A sexually dimorphic ratio of orbitofrontal to amygdala volume is altered in schizophrenia.

BACKGROUND: Neuroanatomic sexual dimorphisms have been correlated with behavioral differences between healthy men and women. We have reported higher orbitofrontal cortex to amygdala ratio (OAR) in women than men. Although gender differences in schizophrenia are evident clinically and correlate with neuroanatomic measures, their relationship to OAR has not been examined. METHODS: Magnetic resonance imaging was performed in 31 neuroleptic-na?ve schizophrenic patients (16 men) and 80 healthy volunteers (34 men), aged less than 50 years. An automated tissue segmentation procedure was combined with expert-guided parcellation of orbitofrontal and amygdala volumes. RESULTS: Men with schizophrenia had increased OAR relative to healthy men, whereas women had decreased OAR. Increased OAR in men with schizophrenia reflected abnormally low amygdala volumes, whereas decreased OAR in women reflected abnormally low orbitofrontal volumes. Less severe negative symptoms were associated with increased OAR in men but with decreased OAR in women. In men, increased amygdala volume was associated with greater symptom severity, whereas in women higher volumes of both amygdala and orbitofrontal regions were associated with lesser severity of negative symptoms. CONCLUSIONS: These opposite OAR abnormalities, whereby men show feminization and women masculinization, suggest gender-mediated effects of the underlying neuropathologic processes. The correlations with symptom severity suggest that neuroanatomic abnormalities in OAR reflect compensatory brain changes.     

Motor blockade associated with continuous epidural infusion after abdominal hysterectomy: a randomized controlled trial comparing 0.1% ropivacaine-plus-fentanyl versus 0.2% ropivacaine-alone

We compared rates of motor blockade, analgesia, adverse effects and patient satisfaction of 0.1% ropivacaine+fentanyl versus 0.2% ropivacaine-alone in a randomized, controlled trial. Fifty-four women who had undergone abdominal hysterectomy were randomly allocated into two groups to receive an epidural block at L_1–2 or L_2–3: group R received 0.2% ropivacaine-alone and group RF received 0.1% ropivacaine plus 2 μg fentanyl/ml, both at 8 ml/h. Rescue analgesia was provided via a morphine-loaded PCA device. Motor blockade (using a modified Bromage scale), pain intensity (visual analogue scale (VAS)), morphine consumption, level of sensory blockade and adverse effects, were measured at 4, 8 and 21 h after infusion. Patient satisfaction with pain management was assessed at the end of the study. The rates of motor blockade were not different at 8 h after infusion but at 21 h, group RF had significantly less motor blockade than group R. There were no differences in VAS, level of sensory blockade, adverse effects and patient satisfaction. Morphine consumption at each measurement was comparable but the total amount used by group RF was less than group R (12 mg versus 20 mg, P=0.049). Therefore, 0.1% ropivacaine with fentanyl 2 μg/ml appears to offer advantages over 0.2% ropivacaine-alone.     

Organization of the callosal connections of visual areas V1 and V2 in the macaque monkey

The interhemispheric efferent and afferent connections of the V1/V2 border have been examined in the adult macaque monkey with the tracers horseradish peroxidase and horseradish peroxidase conjugated to wheat germ agglutinin. The V1/V2 border was found to have reciprocal connections with the contralateral visual area V1, as well as with three other cortical sites situated in the posterior bank of the lunate sulcus, the anterior bank of the lunate sulcus, and the posterior bank of the superior temporal sulcus. Within V1, callosal projecting cells were found mainly in layer 4B with a few cells in layer 3. Anterograde labeled terminals were restricted to layers 2, 3, 4B, and 5. In extrastriate cortex, retrograde labeled cells were in layers 2 and 3 and only very rarely in infragranular layers. In the posterior bank of the lunate sulcus, labeled terminals were scattered throughout all cortical layers except layers 1 and 4. In the anterior bank of the lunate sulcus and in the superior temporal sulcus, anterograde labeled terminals were largely focused in layer 4. Callosal connections in all contralateral regions were organized in a columnar fashion. Columnar organization of callosal connections was more apparent for anterograde labeled terminals than for retrograde labeled neurons. In the posterior bank of the lunate sulcus, columns of callosal connections were superimposed on regions of high cytochrome activity. The tangential extent of callosal connections in V1 and V2 was found to be influenced by eccentricity in the visual field. Callosal connections were denser in the region of V1 subserving foveal visual field than in cortex representing the periphery. In V1 subserving the fovea, callosal connections extended up to 2 mm from the V1/V2 border and only up to 1 mm in more peripheral located cortex. In area V2 subserving the fovea, cortical connections extended up to 8 mm from the V1/V2 border and only up to 3 mm in peripheral cortex.     

氨苯砜综合征诊治探讨——附6例报告

目的：探讨氨苯砜综合征的诊治要点：方法：对6例氨苯砜综合征患者的临床资料进行回顾性分析。结果和结论：6例氨苯砜综合征患者均为中青年，从服药到出现症状的时间较长，为9～55日.6例患者均以高热起病，起病急骤、凶险，病初均有麻疹紫癜样皮疹，皮疹多形，严重者出现尼氏征阳性或阴性的大疱和（或）全身性红皮病样皮疹；均有浅表淋巴结肿大；多数患者有血液系统损害；并均有肝损害：确诊后及时停氨苯砜，给予足量肾上腺皮质激素和（或）大剂量免疫球蛋白静脉注射，以及支持对症处理，住院12～80（中位数53）日，4例痊愈，1例病情得到控制，另1例因治疗第2日自动出院放弃治疗，死于肝功能衰竭？提示氨苯砜综合征需要及时、正确处理，否则预后不良.     

细胞内游离Ca2+在发育中大鼠皮层神经元无镁诱导惊厥性损伤中的作用

目的: 观察细胞内游离Ca2+([Ca2+]i)在培养的不同发育阶段皮层神经元无镁诱导惊厥性损伤中的作用,探讨惊厥性脑损伤年龄依赖性的可能机制.方法:体外培养6 d、17 d的胚胎大鼠皮层神经元用无镁细胞外液处理3 h,或于无镁处理前用NMDA(N-甲基-D-门冬氨酸)受体拮抗剂或Ca2+通道阻滞剂预处理,用MTT代谢率测定的方法检测神经元损伤,以Fluo-3作标记用激光共聚焦显微镜扫描的方法检测[Ca2+]i.结果:体外培养6 d、17 d的神经元单纯无镁组MTT代谢率较同期对照组降低.应用MK-801 10 μmol*L-1、AP-5 50 μmol*L-1、尼莫地平10 μmol*L-1预处理后再给无镁处理,培养6 d、17 d的神经元MTT代谢率均不同程度高于同期单纯无镁组.培养6 d、17 d的神经元相对荧光强度之间差异有显著性,两者与基线荧光强度比较差异亦有显著性.应用上述各种拮抗剂后,[Ca2+]i改变的峰值均明显低于同期单纯无镁组.结论: 在体外不同发育阶段的神经元,短暂无镁处理诱导惊厥样放电所引起的神经元线粒体功能损伤以及[Ca2+]i改变程度不同.这种[Ca2+]i改变的年龄依赖性可能是惊厥导致神经元损伤的年龄依赖性的机制之一.NMDA受体-Ca2+通道激活是导致这种[Ca2+]i改变及神经元损伤的关键环节.     

慢性束缚应激对大鼠行为及前额叶皮质细胞外信号调节激酶磷酸化的影响

目的 探讨慢性束缚应激模型大鼠的行为及前额叶皮质中磷酸化细胞外信号调节激酶（ERK1／2）表达的变化。方法 将雄性SD大鼠随机分为正常对照组和束缚应激组，每组8只。将束缚应激组大鼠放入特制的束缚器中限制其活动，6k／d，连续21d。比较应激前后大鼠旷场行为和Morris水迷宫行为学的改变，用蛋白免疫印迹技术和免疫组织化学方法观察应激后大鼠前额叶皮质P—ERK1／2表达的变化，并与正常对照组比较。结果 （1）行为学改变：应激后，束缚应激组大鼠的水平活动度[（4265±864）mm]少于正常对照组[（8562±502）mm]，中央停留时间[（39．1±4．3）s]长于正常对照组[（24．6±1．6）s]，均P〈0．01；束缚应激组大鼠在Morris水迷宫实验的目标象限活动时间[（57．2±1．7）s]和穿越站台次数[（2．0±0．8）次]均少于正常对照组[分别为（70．7±3．6）s和（6．2±1．0）次；均P〈0．01]。（2）p-ERK1／2蛋白水平：应激后束缚应激组吸光度（A）值[（0．767±0．006）]低于正常对照组[（0．813±0．015）；P〈0．05]。（3）p-ERK1／2阳性细胞数：应激后束缚应激组[（76±5）个]少于正常对照组[（110±14）个；P〈0．05]，且树突染色浅淡。结论 慢性心理应激明显影响动物的活动度和记忆能力；前额叶皮质中p-ERK1／2表达的减少，提示ERK信号转导通路可能参与了应激发生的机制。     

大鼠大脑皮质向脊髓与红核投射的比较

目的 比较大脑皮质向脊髓与红核发出投射的区域并探讨是否有分支投射存在。方法 将。TB及NY分别注入大白鼠的脊髓与红核内，在大脑皮质观察比较标记细胞出现的部位。结果 FB标记细胞出现在24，10，8，6，4，3，1，2，23，29b，29c，18，7，13，39区。NY标记细胞出现于6，4，3，1区，10区的尾侧部及7，18区的颅饲部亦有少量存在。无发现双标记细胞。结论 大脑皮质向脊髓发出投射的区域非常广泛，向红核发出投射的区域全部重叠于皮质脊髓神经元分布的区域内，皮质脊髓神经元无分支投射到红核。     

恢复后期脑卒中综合康复治疗与单纯药物治疗的对比研究

目的 :研究综合康复治疗对恢复后期脑卒中患者运动功能及日常生活能力 (ADL)的影响。方法 :将 92例恢复后期脑卒中患者 ,随机分为康复组 5 0例 ,对照组 4 2例 ,两组一般治疗相同 ,康复组同时配合康复护理、运动疗法、作业疗法和电疗等综合康复治疗 8周。结果 :采用Fugl-Meyer运动功能评分 (FMA)和修订的Barthel指数 (MBI)评分 ,康复组各项指标评分明显优于对照组 (P <0 .0 5 )。结论 :综合康复治疗对于恢复后期脑卒中患者运动功能的恢复有明显效果 ,提高了ADL水平。     

Effect of amyloid peptides on the increase in TrkA receptor expression induced by nicotine in vitro and in vivo

The ability of nicotine to induce a cytoprotective or neuroprotective action occurs through several down-stream mechanisms. One possibility is that the drug increases the expression of tyrosine kinase A (TrkA) nerve growth factor (NGF) receptors. Certain β-amyloid peptides (e.g., Aβ1–42) have been shown to bind with high affinity to α7 nicotinic receptors and thus interfere with a potentially neurotrophic influence. Treatment of differentiated PC-12 cells with nicotine produced a concentration-dependent increase in cell-surface TrkA receptors that occurred concomitantly with cytoprotection. The effect of nicotine was blocked by either of the α7 receptor antagonists α-bungarotoxin (α-BTX) or methyllycaconatine. The cytoprotective action of nicotine also was inhibited by pretreatment with 10–100 nM Aβ1–42. Nicotine also was administered (four injections of 30 μg, spaced evenly over 24 h) to rats by direct injection into a lateral cerebral ventricle. Brain TrkA expression was increased significantly in hippocampus and entorhinal cortex (up to 32% above control), with no changes found in cerebral cortex or hypothalamus. The nicotine-induced increases in TrKA expression in hippocampus and entorhinal cortex were significantly inhibited by 10 μg α-BTX or by 10 nmol Aβ1–42. Therefore, physiologically relevant concentrations of Aβ1–42 can prevent nicotine-induced TrkA receptor expression in brain regions containing cholinergic neurons susceptible to the neurotoxicity associated with Alzheimer’s disease.