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  • 1995-1999  (4)
  • 1996  (4)
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  • 1995-1999  (4)
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  • 1
    Electronic Resource
    Electronic Resource
    Fetal pathology in intrauterine death due to parvovirus B19 infection (1996)
    Oxford, UK : Blackwell Publishing Ltd
    BJOG 103 (1996), S. 0 
    Details
    ISSN: 1471-0528
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Objective To study the pathological features of fetuses dying because of parvovirus B19 infection, with particular reference to the presence of hydrops; to assess the usefulness of immunochemistry as a screening method for the detection of parvovirus infection at post-mortem examination.Design Review of clinical, sonographic, serological and pathological data; immunohistochemical staining of post-mortem tissue.Sample Cases of intrauterine fetal death occurring during the 18-month period January 1993 to June 1994 inclusive, referred for post-mortem examination to the Pathology Department, Royal Victoria Infirmary, Newcastle upon Tyne.Results Eleven cases of fetal death due to parvovirus infection were identified. Seven fetuses were less than 18-week size. Three fetuses showed conspicuous hydropic change. One of the 11 cases was detected for the first time by retrospective immunochemical screening. Of cases originating from the Newcastle district, parvovirus infection was responsible for about 10YO of all non-malformed fetal deaths occurring between 10 and 24 weeks of gestation referred for pathological examination.Conclusions During the period of study, parvovirus infection was a relatively common cause of mid-trimester fetal death. Many fetuses dying because of this infection are not noticeably hydropic, and the possibility of parvovirus infection should be considered in any case of intrauterine fetal death. Immunochemistry can be used to confirm the histopathological diagnosis, and may be of particular help where there is advanced autolysis; immunohistochemical screening may detect occasional cases not initially identified by examination of routinely stained tissue sections.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-0528.1996.tb09664.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Book review (1996)
    Springer
    Pediatric nephrology 10 (1996), S. 252-252 
    Details
    ISSN: 1432-198X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00862099
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    A case of neonatal Bartter’s syndrome (1996)
    Springer
    Pediatric nephrology 10 (1996), S. 414-418 
    Details
    ISSN: 1432-198X
    Keywords: Key words: Prostaglandins ; Tamm-Horsfall protein ; Bartter’s syndrome ; Captopril
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. We describe a child with a neonatal presentation of Bartter’s syndrome. Unlike infants previously described with a similar clinical presentation, the urinary excretion rate of prostaglandin E2 in this child was similar to normal children and Tamm-Horsfall protein was distributed normally in the thick ascending limb of the loop of Henle. The child failed to respond to indomethacin alone, but thrived after the addition of the angiotensin converting enzyme inhibitor, captopril.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004670050131
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Cloning and comparative mapping of a gene from the commonly deleted region of DiGeorge and Velocardiofacial syndromes conserved in C. elegans (1996)
    Springer
    Mammalian genome 7 (1996), S. 639-643 
    Details
    ISSN: 1432-1777
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. We have identified and cloned a gene, ES2, encoding a putative 476 amino acid protein with a predicted M r of 52,568. The gene is localized within the DiGeorge/Velocardiofacial syndrome locus on 22q11.2 and is deleted in all the patients in which a deletion within 22q11 could be demonstrated, with the exception of one patient. ES2 is expressed in all the tissues studied. Sequence comparison showed identity with five ESTs and at the amino acid level the sequence was highly similar to, and collinear with, a hypothetical C. elegans protein of unknown function. Mutation analysis was performed in 16 patients without deletion, but no mutation has been found. The cDNA sequence is conserved in mouse and is localized on MMU16B1-B3, known to contain a syntenic group in common with HSA 22q11.2.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003359900197
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    Paper (German National Licenses)
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