应用PAPS免疫微球法快速诊断家畜锥虫病

ＰＡＰＳ锥虫快速诊断试剂，是中国农业科学院上海家畜寄生虫病研究所研制成功的一种新型的载体微球，它与伊氏锥虫抗原交联所制备的锥虫快速诊断液具有特异性强、敏感性高，重复性好、快速、简便的特点。笔者应用锥虫快速诊断液检测１４９头锥虫阳性病牛（见虫），阳性检出率为９８．７％。对２２５头非疫区阴性牛进行检测，阴性符合率为９９．６％。ＰＡＰＳ试验与间接血凝试验的符合率为９６．１％。对２２７７头耕牛血清和血纸两     

呼吸门控快速自旋回波序列MRCP成像在胆管疾病检查中的应用

目的：评价1．5T MR采用快速自旋回波呼吸门控制T2加权脂肪抑制三维MR水成像技术在胰胆道疾患病人中对胆道的显示及临床诊断效果，方法：采用了FSE序列对32例被怀疑有胆总管疾患的病人用此技术检查成像，然后与术后结果或ERCP图像进行比较评价肝内外胆管的显示情况。结果：32例中均具有诊断性的MR图像，经为59．4％－100．0％，定位诊断率100％,定性诊断率90．6％，结论：1．5 TMR FSE序列重T2加权，呼吸门控，脂肪抑制MRCP成功率高，定位诊断准确，定性率高，是一种无创伤，患者可接受的显影方法。     

禽流感病毒的变异与效应

流感病毒抗原变异与流感的流行大小、预防、控制密切相关.近年来分子生物学技术的发展,越来越多的新方法、新技术用于流感病毒抗原变异的研究,本文对近年来流感病毒抗原变异的原因及其引起的效应作一扼要综述.     

聚合酶链反应对性传播疾病病原体检测的意义

应用聚合酶链反应技术（PCR）对184例男性性传播疾病进行检测，检出单纯淋菌感染79例（43％）；衣原体感染42例（22．8％）；解脲支原体感染28例（15．2％）；混合感染26例（14．1％），认为PCR技术对STD的诊断具有快速、准确的效果。     

180例急腹症的超声显像诊断分析

将１８０例各种病因所致的急腹症患者的超声检查结果与手术和临床最后诊断进行对照分析，结果超声诊断符合率为９１．１％，误诊率５．０％，漏诊率３．９％，讨论了肠梗阻，实质性脏器与空腹脏器破裂的超声图像特征以及探查中的经验和体会，提示超声显像是急腹症的诊断和鉴别诊断的一种重要检查方法。     

传染性法氏囊病病毒分子生物学研究的一些进展

对IBDV近年来的分子生物学方面的研究进展进行概况，主要包括IBDv的基因组结构及理化特性、病毒蛋白、不同型IBDV变异的分子基础和分子生物学诊断技术等，以探讨利用病毒重要基因核酸序列的差异进行IBDV分子流行病学研究及病毒各致病型快速鉴别诊断的可能性．     

磁共振成像诊断听神经瘤的价值

目的：为评价磁共振成像（ＭＲＩ）诊断听神经瘤的价值，本文分析４４例听神经瘤ＭＲＩ表现，探讨该瘤囊性的病理基础及鉴别诊断。方法：采用德国Ｓｉｅｍｅｎｓ１．０Ｔ超导ＭＲ系统，常规ＳＥ序列或快速ＳＥ序列Ｔ１中权，Ｔ２加权成像，层厚３－７ｍｍ，其中３６例静脉内注射Ｇｄ－ＤＴＰＡ增强扫描。结果：本组４６个肿瘤中，有２个（４．３％）地内耳道ＩＡＣ内；６个（１３％）仅限于桥小脑角（ＣＰＡ）；３８个（８２．６％）     

猪瘟病毒分子生物学诊断的研究进展

猪瘟是由猪瘟病毒引起的猪的急性、热性、高度接触性传染病，严重危害我国养猪业。尽管中国很早就研制成功了猪瘟兔化弱毒疫苗。但近年来猪瘟的流行和发病特点发生了很大的变化，很多地区和猪场不断出现非典型猪瘟、温和型猪瘟，给该病的诊断带来了困难。近年来，猪瘟病毒分子生物学诊断方法的研究进展迅速，为猪瘟的快速、准确诊断起到了重要的作用。从聚合酶链式反应技术、核酸探针技术、DNA芯片技术等方面对猪瘟病毒的分子生物学诊断方法进行了综述。     

猴副流感病毒(SV5)研究进展

猴副流感病毒SV5(simian virus 5)在病原学分类上属于副流感病毒5型,它在猴群中常以隐性感染的方式存在,由于该病毒会对猴源细胞生产的生物制品造成污染,在实验动物和生物制品的质量控制中须对该病毒进行监测。本文就猴副流感病毒SV5的生物学,分子生物学特性,遗传复制特征,相关     

外伤性脾破裂超声诊断临床分析

目的：探讨B超检查对脾破裂的诊断率与临床应用价值．方法：对33例B超诊断脾破裂与术后发现进行对照分析，经手术证实与其完全相符．结果：B超检查准确率为95．2％．结论：B超对脾破裂能够做出明确诊断，并能发现损伤的轻重程度及其它合并伤，直观、简单、准确率高．     

Drosophila RNAi screen identifies host genes important for influenza virus replication

All viruses rely on host cell proteins and their associated mechanisms to complete the viral life cycle. Identifying the host molecules that participate in each step of virus replication could provide valuable new targets for antiviral therapy, but this goal may take several decades to achieve with conventional forward genetic screening methods and mammalian cell cultures. Here we describe a novel genome-wide RNA interference (RNAi) screen in Drosophila that can be used to identify host genes important for influenza virus replication. After modifying influenza virus to allow infection of Drosophila cells and detection of influenza virus gene expression, we tested an RNAi library against 13,071 genes (90% of the Drosophila genome), identifying over 100 for which suppression in Drosophila cells significantly inhibited or stimulated reporter gene (Renilla luciferase) expression from an influenza-virus-derived vector. The relevance of these findings to influenza virus infection of mammalian cells is illustrated for a subset of the Drosophila genes identified; that is, for three implicated Drosophila genes, the corresponding human homologues ATP6V0D1, COX6A1 and NXF1 are shown to have key functions in the replication of H5N1 and H1N1 influenza A viruses, but not vesicular stomatitis virus or vaccinia virus, in human HEK 293 cells. Thus, we have demonstrated the feasibility of using genome-wide RNAi screens in Drosophila to identify previously unrecognized host proteins that are required for influenza virus replication. This could accelerate the development of new classes of antiviral drugs for chemoprophylaxis and treatment, which are urgently needed given the obstacles to rapid development of an effective vaccine against pandemic influenza and the probable emergence of strains resistant to available drugs.     

Molecular patterns of avian influenza A viruses

Avian influenza A viruses could get across the species barrier and be fatal to humans. Highly pathogenic avian influenza H5N1 virus was an example. The mechanism of interspecies transmission is not clear as yet. In this research, the protein sequences of 237 influenza A viruses with different subtypes were transformed into pseudo-signals. The energy features were extracted by the method of wavelet packet decomposition and used for virus classification by the method of hierarchical clustering. The clustering results showed that five patterns existed in avian influenza A viruses, which associated with the phenotype of interspecies transmission, and that avian viruses with patterns C and E could across species barrier and those with patterns A, B and D might not have the abilities. The results could be used to construct an early warning system to predict the transmissibility of avian influenza A viruses to humans.     

IFITM3 restricts the morbidity and mortality associated with influenza

The 2009 H1N1 influenza pandemic showed the speed with which a novel respiratory virus can spread and the ability of a generally mild infection to induce severe morbidity and mortality in a subset of the population. Recent in vitro studies show that the interferon-inducible transmembrane (IFITM) protein family members potently restrict the replication of multiple pathogenic viruses. Both the magnitude and breadth of the IFITM proteins' in vitro effects suggest that they are critical for intrinsic resistance to such viruses, including influenza viruses. Using a knockout mouse model, we now test this hypothesis directly and find that IFITM3 is essential for defending the host against influenza A virus in vivo. Mice lacking Ifitm3 display fulminant viral pneumonia when challenged with a normally low-pathogenicity influenza virus, mirroring the destruction inflicted by the highly pathogenic 1918 'Spanish' influenza. Similar increased viral replication is seen in vitro, with protection rescued by the re-introduction of Ifitm3. To test the role of IFITM3 in human influenza virus infection, we assessed the IFITM3 alleles of individuals hospitalized with seasonal or pandemic influenza H1N1/09 viruses. We find that a statistically significant number of hospitalized subjects show enrichment for a minor IFITM3 allele (SNP rs12252-C) that alters a splice acceptor site, and functional assays show the minor CC genotype IFITM3 has reduced influenza virus restriction in vitro. Together these data reveal that the action of a single intrinsic immune effector, IFITM3, profoundly alters the course of influenza virus infection in mouse and humans.     

Avian flu: influenza virus receptors in the human airway

Although more than 100 people have been infected by H5N1 influenza A viruses, human-to-human transmission is rare. What are the molecular barriers limiting human-to-human transmission? Here we demonstrate an anatomical difference in the distribution in the human airway of the different binding molecules preferred by the avian and human influenza viruses. The respective molecules are sialic acid linked to galactose by an alpha-2,3 linkage (SAalpha2,3Gal) and by an alpha-2,6 linkage (SAalpha2,6Gal). Our findings may provide a rational explanation for why H5N1 viruses at present rarely infect and spread between humans although they can replicate efficiently in the lungs.     

Aberrant innate immune response in lethal infection of macaques with the 1918 influenza virus

The 1918 influenza pandemic was unusually severe, resulting in about 50 million deaths worldwide. The 1918 virus is also highly pathogenic in mice, and studies have identified a multigenic origin of this virulent phenotype in mice. However, these initial characterizations of the 1918 virus did not address the question of its pathogenic potential in primates. Here we demonstrate that the 1918 virus caused a highly pathogenic respiratory infection in a cynomolgus macaque model that culminated in acute respiratory distress and a fatal outcome. Furthermore, infected animals mounted an immune response, characterized by dysregulation of the antiviral response, that was insufficient for protection, indicating that atypical host innate immune responses may contribute to lethality. The ability of influenza viruses to modulate host immune responses, such as that demonstrated for the avian H5N1 influenza viruses, may be a feature shared by the virulent influenza viruses.     

计算机病毒解析与防范

计算机病毒被喻为 2 1世纪计算机犯罪的五大手段之一 ,并排序为第二。计算机病毒的攻击性 ,在于它能够破坏各种程序并蔓延于应用领域。目前世界上上亿用户受着计算机病毒的困扰 ,有些还陷入极度的恐慌之中。事实上人们产生上述不安的原因 ,在与对计算机病毒的误解 ,广大计算机用户有必要对计算机病毒的一些知识有一个比较明确的认识和全面的科学态度     

Long-term evolution and transmission dynamics of swine influenza A virus

Swine influenza A viruses (SwIV) cause significant economic losses in animal husbandry as well as instances of human disease and occasionally give rise to human pandemics, including that caused by the H1N1/2009 virus. The lack of systematic and longitudinal influenza surveillance in pigs has hampered attempts to reconstruct the origins of this pandemic. Most existing swine data were derived from opportunistic samples collected from diseased pigs in disparate geographical regions, not from prospective studies in defined locations, hence the evolutionary and transmission dynamics of SwIV are poorly understood. Here we quantify the epidemiological, genetic and antigenic dynamics of SwIV in Hong Kong using a data set of more than 650 SwIV isolates and more than 800 swine sera from 12?years of systematic surveillance in this region, supplemented with data stretching back 34?years. Intercontinental virus movement has led to reassortment and lineage replacement, creating an antigenically and genetically diverse virus population whose dynamics are quantitatively different from those previously observed for human influenza viruses. Our findings indicate that increased antigenic drift is associated with reassortment events and offer insights into the emergence of influenza viruses with epidemic potential in swine and humans.     

Evidence for host-cell selection of influenza virus antigenic variants

Extensive antigenic variability and a capricious epidemiology are characteristics of influenza A and B viruses of man. The haemagglutinin (HA) undergoes frequent and progressive antigenic drift as a result of selection, under immunological pressure, of viruses possessing alterations in the amino acid sequences at specific sites in the molecule. Here we present evidence for an additional selection mechanism for antigenic variants of influenza virus that depends on differing host cell tropisms of virus subpopulations. These studies were initiated after earlier observations of the occurrence of a marked degree of antigenic variation during passage of laboratory strains of influenza virus in eggs and cell cultures (J.C.J., in preparation). We have now shown that cultivation of influenza B viruses in eggs selects subpopulations which are antigenically distinct from virus from the same source grown in mammalian cell cultures. As antigenic characterization of influenza virus strains for epidemiological purposes and for the preparation of influenza vaccines conventionally relies on the cultivation of virus in eggs, our findings may have important practical implications for vaccine design and efficacy.     

Enhanced virulence of influenza A viruses with the haemagglutinin of the 1918 pandemic virus

The 'Spanish' influenza pandemic of 1918-19 was the most devastating outbreak of infectious disease in recorded history. At least 20 million people died from their illness, which was characterized by an unusually severe and rapid clinical course. The complete sequencing of several genes of the 1918 influenza virus has made it possible to study the functions of the proteins encoded by these genes in viruses generated by reverse genetics, a technique that permits the generation of infectious viruses entirely from cloned complementary DNA. Thus, to identify properties of the 1918 pandemic influenza A strain that might be related to its extraordinary virulence, viruses were produced containing the viral haemagglutinin (HA) and neuraminidase (NA) genes of the 1918 strain. The HA of this strain supports the pathogenicity of a mouse-adapted virus in this animal. Here we demonstrate that the HA of the 1918 virus confers enhanced pathogenicity in mice to recent human viruses that are otherwise non-pathogenic in this host. Moreover, these highly virulent recombinant viruses expressing the 1918 viral HA could infect the entire lung and induce high levels of macrophage-derived chemokines and cytokines, which resulted in infiltration of inflammatory cells and severe haemorrhage, hallmarks of the illness produced during the original pandemic.     

Differential roles of MDA5 and RIG-I helicases in the recognition of RNA viruses

The innate immune system senses viral infection by recognizing a variety of viral components (including double-stranded (ds)RNA) and triggers antiviral responses. The cytoplasmic helicase proteins RIG-I (retinoic-acid-inducible protein I, also known as Ddx58) and MDA5 (melanoma-differentiation-associated gene 5, also known as Ifih1 or Helicard) have been implicated in viral dsRNA recognition. In vitro studies suggest that both RIG-I and MDA5 detect RNA viruses and polyinosine-polycytidylic acid (poly(I:C)), a synthetic dsRNA analogue. Although a critical role for RIG-I in the recognition of several RNA viruses has been clarified, the functional role of MDA5 and the relationship between these dsRNA detectors in vivo are yet to be determined. Here we use mice deficient in MDA5 (MDA5-/-) to show that MDA5 and RIG-I recognize different types of dsRNAs: MDA5 recognizes poly(I:C), and RIG-I detects in vitro transcribed dsRNAs. RNA viruses are also differentially recognized by RIG-I and MDA5. We find that RIG-I is essential for the production of interferons in response to RNA viruses including paramyxoviruses, influenza virus and Japanese encephalitis virus, whereas MDA5 is critical for picornavirus detection. Furthermore, RIG-I-/- and MDA5-/- mice are highly susceptible to infection with these respective RNA viruses compared to control mice. Together, our data show that RIG-I and MDA5 distinguish different RNA viruses and are critical for host antiviral responses.