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排序方式: 共有684条查询结果,搜索用时 31 毫秒
641.
Deep venous thrombosis evaluation with limited-flip-angle, gradient- refocused MR imaging: preliminary experience 总被引:1,自引:0,他引:1
Sixteen patients (17 lower extremities) were prospectively examined with venography and limited-flip-angle, gradient-refocused magnetic resonance (MR) imaging for the presence or absence of deep venous thrombosis. Thrombosed vessels showed decreased-to-absent signal intensity, while patent vessels had high signal intensity. In 16 of 17 extremities, MR images allowed accurate detection and localization of the thrombi found with venography. In the remaining extremity, MR imaging allowed correct identification of thrombus in the iliac and femoral veins but incorrectly demonstrated clot in the calf and popliteal veins. MR imaging with limited-flip-angle, gradient-refocused pulse sequences appears to be a sensitive, noninvasive means of detecting deep venous thrombosis. 相似文献
642.
Use of a gradient intensifying screen for scoliosis radiography 总被引:1,自引:0,他引:1
643.
Oshima J; Yu CE; Piussan C; Klein G; Jabkowski J; Balci S; Miki T; Nakura J; Ogihara T; Ells J; Smith M; Melaragno MI; Fraccaro M; Scappaticci S; Matthews J; Ouais S; Jarzebowicz A; Schellenberg GD; Martin GM 《Human molecular genetics》1996,5(12):1909-1913
The Werner syndrome (WS) is a rare autosomal recessive progeroid disorder.
The Werner syndrome gene (WRN) has recently been identified as a member of
the helicase family. Four distinct mutations were previously reported in
three Japanese and one Syrian WS pedigrees. The latter mutation was
originally described as a 4 bp deletion spanning a spliced junction. It is
now shown that this mutation results in a 4 bp deletion at the beginning of
an exon. Nine new WRN mutations in 10 additional WS patients, both Japanese
and Caucasian, are described. These include three compound heterozygotes
(one Japanese and two Caucasian). The new mutations are located all across
the coding region.
相似文献
644.
Vereb M; Agulnik AI; Houston JT; Lipschultz LI; Lamb DJ; Bishop CE 《Molecular human reproduction》1997,3(1):55-59
Sequenced-tagged site (STS) analysis of the Y chromosome long arm (Yq) of
azoospermic males has identified a minimum common deleted region of several
hundred kilobases in approximately 13% of cases. A candidate azoospermia
gene, DAZ (deleted in azoospermia), has been isolated from this region. DAZ
has also been shown to be absent in severely oligozoospermic males albeit
at a much lower frequency. These data, although highly suggestive, do not
constitute formal proof that DAZ actually plays a role in azoospermia, as
no small intragenic deletions, rearrangements or point mutations in the
gene have been found. In this study we report the screening of DNA from 168
azoospermic/oligospermic males for the presence of the DAZ gene. Deletions
involving DAZ were detected in five out of 43 (11.6%) azoospermic males
whereas none were found in the remaining 125 oligospermic patients. We
present the genomic structure of the 5' end of the DAZ gene together with
its sequence analysis in 30 non-obstructed azoospermic males. No mutations
in DAZ were found in any of the patients sequenced. These data provide no
formal proof that DAZ is AZF. Thus the possibility is still valid that
another gene(s) mapping to the deletion interval may be responsible for, or
contribute to, the observed phenotypes. Alternatively, if DAZ is AZF, they
suggest that the most frequent cause of gene inactivation is via large
deletions possibly mobilized by Y chromosome repetitive sequences.
相似文献
645.
646.
Hereditary inclusion body myopathy maps to chromosome 9p1-q1 总被引:5,自引:2,他引:3
Mitrani-Rosenbaum S; Argov Z; Blumenfeld A; Seidman CE; Seidman JG 《Human molecular genetics》1996,5(1):159-163
Hereditary inclusion body myopathy (HIBM) is a unique disorder of unknown
etiology that typically occurs in individuals of Persian Jewish descent.
Distinguishing features of the disorder from other limb girdle myopathies
include elderly age of onset, ethnic predisposition, and sparing of the
quadriceps despite severe involvement of all other proximal leg muscles.
Involved muscles demonstrate fibers with rimmed vacuoles and filamentous
cytoplasmic and nuclear inclusions. Additional histological features are
accumulations of beta-amyloid protein and the absence of inflammatory
cells. To identify the chromosomal location of the gene responsible for
HIBM, nine Persian Jewish families with HIBM were evaluated. Genomewide
linkage analyses identified the recessive IBM locus on chromosome 9 band
p1-q1 (maximum lod score at D9S166 = 5.32, theta = 0.0). This region
contains the Friedreich's Ataxia gene, raising the possibility that HIBM
may be a related neurogenic disorder.
相似文献
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