奥沙利铂联合5-Fu/CF治疗晚期大肠癌的临床观察

目的观察国产奥沙利铂联合5-Fu/亚叶酸钙(CF)治疗晚期大肠癌的疗效及不良反应。方法采用奥沙利铂联合5-Fu／CF治疗晚期大肠癌26例,方案为：奥沙利铂130mg／m^2静脉滴注4h,第1天;CF200mg／m^2静脉滴注2h,第1～5天;后接5-Fu500mg／m^2持续滴液5h,第1～5天;21d为1周期,所有病人平均化疗3～4个周期(中位数3．6周期)。结果本组晚期大肠癌26例,完全缓解(CR)1例,部分缓解(PR)10例,稳定(NC)8例,进展(PD)7例,总有效率42．3％。结论主要不良反应恶心、呕吐、口腔溃烂、外周神经炎、腹泻,大部分均为Ⅰ～Ⅱ度,病人耐受良好,不良反应轻,值得临床推广使用。     

草酸铂联合氟尿嘧啶／亚叶酸钙二线治疗晚期大肠癌临床观察

目的 评价草酸铂（L-OHP）联合氟尿嘧啶（5-FU）／亚叶酸钙（CF）治疗晚期大肠癌的疗效及其毒性反应。方法 采用草酸铂130mg／m^2。，静脉滴注2h第1天；亚叶酸钙200g/m^2。静脉滴注2h（在5-FU前）第2～6天；氟尿嘧啶300—500mg/m^2静脉滴注4h以上第2～6天；治疗经5-FU／CF方案失败后进展的Duke’s D期大肠癌37例，21d为1个周期，连用2～6个周期。结果 37例总有效率（CR＋PR）为32．4％。主要毒性反应：以神经毒性为主，其次为消化道毒性和骨髓抑制，均为可逆性，可以耐受。结论 草酸铂联合氟尿嘧啶／亚叶酸钙二线治疗晚期大肠癌，有较好的疗效；毒性反应可以耐受，值得推广。     

奥沙利铂联合5-氟尿嘧啶和亚叶酸钙治疗晚期大肠癌35例

目的观察奥沙利铂（L-OHP）、5-氟尿嘧啶（5-FU）、亚叶酸钙（CF）联合治疗晚期大肠癌的疗效和不良反应。方法35例晚期大肠癌用L-OHP130mg／m^2加入5％葡萄糖注射液（GS）500mL静脉滴注2—5h，第1天；CF100mg／m^2，第～5天；5-FU500mg／m^2，第1—5天。同时予对症支持治疗，每3周重复用药，每例至少完成3个周期。结果35例共完成123个化疗周期，每例平均3．5个周期，均可评价临床疗效。完全缓解（CR）3例，部分缓解（PR）14例，有效（CR＋PR）率为48．6％；初治24例中，CR3例，PR10例，有效率为54．2％；复治11例中，PR4例，无CR，有效率为36．4％。不良反应主要有恶心呕吐、周围神经毒性、腹泻、白细胞及血小板下降、脉管炎，一般在Ⅰ～Ⅱ度。结论L—OHP联合5-Fu，CF治疗晚期大肠癌疗效肯定，不良反应经处理后均可耐受，无严重不良反应发生，可作为一种供选择方案。     

FOLFOX方案治疗晚期大肠癌临床观察

目的研究奥沙利铂（L-OHP）、5-氟尿嘧啶（5-Fu）、亚叶酸钙（CF）联合组成的FOLFOX方案治疗晚期大肠癌的临床疗效和毒副作用。方法对30例初治或复治晚期大肠癌患者采用L-OHP130mg/m^2,静脉滴注3h,第1天;CF200mg/m^2,静脉滴注第1天至第5天;5-Fu300mg/m^2,静脉滴注第1天至第5天（CF滴完后用）;28d为1个周期,行4个周期治疗后判定疗效。结果 30例患者均可评价疗效及不良反应,总有效率为40.0%。初治患者总有效率41.1%,复治患者总有效率38.3%,不良反应主要表现为骨髓抑制白细胞减少、恶心、呕吐、周围神经炎等,无化疗相关死亡。结论 FOLFOX方案治疗晚期大肠癌疗效肯定,毒副作用能耐受。     

奥沙利铂 5-氟尿嘧啶 亚叶酸钙静脉滴注治疗晚期大肠癌疗效观察

目的 观察奥沙利铂(L-OHP)与5-氟尿嘧啶(5-Fu)及亚叶酸钙(CF)持续用药治疗晚期、复发性大肠癌的疗效.方法 L-OHP 130 mg/m2静脉滴注第1天2h,5-Fu 2.5 g持续静脉滴注120h,CF 100 mg静脉滴注第1～5天,每3周为1个疗程.结果 总有效率达42％.结论 L-OHP与5-Fu及CF持续用药治疗晚期、复发性大肠癌疗效肯定,不良反应轻,可耐受.     

L-OHP+CF+5-Fu方案治疗晚期胃癌临床观察

目的观察亚叶酸钙(CF)、草酸铂(L-OHP)、氟脲嘧啶(5-Fu)组成的方案治疗晚期胃癌的疗效。方法已经病理或手术证实的晚期胃癌24例,采用L-OHP 130mg/m^2静脉滴注2h,第1天：CF150mg／m^2静脉滴注2h,第2—4天,5一Fu200mg/m^2快速静脉滴注,追加900mg／m^2,采用肘静脉穿刺输液泵持续滴注48h,第2—4天。21d为一周期。结果24例患者中,完全缓解(CR)率为16．7％(4／24),部分缓解(PR)率为41．7％(10／24),总有效率(RR)58．3％(14／24)。不良反应：外周感觉神经末梢损害发生率为62．5％(15/24),Ⅰ度静脉炎发生率为33．3％(8／24),骨髓抑制均为Ⅰ级发生率为8．3％(2／24),胃肠道反应均为Ⅰ-Ⅱ级发生率为16．7％(4／24),口腔黏膜炎发生率为4．2％(1／24)。结论L-OHP CF 5-Fu联合化疗方案治疗晚期胃癌疗效好,不良反应轻,患者可耐受。     

草酸铂联合5-FU／CF方案治疗晚期结肠癌的临床观察

目的评价奥沙利铂（L-OHP）联合5-氟脲嘧啶／亚叶酸钙（5-FU／CF）治疗晚期结肠癌的疗效和毒副作用。方法27例晚期结肠癌患者应用奥沙利铂（L-OHP）100mg／m^2，第1天，2h静脉滴注；亚叶酸钙（CF）200mg／m^2，第2-4天静脉滴注2h；5-氟脲嘧啶（5-Fu）500mg／m^2，第2-4天，静脉滴人4h，每3周重复1次。结果27例患者中均可评价疗效，完全缓解1例，部分缓解11例，稳定10例，进展5例。结论奥沙利铂（L-OHP）联合亚叶酸钙（CF）及5-氟脲嘧啶（5-Fu）治疗晚期结肠癌疗效显著，副反应主要是周围神经毒性、中性粒细胞减少及腹泻。     

奥沙利铂联合5-氟脲嘧啶/亚叶酸钙治疗进展期大肠癌的临床体会

目的 观察国产奥沙利铂联合5-氟脲嘧啶(5-Fu),亚叶酸钙(CF)治疗进展期大肠癌的疗效及不良反应。方法 治疗方案为：CF200mg／m^2静脉注射,2h后5-Fu 0．5g静脉注射10min,再予5-Fu 2．5g/m^2经深静脉用输液泵持续静脉输注48h。奥沙利铂130mg／m^2静脉注射2h以上,第1天。以上方案每28天重复1次,所有患者平均2周期。结果 本组中进展期大肠癌42例,完全缓解(氓)2例,部分缓解(PR)13例,稳定(NC)8例,进展(PD)19例,总有效率为35．7％。无治疗相关死亡,主要副反应有：神经毒性、消化道反应、腹泻、恶心、呕吐等,常规对症治疗后缓解。结论 奥沙利铂联合5-Fu／CF治疗进展期大肠癌疗效好、毒副反就轻,多数患者能耐受,是治疗进展期大肠癌较好的联合化疗方案。     

以草酸铂为主的联合化疗方案治疗晚期大肠癌16例

目的 观察草酸铂(OXA)联合醛氢叶酸(CF),5-氟尿嘧啶(5-Fu)治疗晚期大肠癌的近期疗效及不良反映.方法 OXA130mg/m2,iv drip dl;CF100mg,iv dl-5;5-Fu375mg/m2,iv dl-5.以上方案每21d为一周期,至少完成二周期.结果 CR1例,PR5例,SD6例,PD4例.总有效率37.5%,主要不良反应为恶心、呕吐、血白细胞减少、外周神经炎.结论 草酸铂为主联合化疗方案治疗晚期大肠癌疗效较好,不良反应可耐受,值得临床推广应用.     

奥沙利铂联合氟尿嘧啶和亚叶酸钙治疗晚期胃癌

目的：观察奥沙利铂（LOHP）联合氟尿嘧啶（5-Fu）和亚叶酸钙（CF）治疗晚期胃癌的疗效及不良反应。方法：采用FOL-FOX改良方案,第一天采用LOHP130mg/m^2静脉滴注3h,CF200mg静脉滴注2h后,5-Fu500mg快速静脉注射后再用5-Fu 2．4g／m^2 持续静脉滴注泵连续滴注46h,每21天重复,完成2周期后评价疗效。结果：全组46例晚期胃癌患者,CR3例,PR20例,有效率（CR＋PR）50％,中位疾病进展时间（TTP）5．7个月,中位生存期10．5个月。主要不良反应为轻度感觉神经毒性、恶心呕吐及骨髓抑制。结论：LOHP联合5-Fu和CF治疗晚期胃癌疗效较好,不良反应轻,可耐受。     

Nachweis einiger Heilmittel in der Kniegelenksynovialflüssigkeit

Zusammenfassung Mittels Gaschromatographie und Dünschichtchromatographie wiesen die Autoren 11 Substanzen nach, welche durch Injektion oder nach Verabreichung per os in die Kniegelenksynovialflüssigkeit eindrangen. In ihrer Aufstellung konnten sie eine direkte Beziehung zwischen Struktur sowie chemischphysikalischen Eigenschaften der Substanz und ihrer Fähigkeit, aus dem Blut in die Kniegelenksynovialflüssigkeit einzudringen, nicht nachweisen, außer der Tatsache, daß Substanzen mit starker Affinität zu Eiweißstoffen erst in höheren Dosen nachweisbar waren.     

Synthesis,Cytotoxicity and Antileishmanial Activity of Some N-(2-(indol-3-yl)ethyl)-7-chloroquinolin-4-amines

We report herein the condensation of 4,7-dichloroquinoline (1) with tryptamine (2) and D-tryptophan methyl ester (3) . Hydrolysis of the methyl ester adduct (5) yielded the free acid (6) . The compounds were evaluated in vitro for activity against four different species of Leishmania promastigote forms and for cytotoxic activity against Kb and Vero cells. Compound (5) showed good activity against the Leishmania species tested, while all three compounds displayed moderate activity in both Kb and Vero cells.     

Emerging drugs for epilepsy

Epilepsy affects ≤ 1% of the world's population. Antiepileptic drugs (AEDs) are the mainstay of treatment, although more than a third of patients are not rendered seizure free with existing medications. Uncontrolled epilepsy is associated with increased mortality and physical injuries, and a range of psychosocial morbidities, posing a substantial economic burden on individuals and society. Limitations of the present AEDs include suboptimal efficacy and their association with a host of adverse reactions. Continued efforts are being made in drug development to overcome these shortcomings employing a range of strategies, including modification of the structure of existing drugs, targeting novel molecular substrates and non-mechanism-based drug screening of compounds in traditional and newer animal models. This article reviews the need for new treatments and discusses some of the emerging compounds that have entered clinical development. The ultimate goal is to develop novel agents that can prevent the occurrence of seizures and the progression of epilepsy in at risk individuals.     

盐酸达泊西汀中甲磺酸甲酯、甲磺酸乙酯及甲磺酸异丙酯的顶空毛细管GC-ECD法测定

建立了衍生化顶空毛细管气相色谱-电子捕获检测器(ECD)法测定盐酸达泊西汀中的甲磺酸甲酯(MMS)、甲磺酸乙酯(EMS)和甲磺酸异丙酯(IMS).应用碘化钠衍生技术,使用PW-5毛细管柱,载气为氮气,ECD检测,程序升温.MMS、EMS和IMS分别在0.03～0.30、0.05～0.50和0.05～0.50 μg/ml浓度范围内线性关系良好,平均回收率分别为63.5％、100.3％和96.2％,最低检测限分别为0.30、0.50和0.50 ng/ml.     

Lung disease and PKCs

The lung offers a rich opportunity for development of therapeutic strategies focused on isozymes of protein kinase C (PKCs). PKCs are important in many cellular responses in the lung, and existing therapies for pulmonary disorders are inadequate. The lung poses unique challenges as it interfaces with air and blood, contains a pulmonary and systemic circulation, and consists of many cell types. Key structures are bronchial and pulmonary vessels, branching airways, and distal air sacs defined by alveolar walls containing capillaries and interstitial space. The cellular composition of each vessel, airway, and alveolar wall is heterogeneous. Injurious environmental stimuli signal through PKCs and cause a variety of disorders. Edema formation and pulmonary hypertension (PHTN) result from derangements in endothelial, smooth muscle (SM), and/or adventitial fibroblast cell phenotype. Asthma, chronic obstructive pulmonary disease (COPD), and lung cancer are characterized by distinctive pathological changes in airway epithelial, SM, and mucous-generating cells. Acute and chronic pneumonitis and fibrosis occur in the alveolar space and interstitium with type 2 pneumocytes and interstitial fibroblasts/myofibroblasts playing a prominent role. At each site, inflammatory, immune, and vascular progenitor cells contribute to the injury and repair process. Many strategies have been used to investigate PKCs in lung injury. Isolated organ preparations and whole animal studies are powerful approaches especially when genetically engineered mice are used. More analysis of PKC isozymes in normal and diseased human lung tissue and cells is needed to complement this work. Since opposing or counter-regulatory effects of selected PKCs in the same cell or tissue have been found, it may be desirable to target more than one PKC isozyme and potentially in different directions. Because multiple signaling pathways contribute to the key cellular responses important in lung biology, therapeutic strategies targeting PKCs may be more effective if combined with inhibitors of other pathways for additive or synergistic effect. Mechanisms that regulate PKC activity, including phosphorylation and interaction with isozyme-specific binding proteins, are also potential therapeutic targets. Key isotypes of PKC involved in lung pathophysiology are summarized and current and evolving therapeutic approaches to target them are identified.