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61.
The pathogenesis and etiology of Kawasaki disease are unknown, but some studies suggest increased genetic susceptibility. The case is presented of an infant with Kawasaki disease whose father suffered from the same illness 21 years previously. The A, B and C loci of the HLA antigens were examined.  相似文献   
62.
63.
Ibotenate, a glutamatergic agonist, was used to study the spectrum of excitoxic disturbances at different ages of cerebral development. Cultures of whole mouse embryo were submitted to ibotenate at E8 for 20 h: during the phase of early premigratory differentiation; ibotenate did not induce any detectable histological lesion. During migration of supragranular neurons, newborn hamsters intracerebrally injected at P0 with ibotenate display neuronal migration disorders graded from nodular heterotopias to extensive laminar heterotopias mimicking some aspects of lissencephalic and double-cortex syndromes. After completion of neuronal layer V, P0 mice injected with ibotenate exhibit laminar neuronal depopulation of layer V-VIa mimicking human micro-gyria. At P5 in mouse, after completion of neuronal migration of the cortical plate, ibotenate induces neuronal loss in all cortical layers and the formation of porencephalic cysts. This study emphasizes the dramatic role played by glutamate in brain development, in the occurrence of neuronal migration disorders in the cortex. and in grey and white matter damage.  相似文献   
64.
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.  相似文献   
65.
BACKGROUND AND PURPOSE: The Doppler waveform patterns of loss of diastolic flow, appearance of retrograde diastolic flow, or no detectable flow in the cerebral arteries suggest significantly abnormal cerebral blood flow (CBF). A retrospective study was performed to show that significantly abnormal CBF alone, without clinical criteria, is not necessarily specific to brain death in the young pediatric population. PATIENTS AND METHODS: Forty-seven pediatric patients, from newborn to 4 years of age, were found to have significantly abnormal CBF, including 7 patients with loss of diastolic flow, 28 with retrograde diastolic flow, and 23 with no detectable cerebral flow on serial Doppler sonographic examinations. Their clinical data and sonographic results were collected and analyzed. RESULTS: Forty-two patients died, a few of whom had only transient improvement of cerebral flow. All of the patients with no detectable cerebral flow expired. Five patients survived with or without sequelae. Their underlying conditions that caused increased intracranial pressure were treated by medical and/or surgical intervention, and diastolic reversal of CBF corrected within 1 day in all 5. CONCLUSIONS: Although no detectable flow is a lethal sign, pediatric patients with loss or reversal of diastolic flow may survive with prompt and effective treatment. Using Doppler ultrasound to diagnose cerebral circulatory arrest should be done with caution in pediatric patients.  相似文献   
66.
Both systemic and local therapy, for conditions of the breast and unrelated to it, may produce manuno-graphic changes. Some of these are characteristic, such as the pattern of scarring seen in reduction mammo-plasty. In many other instances, however, the changes produced overlap features commonly seen in malignancy. A knowledge of the timing, natural history and spectrum of these changes will aid mammographic interpretation.  相似文献   
67.
The referral pattern of 140 Dutch patients with oral mucosal lesions, who had been referred to a Department of Oral & Maxillofacial Surgery and Oral Pathology, shows that patients with oral mucosal lesions consult the dentist as often as the family doctor as the first source of help or information. Furthermore, family doctors were much more used to refer patients with oral mucosal disease to medical specialists rather than to the dentist or the oral and maxillofacial surgeon.  相似文献   
68.
小包装全氟丙烷气体动力学实验研究   总被引:1,自引:0,他引:1  
为检验塑料小包装全氟丙烷气体(C3F8)在不同包装和储存方法时浓度变化,将装有5~7mlC3F8的聚氯乙烯小袋,根据不同储藏温度和外包装方法随机分成四组:(1)22℃聚乙烯外包装,(2)36℃聚乙烯外包装,(3)22℃铝箔真空外包装,(4)-29℃聚乙烯外包装;每一组C3F8小袋气体存放一定时间后,应用气相色谱分析方法进行浓度测量。结果:第3组C3F8浓度最高和稳定,第2组浓度随放置时间降低最明显,第4组是临床应用气体的储藏和包装方法,其30天样本浓度和第3组相等,但放置一年时浓度降低。结果显示:塑料小包装C3F8予以铝箔真空外包装是一种可行的方法,利于C3F8运输和普及;聚乙烯外包装的C3F8,应放在-29℃保存,时间不超过一年。  相似文献   
69.
Systolic and diastolic blood pressures were measured on 254 monozygotic (MZ) and 260 dizygotic (DZ) male twin pairs, during middle age (average age 48 years) and at two later age points. Genetic and environmental components of covariation were modeled by time series. For both measures, shared environmental influences were absent and specific environmental influences were largely time-specific. Although heritability was about 0.5 at each time point, genetic variation present at middle age contributed only about 60% to that present 9 years later, the remaining 40% being new. Fifteen years later, at the third time point, no new genetic variation was evident, variation in individual differences being entirely attributable to genetic differences laid down at the two earlier ages. © 1993 Wiley-Liss, Inc.  相似文献   
70.
本文对SOD的紫外分光光度法测定进行了实用性研究。结果表明,本文方法具有用血量少,重现性好,快速、灵敏,试剂廉价等优点。西宁地区与平原地区人群的比较测定显示,前者SOD活性明显高于后者(P<0.01)。  相似文献   
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