半夏用量考辨

半夏,<神农本草经>谓其:"气味辛,平,有毒.主伤寒寒热,心下坚.胸胀咳逆,头眩,咽喉肿痛,肠鸣,下气,止汗."现代药理研究证实:法半夏对中枢神经有良好的镇静和安定作用.     

黄精多糖对新生大鼠大脑皮层神经细胞缺氧性凋亡的影响

目的:探讨黄精多糖对体外培养的新生大鼠大脑皮层神经细胞缺氧性凋亡的保护作用.方法:采用"Neurobasal加B27 Supplement"体外培养新生大鼠大脑皮层神经细胞,使用Hoechst 33342荧光染色、免疫细胞化学染色观察黄精多糖对缺氧复氧性神经细胞凋亡的保护作用.结果:缺氧前加入500μg/ml～1.5mg/ml的黄精多糖能显著地降低缺氧复氧培养诱导的神经细胞凋亡率,增加缺氧的神经细胞Bcl-2蛋白的表达,减少Bax蛋白的表达,提高Bcl-2/Bax比值.而缺氧12h后加入黄精多糖则无明显的抗凋亡作用.结论:缺氧前加入黄精多糖可以通过上调缺氧神经细胞Bcl-2表达、下调Bax表达和提高Bcl-2/Bax的比值以避免缺氧的神经细胞凋亡.     

针刺治疗高热30例

高热临床常见。中医称“壮热”、“实热”、“日晡潮热”均属于“高热”的范畴。临床上除病因治疗外，常辅以物理降温和解热镇痛药来退热。而物理降温效果有时并不理想，解热镇痛药长期使用可引起毒副作用及药物依赖性。笔者在处理高热病人时，采用针刺退热，见效快，患者痛苦小，收到了满意效果，现介绍如下。     

《金匮要略》肝虚传脾论

肝虚传脾,乍听起来,似乎不可思议,但理论上客观存在,实践上经得起检验."问曰:上工治未病,何也?师曰:夫治未病者,见肝之病,知肝传脾,当先实脾".<金匮要略>肝病实脾的这个著名论断虽被世代传承,并被不断发掘(或创新),但过去我们曾囿于尤在泾"盖脏病,惟虚者受之,而实则不受,脏邪惟实则能传,而虚则不传"之论,强调肝虚一般不传脾.纵观<金匮要略>全书,肝虚亦可传脾.现特论述之:     

陈国权活用《金匮》方治杂证验案四则

陈国权教授从事医教研30余年,学验具丰,尤擅用<金匮>方辨证治疗临床疑难杂症,现择其验案四则介绍如下. 1 痔疮术后所致顽固性便秘 欧某,女,52岁.2004年1月26日初诊.诉患混合痔,曾先后四次接受手术治疗.在结束最后一次手术的6年中,大便一直不通,因而不敢多食,惧怕远游.最初每周灌肠1～2次.日久了,一则无时间,二则经济上承受不了,索性用手抠大便,痛苦不堪,曾多次想死.诊见面红,尿黄,脉弦略数,舌淡,苔白,中部略黄.证属肝郁血虚,湿郁化热.治宜宣肺疏肝,健脾养血.方用葶苈大枣泻肺汤、丹栀逍遥散、当归贝母苦参丸合四物汤化裁.药用:葶苈子10g,大枣12g,当归36g,赤芍15g,白芍24g,柴胡10g,薄荷8g,炒白术12g,茯苓15g,炙甘草8g,大贝10g,苦参10g,丹皮12g,炒栀子8g,熟地黄10g,川芎10g,炒枳实10g,厚朴10g.三剂.     

Pivotal study of iodine-131-labeled chimeric tumor necrosis treatment radioimmunotherapy in patients with advanced lung cancer.

PURPOSE: Tumor necrosis treatment (TNT) uses degenerating tumor cells and necrotic regions of tumors as targets for radioimmunotherapy. Previous studies in animal tumor models and clinical trials have demonstrated that when linked to the therapeutic radionuclide iodine-131, recombinant chimeric TNT antibody ((131)I-chTNT) can deliver therapeutic doses to tumors regardless of the location or type of malignancy. Therapeutic efficacy and toxicity of (131)I-chTNT in advanced lung cancer patients were studied in this pivotal registration trial. PATIENTS AND METHODS: Patients with advanced lung cancer were treated with systemic or intratumoral injection of (131)I-chTNT in eight oncology centers in China. The objective response rate (ORR) was assessed as the primary end point. RESULTS: All 107 patients who were entered onto the study and completed therapy had experienced treatment failure after prior radiotherapy or chemotherapy a mean of three times. The results showed an ORR of 34.6% (complete response, 3.7%; partial response, 30.8%; no change, 55.1%; and progressive disease, 10.3%) in all patients and 33% in 97 non-small-cell lung cancer patients. A biodistribution study demonstrated excellent localization of the radioactivity in tumors in both systemically and intratumorally injected patients. The most obvious adverse side effect was mild and reversible bone marrow suppression. CONCLUSION: Radioimmunotherapy with (131)I-chTNT was well tolerated and can be used systemically or locally to treat refractory tumors of the lung.     

The p53 codon 72 proline allele is associated with p53 gene mutations in non-small cell lung cancer.

The p53 gene plays a critical role in cell cycle control, the initiation of apoptosis, and in DNA repair. An Arg/Pro polymorphism at codon 72 of the p53 gene alters the ability of the p53 protein to induce apoptosis, influences the behavior of mutant p53, decreases DNA repair capacity, and may be linked with an increased risk of lung cancer. To further define the role of the p53 codon 72 polymorphism on DNA repair, lung cancer risk, and mutant p53 function, we examined the effect of this polymorphism on mutation of the p53 gene and patient survival in non-small cell lung cancer (NSCLC). Tumor and nonneoplastic (lung or lymphocyte) samples were collected from 182 patients with NSCLC. p53 mutations were detected by direct sequencing and/or the Gene Chip p53 assay in 93 of 182 (51%) tumors. p53 codon 72 polymorphisms were identified by PCR/RFLP analysis. p53 mutations were significantly (P = 0.01) associated with the number of codon 72 Pro alleles: Pro/Pro homozygotes, 17 of 26 (65%); Arg/Pro heterozygotes, 45 of 79 (57%); and Arg/Arg homozygotes, 31 of 77 (40%). The number of codon 72 Pro alleles was independently associated with p53 mutations (odds ratio, 1.97; 95% confidence interval, 1.14-3.40; P = 0.01) in a multiple logistic regression model. The codon 72 polymorphism did not influence patient survival in either the entire patient group or among patients with p53 mutant tumors. In summary, the p53 Pro allele is associated with an increased frequency of p53 mutations in NSCLC.     

靶向Survivin基因的短发卡RNA在体内对U251细胞移植瘤的影响

Surivin基因属于凋死蛋白抑制因子（inhibitor of apoptosis,IAP）家族，具有抗细胞凋亡、促细胞增殖和促血管形成等多种生物学活性，其在脑胶质瘤发生和发展过程中的作用尚不完全明确，本研究结盟在观察稳定转染靶向Survivin基因的特异性短发卡RNA（shRNA）真核表达载体对人脑胶质母细胞瘤U251细胞裸鼠体内肿瘤生长和血管形成的影响。方法：将U251细胞，稳定转染Survivin基因shRNA真核表达载体pWHI-SR的U251-SR细胞，以及稳定转染空载体pWHI的U251-P细胞，分别接种于裸鼠背部皮下，建立人脑胶质瘤裸鼠皮下移植瘤模型，定期观察肿瘤生长情况，测定肿瘤体积、绘制肿瘤生长曲线，观察45天后处死动物、称瘤重，采用免疫组化SABC法检测Survivin、增殖细胞核抗原（proliferating cell muclear antigen，PCNA）以及八因子相关抗原（factor Ⅷ related antigen,FⅧRAg）在各组肿瘤标本中的表达，采用TUNEL法检测凋亡细胞，分别计算各组肿瘤标本的增殖指数（proliferative index,PI），凋亡指数（apoptotie index,AI）以及微血管密度（microvessel density,MVD）。结果：与U251、U251-SR组肿瘤标本，U251-SR组裸鼠肿瘤形成时间延迟，肿瘤生长缓慢，肿瘤体积及瘤重均明显减小（P〈0.01）；U251-P组裸鼠相丝，U251-SR组肿瘤标本Survivin蛋白表达明显下调：PI和MVD明显减少，AI明显升高（P〈0.001）。结论：靶向Survivin基因的sbRNA能够在体内明显抑制U251细胞的肿瘤生长和血管形成，Survivn基因可作为脑胶质瘤基因治疗的一个良好靶点，而RNA干涉（RNA interference,RNAi）技术可为脑胶瘤基因治疗的一个良好靶点，而RNA干涉（RNA interference，RNAi）技术可为脑胶质瘤的基因治疗提供新的重点手段。     

益气活血中药能改善慢性心衰症状

慢性充血性心力衰竭是老年人常见病，多发病，是因多种原因造成心脏原发性损害，以心脏功能异常、运动耐力下降及神经内分泌激活为特征的临床综合征。其病机以肾素-血管紧张素系统（RAS）激活为主，RAS作用主要通过血管紧张素Ⅱ（AngⅡ）来实现的。AngⅡ通过收缩血管、促进心肌细胞增生、醛固酮和内皮素分泌等多种机制造成心血管损害。神经内分泌失调是老年人慢性心衰的主要机制，所以治疗慢性充血性心力衰竭以调节神经内分泌为主，降低AngⅡ水平为关键。我们观察益气活血中药对慢性心衰神经内分泌的影响，旨在探讨中药治疗慢性心衰的机理，现总结报告如下。