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排序方式: 共有479条查询结果,搜索用时 17 毫秒
1.
泌尿生殖道炎的病原检查研究 总被引:1,自引:0,他引:1
目的 探讨泌尿生殖道炎多种病原学检查的意义。 方法 沙眼衣原体 (CT)抗原检查采用金标法 ,解脲支原体 (UU)和人型支原体 (MH)的检查采用培养法 ,奈瑟淋球菌 (NG)的检查采用革兰氏染色法。 结果 10 0例被检者中 ,一种病原体阳性率 35 % ,两种或两种以上病原体阳性率 2 9% ,总阳性率达 6 4 % ,一种和多种病原体阳性率之间差异无显著性 (χ2 =0 .82 7,P>0 .0 5 ) ;CT检出率为 16 % ,UU检出率为 39% ,MH检出率为 18% ,NG检出率为 30 %。 结论 泌尿生殖道炎患者解脲支原体和淋球菌的感染率较高 ,可同时由多种病原感染引起 ;对于此类患者有必要同时进行多种病原检查 相似文献
2.
腺病毒载体介导的lacZ基因在NG细胞系及大鼠黑质的表达 总被引:1,自引:0,他引:1
本实验用标记基因lacZ5型重组腺病毒(Ad5CMVlacZ)转染培养的NG细胞系,X-gal染色检测转染效率.在培养的NG细胞系,当病毒滴度为2×108时,转集率达到50%,当滴度为2×109时,转染率达100%,有较好的量效关系;固定病毒液度为1010,培养2~16h,细胞的转染率随时间延长而提高,有较好的时效关系。将Ad5CMVlacZ注射到大鼠黑质部位后,分别于注射后3~120d取脑、切片、X-gal染色,发现黑质局部从第7d开始有部分蓝染,第10d达高峰,注射局部感染率100%;90d时开始下降,持续至120d;纹状体等其它部位无蓝染.上述结果提示,腺病毒载体介导的标记基因可在培养的神经细胞系和中脑黑质部位高效表达,为进一步开展中枢神经系统退变性疾病尤其是帕金森氏病的基因治疗奠定基础。 相似文献
3.
4.
Substance P and somatostatin metabolism in sympathetic and special sensory ganglia in vitro 总被引:4,自引:0,他引:4
Mechanisms regulating the content of the putative peptide transmitters, substance P and somatostatin, were examined in several neuronal populations in culture. Substance P levels increased more than 25-fold within 48 h in sympathetic neurons in the explanted rat superior cervical ganglion, and remained elevated for 4 weeks. Identity of the peptide was authenticated by combined high pressure liquid chromatography-radioimmunoassay. Veratridine prevented the increase of substance P in vitro, and tetrodotoxin blocked the veratridine effect, suggesting that sodium ion influx and membrane depolarization prevent peptide elevation. Veratridine (or potassium)-induced membrane depolarization released substance P into the culture medium through a calcium-dependent process. Consequently, at least some veratridine effects are attributable to release and subsequent depletion of ganglion peptide. However, the inhibitory effects of veratridine were far greater than could be accounted for by the quantity of peptide released, suggesting a separate influence on net synthesis (synthesis less catabolism) of substance P. Viewed in conjunction with previous in vivo studies, our observations suggest that trans-synaptic impulses, through the mediation of postsynaptic sodium flux, release substance P from sympathetic neurons and also regulate intracellular peptide metabolism. To determine whether the processes regulating substance P in sympathetic neurons reflect generalized mechanisms, a different peptide, somatostatin, was examined in sympathetic neurons; moreover, substance P was examined in a different neuronal population, special sensory neurons in the nodose ganglion. Substance P levels increased significantly in both sympathetic and sensory neurons after explantation, and somatostatin levels increased in sympathetic neurons. In each instance, the increase was dependent upon the presence of the calcium ions. Moreover, these increases were all prevented by veratridine, in a tetrodotoxin-sensitive manner. Our observations suggest that common regulatory mechanisms govern peptide transmitter metabolism in diverse neuronal populations. 相似文献
5.
Cellullar deficits are replenished within the central nervous system (CNS) by progenitors to maintain integrity and recover function after injury. NG2 proteoglycan-expressing progenitors replenish oligodendrocyte populations, but the nature of NG2 proteoglycan may not indicate a restricted population of progenitors. After injury, restorative spatiotemporal cues have the potential ability to regulate divergent fate-choices for NG2 progenitors, and NG2 progenitors are known to produce multiple cell types in vitro. Recent data suggest that NG2 expression is attenuated while protein levels remain high within injurious tissue; thus, NG2 expression is not static but transiently controlled in response to a dynamic interplay of environmental cues. Therefore, NG2 proteoglycan expression could label newly generated cells or be inherited by resident cell populations that produce oligodendrocytes for remyelination, astrocytes that provide trophic support and other cells that contribute to CNS function. 相似文献
6.
P J Tyrer I Lee J G Edwards B Steinberg E J Elliott J H Nightingale 《Journal of affective disorders》1980,2(3):149-156
The outcome of antidepressant drug treatment was measured in 200 patients, 145 seen in psychiatric out-patient clinics and 55 in general practice, after 4 weeks of therapy. The results of the 200 patients taken together suggested that prognosis was largely determined by factors dependent on the natural history of the disorder and that clinical symptoms were unimportant, but when the results for patients in each drug group were analysed separately symptoms were more important than natural history factors. We conclude that clinical symptoms are only important predictors of response to antidepressant drugs when the patients studied are homogeneous with regard to natural history factors, particularly duration of illness. 相似文献
7.
目的 观察脱氢表雄酮 (DHEA)是否能增强cAMP的类似物双丁酰环磷酰苷 (DbcAMP)促进神经突起的形成和生长及可能的机制。方法 利用NG10 8 15细胞这一具有神经元形态和功能的细胞系 ,在药物处理后 ,倒置显微镜下观察突起的生长状况 ,并测定突起的长度和有突起的细胞数 ;明胶酶谱分析NG10 8 15细胞在药物处理后 ,上清的基质金属蛋白酶 (MMP)MMP 9和MMP 2的分泌和酶的活性的变化。结果 ①DHEA和DbcAMP可抑制NG10 8 15细胞的增殖 ;②DHEA可增强DbcAMP促进NG10 8突起生长的作用。Db cAMP可以诱导NG10 8细胞突起的形成和生长 ,而DHEA收稿日期 :2 0 0 4-0 2 -0 3 ,修回日期 :2 0 0 4-0 4-19作者简介 :廖 红 ( 1965 -) ,女 ,副教授 ,博士 ,研究方向 :分子药理、神经药理 ,Tel:0 2 5 83 5 93 3 74;E mail:liaohong5 6@hotmail.com与DbcAMP同时作用 ,NG10 8 15细胞突起的长度明显增加 ,而且有突起的细胞数也明显增多 ,DHEA的剂量越高 ,这种促NG10 8 15细胞突起生长的作用越明显。③基质金属蛋白酶参与神经元的分化。DbcAMP能诱导MMP 9和MMP 2的分泌 ,与之相比 ,DHEA +DbcAMP使NG10 8 15细胞的MMP 9和MMP 2的分泌明显增多 ,且具有剂量依赖关系。结论 DHEA具有增强DbcAMP促进NG10 8 15细胞突起形成和生长的作用 相似文献
8.
Polydendrocytes (NG2 cells) are a distinct type of glia that populate the developing and adult central nervous systems (CNS). In the adult CNS, they retain mitotic activity and represent the largest proliferating cell population. Genetic and epigenetic mechanisms regulate the fate of polydendrocytes, which give rise to both oligodendrocytes and astrocytes. In addition, polydendrocytes actively differentiate into myelin-forming oligodendrocytes in response to demyelination. This review summarizes the current knowledge regarding polydendrocyte development, which provides an important basis for understanding the mechanisms that lead to the remyelination of demyelinated lesions. 相似文献
9.
Sabrina Cattaruzza Pier Andrea Nicolosi Roberto Perris 《Connective tissue research》2013,54(3-4):225-229
Proteoglycans (PGs) as a whole, or when considering their GAG chains as single entities, are emerging as key regulators of tumor progression. Expectations on using them as putative prognostic markers and potential therapeutic targets are increasing coincidentally. Due to the multitude of biological roles that they may invest and the ample spectrum of cellular processes that they may control, we still need to learn better how they regulate phenomena such as intracellular signaling, proliferation, apoptosis, motility, and drug resistance. Depending on the type, their expression pattern, and the accessibility of their molecular ligands, PGs can either promote or inhibit tumorigenesis. The structural and functional diversity of PGs coupled with their ubiquitous abundance place them at the crossroads of many critical steps within the metastatic cascade. As this phenomenon is the pivotal factor for patient survivals, particular attention should be given to the understanding of how PGs govern metastasis formation. 相似文献
10.
Zeshan Ahmed Yasmine T. Asi Andrew J. Lees Tamas Revesz Janice L. Holton 《Brain pathology (Zurich, Switzerland)》2013,23(3):263-273
Multiple system atrophy is a neurodegenerative disorder characterized pathologically by abnormal accumulations of α‐synuclein in the cytoplasm of oligodendrocytes, which are termed glial cytoplasmic inclusions (GCIs). Oligodendrocytes are responsible for myelinating axons and providing neurotrophic support, but in MSA, myelin loss, axonal loss and gliosis are consistent features suggesting that GCIs play a central role in disease pathogenesis. Oligodendroglial, myelin and axonal degeneration are also features of multiple sclerosis (MS) in which recent studies have highlighted the robust remyelination capacity of the central nervous system (CNS). The cells responsible for remyelination are called oligodendroglial precursor cells (OPCs). In this study, we investigated the role of OPCs in the pathogenesis of MSA and progressive supranuclear palsy (PSP), a neurodegenerative disease in which neuropathological changes include oligodendroglial inclusions composed of microtubule‐associated protein tau. Despite the lability of OPC‐specific antigens, we successfully identified OPCs and demonstrated that tau and α‐synuclein do not accumulate in OPCs. We also showed that the density of OPCs was increased in a white matter region of the MSA brain, which is also severely affected by GCIs and myelin degeneration. These findings raise the possibility that OPCs could be available to repair disease‐associated damage in MSA, consistent with their biological function. 相似文献