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1.
糖尿病早期肾损害指标的探讨 总被引:1,自引:0,他引:1
目的 探讨早期诊断糖尿病肾损害的方法。方法 采用免疫透射比浊法检测尿转铁蛋白 (TF)和尿微量白蛋白(mALB) ,速率法检测尿N 乙酰 B D 氨基葡萄糖苷酶 (NAG) ,Jaffe速率法测尿肌酐。结果 糖尿病患者尿蛋白定性阴性的尿TF、mALB、NAG均较对照组显著增高 (p <0 0 1) ,单项及双项检测TF、mALB、或NAG这三项指标阳性率偏低 ,联合三项检测阳性率可达 91 1%。结论 检测尿中TF、mALB、NAG是诊断糖尿病早期肾损害指标的敏感指标 相似文献
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3.
Beeri Rachel; Gnatt Averell; Lapidot-Lifson Yaron; Ginzberg Dalia; Shani Moshe; Soreq Hermona; Zakut Haim 《Human reproduction (Oxford, England)》1994,9(2):284-292
Gene amplification occurs frequently in tumour tissues yet is,in general, non-inheritable. To study the molecular mechanismsconferring this restraint, we created transgenic mice carryinga human butyrylcholinesterase (BCHE) coding sequence, previouslyfound to be amplified in a father and son. Blot hybridizationof tail DNA samples revealed somatic transgene amplificationswith variable restriction patterns and intensities, suggestingthe occurrence of independent amplification events, in 31% (11/35)of mice from the FII generation but in only 3.5% (2/58) of theFII and FIV generations. In contrast, >10-fold amplificationsof the BCHE transgene and the endogenous acetylcholinesteraseand c-raf genes appeared in both testis and epididymis DNA from>80% of FIII mice. Drastic, selective reductions in testisBCHEmRNA but not in actin mRNA were detected by the PCR amplificationof testis cDNA from the transgenic mice, and apparently resultedin the limited transmission of amplified genes. The testicularamplification of the BCHE transgene may potentially representa general phenomenon with clinical implications in human infertility. 相似文献
4.
Takashi Ito Ryuji Sakakibara MD Tatsuya Yamamoto Tomoyuki Uchiyama Zhi Liu Masato Asahina Morihiro Higashi Kimihito Arai Shoichi Ito Yusuke Awa Kaori Yamamoto Mika Kinou Tomonori Yamanishi Takamichi Hattori 《Clinical autonomic research》2006,16(1):66-71
Abstract Uro-neurological assessment was performed in four patients with small-fiber neuropathy due to amyloidosis (2 transthyretin-type/2
immunoglobulin light-chain-type). Voiding difficulties were due to detrusor weakness and impaired bladder sensation. In two
patients cholinesterase inhibition treatment caused urge incontinence, indicating detrusor denervation supersensitivity. The
underlying mechanisms of urinary dysfunction seem to involve postganglionic cholinergic and afferent somatic nerves. 相似文献
5.
Alzheimer’s disease (AD) is the most common cause of dementia affecting nearly 18 million people around the world and 4.5 million in the US. It is a progressive neurodegenerative condition that is estimated to dramatically increase in prevalence as the elderly population continues to grow. As the cognitive and neuropsychiatric signs and symptoms of AD progresses in severity over time, affected individuals become increasingly dependent on others for assistance in performing all activities of daily living. The burden of caring for someone affected by the disorder is great and has substantial impact on a family’s emotional, social and financial well-being. In the US, the currently approved medications for the treatment of mild to moderate stages of AD are the cholinesterase inhibitors (ChEIs). Cholinesterase inhibitors have shown modest efficacy in terms of symptomatic improvement and stabilization for periods generally ranging from 6 to 12 months. There are additional data that have emerged, which suggest longer-term benefits. For the moderate to severe stages of AD, memantine, an N-methyl-D-aspartate (NMDA) receptor antagonist is in widespread use and has shown modest benefit as monotherapy and in combination with ChEIs. The cost effectiveness of the currently available therapeutic agents for AD has undergone great scrutiny and remains controversial, especially outside the US. Neuropsychiatric symptoms such as agitation and psychosis are common in AD. Unfortunately, in the US there are no Food and Drug Administration (FDA)-approved agents for the treatment of these symptoms, although atypical antipsychotics have shown some efficacy and have been widely used. However, the use of these agents has recently warranted special caution due to reports of associated adverse effects such as weight gain, hyperlipidemia, glucose intolerance, cerebrovascular events, and an increased risk for death. Alternative agents used to treat neuropsychiatric symptoms include serotonergic antidepressants, benzodiazepines, and anticonvulsant medications. 相似文献
6.
Cholinergic therapy in dementia 总被引:4,自引:0,他引:4
P. J. Whitehouse 《Acta neurologica Scandinavica》1993,88(S149):42-45
After reviewing the evidence for cholinergic pathology in Alzheimer's disease and related disorders, this paper reviews strategies for treating dementia using cholinomimetic drugs. Special attention is paid to cholinesterase inhibitors, particularly tacrine, the drug recently approved by the FDA. New studies suggesting that muscarinic and nicotinic cholinergic receptor active drugs may be more effective will be reviewed. Brief mention will be made of strategies to slow the progression of Alzheimer's disease. 相似文献
7.
Regina Alber Olaf Sporns Thomas Weikert Elmar Willbold Paul G. Layer 《Anatomy and embryology》1994,190(5):429-438
Embryonic cholinesterases are assigned important functions during morphogenesis. Here we describe the expression of butyrylcholinesterase and acetylcholinesterase, and the binding of peanut agglutinin, and relate the results to mitotic activity in chick wing and leg buds from embryonic day 4 to embryonic day 9. During early stages, butyrylcholinesterase is elevated in cells under the apical ectodermal ridge and around invading motoraxons, while acetylcholinesterase is found in the chondrogenic core, on motoraxons and along the ectoderm. Peanut agglutinin binds to the apical ectodermal ridge and most prominently to the chondrogenic core. Measurements of thymidine incorporation and enzyme activities were consistent with our histological findings. Butyrylcholinesterase is concentrated near proliferative zones and periods, while acetylcholinesterase is associated with low proliferative activity. At late stages of limb development, acetylcholinesterase is concentrated in muscles and nonexistent within bones, while butyrylcholinesterase shows an inverse pattern. Thus, as in other systems, in limb formation butyrylcholinesterase is a transmitotic marker preceding differentiation, acetylcholinesterase is found on navigating axons, while peanut agglutinin appears in non-invaded regions. These data suggest roles for cholinesterases as positive regulators and peanut-agglutinin-binding proteins as negative regulators of neural differentiation. 相似文献
8.
Steffen Roiner Nikolas Bakinde Ulrike Zeitschel Reinhard Schliebs Volker Bigl 《International journal of developmental neuroscience》1998,16(7-8):669-673
The present study was conducted to test the hypothesis that cholinergic basalforebrain neurons are a major source of cerebrospinal fluid (CSF) cholinesterases. To address thisquestion enzyme activities of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) inboth CSF and parietal cortex were assayed following selective lesion of basal forebrain cholinergicneurons by a single intracerebroventricular application of the cholinergic immunotoxin192IgG-saporin. Cholinergic immunolesions led to a dramatic decrease in total AChE activity inparietal cortex, which was due to the specific loss of the G4 molecular form while the activity ofthe G1 form was increased as compared to nonlesioned animals. In contrast, the total enzymeactivity of BChE and its molecular forms were not affected by cholinergic lesion in both parietalcortex and CSF. The data suggest, that cholinergic basal forebrain neurons are seemingly not amajor source of cholinesterases in the CSF, and do not provide any evidence for using CSFcholinesterases as a diagnostic marker of basal forebrain cholinergic cell loss in humans. 相似文献
9.
孙长荣 《军事医学科学院院刊》1988,(4)
本文报告了我所自己合成的可逆性胆硷酯酶抑制剂——二甲氨基甲酸-3-叔丁基-4-〔2-(1-哌啶基)乙氧基〕苯酯(代号"8294")与生理对抗剂或胆硷酯酶重活化剂伍用,对不同神经性毒剂中毒的预防效价、安全系数、有效时间以及与催醒宁("705")比较等所进行的观察.结果显示,"8294"比"705"的毒性小,安全系数大,效价高,有效时间长. 相似文献
10.
Relaxation times of choline, creatine and N-acetyl aspartate in human cerebral white matter at 1.5 T
Several studies have investigated the T1 and T2 relaxation time of choline, creatine and N-acetyl aspartate in cerebral white matter in normal human subjects. However, these studies demonstrate a large variation in T1 and T2 values. In the present study, relaxation times of choline, creatine and N-acetyl aspartate were determined in cerebral white matter in 15 control subjects (age 21 +/- 2 y, mean +/- SD) at 1.5 T. Using PRESS, seven or eight data points were obtained to fit the T1 and T2 relaxation curves to, respectively. The mean voxel size was 14 cm3. The T1 relaxation times of choline, creatine and N-acetyl aspartate were 1091 +/- 132 (mean +/- SD), 1363 +/- 137 and 1276 +/- 132 ms. The T2 relaxation times were 352 +/- 52, 219 +/- 29 and 336 +/- 46 ms, respectively. 相似文献