综合性医院抑郁症的特点及疗效分析

目的:了解综合性医院神经内科门诊抑郁症的临床特点及抗抑郁治疗的临床疗效.方法:对46例抑郁症患者的临床特点进行研究分析,同时对其中24例患者给予帕罗西汀治疗,对汉密尔顿抑郁评定表(HAMD)的平均总分数、汉密尔顿4因子及临床总体印象量表(CGI)评分在治疗前后进行比较.结果:46例抑郁症患者均以不同程度的躯体症状为主诉,临床表现多种多样,可涉及全身各系统;其中24例抑郁症患者给予帕罗西汀治疗后,汉密尔顿抑郁评定表的平均总分数、汉密尔顿4因子及临床总体印象量表评分分数在治疗后较治疗前显著减少(P＜0.01).结论:了解抑郁症患者躯体症状的临床特点,对于抑郁症的诊断和治疗至关重要.帕罗西汀对抑郁症患者具有明显的抗焦虑作用及早期改善睡眠的作用且整体抗抑郁疗效好.     

Ca~(2+)在大鼠应激性胃粘膜损伤中作用的研究

目的 :探讨大鼠胃粘膜与急性胃粘膜损伤之间的关系。方法 :采用原子吸收光谱分析法 ,测定胃粘膜Ca2 +含量。结果 :胃粘膜损伤程度随应激时间延长而加重 ,胃粘膜Ca2 + 含量却下降 ,二者呈明显负相关 ,但是 ,CaCl2 预应激或应用钙通道阻断剂 ,可减轻胃粘膜损伤程度。结论 :Ca2 + 在急性胃粘膜损伤中有一定的作用。     

Plasmid DNA encoding transforming growth factor-beta1 suppresses chronic disease in a streptococcal cell wall-induced arthritis model.

Transforming growth factor beta is a potent immunomodulator with both pro- and antiinflammatory activities. Based on its immunosuppressive actions, exogenous TGF-beta has been shown to inhibit autoimmune and chronic inflammatory diseases. To further explore the potential therapeutic role of TGF-beta, we administered a plasmid DNA encoding human TGF-beta1 intramuscularly to rats with streptococcal cell wall-induced arthritis. A single dose of 300 microg plasmid DNA encoding TGF-beta1, but not vector DNA, administered at the peak of the acute phase profoundly suppressed the subsequent evolution of chronic erosive disease typified by disabling joint swelling and deformity (articular index = 8.17+/-0. 17 vs. 1.25+/-0.76, n = 6, day 26, P < 0.01). Moreover, delivery of the TGF-beta1 DNA even as the chronic phase commenced virtually eliminated subsequent inflammation and arthritis. Both radiologic and histopathologic as well as molecular evidence supported the marked inhibitory effect of TGF-beta1 DNA on synovial pathology, with decreases in the inflammatory cell infiltration, pannus formation, cartilage and bone destruction, and the expression of proinflammatory cytokines that characterize this model. Increases in TGF-beta1 protein were detected in the circulation of TGF-beta1 DNA-treated animals, consistent with the observed therapeutic effects being TGF-beta1 dependent. These observations provide the first evidence that gene transfer of plasmid DNA encoding TGF-beta1 provides a mechanism to deliver this potent cytokine that effectively suppresses ongoing inflammatory pathology in arthritis.     

马尔尼菲青霉病不同类型病变中免疫反应观察

选用２组病变类型不同的６例马尔尼菲青霉病人病变组织，采用免疫组化ＰＡＰ法，观察病变组织中ｌ８淋巴细胞、巨噬细胞、ＩｇＧ、ＩｇＭ、乙等免疫指标。结果发现马尔尼菲青霉病的病变类型取决于机体的免疫功能状态，人体抗马尔尼菲青霉免疫以细胞免疫为主，组织中Ｔ细胞的存在对于杀灭真菌、局限病变具有积极意义；体液免疫特别是特异性抗体的出现除具有促进细胞免疫功能外，可能也是脓肿成因之一。     

脑卒中急性期白细胞反应及临床意义

脑卒中急性期大多数患者白细胞增多，表现为中性粒细胞计数与白细胞总数增高，脑出血组白细胞增高姓率高于脑梗塞组，而中性粒细胞增高发生率二组间无差别，外周血白细胞增高与临床神经功能缺损程度评分有密切关系，中性粒细胞计数越高，近期神经功能预后则越差。     

豚鼠耳蜗微血管内皮细胞体外通透性的研究

目的　研究豚鼠耳蜗微血管内皮细胞的体外通透性特征。方法　在成功建立豚鼠耳蜗微血管内皮细胞体外通透性模型的基础上 ,研究该体外模型跨细胞电阻及对12 5I 牛血清白蛋白的通透性。结果　①耳蜗微血管内皮细胞在培养增殖过程中其跨细胞电阻呈动态变化过程 ,以 5× 10 4/cm2 的细胞密度接种时 ,7d左右电阻到达峰值 ,其跨细胞电阻峰值大小为 (118 9± 18 5 )Ω/cm2 ;②体外模型中加入12 5I 牛血清白蛋白后 ,其通透性呈上升期抛物线型曲线 ,90min内几乎呈直线。结论　跨细胞电阻及对12 5I 牛血清白蛋白变化曲线能反映体外耳蜗微血管内皮细胞的通透性特征     

Acute effects of serotonin on rat bladder contractility.

INTRODUCTION: The purpose of this study is to investigate in vitro the effects of serotonin on the rat detrusor. In particular, it examines which drugs inhibit the serotonin-induced detrusor contractions. MATERIALS AND METHODS: Isometric tension changes of isolated rat bladder muscle strips were recorded in an organ bath using a force transducer. Acute effects of serotonin (0.0001-0.01 mM) on resting tension were assessed. Electrical field stimulation (EFS); bethanechol (0.0001-0.01 mM); ATP (1-3 mM)- or KCl (63.5-254 mM)-induced contractions using an application in an organ bath were compared with serotonin-induced contractions. In order to examine the action mechanism of serotonin-induced stimulation, EFS-, bethanechol-, ATP- or KCl-induced contraction on serotonin treatment (0.001 mM) was assessed and serotonin (0.001-0.1 mM) was cumulatively added to the organ bath following preincubation with propranolol, ketanserin, tropisetron, propiverine, sodium nitroprusside or doxazosin. RESULTS: The serotonin-induced response has two phases: an initial transient contraction and a prolonged tonic phase. Serotonin produced a reversible and dose-dependent contraction of the detrusor strips. Responses to bethanechol significantly increased with a concentration of 0.001 mM serotonin (p < 0.05). There was no effect on the responses to ATP, KCl, or EFS on 0.001 mM serotonin. The 5-HT(2) receptor is mainly responsible for serotonin-induced contractions of the detrusor (p < 0.05), while the 5-HT(1) receptor is partially responsible. Doxazosin and propiverine each significantly suppressed the response to serotonin, while sodium nitroprusside and tropisetron each had no effect (p < 0.05). CONCLUSIONS: Because the 5-HT(2) antagonist blocked the effect of serotonin-induced bladder contractions and the stimulation of the adrenoreceptors, the 5-HT(2) antagonist seems to improve lower urinary tract symptoms.