冯崇廉主任应用小柴胡汤经验浅释

小柴胡汤出自《伤寒论》,是仲景为少阳伤寒而设的主方。原为治疗少阳证而设,其组方合理,疗效卓著,后世医家对其适应症有了广泛的发展,冯崇廉主任医师深刻领会方义,略有加减,在临床各科疾病的治疗方面取得了良好的疗效。     

苦针汤的组方研究

目的：对苗药苦针汤进行组方基础研究和新药开发研究。方法：以该方对金黄色葡萄球菌、痢疾杆菌、白色葡萄球菌、致病性大肠杆菌（1）的抑制作用为考察指标，运用混料均匀设计法将组成苦针汤中的4味药配制成12种不同比例的复方，通过抗菌实验，测试用药抗菌能力。结果：建立回归方程．对回归方程及其中各项系数进行检验，求抗菌效果最佳时的变量取值。结论：回归方程通过检验，有意义、可用；苦参、黄芩对抑菌效果的贡献不显著，其余两味药以19．56g和11．84g组方时抗菌效果最佳，优于理论计算值。     

大柴胡汤加减治疗内科杂证

大柴胡汤加减治疗胆囊炎、胆石症、急性胰腺炎、便秘、肺炎、偏头痛等内科杂证。     

《医林改错》方药临床运用

清代医学家王清任之《医林改错》,阐发气血理论,其方药临床实用性较强,治疗疑难病,常获较好疗效,笔者在临床中学习取得一定体会,列举病案4例。     

膈下逐瘀汤联合环磷酰胺对EAC肝癌小鼠肿瘤间质血管生成的影响

目的 探讨膈下逐瘀汤联合环磷酰胺对EAC肝癌模型小鼠的抗癌作用及其机制.方法 选EAC肝癌小鼠细胞株,建立肿瘤动物模型后,按完全随机化原则分为空白组、模型组、中药组、CTX组、中药+ CTX组.空白组、模型组给予生理盐水灌胃0.4 ml/d;中药组给予膈下逐瘀汤(11 g/kg体重)0.4 ml/d灌胃;CTX组给予环磷酰胺(2 mg/ml)腹腔注射0.4 ml/d;中药+CTX组给予膈下逐瘀汤0.4 ml/d灌胃、CTX腹腔注射0.4 ml/d.给药10d后,检测各组小鼠的体重、一般状态、光镜下进行形态学观察,电镜下观察肿瘤间质血管生成情况.结果 中药+CTX组可改善小鼠食欲,增加体重(33.60±2.14)g.中药+CTX组可减少肿瘤间质中毛细血管数量;电镜下可见中药+ CTX组肿瘤组织内新生的毛细血管结构破坏最为严重.结论 中药+ CTX组可提高EAC肝癌模型小鼠的生活质量,抑制肿瘤间质毛细血管的生长.     

益经汤治疗卵巢早衰20例

目的:观察益经汤治疗卵巢早衰的临床疗效。方法:20例卵巢早衰患者连续服用益经汤治疗3个月,观察月经恢复情况及血清生殖内分泌激素FSH及E2的变化。结果:治疗后有规律月经的6例,半年内2次以上的5例,半年内1次的5例,仍闭经的4例;所有患者FSH均下降,与治疗前相比差异有显著性(P0.05),E2均上升,与治疗前相比有差异(P0.05)。结论:益经汤能促进月经来潮,调节血清生殖内分泌激素FSH及E2的水平,治疗卵巢早衰安全、有效。     

促排卵汤联合生活方式干预对多囊卵巢综合征妇女血清SAP、Apelin与IL-18水平的影响

目的 研究促排卵汤联合生活方式干预对多囊卵巢综合征妇女血清SAP、Apelin与IL-18水平含量的影响.方法 选择2016年1月—2016年12月就诊的多囊卵巢综合征患者80例,分为2组各40例.其中,试验组患者在对照组常规理疗的同时添加促排卵汤联合生活方式干预,比较2组患者血清SAP、Apelin与IL-18水平含...     

扶正消癌Ⅰ号方对GP方案治疗老年非小细胞肺癌减毒增效的临床研究

目的:研究扶正消癌Ⅰ号方对GP方案治疗老年非小细胞肺癌(NSCLC)的减毒增效作用。方法:选择2006年1月—2006年12月住院的老年NSCLC患者35例,按随机设计分为研究组和对照组,分别为20例和15例,研究组给予扶正消癌Ⅰ号方,药用:茯苓10g,白术10g,山药10g,黄芪15g,太子参15g,白花蛇舌草30g,山慈菇15g,蜈蚣2条,每日1剂,连服14天,同时给予GP方案:吉西他滨(GEM)1000mg/m2,第1,8天,卡铂(CBP)AUC 5,第1天,3周为1个周期,至少完成2个周期治疗的病例进入统计学处理,对照组给予GP方案,方法同研究组,观察近期疗效,毒副反应,生存质量(QOL)和总生存时间(OS)。结果:进入统计学处理的病例数研究组与对照组分别为18例和13例,研究组与对照组在近期疗效方面无显著差异(44.44%vs 38.46%,χ2=0.111,P=0.739),研究组毒副反应发生率显著低于对照组(P0.05)、QOL优于对照组(P0.05),在中位生存时间(MST)和OS方面无显著性差异(P0.05)。结论:扶正消癌Ⅰ号方对GP方案治疗老年NSCLC患者能够显著降低毒副反应发生率,提高QOL,具有肯定的减毒增效作用,有一定的临床应用价值。     

Exploring the mechanism of Buyang Huanwu decoction in the treatment of lumbar disc herniation based on network pharmacology and molecular docking

Buyang Huanwu decoction (BYHWD), as one of the traditional Chinese medicine formulas, is widely used in the clinical treatment of lumbar disc herniation (LDH) with curative effect. It has the characteristics of multi-component, multi-target, and mutual synergy, but the mechanism of action is often unclear. It needs some research to explore the molecular mechanism of BYHWD in the treatment of LDH based on network pharmacology and molecular docking. Screen the active compounds of BYHWD and predict drug-related gene/protein targets, which could determine the specific target of BYHWD in the treatment of LDH. Construct the “Drugs-Compounds-Targets” network and search for the core targets. Use Gene Ontology functional enrichment analysis, Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis, and molecular docking verification to explore the possible molecular mechanism. Eighty-two effective compounds and 666 targets of BYHWD, 187 targets for LDH treatment, and 20 core candidate targets were excavated. A total of 3414 entries were identified by Gene Ontology enrichment analysis, 173 related signal pathways were identified by Kyoto Encyclopedia of Genes and Genomes enrichment analysis, and 5 core compounds were identified by molecular docking, which had a good affinity with core genes STAT3, JUN, AKT1, MAPK1, RELA, and PIK3CA. BYHWD may play the role of analgesic and improving function by synergistic anti-inflammatory and analgesic compounds, regulating cell metabolic differentiation, regulating immunity, and anticoagulation. BYHWD in the treatment of LDH may play a role in analgesia and improve function through multiple signaling pathways, including PI3K-Akt, mitogen-activated protein kinase, tumor necrosis factor, and interleukin-17. The PI3K-Akt signaling may be one of the key mechanisms.     

Dual leucine zipper kinase (MAP3K12) modulators: a patent review (2010–2015)

Introduction: The dual leucine zipper kinase (DLK, MAP3K12) is essential for neuronal development and has been shown to mediate axon regeneration. On the other hand, DLK is involved in the pathogenesis of neurodegenerative disease and diabetes mellitus. Several patents have been published claiming to modulate or inhibit DLK by various approaches including ATP competitive inhibitors. In addition, two publications describe SAR of highly selective DLK inhibitors with efficacy in distinct mouse models of neurodegeneration.

Areas covered: This review summarized patents claiming to modulate DLK activity published between 2010 and 2015. Peer-reviewed publications related to the patents and additional peer-reviewed publications are included. This article describes 18 patents from three pharmaceutical companies and three academic research groups.

Expert opinion: Several methods are proposed to modulate DLK activity, some of them very experimental and not suitable for easy application in patients. ATP competitive kinase inhibitors exert high affinity, but for the majority, no information about their selectivity is available. To date, two inhibitors have been tested in mice. Given the controversial findings that DLK is required for neurodegeneration and for axon regeneration, more research is needed to further elucidate the regulation and the function of this kinase in diverse organs/tissues and under physiological and pathological conditions.