健脾导滞方对人胃癌细胞的作用

目的:观察中药健脾导滞方对胃癌细胞生长、对P53和VEGF及其受体表达的作用.方法:分别以高、中、低等不同剂量的健脾导滞方制剂对Wistar雄性大鼠进行灌胃,制备含药血清,然后分别用不同剂量组的含药血清培养胃癌细胞,以倒置显微镜及流式细胞仪观测各组胃癌细胞的生长状况,并用免疫组化法检测各组胃癌细胞中P53和VEGF及其受体Flt的表达.结果:与对照组比较,用药组胃癌细胞的生长及细胞周期明显改变;P53和VEGF及其受体的表达明显减弱(P＜0.05).结论:健脾导滞方对胃癌细胞的生长,对P53和VEGF及其受体的表达均有抑制作用.     

Genetic epidemiology of alpha-1 antitrypsin deficiency in North America and Australia/New Zealand: Australia, Canada, New Zealand and the United States of America

Alpha-1-antitrypsin deficiency (AAT deficiency) is one of the most common serious hereditary disorders in the world, as its affects all major racial subgroups worldwide, and there are an estimated 120.5 million carriers and deficient subjects worldwide. This genetic disease is related to susceptibility for development of jaundice in infants, liver disease in children and adults and pulmonary emphysema in adults. Moreover, AAT deficiency carrier phenotypes (PiMS and PiMZ) and deficiency allele phenotypes (PiSS, PiSZ and PiZZ) are suspected to predispose subjects to a variety of other adverse health effects. Because there is a limited database on the number of individuals affected by this disease worldwide, we have collected data on control cohorts in genetic epidemiological studies published on case-control studies in the peer-reviewed literature worldwide. Based on these data, we estimated the numbers of carriers and deficiency allele combinations for the two most common defective alleles, namely PiS and PiZ in 58 countries worldwide. The present paper focuses on the distribution of the PiS and PiZ deficiency alleles in Australia, Canada, New Zealand and the United States of America. A total of 31,042,232 individuals at risk for adverse health effects have been calculated in these four countries: 2,144,158 in Australia, 3,258,564 in Canada, 430,922 in New Zealand and 24,909,548 in the United States of America. The prevalences for all five phenotypic classes of AAT deficiency in each of these countries is as follows: Australia 1 out of 8.9, Canada 1 out of 9.8, New Zealand 1 out of 8.5 and the United States of America 1 out of 11.3. The geographical distribution of individual control cohorts and estimates of the numbers of carriers and deficiency allele phenotypes in each of these four countries are given in individual tables.     

补肾、健脾、益气、活血法对衰老细胞周期基因表达的调控作用

目的：比较补肾、健脾、益气、活血法对衰老细胞周期基因表达的调控作用。方法：采用上述4种不同的含药血清对衰老的人胚肺二倍体成纤维细胞2Bs细胞株进行处理,通过细胞寿命实验、流式细胞仪、RT—PCR、Westemblot方法研究不同中药对衰老细胞周期及其相关基因(P16^INK4、Cyclin D1及PCNA)的mRNA转录和蛋白表达的影响。结果：补肾、益气中药对衰老细胞周期有一定的促进作用,并可下调衰老细胞增殖抑制基因P16和周期蛋白Cyclin D1的mRNA／蛋白表达;上调细胞周期促进增殖基因PCNAmRNA／蛋白的表达。而健脾、活血中药对细胞周期及其相关基因和蛋白表达的作用不明显。结论：补肾、益气方药对细胞周期有促进作用,其中的作用可能是通过促进P16途径的基因表达来实现。     

魏建功《古音系研究》的科学精神

《古音系研究》是已故著名语言学家魏建功先生的一部力作。该书以如何研究古音系及如何建立语音史和语言史为宗旨 ,详述古音系的分期和内容 ,论列古音系材料十种 ,其中五种均为旧音韵学书籍难以觅见的 ,弥足珍贵。书中所征引、所讨论的中外时贤的论著达数十种之多 ;所讨论的范围、所涉及的资料上自甲骨文 ,下迄婴儿学语的讹音 ,东自日语、朝鲜语汉字音 ,西至敦煌遗书 ,可谓囊括古今 ,包举宇内。《古音系研究》堪称音韵学乃至语言学领域内最富时代气息和战斗精神的著作 ,书中一以贯之的“综论古今通塞 ,尚论群贤得失”的科学精神 ,尤为可贵     

《伤寒论》中的一方多治探讨

《伤寒论》中桂枝汤等10个代表方均为一方多治的典型应用。论中所述诸证病因不同、症状不同，其病机则一。这为后世立法处方开了先河。后学者应以仲景之法为我法，见病知源，活学活用，使其立法，辨证、处方更加合理。     

萎缩康冲剂治疗萎缩性胃炎癌前病变的临床与实验研究

１００例患者均经胃镜与病理确诊为萎缩性胃炎（ＣＡＧ）伴中重度肠化（ＩＭ）和／或不典型增生（ＡＴＰ）,随机分为萎缩康治疗组和维酶素对照组,各５０例,治疗１疗程后,两组显效率分别为４２％,８％,总有效率为９０％,４０％（Ｐ均〈０．０５）。将Ｗｉｓｔａｒ大鼠１４只,随机分为６组,饮用５０μｇ／ｍｌ的甲基硝基亚硝基胍（ＭＮＮＧ）溶液,喂含０．０１％雷尼替丁标准颗粒饲料制成癌前病变模型,以萎缩康与维权衡利弊     

明代六部综合性医书的传日及其影响

明代传日医书众多,以《医书大全》、《南北经验医方大成》、《玉机微义》、《医学正传》、《医学入门》、《万病回春》等综合性医书,传播最快,影响最大。它们促进了16世纪以降日本开始对中国医籍的大量翻刻;为日本当时医师培养提供了便捷教本;丰富了道三学派的理论与实践,从而为日本医学中兴增添了砖瓦。     

安宫牛黄丸治疗蛛网膜下腔出血后脑血管痉挛疗效观察

目的 :观察安宫牛黄丸治疗蛛网膜下腔出血后脑血管痉挛的疗效。方法 :4 8例患者随机分为治疗组和对照组 ,各 2 4例 ,治疗组给安宫牛黄丸 ,每次 3 g,2次 /日 ,对照组给尼莫地平 ,每次 60 mg,4次 /日。分别测 2组用药前 3 0分钟 ,用药后 3日及 12日脑血流速度并评定疗效。结果 :治疗组大脑中动脉平均血流速度由 ( 168± 4 9) cm/s降至 ( 96± 2 5 ) cm/s;对照组由 ( 171± 3 8) cm/s降至 ( 117± 3 4) cm/s,2组比较有显著性差异 ( P<0 .0 1)。同时治疗组疗效优于对照组。结论 :安宫牛黄丸治疗蛛网膜下腔出血后脑血管痉挛有较好疗效     

Plasma calcium and phosphate levels in an adult noninsulin-dependent diabetic population

Summary Duplicate or triplicate measurements of fasting plasma glucose, calcium (Ca), phosphate (Pi), and glycosylated hemoglobins were performed on a group of non-insulin dependent diabetic patients and controls at 3–6 month intervals. In the diabetic group (48 males and 44 females), 18 were on diet only, 21 on diet and oral hypoglycemic treatment, and 51 on diet and insulin. These were a total of 217 measurements for each parameter. Results were compared to 416 measurements obtained from sex and age-matched controls. Plasma Ca levels were higher in the diabetic group (2.48±0.004 vs 2.38±0.006 mmol/liter)P<0.001; plasma Pi levels were similar to those of controls. The difference in plasma Ca was not influenced by age, sex, or mode of treatment. No correlation was found in the three treatment groups between plasma Ca and duration of diabetes nor with patients' weights. The results are consistent with the view that an alteration in calcium homeostasis accompanies the diabetic state.