方法来诊断肾移植急性排斥反应。我们采用双抗体夹心ＥＬＩＳＡ分别于术前、术后第３、７天及以后每周１次，连续２个月动态监测２４例肾移植患者１１４例次血清可溶性白介素－２受体（ｓＩＬ－２Ｒ），以探讨其对移植肾急性排斥反应诊断和鉴别诊断的临床意义。结果表明ｓｌＬ－２Ｒ水平移植前高于正常对照组，移植后随着移植肾功能的恢复而明显降低（Ｐ＜０．０１），当发生急性排斥反应时则显著升高，而环孢素肾中毒、急性肾小管坏死时则变化不明显。特别强调了动态检测ｓＩＬ－２Ｒ变化百分率对急性排斥反应的预测、诊断和鉴别诊断具有更重要意义。     

大脑中动脉M1段闭塞患者血清血小板衍生生长因子、胰岛素样生长因子1水平与侧支循环形成及预后的关系

目的 探讨大脑中动脉M1段闭塞（M1CAO）患者血清血小板衍生生长因子（PDGF）、胰岛素样生长因子1（IGF-1）水平与侧支循环形成及预后的关系。方法 选取2017年2月～2018年8月我科收治的M1CAO患者158例作为疾病组,另取169例门诊健康体检者作为对照组。所有M1CAO患者均于发病1周后行磁共振血管成像（MRA）检查确诊,根据软脑膜侧支循环代偿形成情况,将其分为无代偿组、单纯大脑前动脉（ACA）代偿组、单纯大脑后动脉（PCA）代偿组及ACA+PCA代偿组。采用酶联免疫吸附试验（ELISA）检测所有受试者的血清PDGF、IGF-1水平;采用美国国立卫生研究院卒中量表（NIHSS）对住院当天及15d时M1CAO患者的神经功能缺损情况进行评分;采用改良Rankin量表（mRS）对M1CAO患者出院后90d的预后进行评估,将其分为预后良好组和预后不良组。比较各组受试者的临床资料。血清PDGF、IGF-1水平的相关性分析采用Pearson相关分析;M1CAO患者预后的影响因素分析采用logistic回归分析。结果 与对照组比较,疾病组患者血清PDGF、IGF-1水平均明显降低（P＜0.05）。与无代偿组比较,单纯ACA代偿组、单纯PCA代偿组、ACA+PCA代偿组患者血清PDGF、IGF-1水平依次升高,NIHSS评分依次降低（P＜0.05）。与预后不良组比较,预后良好组患者血清PDGF、IGF-1水平均明显升高（P＜0.05）。Pearson相关分析结果显示,M1CAO患者血清PDGF水平与IGF-1水平呈正相关（r=0.414,P＜0.05）。Logistic回归分析结果显示,血清高PDGF、IGF-1水平及侧支循环形成是M1CAO患者预后良好的独立保护因素（P＜0.05）,糖尿病是M1CAO患者预后不良的独立危险因素（P＜0.05）。结论 M1CAO患者血清PDGF、IGF-1水平明显降低,二者水平升高与侧支循环形成及良好预后有关,是M1CAO患者预后的独立影响因素。     

钼对克山病病区粮养大鼠红细胞NADH－细胞色素b_5高铁血红蛋白还原酶活力的影响

Ｗｉｓｔａｒ大鼠３０只，雌雄各半分层均匀分为非病区粮组、病区粮组和病区粮补相组（１００ｍｇ／ｋｇ），分别喂以克山病非病区粮和克山病病区粮，实验期为４个月。病区粮养大鼠红细胞还原高铁血红蛋白的能力，ＮＡＤＨ—细胞色素ｂ_５高铁血红蛋白还原酶活力均低于非病区粮组。病区粮补钼可升高此酶活力，提高红细胞还原高铁血红蛋白的能力，在一次性失血的应激情况下，程度达到显著。病区粮补钼（１００ｍｇ／ｋｇ）对红细胞谷胱甘肽过氧化物酶活力无明显影响。     

硒蛋亚硒酸钠对云南克山病病区儿童全血谷胱甘肽过氧化物酶活性影响的动态观察

选择云南楚雄克山病病区６～１０岁儿童作为观察对象，分为四组；服硒蛋组，服普通鸡蛋组．服亚硒酸钠药片组及对照组，连续３年动态观察将胱甘肽过氧化物酶（ＧＳＨ－ＰＸ）的活性，结果表明：服硒蛋组全血ＧＳＨ－ＰＸ活性显著增高，显著高于其它各组，服硒片组ＧＳＨ－ＰＸ的活性也增高，与服普通鸡蛋组、对照组比有差异，但不如服硒蛋组明显。结果提示：病区长期服硒蛋和硒片都能提高全血ＧＳＨ－Ｐｘ的活性，但服硒蛋比单纯服硒片效果更好。     

Loss of muscarinic cholinergic receptors from the temporal cortex of alcohol abusers

It is currently controversial whether all the brain damage in alcohol abusers in the result of thiamine deficiency (Wernicke-Korsakoff's disease) or whether, in addition, alcohol abuse may affect the brain by other mechanisms as well. The purpose of this study was to determine if alcohol abuse affects muscarinic cholinergic and benzodiazepine receptors in histologically normal brains obtained at autopsy in a general hospital population. Patients were excluded from this study if they had clinical brain diseases (including Wernicke's disease), died in coma, or had liver disease, significant brain atrophy, or dementia severe enough to require institutionalization. We found that muscarinic cholinergic synaptic receptor density determined with [³H] quinuclidinly benzilate was decreased by 40% in homogenates of the tempeoral cortex of 26 alcohol abusers compared with 26 matched nonalcoholic controls. The affinities of the muscarinic receptors were not significantly different between the two groups. In contrast, receptor densities and affinities of benzodiazepine receptors determined with [³H]flunitrazepam were not significantly different in the two groups. Age and death-autopsy time interval had no significant effects on either wet tissue protein concentrations, yields of protein after centrifugation, or receptor binding. The contributions of age and time interval were each less than 2% of the total variance of protein concentrations and receptor binding. When patients were excluded or included who had received cholinergic, anti-cholinergic, or benzodiazepine medications before death, no significant effects on the final results were observed. Pneumonia, known to be associated with acute hypoxia, and chronic obstructive pulmonary disease, known to be associated with chronic hypoxia, where approximately equally distributed between the two groups and had no significant effects on the results reported here. The loss of muscarinic and the sparing of benzodiazepine receptors occurs in the temporal cortex of histologically normal brains in the absence of significant atrophy and of gross dementia. This means that these changes are early in the development of an alcohol encephalopathy. We have previously reported a decrease in both muscarinic and benzodiazepine receptor binding in the frontal cortex and a decreasing muscarinic but not benzodiazepine receptors in the temporal cortex of alcohol abusers. Taken together, these findings suggest that alcohol neurotoxicity does not simply result in a random loss of neurons and/or their associated synapses with their receptors. Instead, different types of receptors, depending upon their location in different brain regions, are specifically affected or spared. This suggests the involvement of region- and receptor-specific mechanisms in chronic alcohol toxicity. These and other changes in synaptic receptors may be the molecular basis for some of the specific behavior patterns of certain alcohol abusers.     

Pre- and postsynaptic markers of cholinergic neurons in the cerebral cortex of rats of different ages

In order to investigate the effect of aging on postsynaptic muscarinic binding, we measured 3H-PZ binding in the cerebral cortex of male Fisher 344 rats of different ages. ChAT activity was measured as a presynaptic marker of the cholinergic system. Total and salt-soluble AChE activities were also measured. Maximal binding of 3H-PZ and ChAT activity did not change during aging. The ratio of detergent-soluble AChE to salt-soluble AChE was lower in 30-month-old rats than in 4-month-old rats. The results of the present study do not indicate that the amount of M1 muscarinic receptors proposed to be located postsynaptically decreases during aging. In senescent rats, however, the proportions of salt-soluble and detergent-soluble AChE may differ form those in young rats.     

Studies of the cholinergic receptors involved in the secretion of insulin using isolated perfused rat pancreas

Summary Studies of the role and nature of the cholinergic receptors acting on the secretion of isolated perfused rat pancreas have shown the following: The infusion of acetylcholine at a dose of 2.5 M in the presence of a concentration of glucose of 1.5 g/1, provoked a first phase of immediate and important stimulation of the secretion of insulin; this initial peak of insulin secretion was followed by a second phase during which a new less intense stimulation occurred; the latter was followed by an inhibition appearing at a time that depended on the pancreas used. At a dose of 0.5 M of acetylcholine, the first phase of stimulation always appeared; during the second phase some pancreases were inhibited, others remained stimulated. — The peak of insulin secretion obtained by stimulation with acetylcholine during the first phase was dose related. — Eserine intensified the effects of acetylcholine. — The presence of glucose was essential for the insulinsecretory action of acetylcholine. The muscarinic nature of the cholinergic receptors implicated in the secretion of insulin was demonstrated by the use of: — Atropine which completely blocked the effects of acetylcholine, — Muscarine which produced the same effects as acetylcholine on our pancreas preparation, effects which were equally inhibited by atropine. The cholinergic receptors of the endocrine beta cell of the islet of Langerhans of the pancreas are therefore of the muscarinic type.     

心力衰竭患者M2乙酰胆碱受体的自身抗体对豚鼠心肌细胞L型钙通道的影响

目的观察心力衰竭患者M2乙酰胆碱能受体的自身抗体(Abs)阳性血清以及M2乙酰胆碱能受体激动剂碳酰胆碱对心肌细胞的影响.方法应用全细胞钳制技术,定量观察并比较碳酰胆碱和心力衰竭患者Abs阳性血清对豚鼠单个心室肌细胞的L型钙电流强度的影响.结果M2受体激动剂碳酰胆碱使预先由异丙肾上腺素增大的L型钙电流峰值电流强度和标准电流密度从(2111.65±203.13)pA和(18.83±1.14)pA/pF下降为(1230.87±208.14)pA(P＜0.01)和(10.72±1.06)pA/pF(P＜0.01),M2受体阻滞剂阿托品可以阻断碳酰胆碱的这一作用.同样,心力衰竭患者的Abs阳性血清能使L型钙电流的峰值电流强度由(1995.21±195.13)pA下降至(636.42±110.07)pA,P＜0.01,标准电流密度由(18.13±1.03)pA/pF下降至(5.54±0.81)pA/pF,P＜0.01;阿托品也可阻断此作用.结论心力衰竭患者Abs阳性血清对豚鼠心室肌细胞的作用与碳酰胆碱相似,对心肌细胞M2受体有"激动剂样"效应,能使心肌细胞的L型钙电流减小,产生负性肌力作用;阿托品可以阻断它们对豚鼠心室肌细胞的作用.