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排序方式: 共有409条查询结果,搜索用时 31 毫秒
1.
C. Caroline Blackwell Donald M. Weir Anthony Busuttil Abdulrahman T. Saadi Steven D. Essery Mohammed W. Raza V.S. James D.A.C. Mackenzie 《FEMS immunology and medical microbiology》1994,9(2):91-100
Abstract Epidemiological factors associated with susceptibility to respiratory infections are similar to those associated with Sudden Infant Death Syndrome. Here we review the evidence that respiratory pathogens might be involved in some cases of Sudden Infact Death Syndrome in the context of factors identified in epidemiological studies of cot deaths: the age range affected; mother's smoking; respiratory viral infections; immunisation status. Both laboratory and epidimiological evidence suggests that vulnerability of infants to infectious agents depends on interactions between genetic, developmental and environmental factors that contribute to colonisation by microorganisms, the inflammatory and specific immune responses and the infants' physiological responses to inflammatory mediators. A model is proposed to explain how microorganisms might trigger a series of events resulting in some of these unexpected deaths and discusses how the present recommendations regarding child care practices might help reduce the numbers of Sudden Infant Death Syndrome cases associated with infectious agents. 相似文献
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S.D. Essery D.M. Weir V.S. James C.C. Blackwell A.T. Saadi A. Busuttil G. Tzanakaki 《FEMS immunology and medical microbiology》1994,9(1):15-22
Abstract There is evidence that the Lewisa blood group antigen is one of the receptors for a number of potentially pathogenic microorganisms. To determine how widely distributed the microbial adhesins are that bind this antigen, anti-idiotypic antibodies produced against monoclonal anti-Lewisa were used in coagglutination assays to screen a variety of species. The following were agglutinated: 7/7 strains of Staphylococcus aureus ; 10/19 (53%) strains of Neisseria meningitidis ; 8/13 (62%) strains of Haemophilus influenzae ; 1/3 strains of Helicobacter pylori ; 1/2 strains of Neisseria gonorrhoeae ; 1/2 strains of Candida albicans . The application of the anti-idiotypic antibodies to studies of host cell receptors, isolation of adhesins and development of new epidemiological typing reagents is discussed. 相似文献
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Muhammad W. Raza C. Caroline Blackwell Marie M. Ogilvie Abdulrahman T. Saadi John Stewart Robert A. Elton Donald M. Weir 《FEMS immunology and medical microbiology》1994,10(1):25-30
Abstract Viral glycoproteins G and F are expressed on the surface of cells infected with respiratory syncytial virus (RSV). We investigated the role of these proteins in the previously reported enhanced binding of Neisseria meningitidis to RSV-infected HEp-2 cells. Virus particles attached to bacteria were detected by immunofluorescence with flow cytometry. Binding of FITC-labelled bacteria to RSV-infected cells was significantly inhibited by monoclonal antibody against glycoprotein G. Unlabelled bacteria interfered with binding of the anti-G monoclonal antibody to these cells. These interactions were not found with a monoclonal antibody against glycoprotein F. We propose that glycoprotein G of RSV expressed on the surface of infected cells might act as an additional receptor for meningococci. 相似文献
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Christophe Biju-Duval Hajer Ennafaa Nicole Dennebouy Monique Monnerot Françoise Mignotte Ramon C. Soriguer Amel El Gaaïed Ali El Hili Jean-Claude Mounolou 《Journal of molecular evolution》1991,33(1):92-102
Summary A characterization was conducted on mitochondrial DNA (mtDNA) molecules extracted separately from 107 European rabbits (Oryctolagus cuniculus) both wild and domestic, 13 European hares (Lepus capensis), and 1 eastern cottontail (Sylvilagus floridanus). Experimentally this study took into account restriction site polymorphism, overall length variation of the noncoding region, and numbers of repeated sequences. Nucleotide divergences indicate that the mtDNAs from the three species derived from a common ancestor some 6–8 million years (Myr) ago. Every animal appeared heteroplasmic for a set of molecules with various lengths of the noncoding region and variable numbers of repeated sequences that contribute to them. This systematic heteroplasmy, most probably generated by a rate of localized mtDNA rearrangements high enough to counterbalance the cellular segregation of rearranged molecules, is a shared derived character of leporids.The geographic distribution of mtDNA polymorphism among wild rabbit populations over the western European basin shows that two molecular lineages are represented, one in southern Spain, the second over northern Spain, France, and Tunisia. These two lineages derived from a common ancestor some 2 Myr ago. Their present geographical distribution may be correlated to the separation of rabbits into two stocks at the time of Mindel glaciation.Finally the distribution of mtDNA diversity exhibits a mosaic pattern both at inter- and intrapopulation levels. 相似文献
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Summary Sequential cytogenetic studies of four patients with ataxia telangiectasia showed the progressive development of lymphocyte clones, each marked with a rearranged chromosome 14. Initial studies had shown random chromosomal breaks and rearrangements. Later studies in all patients showed nonrandom rearrangement of chromosome 14 with a breakpoint at 14q12 and with the distal segment translocated to either chromosome 14 or 7. The proportion of circulating lymphocytes carrying the marker tended to increase with time, accounting for the majority of the lymphocytes eventually in one case. The marked lymphocyte clones evolved further, as a result of loss of the small centric portions of the rearranged chromosome 14 (14pter14q12).Perhaps the abnormal clones in ataxia telangiectasia escape immunologic surveillance and flourish in an immunologically impaired environment. Subsequent to the loss of the centric portion of the rearranged chromosome 14, the cells may acquire additional capabilities that enhance malignant transformation. 相似文献
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H Elmahmoudi H Khodjet-El-Khil E Wigren A Jlizi K Zahra D Pellechia C Vinciguerra B Meddeb A Elgaaied Ben Ammar E Gouider 《Diagnostic pathology》2012,7(1):93
ABSTRACT: INTRODUCTION: Hemophilia A is an X linked recessive hemorrhagic disorder caused by mutations in the F8 gene that lead to qualitative and/or quantitative deficiencies of coagulation factor VIII (FVIII). Molecular diagnosis of hemophilia A is challenging because of the high number of different causative mutations that are distributed throughout the large F8 gene. Molecular studies of these mutations are essential in order to reinforce our understanding of their pathogenic effect responsible for the disorder. Aim In this study we have performed molecular analysis of 28 Tunisian hemophilia A patients and analyzed the F8 mutation spectrum. METHODS: We screened the presence of intron 22 and intron 1 inversion in severe hemophilia A patients by southern blotting and polymerase chain reaction (PCR). Detection of point mutations was performed by dHPLC/sequencing of the coding F8 gene region. We predict the potential functional consequences of novel missense mutations with bioinformatics approaches and mapping of their spatial positions on the available FVIII 3D structure. RESULTS: We identified 23 different mutations in 28 Tunisian hemophilia A patients belonging to 22 unrelated families. The identified mutations included 5 intron 22 inversions, 7 insertions, 4 deletions and 7 substitutions. In total 18 point mutations were identified, of which 9 are located in exon 14, the most mutated exonic sequence in the F8 gene. Among the 23 mutations, 8 are novel and not deposited in the HAMSTeRS database nor described in recently published articles. CONCLUSION: The mutation spectrum of Tunisian hemophilia A patients is heterogeneous with the presence of some characteristic features. Virtual slides The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1693269827490715. 相似文献
10.
ObjectivesTo assess the prevalence of noncommunicable disease (NCD) risk factors among Saudi university employees and their families; to estimate the cardiovascular risk (CVR) amongst the study population in the following 10years.MethodsThe NCD risk factors prevalence was estimated using a cross-sectional approach for a sample of employees and their families aged ≥ 18 years old, in a Saudi university (Riyadh in Kingdom of Saudi Arabia; KSA). WHO STEPwise standardized tools were used to estimate NCD risk factors and the Framingham Coronary Heart Risk Score calculator was used to calculate the CVR.ResultsFive thousand and two hundred subjects were invited, of whom 4,500 participated in the study, providing a response rate of 87%. The mean age of participants was 39.3±13.4 years. The majority of participants reported low fruit/vegetables consumption (88%), and physically inactive (77%). More than two thirds of the cohort was found to be either overweight or obese (72%), where 36% were obese, and 59% had abdominal obesity. Of the total cohort, 22–37% were found to suffer from dyslipidaemia, 22% either diabetes or hypertension, with rather low reported current tobacco use (12%). One quarter of participants was estimated to have >10% risk to develop cardiovascular disease within the following 10-years.ConclusionThe prevalence of NCD risk factors was found to be substantially high among the university employees and their families in this study. 相似文献