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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
Observational Model: Cohort, Time Perspective: Prospective
Vancouver General Hospital, Orthopaedics Dept.
University of British Columbia
Published on BioPortfolio: 2010-07-15T17:00:00-0400
The purpose of this prospective, randomized, controlled trial is to compare subjective patient-reported outcomes and objective clinical results between arthroscopic Bankart repair with and...
Adult Tay-Sachs disease and Sandhoff diseases are caused by deficiency of an enzyme called β-hexosaminidase A, or Hex A in short. This enzyme is located in a particular cellular componen...
We want to see if Zavesca (or miglustat) is safe and can be tolerated by patients with acute infantile onset GM2 gangliosidosis - classical Tay-Sachs and infantile onset Sandhoff disease. ...
Primary: Evaluate the degree of correction attainable with Poly-L-Lactic Acid(Sculptra) for the correction of hill and valley acne scarring Secondary: Document types and inc...
To investigate different strategies of body positioning associated to early corporal mobilization and verify the impact int the time and quantification of thoracic and mediastinal draina...
Off-track Hill-Sachs lesions have been associated with high rates of recurrent shoulder instability. Both arthroscopic Bankart with remplissage and modified Latarjet have been described to treat off-t...
The glenoid track concept was used to confirm the engaging Hill-Sachs lesion (HSL) as a risk factor for recurrent instability following arthroscopic Bankart repair (ABR). However, the post-operative c...
Arthroscopic remplissage of a Hill-Sachs lesion (HSL) associated with a Bankart repair (BR) has been recently introduced as a surgical option to treat chronic anterior shoulder instability. The purpos...
There is increasing evidence to suggest that the amount of glenoid bone loss to indicate bone block procedures may be lower than previously thought, particularly in the presence of a Hill-Sachs defect...
The year 2018 marks the 150th anniversary of the first publication of Julius von Sachs' (1832-1897) Lehrbuch der Botanik (Textbook of Botany), which provided a comprehensive summary of what was then k...
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.