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Hung J. Kim Torrance Jackson Konrad Noben–Trauth 《Journal of the Association for Research in Otolaryngology》2003,4(1):83-90
Genetic studies on spontaneous mouse mutants with hearing defects have provided important insights into the function of genes
expressed in inner ear hair cells. Here we report on our genetic analyses of the deaf mutants varitint-waddler (Va) and jerker
(Espnje). A high-resolution genetic map localizes VaJ to a 0.14 ± 0.08 cM region between D3Mit85 and D3Mit259 on distal chromosome
3. By comparative mapping, the human ortholog resides at 1p22.3 between markers D1S3449 and D1S2252. To study the effect of
different genetic backgrounds on the hearing phenotype, Espnje and VaJ were crossed to various inbred strains. Auditory-evoked
brainstem response tests on F2 progeny demonstrate that expression, inheritance, and penetrance of the hearing phenotype are
solely controlled by the mutant allele. To test for a genetic interaction between Espnje and Cdh23v, auditory function was
analyzed in double heterozygotes; no significant increases of thresholds of sound pressure levels were observed. The results
establish the framework for cloning the Va gene and provide valuable insights into the genetics of deafness mutations in the
mouse. 相似文献
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Transcatheter Closure of Atrial Septal Defects by the “Buttoned” Device: Complications and Need for Surgical Revision 总被引:2,自引:0,他引:2
H. P. Gildein S. Däbritz A. Geibel K. Sarai J. Vazquez–Jimenez W. Hügel R. Mocellin 《Pediatric cardiology》1997,18(5):328-331
Immediate and medium-term experience with transcatheter closure of a secundum atrial septal defect by the ``buttoned' device
in seven patients is reported. Complications occurred in two patients during the procedure. In one patient with complications,
the occluder was partly released in the right atrium. All efforts to correct its position were unsuccessful and caused considerable
deformation of the device, which had to be removed surgically. In the other patient with complications, disconnection of the
occluder and counteroccluder occurred immediately after removal of the loading wire. Both parts were retrieved by catheter.
Five patients had uneventful closure of the atrial septal defect. On follow-up, however, displacement of the device towards
the mitral valve was observed in two patients, which caused mitral regurgitation. Surgical removal of the device and repair
of the mitral valve was necessary in both patients. Two years after the procedure, the atrial septal defect was closed completely
in two of the remaining three patients and a small residual defect persisted in one patient. 相似文献
5.
Maneesha Bhaya M.D. Ferit Onur Mutluer M.D. Edward Mahan M.D. Luke Mahan Ming C. Hsiung M.D. Wei–Hsian Yin M.D. Ph.D. Jeng Wei M.D. MsD Shen–Kou Tsai M.D. Ph.D. Guang–Yu Zhao M.D. Wei–Hsian Yin M.D. Manish Pradhan M.D. Rajesh Beniwal M.D. Deepak Joshi M.D. Fatemeh Nabavizadeh M.D. Amitoj Singh M.B.B.S. Navin C. Nanda M.D. 《Echocardiography (Mount Kisco, N.Y.)》2013,30(3):345-353
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Gary Mierau E.J. Wills Josephine Wyatt–Ashmead Edward Hoffenberg Ernest Cutz 《Ultrastructural pathology》2013,37(6):517-521
Microvillous inclusion disease is a rare lethal disorder characterized by intractable, severe, watery diarrhea beginning in early infancy. The underlying defect is thought to be an autosomal recessive genetic abnormality resulting in defective brush-border assembly and differentiation. Normally, this diagnosis is easily established through the electron microscopic demonstration of characteristic microvilli-lined inclusions lying within the apical cytoplasm of surface enterocytes. In a small number of patients appearing to have microvillous inclusion disease it has not proven possible to demonstrate the typical inclusions. The existence of another entity, termed intestinal microvillous dystrophy, has been proposed to account for such occurrences. This assertion was founded in large part upon the observation that the few subjects studied all displayed a slightly atypical clinical presentation. The case now being presented exhibited the morphologic features ascribed to intestinal microvillous dystrophy but had a clinical presentation that was entirely typical of microvillous inclusion disease. It serves thus to conceptually unite intestinal microvillous dystrophy with microvillous inclusion disease. 相似文献