左旋多巴的合成与提取

左旋多巴 (L DOPA)是治疗帕金森病的有效药物。L DOPA的生产方法有化学合成、从植物中提取和微生酶物转化等 ,其中利用微生物的酪氨酸酚解酶以邻苯二酚、丙酮酸和氨为底物合成L DOPA被证明是一种最经济且最有前途的方法。应用基因工程技术构建高效菌株。左旋多巴的提取有多种方法 ,其中向反应体系中加入晶种使多巴从反应体系中析出 ,除去菌体和杂质 ,再进行重结晶可得到纯度较高的多巴是一种很好的方法。     

细胞分裂图形图像的判断及应用

细胞分裂图形图像的判断,是教学的重点,也是学习的难点.掌握一套行之有效的判断方法,将提高解题速度和正确率.     

蛋白酶体结构和活性调节机制的研究进展

蛋白酶体负责细胞内绝大多数蛋白质的降解,几乎对生物体所有的生命活动都具有调控作用.蛋白酶体功能异常能够导致很多疾病.近期,研究者们在蛋白酶体的结构分析和活性调节机制等方面的研究都获得了重要的突破.本文综述了有关蛋白酶体结构和活性调控机制,包括转录调控、翻译后修饰、组装机制等的研究进展,这些对蛋白酶体新的认识将为蛋白酶体相关疾病的研究及相应药物的开发带来新的思路.对于目前蛋白酶体抑制剂的研发本文也做了简要的介绍.     

Differentiation of Two Types of Basophils In The Adenohypophysis of The Rat and The Mouse

Pituitaries are fixed for 24 hr. in Bouin's fluid containing 0.5% trichloroacetic acid instead of 5% acetic acid, or in a mixture of 9 parts SUSA and 1 part saturated aqueous solution of picric acid. They are embedded in paraffin and horizontal sections are cut at 3-4 μ. The staining method consists of 3 phases: (a) immersion in aldehyde-fuchsin for the selective demonstration of the beta cell granules, (b) staining of the nuclei with Ehrlich's hematoxylin and (c) a rapid one-step counterstain with light green and orange G dissolved in a phosphotungstic-acetic acid mixture for the differentiation of the acidophilic and the delta cell granules.     

The Atlatl: The Physics of Function and Performance

Abstract

An examination of the physical laws behind the function and performance of the atlatl-both with and without weights-is presented. The increased distance a dart can be thrown with the atlatl is a function of the increased mechanical advantage which the atlatl provides by increasing the length of the moment arm. The location of weight on an atlatl is shown to produce a performance less than or equal to that achieved without a weight. It is proposed, although unproven, that the addition of a weight to an atlatl acts as a stabilizing device to reduce side to side oscillations and thereby providing greater control. The penetration of a projectile thrown with an atlatl is greater than that of one thrown by hand and about equal to that of an arrow shot from a bow.     

三峡库区植物资源及保护

三峡库区有丰富的植物资源。据资料统计表明：库区有维管束植物6088种,分属于208科,1428属,约占全国植物总数的20％左右;有珍稀植物57种,占全国珍稀植物的14.7％。库区有植被类型78个,有药用植物3500种,隶属于603属,174科,同时有丰富的粮食经济植物和野生香料植物资源．随着三峡工程的修建,直接或间接地破坏了植物的生存环境,因此,加强法制宣传教育,提高环境保护意识．建立自然保护区和植物园等措施,有效的保护了库区植物资源,改善了生态环境的质量,促进了人与自然的和谐发展。     

脱落酸应答基因的表达调控及其与逆境胁迫的关系

本文对生长调节物质脱落酸应答基因的类型、结构和功能特征、表达调控的分子机理,以及近年来的热点问题：ABA在逆境胁迫反应中的作用机制,ABA应答基因与逆境胁迫的关系等作了较全面的综述。     

A型流感病毒非结构蛋白的功能及临床应用

NS1蛋白作为A型流感病毒的非结构蛋白,最初的研究着重于它对宿主细胞蛋白质合成的抑制作用方面考虑.随着研究的深入,对其基因的进化、蛋白质的抗原性作了详细的研究,同时发现流感病毒的NS1蛋白与流感病毒所诱导的细胞凋亡之间存在一定的联系,其对凋亡的调节作用与流感病毒感染的细胞是否产生干扰素及其所感染的细胞系直接相关.NS1蛋白能够抑制病毒感染细胞干扰素的产生,在流感病毒拮抗干扰素的抗病毒效应中发挥了重要的作用,许多研究表明,这种干扰素拮抗作用可能与流感病毒的毒力有关.由于传统疫苗的广泛应用,NS1蛋白在临床应用中作为鉴别诊断免疫禽和自然感染禽的检测抗原具有广阔的前景.     

老年人冠状动脉狭窄程度与超敏C反应蛋白及脂蛋白(a)水平的研究

目的:探讨老年人冠脉狭窄程度与超敏C反应蛋白(hs-CRP)及脂蛋白(a()LP(a))水平的关系。方法:分析研究260例年龄>60岁的经行冠脉造影检查明确诊断冠心病的患者的冠脉狭窄程度,以及术前空腹采血测定其hs-CRP及LP(a)的水平。结果:①冠脉病变组(186例)与对照组(76例)比较,冠脉病变组Lp(a)和hs-CRP水平分别为(3.30±4.30)mg/L和(146.30±3.21)mg/L,对照组分别为(1.32±2.32)mg/L和(40.26±2.44)mg/L,二者存在差别(P<0.01),差别有统计学意义。②各个亚组病与对照组比较各亚组(单支病变组、双支病变组、三支病变组)hs-CRP和LP(a)与对照组相比较存在明显差异,单支病变组51例,双支病变组72例,三支病变组63例。单支病变组hs-CRP和Lp(a)水平分别为(2.11±1.31)mg/L和(41.58±2.32)mg/L,双支病变组分别为(2.97±2.11)mg/L和(47.12±1.21)mg/L,三支病变组分别为(3.42±2.16)mg/L和(60.13±3.54)mg/L,P<0.05,差别有统计学意义,且随着病变支数的增加,hs-CRP和LP(a)呈增高趋势。并行单因素相关分析,hs-CRP和LP(a)与冠脉病变支数有正相关关系(P<0.05)。③男性病变组(107例)和女性病变组(79例),男性组hs-CRP和LP(a)水平分别为(1.87±2.11)mg/L和(43.60±2.18)mg/L,女性病变组hs-CRP和LP(a)水平分别为(3.33±1.70)mg/L和(50.77±2.47)mg/L,二者存在差别,P>0.05,差别无统计学意义。结论:老年人冠脉狭窄程度与血清Lp(a)和hs-CRP水平变密切相关,呈正相关,老年男性冠心病患者与女性冠心病患者相比,血清Lp(a)和hs-CRP水平无显著差异。     

The Causes and Prevention of Cancer: The Role of Environment

The idea that synthetic chemicals such as DDT are major contributors to human cancer has been inspired, in part, by Rachel Carson's passionate book, Silent Spring. This chapter discusses evidence showing why this is not true. We also review research on the causes of cancer, and show why much cancer is preventable.Epidemiological evidence indicates several factors likely to have a major effect on reducing rates of cancer: reduction of smoking, increased consumption of fruits and vegetables, and control of infections. Other factors are avoidance of intense sun exposure, increases in physical activity, and reduction of alcohol consumption and possibly red meat. Already, risks of many forms of cancer can be reduced and the potential for further reductions is great. If lung cancer (which is primarily due to smoking) is excluded, cancer death rates are decreasing in the United States for all other cancers combined.Pollution appears to account for less than 1% of human cancer; yet public concern and resource allocation for chemical pollution are very high, in good part because of the use of animal cancer tests in cancer risk assessment. Animal cancer tests, which are done at the maximum tolerated dose (MTD), are being misinterpreted to mean that low doses of synthetic chemicals and industrial pollutants are relevant to human cancer. About half of the chemicals tested, whether synthetic or natural, are carcinogenic to rodents at these high doses. A plausible explanation for the high frequency of positive results is that testing at the MTD frequently can cause chronic cell killing and consequent cell replacement, a risk factor for cancer that can be limited to high doses. Ignoring this greatly exaggerates risks. Scientists must determine mechanisms of carcinogenesis for each substance and revise acceptable dose levels as understanding advances.The vast bulk of chemicals ingested by humans is natural. For example, 99.99% of the pesticides we eat are naturally present in plants to ward off insects and other predators. Half of these natural pesticides tested at the MTD are rodent carcinogens. Reducing exposure to the 0.01% that are synthetic will not reduce cancer rates. On the contrary, although fruits and vegetables contain a wide variety of naturally-occurring chemicals that are rodent carcinogens, inadequate consumption of fruits and vegetables doubles the human cancer risk for most types of cancer. Making them more expensive by reducing synthetic pesticide use will increase cancer. Humans also ingest large numbers of natural chemicals from cooking food. Over a thousand chemicals have been reported in roasted coffee: more than half of those tested (19/28) are rodent carcinogens. There are more rodent carcinogens in a single cup of coffee than potentially carcinogenic pesticide residues in the average American diet in a year, and there are still a thousand chemicals left to test in roasted coffee. This does not mean that coffee is dangerous but rather that animal cancer tests and worst-case risk assessment, build in enormous safety factors and should not be considered true risks.The reason humans can eat the tremendous variety of natural chemical "rodent carcinogens" is that humans, like other animals, are extremely well protected by many general defense enzymes, most of which are inducible (i.e., whenever a defense enzyme is in use, more of it is made). Since the defense enzymes are equally effective against natural and synthetic chemicals one does not expect, nor does one find, a general difference between synthetic and natural chemicals in ability to cause cancer in high-dose rodent tests.The idea that there is an epidemic of human cancer caused by synthetic industrial chemicals is false. In addition, there is a steady rise in life expectancy in the developed countries. Linear extrapolation from the maximum tolerated dose in rodents to low level exposure in humans has led to grossly exaggerated mortality forecasts.Such extrapolations can not be verified by epidemiology. Furthermore, relying on such extrapolations for synthetic chemicals while ignoring the enormous natural background, leads to an imbalanced perception of hazard and allocation of resources. It is the progress of scientific research and technology that will continue to lengthen human life expectancy.Zero exposure to rodent carcinogens cannot be achieved. Low levels of rodent carcinogens of natural origin are ubiquitous in the environment. It is thus impossible to obtain conditions totally free of exposure to rodent carcinogens or to background radiation. Major advances in analytical techniques enable the detection of extremely low concentrations of all substances, whether natural or synthetic, often thousands of times lower than could be detected 30 years ago.Risks compete with risks: society must distinguish between significant and trivial risks. Regulating trivial risks or exposure to substances erroneously inferred to cause cancer at low-doses, can harm health by diverting resources from programs that could be effective in protecting the health of the public. Moreover, wealth creates health: poor people have shorter life expectancy than wealthy people. When money and resources are wasted on trivial problems, society's wealth and hence health is harmed.     

干扰素通路调控与自身免疫疾病

干扰素信号通路是细胞抵抗病原微生物侵染的重要防线。通过识别病源相关模式分子、激活下游通路,干扰素的表达被显著上调并分泌于细胞外,作用于自身和周围细胞,引发众多下游基因的转录激活。这些基因产物直接参与抗侵染过程或调控机体免疫反应。干扰素信号通路需要被正确调控,其异常激活会导致炎症和自身免疫疾病的发生。正确地识别“自己”和“非己”分子是首要的一步。鉴于干扰素通路所抵抗的微生物侵染中,核酸分子是重要的免疫原性分子,内源性核酸分子的代谢调控显得尤为重要。细胞编码一系列参与核酸代谢的酶,这些蛋白质功能的发挥对保持细胞核酸稳态至关重要。以单基因突变引发的自身免疫疾病Aicardi-Goutières综合征为例,目前发现9种基因可突变致病,均来自DNA代谢相关的和RNA代谢相关的基因。尽管这9种基因突变都导致干扰素通路的异常激活,但中间所依赖的参与蛋白并不相同。可见,同样症状的疾病,其致病机理也可能不同,这也将影响有效治疗方案的确定,凸显基因检测在诊治自身免疫疾病中的必要性。本综述通过阐述细胞内环境稳态对干扰素通路正确识别“自己”和“非己”的重要作用,帮助理解自身免疫疾病的发病机理。