FDA：长效β受体激动剂需限制使用

适当使用时,LABAs利大于弊,可继续用于治疗哮喘。FDA建议仅用于哮喘控制药物如吸入性皮质激素不能有效缓解病情的患者。     

The 18- to 23-kb deletion of the Macedonian delta beta-thalassemia includes the entire delta and beta globin genes

Restriction endonuclease mapping analyses were made of DNA from a few members of a Macedonian family with hematological characteristics of delta beta-thalassemia, ie, microcytosis, normal HbA2 levels, and elevated levels of HbF (7% to 14%) with G gamma (average 40.5%) and A gamma T chains (average 59.5%). A large deletion of 18 to 23 kb was present with a 5' breakpoint within a 670-bp segment of DNA between the HpaI and NcoI restriction sites 5' to the delta globin gene, and a 3' breakpoint between the BamHI and HpaI restriction sites located some 9 to 13 kb 3' to the beta globin gene. This deletion is different from those present in other types of G gamma A gamma(delta beta)zero- thalassemia. The similarity of the hematological expression of these delta beta-thalassemic conditions which have somewhat comparable 5' breakpoints supports the idea that an important fetal hemoglobin- controlling region lies between the psi beta and delta globin genes.     

傣药小灯台中的吲哚生物碱

从傣药小灯台(Winchia catophylla A. DC.)中分到4个吲哚生物碱,经理化常数测定,光谱分析和化学转化,分别鉴定为echitamine chloride(Ⅰ),echitamidine(Ⅱ),N_B-demethyl-echitamine(Ⅲ)和22-O-acetyl-N_b--demethyl-echitamine(Ⅳ),其中Ⅳ为新的吲哚生物碱。     

医用聚乳酸类高分子材料的应用

目的:阐述医用聚乳酸类高分子材料的需求,综述聚乳酸类高分子材料在生物医学领域的应用,并对其在医学领域的应用前景进行展望。资料来源:应用计算机检索ACS美国化学学会数据库2000-01/2006-12关于医用聚乳酸类高分子材料的文章,检索词“polylactide”;利用Elsevier Science全文电子期刊数据库2000-01/2006-12进行检索,检索词“polylactide”和全文检索“Medical polymeric material”。同时利用计算机检索中国期刊全文数据库1994-01/2005-12的相关文章,限定文章语言种类为中文,检索词“聚乳酸类医用高分子材料”。资料选择:对资料进行初审,纳入标准:①关于聚乳酸类医用高分子材料的需求。②医用聚乳酸类高分子材料的合成及应用。排除标准:重复性研究。资料提炼:共收集到符合上述要求的文献100篇,排除70篇重复性研究。30篇符合纳入标准:其中6篇关于聚乳酸类医用高分子材料的需求,24篇关于医用聚乳酸类高分子材料的合成及应用。资料综合:聚乳酸是一种具有良好的生物相容性和可生物降解的聚合物,最终的降解产物是二氧化碳和水,对人体无毒、无刺激。目前,聚乳酸类材料产品在医学领域广泛用于药物控制释放载体、组织工程、骨内固定、修复、手术缝合线、人造皮肤以及三维多孔支架等。结论:医用聚乳酸类高分子材料有非常广阔的应用前景,今后研究的重点是研发高效低成本的聚乳酸制备方法,合成适应于不同医疗或其他用途的、具有优良生物相容性的聚乳酸共聚物高分子材料。     

健胃愈疡颗粒干预下大鼠胃溃疡黏膜乳癌相关肽和血小板活化因子的表达及与胃黏膜疏水性的相关性研究

目的:观察对胃溃疡复发有较好疗效的健胃愈疡颗粒对溃疡黏膜乳腺癌相关肽和血小板活化因子表达的影响,分析其可能的作用机制。方法:实验于2005-07/2006-07在湘雅医院中心实验室完成。SD大鼠110只,雌雄各半,随机抽签法分为5组,即正常对照组、假手术组、雷尼替丁组、健胃愈疡组,各20只;模型组30只。以Okabe改良法复制大鼠实验性胃溃疡,假手术组仅以生理盐水代替乙酸注入玻管内。造模后24h,雷尼替丁组、健胃愈疡组大鼠分别灌服盐酸雷尼替丁和健胃愈疡颗粒(药物组成为:柴胡、党参、白芍、延胡索、白芨、珍珠层粉、青黛、甘草,湖南湘雅制药有限公司生产)药液10mL/kg,分别相当于2.70,1.62g/kg,1次/d。假手术组、模型组灌服蒸馏水10mL/kg。10d后各组中随机取出10只大鼠剖腹取胃(处死前大鼠禁食24h),90d时将模型组20只大鼠再分为模型复发组和模型非复发组,各10只;除正常对照组、假手术组、模型非复发组大鼠腹腔内注射生理盐水外,其余各组大鼠腹腔内注射白细胞介素1,1μg/kg;在注射48h,大鼠禁食24h后,剖腹取胃。观察其对胃溃疡大鼠胃黏膜氨基己糖及磷脂含量、溃疡指数和胃黏膜血流的影响,并用RT-PCR观察乳癌相关肽乳癌相关肽和血小板活化因子表达的变化。结果:实验动物110只,全部进入结果分析。①模型组10,92d胃黏膜血流均低于正常对照组(P<0.01);健胃愈疡组同期胃黏膜血流均高于模型组(P<0.01)。②健胃愈疡组和雷尼替丁组10d溃疡指数均低于模型组(P<0.01,P<0.05);模型复发组、健胃愈疡组和雷尼替丁组92d溃疡指数均高于模型组(P<0.01);健胃愈疡组10,92d溃疡指数及复发率均低于雷尼替丁组(P<0.05,P<0.01)。③模型组10,92d氨基己糖和磷脂含量均低于正常对照组(P<0.01)。健胃愈疡组10,92d氨基己糖和磷脂含量均高于模型组和雷尼替丁组(P<0.01)。溃疡指数与氨基已糖、磷脂含量呈负相关(r=-0.957,-0.960,P<0.01)。④健胃愈疡组和雷尼替丁组10d乳癌相关肽mRNA表达较正常组和假手术组提高,血小板活化因子mRNA的表达下调(P<0.01),健胃愈疡组两指标表达变化较雷尼替丁组显著(P<0.01);模型复发组、健胃愈疡组和雷尼替丁组92d乳癌相关肽mRNA、血小板活化因子mRNA的表达同组10d比较差异无显著性意义(P>0.05);模型组乳癌相关肽mRNA、血小板活化因子mRNA的表达同组10d比较差异有显著性意义(P<0.01)。结论:健胃愈疡颗粒可提高乳癌相关肽mRNA及下调血小板活化因子mRNA的表达,影响胃黏膜氨基己糖及磷脂含量,可能是其促进溃疡愈合的机制之一。     

Desmoplastic fibroma of the proximal ulna

A young man presented with desmoplastic fibroma in the proximal ulna. This rare tumour was treated by curettage and bone grafting.     

3,5-甾二烯化合物的合成及抗早孕活性

以18-甲基-17β-羟基-17α-乙炔基-雌甾-4-烯-3-酮(18-甲基炔诺酮),17β-羟基-17α-乙缺基-雌甾-4-烯-3-酮(炔诺酮),17β-羟基-17α-乙炔基-雄甾-4-烯-3-酮(妊娠素)和17a-羟基孕甾-4-烯-3,20二酮(17α-羟基黄体酮)为原料,经NaBH,还原、脱水、双键转位和酯化等反应合成一系列3,5-甾二烯化合物,用¹HNMR和MS证明了它们的结构。动物筛选结果表明,17β-丙酰氧基-17α-乙炔基-雌甾-3,5-二烯(IV_b2有明显的抗早孕活性。中断早期妊娠的作用似与其雌激素活性有关。     

Prostate Tumor Growth Can Be Modulated by Dietarily Targeting the 15-Lipoxygenase-1 and Cyclooxygenase-2 Enzymes

The main objectives of our study were to determine the bioavailability of omega-3 (ω-3) to the tumor, to understand its mechanisms, and to determine the feasibility of targeting the ω-6 polyunsaturated fatty acids (PUFAs) metabolizing 15-lipoxygenase-1 (15-LO-1) and cyclooxygenase-2 (COX-2) pathways. Nude mice injected subcutaneously with LAPC-4 prostate cancer cells were randomly divided into three different isocaloric (and same percent [%] of total fat) diet groups: high ω-6 linoleic acid (LA), high ω-3 stearidonic acid (SDA) PUFAs, and normal (control) diets. Tumor growth and apoptosis were examined as end points after administration of short-term (5 weeks) ω-3 and ω-6 fatty acid diets. Tumor tissue membranes were examined for growth, lipids, enzyme activities, apoptosis, and proliferation. Tumors from the LA diet-fed mice exhibited the most rapid growth compared with tumors from the control and SDA diet-fed mice. Moreover, a diet switch from LA to SDA caused a dramatic decrease in the growth of tumors in 5 weeks, whereas tumors grew more aggressively when mice were switched from an SDA to an LA diet. Evaluating tumor proliferation (Ki-67) and apoptosis (caspase-3) in mice fed the LA and SDA diets suggested increased percentage proliferation index from the ω-6 diet-fed mice compared with the tumors from the ω-3 SDA-fed mice. Further, increased apoptosis was observed in tumors from ω-3 SDA diet-fed mice versus tumors from ω-6 diet-fed mice. Levels of membrane phospholipids of red blood cells reflected dietary changes and correlated with the levels observed in tumors. Linoleic or arachidonic acid and metabolites (eicosanoid/prostaglandins) were analyzed for 15-LO-1 and COX-2 activities by high-performance liquid chromatography. We also examined the percent unsaturated or saturated fatty acids in the total phospholipids, PUFA ω-6/ω-3 ratios, and other major enzymes (elongase, Delta [Δ]-5-desaturase, and Δ-6-desaturase) of ω-6 catabolic pathways from the tumors. We observed a 2.7-fold increase in the ω-6/ω-3 ratio in tumors from LA diet-fed mice and a 4.2-fold decrease in the ratio in tumors from the SDA diet-fed mice. There was an increased Δ-6-desaturase and Δ-9 desaturase enzyme activities and reduced estimated Δ-5-desaturase activity in tumors from mice fed the SDA diet. Opposite effects were observed in tumors from mice fed the LA diet. Together, these observations provide mechanistic roles of ω-3 fatty acids in slowing prostate cancer growth by altering ω-6/ω-3 ratios through diet and by promoting apoptosis and inhibiting proliferation in tumors by directly competing with ω-6 fatty acids for 15-LO-1 and COX-2 activities.