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Assessment of Weber Humeral Derotational Osteotomy Using CT Scan

2010-07-15 17:00:00 | BioPortfolio

Summary

Subjects who have had the Weber osteotomy for Hill-Sachs lesions will have CT of Both shoulders. Amount of rotation in operative shoulder will be compared to contralateral. QOL will be assessed

Study Design

Observational Model: Cohort, Time Perspective: Prospective

Conditions

Hill Sachs

Location

Vancouver General Hospital, Orthopaedics Dept.
Vancouver
British Columbia
Canada

Status

Recruiting

Source

University of British Columbia

Results (where available)

View Results

Links

Published on BioPortfolio: 2010-07-15T17:00:00-0400

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Medical and Biotech [MESH] Definitions

A glycosphingolipid that accumulates due to a deficiency of hexosaminidase A or B (BETA-N-ACETYLHEXOSAMINIDASES), or GM2 activator protein, resulting in GANGLIOSIDOSES, heredity metabolic disorders that include TAY-SACHS DISEASE and SANDHOFF DISEASE.

An essential cofactor for the degradation of G(M2)GANGLIOSIDE by lysosomal BETA-N-ACETYLHEXOSAMINIDASES. Genetic mutations resulting in loss of G(M2) activator protein are one of the causes of TAY-SACHS DISEASE, AB VARIANT.

The alpha subunit of hexosaminidase A. Mutations in the gene that encodes this protein can result in loss of hexosaminidase A activity and are linked to TAY-SACHS DISEASE.

An autosomal recessive neurodegenerative disorder characterized by an accumulation of G(M2) GANGLIOSIDE in neurons and other tissues. It is caused by mutation in the common beta subunit of HEXOSAMINIDASE A and HEXOSAMINIDASE B. Thus this disease is also known as the O variant since both hexosaminidase A and B are missing. Clinically, it is indistinguishable from TAY-SACHS DISEASE.

An autosomal recessive neurodegenerative disorder characterized by the onset in infancy of an exaggerated startle response, followed by paralysis, dementia, and blindness. It is caused by mutation in the alpha subunit of the HEXOSAMINIDASE A resulting in lipid-laden ganglion cells. It is also known as the B variant (with increased HEXOSAMINIDASE B but absence of hexosaminidase A) and is strongly associated with Ashkenazic Jewish ancestry.

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