نتایج جستجو برای: mucopolysaccharidosis type i

تعداد نتایج: 2218703  

Journal: :The Journal of the Association of Physicians of India 2013
Rajesh Patil Nilesh Wasekar S G Jadhav Ravindra Zore Parin Sangoi Deepti Vishwanathan

+Pg Resident, *Head of unit, **assistant Professor, Dept. of Medicine, grant Medical College and sir J.J. group of Hospitals, Mumbai. Received: 01.10.2011; Revised: 16.07.2012; Re-revised: 03.12.2012; accepted: 11.01.2013 Abstract Introduction : We present a very rare case of mucopolysaccharidosis type II (Hunter syndrome). which presented as short stature, coarse facies, mild mental retardatio...

Journal: :Brain : a journal of neurology 2018
Rebecca J Holley Stuart M Ellison Daniel Fil Claire O'Leary John McDermott Nishanthi Senthivel Alexander W W Langford-Smith Fiona L Wilkinson Zelpha D'Souza Helen Parker Aiyin Liao Samuel Rowlston Hélène F E Gleitz Shih-Hsin Kan Patricia I Dickson Brian W Bigger

Mucopolysaccharidosis IIIB is a paediatric lysosomal storage disease caused by deficiency of the enzyme α-N-acetylglucosaminidase (NAGLU), involved in the degradation of the glycosaminoglycan heparan sulphate. Absence of NAGLU leads to accumulation of partially degraded heparan sulphate within lysosomes and the extracellular matrix, giving rise to severe CNS degeneration with progressive cognit...

2013
Carole A. Vogler Babette Gwynn

We have characterized a new mutant mouse that has virtually no /-glucuronidase activity. This biochemical defect causes a murine lysosomal storage disease that has many interesting similarities to human mucopolysaccharidosis type VII (MPS VII; Sly syndrome; fl-glucuronidase deficiency). Genetic analysis showed that the mutation is inherited as an autosomal recessive that maps to the fl-glucuron...

Journal: :International Journal of Clinical Biochemistry and Research 2023

Mucopolysaccharidosis is a lysosomal storage disorder, caused due to deficiency of enzymes required for the breakdown Mucopolysaccharides. These undegraded Mucopolysaccharides accumulate in various tissues and cause characteristic features like neurological deficit, impaired motor function, developmental delay, hearing loss, behavioral problems, corneal clouding, glaucoma, respiratory distress,...

2015
Pamela Arn Iain A. Bruce James E. Wraith Helen Travers Shari Fallet

OBJECTIVE Mucopolysaccharidosis I (MPS I) is a progressive, debilitating, and life-threatening genetic disease, which, owing to the nonspecific nature of the early symptoms, is often unrecognized and associated with significant diagnostic delays. To improve early recognition leading to early diagnosis and initiation of treatment, we characterized the extent of airway-related symptoms and surger...

Journal: :Molecular therapy : the journal of the American Society of Gene Therapy 2007
Xiucui Ma Yuli Liu Mindy Tittiger Anne Hennig Attila Kovacs Sarah Popelka Baomei Wang Ramin Herati Mark Bigg Katherine P Ponder

Mucopolysaccharidosis I (MPS I) is caused by deficient alpha-L-iduronidase (IDUA) activity and results in the accumulation of glycosaminoglycans and multisystemic disease. Gene therapy could program cells to secrete mannose 6-phosphate-modified IDUA, and enzyme in blood could be taken up by other cells. Neonatal retroviral vector (RV)-mediated gene therapy has been shown to reduce the manifesta...

2012
R.M. Castilhos D. Blank C.B.O. Netto C.F.M. Souza L.N.T. Fernandes I.V.D. Schwartz R. Giugliani L.B. Jardim

Progressive myelopathies can be secondary to inborn errors of metabolism (IEM) such as mucopolysaccharidosis, mucolipidosis, and adrenomyeloneuropathy. The available scale, Japanese Orthopaedic Association (JOA) score, was validated only for degenerative vertebral diseases. Our objective is to propose and validate a new scale addressing progressive myelopathies and to present validating data fo...

Journal: :The American journal of pathology 1983
M E Haskins G D Aguirre P F Jezyk R J Desnick D F Patterson

Five cats with feline alpha-L-iduronidase-deficient mucopolysaccharidosis were studied. Membrane-bound cytoplasmic inclusions were present in central nervous system neurons, hepatocytes, chondrocytes, vascular and splenic smooth muscle cells, bone marrow leukocytes, and fibroblasts of the skin, eye, and cardiac valves. The lesions in these cats closely resemble those described in human patients...

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