新生SD大鼠缺氧缺血性脑损伤早期线粒体内膜跨膜电势的变化

【目的】　了解缺氧缺血性脑损伤 (HIBD)早期脑细胞△Ψm的变化。　【方法】　 7日龄新生大鼠随机分为正常对照组 (n =6) ,HIBD组 (n =3 6,分为HIBD后 0、1、2、3、4h时间点组 )。予以右颈总动脉分离结扎后再置8%O2 低氧舱 2 .5h ;断头处死后分离左右大脑半球制成单细胞悬液 ,加入终浓度为 1μmol的罗丹明 12 3于 3 7℃避光孵育 45min后 ,以流式细胞仪测定△Ψm并计算左右大脑半球△Ψm比值。　【结果】　正常P7SD大鼠左、右侧大脑半球脑细胞△Ψm分别为 ( 18.2 1± 1.2 6)MFL和 ( 18.93± 0 .74)MFL ,右∶左比值为 1.0 6。HIBD损伤使双侧大脑半球脑细胞△Ψm降低程度更明显 ,其中HIBD后 0h时△Ψm右∶左比值比正常时降低了 2 4.5 %(P <0 .0 5 )。HIBD后 1～ 3h时间内 ,△Ψm稍有回升。HIBD后 4h时HI损伤侧△Ψm值及右∶左比值均出现第二次降低现象 ,且程度更重 ,其中右 :左比值比正常时降低了 3 4%(P <0 .0 5 )。　【结论】　HIBD早期脑细胞△Ψm出现两次降低 (初次及二次降低 ) ,分别发生在HI损伤 0h和 4h时 ,提示有关改善线粒体功能的治疗尽量在△Ψm出现第二次降低前应用     

体外培养的小鼠骨髓基质细胞对血细胞集落形成的支持

为探讨骨髓基质细胞在液体条件下支持造血的能力,对小鼠骨髓有核细胞体外培养,在液体培养基中形成基质细胞贴壁层,更换培养液,再种植骨髓有核细胞。结果在贴壁的基质细胞上形成了细胞集落。按细胞形态特征分为两类:一类为基质细胞集落,仅为偶见。另一类为造血细胞集落,数量较多,并且集落通过一定的结构与贴壁的基质细胞连接。结果提示,造血细胞集落的形成,需要有与骨髓基质细胞接触的微环境,并可对基质细胞的生长发育有一定的反作用。本文提出了造血细胞集落的液体培养法。     

一种新的正交参数选优法及其在非线性回归分析中的应用

非线性回归分析是工程中经常采用的一种用来估计数学模型参数的方法，该方法能否顺利运用与参数初始值的选择有极大关系。本研究提出一种新的正交参数选优法——阻尼正交表法，它不仅可以保证非线性回归分析算法的顺利收敛，而且能够显著提高后者的收敛速度，进而极大改善非线性回归分析算法的应用性能。本研究的数值试验及心肌造影超声心动图定量分析应用实例表明，作为对传统正交参数选优法的一种改进，阻尼正交表法在科学与工程计算或信号与信息处理领域有着很好的应用前景。     

Histological Changes and Differential Diagnosis of Mesenchymal Chondrosarcoma

Eight cases of mesenchymal chondrosarcoma either of skeletal(5 cases) or extrasketetalorigin (3 cases) are reported. According to histopathological and diagnostic criteria,mesenchymal chondrosarcoma were classified into two types cartilage isiand cell type andundifierentiated small cell type It is believed that the application of this classification in the study ofmesenchymal chondrosarcoma is helptul the estimation of its malignancy and choice of treatmentas well al in the prediction of its prognosis. Mesenchymal chondrosarcoma is a highly malignant neoplasm with poor prognosis. None ofthe patients in this series survived more than five years after they were diagnosed. The diffentialdiagnosis of malignant lymphoma, chondrosarcoma, hemangiopericytosarcoma, etc. was discussed.My data support the assumption that mesenchymal chondrosarcoma originates from the secondarymesenchyme rather than the primary mesenchyme.     

人胎儿前庭器超微结构的观察

对人胎儿前庭器超微结构的研究,国内外报道甚少。本文对18至36周人胎儿颞骨10具进行了扫描电镜和透射电镜的观察,并对应用Surface preparation法制做人胎儿前庭器标本的方法进行了探讨。本文观察所见:豚鼠平衡斑的生理状态与人胎儿很近似,体面积比人胎儿平衡斑小,感觉毛长,细胞排列更整齐。28周以后的胎儿因前庭周围骨质变硬,制做标本时可以分别取出两囊斑和壶腹嵴。     

胆汁胆固醇对胆囊收缩素受体表达的影响

目的：探讨胆汁胆固醇对胆囊收缩素受体（CCK－R）表达的影响。方法 采用放射免疫分析法和受体放射配基结合法检测对照组、高胆固醇组、自然恢复组及治疗组豚鼠门静脉血CCK水平、胆囊CCK－R的最大结合容量（Bmax）和亲和力（Kd），同时观察空腹胆囊体积（FV）、胆囊胆汁量（FB）和餐后胆囊体积（RV）、胆囊胆汁量（RB）及胆囊收缩率（E％）、胆汁胆固醇浓度的变化。结果 与对照组比较，高胆固醇组豚鼠FV、FB增大（P＜0.05），RV、RB也增大，胆囊收缩率下降（P＜0.01），胆汁胆固醇浓度升高（P＜0.05），门静脉血CCK水平及CCK－R的Kd无改变，而CCK－R的Bmax下降（P＜0.01）；治疗组上述各项指标正常。结论 胆汁中的高胆固醇通过下调胆囊CCK－R表达而导致胆囊收缩功能障碍，降低胆汁高胆固醇浓度可以促进胆囊动力功能的恢复。     

全国细菌药敏试验的室间质量评价

目的：了解全国大中型医院细菌药敏试验（AST）状况，提高检测水平和质量。方法：定期向全国各参加评价实验室发放冻干标本，要求在规定时间内报告可疑感染的病原菌及其药敏结果，对回报结果给予数据统计、分析和评价。结果：2000年全国489个细菌室对常见耐药菌的检测正确率分别为：超广谱β－内酰胺酶63％（ESBLs)；苯唑西林敏感金黄色葡萄球菌（MSSA）74％；苯唑西林耐药凝固酶阴性葡萄球菌（MRSCoN)48％；对青霉素不敏感肺炎链球菌7％；氨基糖苷类高水平耐药肠球菌95％；产β－内酰胺酶流感嗜血杆菌正确率35％。结论：通过细菌药敏试验的室间质量评价反映出我国的细菌耐药性检测水平急待提高。     

32例出血性梗塞研究分析

对32例出血性梗塞研究分析，发现常出现于脑栓塞及大面积脑血栓病人。以治疗中病情突然加重或持久症状不改善为特征，动态CT检查对本病的诊断及治疗有重要意义。     

诺氟沙星的吸附伏安法研究

在ｐＨ＝７．４９氨－氯化铵缓冲液中，诺氟沙星在滴汞电极上产生一灵敏的还原峰，峰电位为－１．５２Ｖ（ｖｓ．ＳＣＥ）。在１．９８×１０（－７）～４．８８×１０（－６）ｍｏｌ／Ｌ之间有良好的线性关系。本文对其极谱性质和电极过程进行了研究，用于诺氟沙星的测定，方法简便，结果准确、可靠。     

N-methyl-D-aspartate exposure blocks glutamate toxicity in cultured cerebellar granule cells.

Exposure of cultured cerebellar granule cells to glutamate results in a concentration-dependent (EC50 = 22.7 +/- 0.4 microM) and delayed (24-72 hr) neurotoxicity, which is blocked by the specific N-methyl-D-aspartate (NMDA) receptor antagonists 2-amino-5-phosphovalerate and MK-801 but is unaffected by the non-NMDA receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione and 6,7-dinitroquinoxaline-2,3-dione. Although glutamate toxicity in these cells is mediated by the NMDA subtype of glutamate receptor, pretreatment of cerebellar granule cells with subtoxic concentrations of NMDA markedly antagonizes the neurotoxic actions of glutamate, with an IC50 of 55 +/- 4 microM. The neuroprotective effect of NMDA requires a preincubation time of approximately 120 min to be fully manifested and does not require the presence of NMDA during glutamate exposure. These data demonstrate that NMDA receptors mediate both neurotoxicity and neuroprotection in cerebellar granule cells. Among four glutamate receptor agonists tested (NMDA, quisqualate, ibotenate, and kainate), only NMDA was able to provide a robust neuroprotection against glutamate toxicity. Quisqualate was neither neurotoxic nor neuroprotective, whereas ibotenate, which was nontoxic by itself, induced a small degree of neuroprotection. In contrast, kainate, which was neurotoxic to cerebellar granule cells, also provided considerable neuroprotection against glutamate toxicity. Because preincubation of cerebellar granule cells with NMDA fails to alter NMDA receptor-mediated phosphoinositide hydrolysis or the specific binding of [3H]MK-801 to NMDA receptors, it appears that the neuroprotective effects of NMDA are not due to NMDA receptor desensitization.