SARS家庭聚集型病例8例报告分析

SARS是由变异冠状病毒引起的新型烈性传染病，具有在家庭和医院内聚集发病的特点。其影像学表现对于临床诊断和随诊观察具有重要价值。本文报告了分属3个家庭的8个病例发病早期(1周)影像学表现(包括胸部平片和CT)和部分临床表现资料，讨论并分析SARS早期影像学表现的若干特点及与临床表现之间的关系。     

持续性脑脊液耳漏的诊断与治疗

目的：探讨持续性脑脊液耳漏的发病原因、临床表现、诊断及手术处理方法。方法：分析1987年6月－2000年12月收治26例持续性脑脊液耳漏的临床资料，男16例，女10例。成人18例，儿童8例。结果：26例中自发性脑脊液耳漏14例，因乳突及侧颅底手术引起的12例。15例伴有复发性脑膜炎。26例中25例在我院1次手术修补成功，1例听神经瘤术后脑脊液鼻漏行2次手术修补成功。结论：手术是主要的治疗方法，术中应注意颅底的修复，尤其对内听道、鼓室、咽鼓管、乳突尖等重要部位的处理，以预防术后脑脊液耳漏的发生。     

运动性中枢疲劳及乳酸对大鼠大脑皮质神经细胞MCT mRNA表达的影响

目的:探讨运动性中枢疲劳时大鼠大脑皮质MCT1、MCT2mRNA表达的变化以及乳酸对大鼠大脑皮质神经元MCT2mRNA表达的影响。方法:12只Wistar大鼠随机分为对照组和力竭训练1周组,每组6只。通过7天力竭训练建立中枢疲劳模型,观察中枢疲劳时大鼠大脑皮质MCT1、MCT2mR-NA表达变化;采用原代培养的大鼠大脑皮质神经元,观察不同浓度乳酸作用后大鼠大脑皮质神经元MCT2mRNA表达的变化。采用Trizol法提取大脑皮质和神经元总RNA;用SYBRAgreenI荧光定量RT-PCR测定MCT1及MCT2mRNA表达变化。结果:整体水平:力竭训练1周组MCT1mRNA表达无明显变化,而MCT2mRNA表达较对照组显著升高6·35±3·54倍(P<0·05)。细胞水平:乳酸作用后,神经元MCT2mRNA表达在pH=7·25时较对照组(pH=7·35组)升高3·08±2·38倍(P<0·05)。但随着乳酸浓度进一步升高,MCT2mRNA表达无明显增加。结果提示,中枢疲劳可能引发大脑皮质神经元MCT2mRNA表达升高,MCT2基因表达可能与乳酸在中枢疲劳中的作用有关。     

Potential contribution of nuclear factor-kappaB to cerebral vasospasm after experimental subarachnoid hemorrhage in rabbits.

Nuclear factor-kappaB (NF-kappaB) plays a key role in inflammation, which is involved in the development of cerebral vasospasm after subarachnoid hemorrhage (SAH). In the present study, we assessed the potential role of NF-kappaB in regulation of cerebral vasospasm. Nuclear factor-kappaB DNA-binding activity was measured in cultured vascular smooth muscle cells (VSMCs) treated with hemolysate and pyrrolidine dithiocarbamate (PDTC, 80 micromol/L), an inhibitor of NF-kappaB. Forty-two rabbits were divided into three groups: control, SAH, and PDTC groups (n=14 for each group). The caliber of the basilar artery was evaluated. Nuclear factor-kappaB DNA-binding activity and the gene expression levels of cytokines and adhesion molecules in the basilar artery were measured. Immunohistochemical study was performed to assess the expression and localization of tumor necrosis factor (TNF)-alpha, intercellular adhesion molecule (ICAM)-1, and myeloperoxidase (MPO). It was observed that NF-kappaB DNA-binding activity was significantly increased by treatment with hemolysate in cultured VSCMs, but this increase was suppressed by pretreatment with PDTC. Severe vasospasm was observed in the SAH group, which was attenuated in the PDTC group. Subarachnoid hemorrhage could induce increases of NF-kappaB DNA-binding activity and the gene expression levels of TNF-alpha, interleukin (IL)-1 beta, ICAM-1, and vascular cell adhesion molecule (VCAM)-1, which were reduced in the PDTC group. Immunohistochemical study demonstrated that the expression levels of TNF-alpha, ICAM-1, and MPO were all increased in the SAH group, but these increases were attenuated in the PDTC group. Our results suggest that NF-kappaB is activated in the arterial wall after SAH, which potentially leads to vasospasm development through induction of inflammatory response.     

局部亚低温治疗急性脑出血的临床研究

目的观察冰帽加双侧颈动脉区冰敷治疗急性脑出血的临床疗效和探讨最佳治疗时机。方法 174例急性脑出血患者随机分为治疗组和对照组 ,每组 87例。对照组给予常规治疗 ,治疗组在常规治疗的基础上同时给予亚低温治疗 ;治疗组中 46例在发病 3小时内治疗 ,41例在发病 3小时后治疗。观察治疗组与对照组以及治疗组中发病 3小时内与发病 3小时后两组的临床疗效和预后情况。结果亚低温治疗组与对照组比较 ,神经功能改善 (P <0 0 5 ) ,生存率及恢复良好率提高 (P <0 0 5 )。发病 3小时内开始治疗者优于 3小时后开始者 (P <0 0 5 )。结论亚低温治疗能有效减轻急性脑出血后的神经功能缺损 ,降低病死率和致残率 ;最佳治疗时机在发病 3小时以内。     

高血压患者左室舒张功能与左室肥厚的关系及随龄改变

为探讨原发性高血压 (以下简称高血压 )患者的左室舒张功能和左室肥厚的关系及其随龄改变 ,抽取 1995年 2月至 2 0 0 2年 7月间门诊高血压患者 4 81例为高血压组 ,以同期体检健康者 2 54 3例为对照组 ,年龄 10～ 80岁 ,并将原发性高血压患者分为 3级 ,每级中按性别分 2组。采用惠普 2 50 0彩色多普勒超声诊断系统检测 2组的室间隔厚度、左室后壁厚度、E/A等指标。使用SPSS软件进行统计学处理分析。结果 :高血压和正常对照组相比E/A显著下降 ,室间隔和左室后壁显著增厚 (P <0 .0 1)。 2个组的E/A均随年龄下降 ,而室间隔厚度随年龄增厚 ,且室间隔厚度和E/A呈显著负偏相关 (P <0 .0 1)。在高血压分级组中 ,Ⅰ～Ⅲ级高血压组中男性的室间隔厚度均厚于女性 (均P <0 .0 1) ,Ⅰ、Ⅱ级高血压组中男性的左室后壁厚度厚于女性 (P <0 .0 5,P <0 .0 1) ,Ⅰ级高血压组中女性的E/A低于男性 (P <0 .0 5)。提示 :左室舒张功能随着年龄的增加而降低 ,而且和高血压左室肥厚呈负偏相关关系 ,性别对其也有一定的影响     

Cortical Reorganization Allows for Motor Recovery after Crossed Cerebrocerebellar Atrophy

The authors report the case of a 33-year-old woman who exhibited, at the age of 17, a left-sided hemiplegia, which was followed by good motor recovery, though with a permanent deficit in fine finger movements. She had a widespread loss of neural tissue in the right hemisphere (crossed cerebrocerebellar atrophy), including (1) marked atrophy and thinning of the precentral and postcentral gyri; (2) widespread deep white matter destruction, including the corticospinal tract; and (3) crossed cerebellar atrophy. Except over the supplementary motor area (SMA), transcranial magnetic stimulation did not elicit motor evoked potentials in the affected hand. Nevertheless, during opening and closing of the affected hand, functional magnetic resonance imaging showed an activation of the lesioned primary sensorimotor cortex (SMC), as well as of the intact SMA and the parietal areas, but not of the ipsilateral motor areas. The authors speculate that recovery was achieved by a motor command generated in the SMC and the parietal cortex, passing through corticospinal axons originating in the SMA.