认识配方施肥 树立科学施肥观

文章分析了山西省农业施肥中存在的问题，指出树立科学的施肥观，实行配方施肥的方法。     

奶牛养殖规模户高产高效技术

从奶牛良种选购、奶牛产奶期饲养管理、干乳期饲养管理、平时饲养管理、疾病预防等方面进行了概述,提出对奶牛采取高产高效技术进行养殖,从而提高养殖效率的观点。并对奶牛养殖高效高产技术进行了概述。     

枯草芽孢杆菌水剂对西瓜枯萎病的田间防效研究

本试验通过35亿活芽孢／ml枯草芽孢杆菌水剂以浸种、灌根并用的方式防治西瓜枯萎病，田间试验结果表明：枯草芽孢杆菌水剂250倍液、500倍液对西瓜枯萎病具有明显的防治效果，同时对黄瓜秧苗正常生长无任何不良影响。此外，枯草芽孢杆菌水剂还对西瓜植株具有一定的促进生长作用。     

圈养野生动物传染病流行因素浅析

根据动物园的现状及对一些具体病例进行调查分析，将圈养野生动物传染病流行因素主要归纳为以下几个方面：广泛收集野外动物进行动物交换、饲养管理不当、观赏展览与游人接触。控制好以上几个方面的流行环节，是杜绝圈养野生动物传染病流行的关键。     

物欲的困扰与心灵的挣扎--徐坤城市题材小说论

以往对徐坤小说的研究中,对她创作中所揭示的社会转型期与知识分子“边缘化”问题、商业文化与男权文化境遇中的城市女性的生存困境与精神困境两个方面论的研究论述比较普遍深入,而对徐坤小说中所揭示的城市化进程中城市的变迁及城市人的异化现象和都市文明病关注、论述甚少,实际上,徐坤小说的背景是城市,因此,徐坤的小说对90年代以来,商品经济大潮中城市人面临的价值观的变迁、物欲的困扰和精神的异化及现代城市文明病等也有切身的感受,并在其创作中有独特的思考与文学表达。     

2型糖尿病合并冠心病患者的血脂异常分析

目的探讨2型糖尿病合并冠心病与血脂异常的关系。方法收集常熟市中医院老年康复中心2004年3月至2005年10月住院病人中2型糖尿病合并冠心病患者共77例,从本中心健康体检者中选取35例作为正常对照组(Ⅲ组),测定血脂水平并进行比较。结果Ⅰ组糖尿病合并心肌梗死组血浆甘油三酯(TG)、血浆总胆固醇(TC)、载脂蛋白B(ApoB)、低密度脂蛋白(LDL)明显升高,高密度脂蛋白(HDL)、载脂蛋白A(ApoA)显著降低,与Ⅱ组无心肌梗死组相比,差异显著(P<0.01),与Ⅲ组正常对照组相比较血TG水平升高,HDL降低(P<0.01)。结论TG升高及HDL的降低是2型糖尿病合并冠心病等心血管疾病发生、发展的主要危险因素。     

Regression of genetically determined polycystic kidney disease in murine organ culture

Summary Cystic kidneys from the mutant CPK strain of C57BL/6J mice were cultured in serum-free organ culture. During 120 h of incubation in chemically-defined medium, CPK cystic tubular changes underwent complete regression. Environmental factors regulate the expression of genetically determined polycystic kidney disease in this model.     

慢性肺心病的腹部体征

本文无选择的、随机的收集了1982年11月～1983年2月间,广州市、吉林市和通化市等11间医院571例患者,其中包括慢性肺心病320例,阻塞性肺气136例,其它心脏病115例,就腹部体征进行了互相间的对比观察。结果是慢性心病组288例(90.0％),阻塞性气肿组62例(45.5％)表现有剑突下搏动,而其它心脏病组只15例(13.0％)有此体征。此种搏动来源于垂悬的、搏动着的心脏(有时伴有右室肥厚),乃是心脏前下壁的搏动经膈肌传导而来,认为此征在慢性肺心病与其它性质心脏病之间可具诊断及鉴别诊断意义。同时发现慢性肺心病组241例(7.53％)阻塞性肺气肿组63例(46.3％)有明显腹壁紧张,其它心脏组18例(15.6％)有此征。这是由于长期的咳嗽、咳痰动作和腹式呼吸,致使腹肌运动过度所造成的。此征在慢性肺心病与其他性质心脏病间也有一定的诊断及鉴别诊断意义。至于肝脾肿大、腹水则无鉴别诊断意义。还指出在慢性肺心病并发严重支气管肺部感染的2例患者(0.62％),由于剧烈的毒血症和伴存的瀰漫性血管内凝血及低钾发生了麻痹性肠梗阻。表现明显腹部胀气、肠鸣音消失及便秘,连同患者本来就有的腹肌紧张体征,可能给人以“急腹症”的印象,对这类病例不要误作手术。     

Proteolytic generation and aggregation of peptides from transmembrane regions: lung surfactant protein C and amyloid β-peptide

The formation of amyloid fibrils is associated with several devastating diseases in humans and animals, including e.g. Alzheimers disease (AD) and the spongiform encephalopathies. Here, we review and discuss the current knowledge on two amyloid peptides: lung surfactant protein C (SP-C) and the amyloid -peptide (A), implicated in human lung disease and in AD, respectively. Both these hydrophobic peptides are derived from the transmembrane region of their precursor protein, and can transit from a monomeric -helical state to a -sheet fibril. The helices of SP-C and A are composed of amino acid residues with inherently higher propensities for strand than helix conformation. Their helical states are stabilized by a membrane environment, and loss of membrane association thus promotes structural conversion and fibril formation. We speculate that the loss of structural context for sequences with a high propensity for formation of sheets may be a common feature of amyloid formation in general.Received 9 July 2003; received after revision 15 August 2003; accepted 3 September 2003     

Unraveling the pathogenesis of Parkinson’s disease – the contribution of monogenic forms

The field of Parkinsons disease pathogenesis is rapidly evolving from the one of a monolithic and obscure entity into the one of a complex scenario with several known molecular players. The ongoing systematic exploration of the genome holds great promise for the identification of the genetic factors conferring susceptibility to the common non-Mendelian forms of this disease. However, most of the progress of the last 5 years has come from the successful mapping and cloning of genes responsible for rare Mendelian variants of Parkinsons disease. These discoveries are providing tremendous help in understanding the molecular mechanisms of this devastating disease. Here we review the genetics of the monogenic forms of Parkinsons disease. Moreover, we focus on the mechanisms of disease caused by -synuclein and parkin mutations, and the implications of this growing body of knowledge for understanding the pathogenesis of the common forms of the disease. Received 10 March 2004; received after revision 26 April 2004; accepted 29 April 2004