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151.
The complete sequence of the cDNA encoding the neuropeptide Y (NPY) Y1-receptor has recently been deduced from a rat brain library, and the presence of messenger ribonucleic acid (mRNA) encoding Y1-receptor protein has been demonstrated within the brain. Using quantitative in situ hybridization histochemistry, the content and distribution of Y1receptor and preproNPY mRNAs have been investigated in the hypothalamic arcuate nucleus of adrenalectomized rats receiving glucocorticoid replacement therapy for 12 days by means of either high doses of dexamethasone in their drinking water or by subcutaneous corticosterone pellets. Basal metabolic parameters such as weight gain or loss, blood glucose and plasma insulin were monitored: Dexamethasone treatment induced weight loss and a state of hyperinsulinemia with normoglycemia, while corticosterone treated animals displayed metabolic parameters identical to sham ADX animals. Within the arcuate nucleus of glucocorticoid treated animals, levels of Y1receptor and preproNPY mRNAs were increased. In contrast, adrenalectomy itself had no effect upon Y1-receptor mRNA levels or preproNPY mRNA levels in the arcuate nucleus. These studies demonstrate that glucocorticoids exert a stimulatory action on levels of Y1-receptor mRNA and preproNPY mRNA levels in the hypothalamic arcuate nucleus. This is the first evidence to suggest that the expression of a neuropeptide-receptor gene in the central nervous system may be directly sensitive to peripheral hormonal signals.  相似文献   
152.
本文报告口服Sumatriptan 100mg对偏头痛急性发作119例次的治疗结果。治疗后4h内显效91例次(76.5%),好转16例次(13.4%),无效12例次(10.1%),总有效率为89.9%。对偏头痛伴随症状恶心、呕吐和畏光、畏声的缓解率分别为94.2%、96%和94.3%。  相似文献   
153.
Summary: In situ hybridization of mRNA for collagen IV, collagen VI, stromelysin (MMP-3) and TIMP1 was examined in renal biopsy specimens from patients with IgA nephropathy (IgAN) or diabetic nephropathy with various degrees of tissue damage. The majority of cells in the glomeruli expressed these mRNA almost simultaneously, but a few cells demonstrated positive expression for only one of these probes. There was a parallel relationship between the degree of tissue damage and that of mRNA expressions of these probes in patients with IgAN, while patients with diabetic nephropathy showed a reverse relationship between these two parameters. It is concluded that patients with mesangial proliferative glomerulonephritis expressed mRNA for collagen collagenase and its inhibitor in the glomeruli in parallel with the progress of tissue damage. In contrast, glomerular samples from patients with diabetic nephropathy showed that there was an inverse relationship between tissue damage and expression of mRNA. It is concluded that expression of collagen, collagenase and its inhibitor parallels the progression of glomerular changes in IgAN, but such parallel expression was not observed in patients with diabetic nephropathy.  相似文献   
154.
155.
乌苯美司体外对人单核细胞功能的活化作用   总被引:1,自引:0,他引:1  
观察了国产乌苯美司(乌比美克)体外对人单核细胞功能的影响:①0.01 ̄100μg/ml乌苯美司能直接诱导人单核细胞生成IL-1;②经0.1μg/ml乌苯美司作用4h后,人单核细胞即开始分泌IL-1,24h达到高峰,以后逐渐下降;③经10 ̄100μg/ml乌苯美司预处理,单核细胞可促进NK细胞活性,而经0.01 ̄0.1μg/ml乌苯美司处理,单核细胞则抑制NK细胞活性。  相似文献   
156.
In this study, the behavioural response to dopamine D1-like receptor agonists (SKF 38393, SKF 81297 and SKF 77434) and D2-like receptor agonists (quinpirole and RU 24213), administered alone and in combination to rats treated repeatedly with electroconvulsive shock (five ECS over 10 days) or sham, was tested. Agonist-induced behaviour was monitored by automated activity meters and direct observation using a checklist scoring method. Repeated ECS (compared to sham controls) had no significant effect on the behavioural response to SKF 38393 (7.5 mg/kg SC), SKF 81297 (0.2 mg/kg SC), SKF 77434 (0.1 mg/kg SC), quinpirole (0.1 and 0.25 mg/kg SC) or RU 24213 (0.3 mg/kg SC), when administered alone. In contrast, repeated ECS markedly increased locomotion (activity counts and scores) induced by the non-selective dopamine agonist apomorphine (0.5 mg/kg SC) and by co-administration of a D1-like agonist plus a D2-like agonist [SKF 38393 (7.5 mg/kg SC) plus quinpirole (0.25 mg/kg SC), SKF 81297 (0.2 mg/kg SC) plus quinpirole (0.1 mg/kg SC), and SKF 77434 (0.1 mg/ kg SC) plus RU 24213 (0.3 mg/kg SC)]. This ECS-induced enhancement of dopamine-mediated behaviour was observed for up to 3 weeks after cessation of ECS treatment. In addition, ECS also enhanced the locomotor response to intra-accumbens SKF 38393 plus quinpirole (0.4 and 1.0 μg/side, respectively). These results provide evidence that the enhancement of dopamine function by repeated ECS requires concomitant stimulation of both D1-like and D2-like receptors, and that this effect is long-lasting. Received: 24 January 1997 /Final version: 5 March 1997  相似文献   
157.
本文利用细胞集落形成测定细胞存活率的方法,检测了仓鼠细小病毒(PVH-1)对2株不同分化程度的胃癌细胞的抑制作用。同时收集感染后48h、72h、96h、144h的胃癌细胞,利用电镜观察胃癌细胞的变化。结果表明,PVH-1能抑制不同分化程度的胃癌细胞株,其敏感性与胃癌细胞的分化程度有关。  相似文献   
158.
The opioid transmitters enkephalin and dynorphin are known to regulate pallidal output and consequently cortical excitability. Indeed, abnormal basal ganglia opioid transmission has been reported in several involuntary movement disorders, including levodopa-induced dyskinesias in Parkinson's disease (PD), tardive dyskinesias/dystonia, Huntington's disease, and Tourette's syndrome. Moreover, a previous 11C-diprenorphine PET study investigating levodopa-induced dyskinesias found reduced opioid receptor availability in PD with but not without dyskinesias. We wished to investigate if a similar alteration in basal ganglia opioid binding was present in DYT1 primary torsion dystonia (PTD). Regional cerebral 11C-diprenorphine binding was investigated in 7 manifesting carriers of the DYT1 gene and 15 age-matched normal controls using a region-of-interest (ROI) approach and statistical parametric mapping (SPM). No difference in regional mean 11C-diprenorphine binding was found between DYT1-PTD and controls, and no correlation between the severity of dystonia and opioid binding was seen. We conclude that aberrant opioid transmission is unlikely to be present in DYT1-PTD and altered opioid transmission is not a common mechanism underlying all disorders of involuntary movement.  相似文献   
159.
160.
Objective To investigate the roles of lipoxin A4, an endegenous lipid mediator with wide anti-inflammatory fea- tures, in attenuating myocardial ischemia-reperfusion injury and the possible mechanisms. Methods Thirty male KM mice were divid- ed randomly into three groups, 10 in each: ischemia-reperfusion group (group A), lipoxin A4 (0.1 mg/kg) group (group B) and Zn- PP (Zinc protoporphyrin Ⅸ, 25 mg/kg)phus lipoxin A4 (0.1 mg/kg)group (group C). A ischemia-reperfusion heart model was de- veloped by ligating the lift anterior descending branch of the coronary artery. A dine of 10% dehydrated alcohol in 0.2 ml for group A, a dose of isochoric lipoxin A4 for group B and a dose of isochoric ZnPP + lipoxin A4 for group C was infused into the ascending aorta through a catheter, which was kpassing the right common carotid artery, 30 minutes after reperfusion. The concentration of serum TNF-α, activities of serum crestine kinase(CK) and lactate dehydrogenase (LDH), activities of myeloperoxidase (MPO) and malond- ialdehyde (MDA) and the cell apoptosis rate in the myocardial tissue were measured 5 hours after reperfusion. Pathological features of the inflammatory infiltration in the myocardium were also observated.Results As compared with group A, the inflammatoryry infiltra- tion in the ischemic and necrotic regions tithe myocardium was reduced, with group C in the intermediate range. The serum activities of CK and LDH wine significantly lower in group B and C than that in group A, and the lowest activities were detected in group B. Similar findings were observed for MPO, an indicator for neutrophil infiltration, and MDA, an indictor for cell injury caused by oxy- gen radicals, in the myocardium. The concentration of TNF-α and the rate of cadiocyte apoptosis were decreased significantly in group B(P < 0.01). ZnPP, an inhibitor of heine oxygenase (HO)-1, attenusted the above protective effects of lipoxin A4 significantly (P<0.05). Conclusion Lipoxin A4 has protective effects against myocardial ischemia-reperfusion injury, and HO-1 may have a potential role in the protectve mechanisms of lipoxin A4, probably pertly by means of reducing the production of reactive oxygen spe- cies and TNF-α, decreasing the activation and infiltration of neutrophils, alleviating inflammatory damage and avoiding apoptosis.  相似文献   
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