杨牧祥治疗高脂血症经验

高脂血症属中医痰浊、瘀血证范畴,与肝脾肾的功能失调相关,因脾失健运,痰瘀互结导致。杨老提出"从痰瘀论治",化痰降浊、活血化瘀治其标,健脾益气、强本清源治其本。每用皆获疗效。     

《唇舌症候图》考证

<唇舌症候图>一直被工具书著录为"清力钧绘",定为清代的著作.本文从有关力钧的史料、图书特征和全书内容等办面进行论证,证明该书并非力钧所著,而是日本的汉医著作.     

血液粘滞性与中医证的研究

本研究按全国统编教材《中医诊断学》的辨证标准,采用上海第一医科大学生产的毛细管式粘度计,对气血两虚、脾肾阳虚、阴虚阳亢、痰湿内阻及气滞血瘀证患者进行了血液粘滞性测定。结果发现随证的不同,血液粘滞性的改变有明显差异。气血两虚与脾肾阳虚证处于低血粘状态,而其他各证则处于高血粘状态。从血液流变学角度揭示了虚、实证的实质不同,它们的形成与血液粘滞性的降低或升高直接相关。从血液粘度微观指标分析,各证又呈现特异性改变,气血两虚与脾肾阳虚证是因红细胞压积的减少引起低粘状态,它们有共同的病理基础,与脾肾功能低下气血化生不足,致使血液中有形成份减少直接相关。而阴虚阳亢证则红细胞压积显著增加,使血液表现出高浓状态,是引起肝风内动的病理基础。痰湿证血浆粘度明显增高,使血液中表现出高粘状态及临床上表现出“重浊而粘腻”的特性,与脾为湿困,健运失调,机体对(?)微物质的代谢紊乱有关。气滞血瘀证之红细胞聚集能力最强,使血细胞易于聚集成堆、淤滞不通而成瘀,与肝之疏泄、藏血、调血功能失调有关。这一规律性改变,反映出机体内血液中有形或无形成份的异常是中医证病理变化的物质基础,在某种意义揭示了有关证的实质,认为血液粘滞性的测定似可作为辨别有关证的客观指标,无论在临床或在理论上对中医证的认识或研究都是有意义的。     

阿朴吗啡对颈动脉体球细胞帕金森病大鼠纹状体移植区C-FOS和JUN-B表达的影响

目的 :探讨帕金森病 (PD)大鼠颈动脉体球细胞移植治疗后多巴胺细胞的功能状况。方法 :采用 6 -羟多巴胺损毁制备 PD大鼠模型 ,腹腔注射阿朴吗啡 2 h后诱导移植后 12周纹状体组织内 c- fos和 Jun- B的表达 ,分析其分布和阳性细胞数目。结果 :移植后 12周 ,移植物内和与宿主接触面 c- fos表达增高 ,而 Jun- B的表达没有变化。结论 :移植物内和与宿主接触面 c- fos表达增高表明移植细胞仍保持着其生理功能     

杨洪涛从脾肾论治慢性肾脏病医案举隅

慢性肾脏病主要临床表现为血尿、蛋白尿、水肿及肾功能损害等。在现代医学积极治疗的情况下,肾脏疾病的患病率及病死率仍然就高,中医药独具特色的辨证论治在治疗慢性肾脏病方面有着较好的疗效。杨洪涛教授认为,慢性肾脏病病程日久,病机总属本虚标实,虚实夹杂。杨师临证时精于辨证,在治疗慢性肾脏病时注重健脾补肾,屡获良效。     

杨志宏教授治疗帕金森病经验

帕金森病是一种多发于中老年的神节系统变性疾病。杨志宏教授治疗帕金森病独具特色,注重滋补肝肾以固本;在化痰祛瘀的同时,注重益气;倡导清热除湿、解毒排毒以护脑;常用解表除湿的方法治疗汗出,疗效显著。     

国医大师杨春波察舌辨湿热案经验

杨春波教授系全国第三届国医大师,脾胃病名家,临床经验丰富,对脾胃湿热证有较深入研究。舌诊是中医诊病的特色诊法,文章介绍国医大师杨春波教授察舌辨湿热泄泻验案1则,并在此基础上梳理杨春波教授运用舌诊辨治湿热病经验,突出舌诊在湿热病中的优势。文章对其临床运用经验与学术观点进行总结,为湿热病的临床诊断与治疗提供参考与借鉴。     

FIST/HIPK3: a Fas/FADD-interacting serine/threonine kinase that induces FADD phosphorylation and inhibits fas-mediated Jun NH(2)-terminal kinase activation

Fas is a cell surface death receptor that signals apoptosis. Several proteins have been identified that bind to the cytoplasmic death domain of Fas. Fas-associated death domain (FADD), which couples Fas to procaspase-8, and Daxx, which couples Fas to the Jun NH(2)-terminal kinase pathway, bind independently to the Fas death domain. We have identified a 130-kD kinase designated Fas-interacting serine/threonine kinase/homeodomain-interacting protein kinase (FIST/HIPK3) as a novel Fas-interacting protein. Binding to Fas is mediated by a conserved sequence in the COOH terminus of the protein. FIST/HIPK3 is widely expressed in mammalian tissues and is localized both in the nucleus and in the cytoplasm. In transfected cell lines, FIST/HIPK3 causes FADD phosphorylation, thereby promoting FIST/HIPK3-FADD-Fas interaction. Although Fas ligand-induced activation of Jun NH(2)-terminal kinase is impaired by overexpressed active FIST/HIPK3, cell death is not affected. These results suggest that Fas-associated FIST/HIPK3 modulates one of the two major signaling pathways of Fas.     

3D-QSAR studies of JNK1 inhibitors utilizing various alignment methods

We report our three-dimensional quantitative structure activity relationship (3D-QSAR) studies of the series of anilinopyrimidine derivatives of JNK1 inhibitors. The comparative molecular field analysis (CoMFA) and comparative molecular similarity indices analysis (CoMSIA) were applied using different alignment methods. The ligand-based atom-by-atom matching alignment has produced better values for CoMFA (q(2) = 0.646 and r(2) = 0.983), while in CoMSIA it has achieved only lower statistical values. The pharmacophore-based model has produced (q(2) = 0.568, r(2) = 0.938) and (q(2) = 0.670, r(2) = 0.982) for CoMFA and CoMSIA models, respectively. As the model was based on the receptor-guided alignment, all the compounds were optimized within the receptor, resulting in q(2) = 0.605 and r(2) = 0.944 for CoMFA, and q(2) = 0.587 and r(2) = 0.863 for CoMSIA. Molecular Dynamic simulation studies suggested that the generated models were consistent with the low-energy protein ligand conformation. The CoMFA and CoMSIA contour maps indicated that the substitutions of the electropositive groups in the phenyl ring, and an addition of hydrophobic groups in the pyrimidine ring, are important to enhance the activity of this series. Moreover, the virtual screening analysis against NCI database yields potentials hits, and the results obtained would be useful to synthesize selective and highly potent c-Jun N-terminal kinase 1 analogs.     

Intracisternal administration of mitogen-activated protein kinase inhibitors reduced mechanical allodynia following chronic constriction injury of infraorbital nerve in rats

The present study investigated the role of mitogen-activated protein kinase (MAPK) in orofacial neuropathic pain following chronic constriction injury of the infraorbital nerve (ION-CCI). Experiments were carried out on male Sprague-Dawley rats weighing between 200 and 230 g. The ION was separated from adhering tissue, and two ligatures (5-0 chromic gut) were tied loosely around it. We examined the air-puff thresholds (mechanical allodynia), scores of pinprick (mechanical hyperalgesia), and face grooming frequency for acetone application (hypersensitivity for cold stimulation) - 3, 3, 6, 9, 12, 15, 20, 25, 30, and 40 days after surgery. ION-CCI produced mechanical allodynia, hyperalgesia, and cold hypersensitivity. We investigated whether administration of MAPKs inhibitors blocks ION-CCI-induced mechanical allodynia. Intracisternal administration with PD98059 or SB203580, a MEK inhibitor or a p38 MAPK inhibitor, respectively, significantly inhibited ION-CCI-induced mechanical allodynia in the orofacial area. These results indicate that the ION-CCI produced behavioral alterations in the orofacial area and those central MAPKs pathways contribute to orofacial neuropathic pain. Our findings suggest that MAPKs inhibitors have a potential role in treatment for orofacial neuropathic pain.