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1.
F R Ochsendorf H Sch?fer R Milbradt 《Der Hautarzt; Zeitschrift für Dermatologie, Venerologie, und verwandte Gebiete》1987,38(7):400-403
In an 80-year-old woman with pemphigus erythematosus, we demonstrated ANA as well as anti-DNA antibodies in the serum. This finding supports the argument that this skin disorder represents a combination of a disease of the pemphigus group with systemic lupus erythematosus. 相似文献
2.
Summary 84 forensic necropsy cases with a history of sudden unexpected death and where no acceptable cause of death was found at autopsy (= cases of sudden unexplained death, SUD) were found to have a significantly higher rate of influenza A (H 3 N 2) infection than did matched controls of the general population and a group of forensic necropsy cases with known cause of death (NON-SUD cases).By contrast, the group of SUD cases was found to have no significantly increased infection rate with influenza H 1 N 1 and B virus, parainfluenza viruses, RS virus, adenovirus, and cytomegalovirus.The influenza A associated SUD cases had a significantly higher rate of pathological and histological findings previously described for cases of primary viral pneumonia than did SUD cases without recent influenza A infection and NON-SUD cases.These findings suggest that virological examination of SUD cases could be helpful in order to determine the probable cause of death.A considerable portion of the influenza associated SUD cases occurred during interepidemic influenza periods. Therefore, such cases could be a useful source for monitoring the interepidemic spread of influenza virus. 相似文献
3.
Two fast magnetic resonance (MR) imaging techniques, advanced Fourier and partial-flip imaging, were used at 0.35 T to examine 21 patients with suspected intracranial lesions; the results were quantitatively compared with a conventional spin-echo study. Both of the fast MR techniques yielded a fourfold reduction in imaging time per section. The advanced Fourier sequence showed contrast that was identical to the conventional spin-echo study with signal-to-noise ratios of 58% and 57% for the first and second echoes, respectively. The partial-flip sequence showed a contrast of 109% and 57% for lesions versus substantia alba, and 107% and 78% for substantia grisea versus substantia alba relative to the first and second echoes of the conventional spin-echo study. The partial-flip sequence was particularly sensitive to magnetic susceptibility; this produced artifacts that may undermine the usefulness of partial flip for routine screening in certain parts of the brain. However, this susceptibility significantly improved the detection of intracranial hemorrhage when compared with the spin-echo sequence, particularly when combined with phase mapping of the partial-flip study. 相似文献
4.
Missense mutation in a von Willebrand factor type A domain of the alpha 3(VI) collagen gene (COL6A3) in a family with Bethlem myopathy 总被引:2,自引:0,他引:2
Pan TC; Zhang RZ; Pericak-Vance MA; Tandan R; Fries T; Stajich JM; Viles K; Vance JM; Chu ML; Speer MC 《Human molecular genetics》1998,7(5):807-812
The Bethlem myopathy is a rare autosomal dominant proximal myopathy
characterized by early childhood onset and joint contractures. Evidence for
linkage and genetic heterogeneity has been established, with the majority
of families linked to 21q22.3 and one large family linked to 2q37,
implicating the three type VI collagen subunit genes, COL6A1 (chromosome
21), COL6A2 (chromosome 21) and COL6A3 (chromosome 2) as candidate genes.
Mutations of the invariant glycine residues in the triple-helical
domain-coding region of COL6A1 and COL6A2 have been reported previously in
the chromosome 21-linked families. We report here the identification of a
G-->A mutation in the N-terminal globular domain-coding region of COL6A3
in a large American pedigree (19 affected, 12 unaffected), leading to the
substitution of glycine by glutamic acid in the N2 motif, which is
homologous to the type A domains of the von Willebrand factor. This
mutation segregated to all affected family members, to no unaffected family
members, and was not identified in 338 unrelated Caucasian control
chromosomes. Thus mutations in either the triple-helical domain or the
globular domain of type VI collagen appear to cause Bethlem myopathy.
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CC Thorn M Smith O Aziz TC Holme 《Annals of the Royal College of Surgeons of England》2013,95(1):52-56