器质性脑损害对老年人智力的影响

用长谷川式老年人用简易智力表,对53例器质性脑损害的老年人进行测验。结果表明,器质性脑损害对老年人的智力有显著影响。智力障碍的发生率明显高于对照组(P<0.01),且大脑左右半球及病程长短对智力的影响无显著性差异。多发性脑梗塞对智力的影响最明显,脑出血居第二位。     

Substantia nigra regulates action of antiepileptic drugs

The cholinergic agonist pilocarpine triggers sustained limbic seizures in rodents. Pilocarpine seizures were blocked by systemic administration of benzodiazepines, barbiturates, valproate and trimethadione, while diphenylhydantoin did not affect, and ethosuximide increased the susceptibility of rats to such seizures. This pattern of action antiepileptic drugs is characteristic for pilocarpine seizures and different from other rodent models of epilepsy. Although the anatomical substrates in the forebrain involved in the expression of anticonvulsant activity are unknown, the basal ganglia are believed to be essential for the motor expression of pilocarpine seizures. Bilateral microinjections into the substantia nigra, a major output station of the basal ganglia, of midazolam (ED₅₀ 38.5 nmol; range 29–52 nmol), phenobarbital (ED₅₀ 16 nmol; range 7–39 nmol) and trimethadione (ED₅₀ 30 nmol; range 16–56 nmol) protected rats against pilocarpine seizures (380 mg/kg i.p.). Diphenylhydantoin (up to 100 nmol) remained inactive, while ethosuximide (ED₅₀ 38 nmol; range 22–65.5 nmol) reduced the threshold for pilocarpine seizures, converting subconvulsant doses of pilocarpine (200 mg/kg i.p.) into convulsant ones. The profiles of action of antiepileptic drugs on pilocarpine seizures were similar following intranigral and systemic administration. These observations suggest that the substantia nigra may mediate some actions of antiepileptic drugs.     

蛋白酶体抑制剂诱导多巴胺能神经元变性及诱导型一氧化氮合酶变化

目的探讨蛋白酶体（proteasome）功能下降在帕金森病（PD）发病机制中的作用，以及模型大鼠脑内黑质部位诱导型一氧化氮合酶（iNOS）是否参与蛋白酶体抑制剂Lactacystin诱导的多巴胺能神经元变性。方法将30只健康雄性SD大鼠分为5组（生理盐水对照组，1d组、3d组、1周组、3周组），每组6只。将蛋白酶体抑制剂Lactacystin立体定向注射至大鼠黑质部位，记录大鼠在不同时间点的行为学改变，并用免疫组化方法观察生理盐水对照组及不同时间点组（1d、3d，1周、3周）大鼠黑质区多巴胺能神经元变性及iNOS变化。结果Lactacystin注射1周后大鼠开始出现自发性活动减少，阿朴吗啡可诱导出旋转行为；3周后，30min旋转次数为258．90±11．56；实验3周组黑质部位TH阳性细胞减少。1d后iNOS阳性细胞明显增多，3d时达高峰，1周后开始下降，3周时基本消失。结论蛋白酶体功能下降可能是多巴胺能神经元变性的始动因素，而iNOS上调可能是多巴胺能神经元变性的重要过程。     

系统性硬皮病的肾脏损害

目的：研究系统性硬皮病（ＳＳｃ）的肾脏损害、肾危象的发生、临床表现及可能的发病原因。方法：对１０５例ＳＳｃ临床及实验室资料作回顾性分析。对４例ＳＳｃ用浆水激发雷诺现象后观察肾眼质血流情况。结果：１０５例ＳＳｃ中２５例有肾丰，其中３例发生肾危象。冷水激后肾皮质血流减少。结论：ＳＳｃ肾脏损害发生率为２４％。严重者短期引起死亡。其发生可能是由于自身免疫致肾血管为以及遇冷时肾血管收缩致肾损害加重     

Rebamipide prevents occurrence of gastric lesions following transcatheter arterial embolization in the hepatic artery

BACKGROUND: Transcatheter arterial embolization (TAE) of the hepatic artery is a common treatment method for hepatocellular carcinoma (HCC), but it often induces gastric mucosal injury. We examined whether or not rebamipide administration, beginning 1 week before and ending 2 weeks afterTAE, can prevent worsening of gastric mucosal disorders. METHODS: The subjects were 73 chronic hepatitis C or type C liver cirrhosis patients who concomitantly had HCC and received TAE in our hospital. The patients were randomly allocated to the rebamipide group (oral, 300 mg/day for 3 weeks starting 1 week before TAE) or the non-rebamipide group. Gastric endoscopy was performed 1 week before and 2 weeks afterTAE and the presence of erythema, erosion and/or submucosal haemorrhagic spots was monitored. Based on the findings, gastric mucosal disorder before and after TAE was quantitatively evaluated using the modified Lanza score (MLS). RESULTS: Overall, MLS after TAE increased significantly (P< 0.05). However, in the rebamipide group, MLS did not change. The MLS after TAE increased significantly in patients who had either liver cirrhosis, oesophageal varices or gastropathy (P< 0.01 or < 0.05). In the non-rebamipide group, a significant increase in MLS after TAE was observed in patients who had one of the above-mentioned three diseases (P< 0.01 or < 0.05). CONCLUSIONS: Gastric lesions which were present before TAE were significantly worsened after TAE. Rebamipide administration prevents TAE-induced aggravation of gastric lesions.     

肩关节脱位合并肩袖与Bankart损伤的诊治

目的 探讨关节镜下修复肩关节前脱位合并肩袖与Bankart损伤的疗效.方法 1999年9月至2007年7月收治16例肩关节脱位合并肩袖与Bankart损伤患者,男14例,女2例;左肩6例,右肩10例.交通伤8例,运动伤4例,牵拉伤4例.受伤至手术时间平均4.5个月(1.5～11.0个月).肩关节x线片显示肩盂撕脱骨折3例.16例患者肩关节核磁共振造影显示肩袖与Bankart损伤.关节镜探查发现肩袖于肱骨大结节处撕脱伴肩袖挛缩12例.采用关节镜下松解、缝合锚钉和骨锚钉同定缝合9例;因肩袖挛缩明显,进行关节镜与小切口辅助下肩袖缝合固定术3例;肩衲组织因牵拉松弛抬肩无力,采用等离子刀皱缩和肩袖缝合紧缩术4例.Bankart损伤采用关节镜下可吸收Bankart钉固定3例,钛合金缝合锚钉固定3例,关节镜下直接缝合修补盂唇3例,骨锚钉加会属锚钉固定7例.结果 16例患者术后获平均16.5个月(7～34个月)随访.肩关节稳定,肩外展和上举功能恢复正常12例,术后肩关节外展、抬举活动轻度受限2例,前伸活动疼痛2例.金属锚钉拔出再手术2例.采用美国加州洛杉矶大学UCLA肩关节功能评分:术前平均(21.5±5.5)分;术后平均(32.4±5.6)分,优12例,良4例.结论 肩关节脱位合并肩袖与Bankart损伤核磁共振造影有助于诊断;肩袖挛缩者应进行充分松解,无张力缝合固定有利于肩袖愈合;异体骨锚钉修复肩袖与Bankart损伤,生物固定、费用低廉,具有重要的价值.     

Nerve growth factor (NGF) potentiates the changes in striatal proenkephalin mrnas subsequent to 6-hydroxydopamine-induced lesions of the substantia nigra

The topographical changes in proenkephalin (PEK) mRNAs which occur in the caudate-putamen (CPu) after 6-hydroxydopamine (6-OHDA)-induced unilateral lesion of the mesostriatal dopamine (DA) pathway were evaluated by quantitative in situ hybridization. These lesions caused significant increases in PEK mRNA in all regions of the caudate-putamen (CPu). The chronic intraventricular administration of NGF potentiated the increases in PEK mRNA, with the magnitude of changes being greater in the dorsomedial and dorsolateral regions of the striatum. NGF did not affect the loss of tyrosine hydroxylase mRNA observed in the substantia nigra ipsilateral to the 6-OHDA-induced lesion. These results demonstrate that alterations which occur in a neuropeptide system as a consequence to 6-OHDA-induced denervation of the striatum can respond to NGF administration in a topographical fashion.     

Beeinflussung der degenerativen und regenerativen Vorgänge an peripheren Nerven unter Behandlung mit B-Vitaminen

Summary Degenerative and regenerative changes in the saphenous nerve of the rabbit following systemic treatment with either a combination of the vitamins B₁, B₆ und B₁₂ or physiological saline solution were investigated. Cold lesion of the nerve (–196°C), which led to an optimal axonotmesis, was used to cause a secondary degeneration.The nerves were removed and investigated by light and electron microscopy after 4, 10 and 21 days. Morphological results show that the number of regenerating axons is higher and that of degenerating axons lower in the group treated with the given doses of vitamins than in the comparable control group.An explanation of the underlying metabolic processes is as yet not possible. Further investigations considering the contribution of the individual vitamins to the enhancement of degenerative and regenerative processes are necessary. Clinical indications of neurotoxicity due to the dose levels used here were not observed.

     

Central vasopressin V1a receptors modulate neural processing in mothers facing intruder threat to pups

Vasopressin V1a receptors in the rat brain have been studied for their role in modulating aggression and anxiety. In the current study blood-oxygen-level-dependent (BOLD) functional MRI was used to test whether V1a receptors modulate neural processing in the maternal brain when dams are exposed to a male intruder. Primiparous females were given an intracerebroventricular (ICV) injection of vehicle or V1a receptor antagonist ([deamino-Pen¹, O-Me-Tyr, Arg⁸]-Vasopressin, 125 ng/10 μL) 90-120 min before imaging. During fMRI, awake dams were presented with a male intruder threat to pups using a specialized chamber that contained separate compartments for pups and a male intruder. Our results indicate that the number of activated voxels was reduced in the cortical amygdala with V1a receptor blockade, while an increase was observed in the anterior olfactory nucleus and other areas. Dams treated with V1a antagonist showed significantly greater BOLD responses in the anterior olfactory nucleus, infralimbic prefrontal cortex, gustatory cortex, somatosensory cortex, and substantia innominata when presented with a novel male intruder. BOLD responses were reduced in the cortical amygdala and ventromedial hypothalamus. The V1a receptor sensitive areas play roles in the processing of smell, taste and touch and emotional reactivity. Thus one interpretation of the present fMRI data is that vasopressin, acting through V1a receptors, may modulate sensory processing and perhaps coordinate this effect with changes in visceromotor activity during the initial stages of maternal aggressive motivation and/or anxiogenic responses.