基于概率神经网络的核保风险分析模型

运用多元统计和概率神经网络的方法，结合实际研究项目，提出医疗保险中的核保风险分析模型．它是利用已知信息对投保人的患病风险以及属于何种风险类别进行分析和判别．其做法是首先对数据库用Kendall（tau-b）进行相关性检验，剔除导致疾病发牛的相关性较小的因素，然后选取17000条数据作为训练集，应用概率神经网络进行训练．训练完成后，选取另外1000条数据作为测试集，检验预测结果．这种模型用MATLAB软件实现，具有呵操作性，并可推广到相应的保险和余融等领域的风险分析问题中去。     

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     

Molecular basis of Alzheimer's disease

Despite an exponential production of data, Alzheimer's disease (AD) remains an enigma. Unresolved questions persist in the face of the heterogeneity of this neuropathology. Recent progress in understanding mechanisms for AD results from the study of amyloid precursor protein (APP) metabolism and the involvement of senile plaque-associated proteins. In addition to the amyloid cascade hypothesis, alternative schemes emerge, in which the amyloid peptide is not the primary effector of the disease. Perturbations of vesicular trafficking, the cytoskeletal network, and membrane cholesterol distribution could be central events. Furthermore, since the physiological role of APP, presenilins, and apolipoprotein E in the central nervous system are not completely understood, their involvement in AD etiology remains speculative. New actors have to be found to try to explain sporadic cases and non-elucidated familial cases.     

Molecular modeling of the ion channel-like nanotube structure of amyloid β-peptide

The ion channel-like nanotube structure of the oligomers of amyloid β-peptide (Aβ) was first investi-gated by molecular modeling. The results reveal that the hydrogen bond net is one of the key factors to stabilize the structure. The hydrophobicity distribution mode of the side chains is in favor of the structure inserting into the bilayers and forming a hydrophilic pore. The lumen space is under the control of the negative potential,weaker but spreading continuously,to which the cation selectivity attributes; meanwhile,the alternate distribution of the stronger positive and negative potentials makes the electrostatic distribution of the structure framework balance,which is also one of the key factors stabilizing the structure. The results lay the theoretical foundation for illuminating the structure stability and the ion permeability,and give a clue to elucidating the molecular mechanism of Alzheimer's dis-ease (AD) and designing novel drugs to prevent or reverse AD at the root.     

Immune response in cattle inoculated with the recombinant complete polyprotein of foot-and-mouth disease virus from Bombyx mori larvae

The intact open reading frame (ORF) of foot-and-mouth disease virus (FMDV) Asia I/XJ strain was am- plified by RT-PCR and inserted into the transfer vector pVL1393 to generate plasmid pVL-ORF. Bm-N cells were transfected with pVL-ORF and linearized Bm-BacPAK6 DNA, and the recombinant silkworm baculovirus Bm-ORF containing the full ORF of FMDV was obtained. The results of indirect im- munofluorescence assay (IFA) showed that Bm-ORF could be expressed efficiently in Bm-N cell. After inoculating the early 5th instar larvae of silkworm, the polyprotein of FMDV could be detected by sandwich ELISA and empty capsid-like particles could be observed under the electron microscope. Expression products from silkworm were used as the antigen to immunize the cattle. The specific an- tibody was induced in all vaccinated animals. The immunized cattle were challenged with the virulent FMDV Asia I/XJ strain, two of the four cattle were completely protected and clinical symptoms were alleviated and delayed in the others. The results suggest that this strategy might be used to develop the new subunit FMDV vaccine.     

Molecular mechanism of abnormal aggresation of α-synuclein

The abnormal aggregation of α-synuclein （α-Syn） is thought to be closely associated with Parkinson＇s disease, but the pathogenesis is still unclear. In this review, we survey the latest development in the molecular mechanism of abnormal α-Syn aggregation, especially in the aspects of the core sequences, aggregation inhibitors, structural transformation and filament morphologies. By exploring the mechanism of α-Syn aggregation, we will have a better understanding of the disease pathogenesis, and develop strategies for preventing and treating this severe disease.