نتایج جستجو برای: tyrosinemia type ii

تعداد نتایج: 1796109  

Journal: :Proceedings of the National Academy of Sciences of the United States of America 1998
S Kubo M Sun M Miyahara K Umeyama K Urakami T Yamamoto C Jakobs I Matsuda F Endo

Tyrosinemia type 1, caused by mutations in the fumarylacetoacetate hydrolase gene (Fah), is characterized by severe liver injury. We earlier developed a tyrosinemic mouse model with two genetic defects, Fah and 4-hydroxyphenylpyruvate dioxygenase (Hpd) deficiencies. Apoptosis of hepatocytes was induced and an acute onset of liver failure occurred after administration of homogentisic acid (HGA),...

پایان نامه :وزارت علوم، تحقیقات و فناوری - دانشگاه فردوسی مشهد - دانشکده مهندسی 1389

abstract type-ii fuzzy logic has shown its superiority over traditional fuzzy logic when dealing with uncertainty. type-ii fuzzy logic controllers are however newer and more promising approaches that have been recently applied to various fields due to their significant contribution especially when the noise (as an important instance of uncertainty) emerges. during the design of type- i fuz...

Journal: :Orphanet Journal of Rare Diseases 2020

Journal: :Clinical chemistry 2008
Kenneth A Pass Mark Morrissey

Hepatorenal tyrosinemia, also known as tyrosinemia type I (Tyr-I) is an autosomal recessive inborn error of metabolism. The primary enzyme defect has been attributed to a deficiency of fumarylacetoacetase (EC 3.7.1.2) (1 ). Tyr-I is usually asymptomatic in newborns, but if left untreated it affects liver, kidney, bone, and peripheral nerves; in its most severe form, affected infants may die fro...

2017
Hakim Rahmoune Nada Boutrid Mounira Amrane Belkacem Bioud Habibe Koç Uçar

Address for Correspondence: Dr. Hakim Rahmoune, Department of Pediatrics, Setif University Hospital, Setif, Algeria Phone: +213-550123279 e-mail: [email protected] Received: 7 August 2016 Accepted: 16 January 2017 • DOI: 10.4274/balkanmedj.2016.1209 Available at www.balkanmedicaljournal.org Cite this article as: Rahmoune H, Boutrid N, Amrane M, Bioud B. Comment on Pancreatitis in Type 1 T...

Journal: : 2022

Tyrosinemia is a rare metabolic disease resulting from disorder of amino acids, which can occur under the «masks» various diseases, debut as hemorrhagic syndrome in children all age groups, hepatolienal syndrome, hypoglycemia, rickets-like disease, peripheral neuropathy. Clinical case. In our publication, we report on girl at 1 year 7 months who had recurrent nosebleeds, led to referral hematol...

Journal: :Neurochemistry International 2012
Gabriela K. Ferreira Milena Carvalho-Silva Cinara L. Gonçalves Júlia S. Vieira Giselli Scaini Fernando V. Ghedim Pedro F. Deroza Alexandra I. Zugno Talita C.B. Pereira Giovanna M.T. Oliveira Luiza W. Kist Maurício R. Bogo Patrícia F. Schuck Gustavo C. Ferreira Emilio L. Streck

Tyrosinemia is a rare genetic disease caused by mutations on genes that codify enzymes responsible for tyrosine metabolism. Considering that tyrosinemics patients usually present symptoms associated with central nervous system alterations that ranges from slight decreases in intelligence to severe mental retardation, we decided to investigate whether acute and chronic administration of L-tyrosi...

Journal: :Archives of Disease in Childhood 2012

Journal: :Clinical chemistry 1976
A Grenier L Bélanger C Laberge

We describe an electroimmunodiffusion technique for measuring alpha1-fetoprotein in blood spotted on chromatography paper. The system is being used as a complementary test in a neonatal mass-screening program for detection of inborn metabolic diseases in the Province of Quebec. In a series of 102 cases of neonatal hypertyrosinemia, the test has proven to be highly discriminative for hereditary ...

Journal: :Eukaryotic cell 2006
Márcia Eliana da Silva Ferreira Marcela Savoldi Pierina Sueli Bonato Maria Helena S Goldman Gustavo H Goldman

Mutations in the human HPD gene (encoding 4-hydroxyphenylpyruvic acid dioxygenase) cause hereditary tyrosinemia type 3 (HT3). We deleted the Aspergillus nidulans homologue (hpdA). We showed that the mutant strain is not able to grow in the presence of phenylalanine and that it accumulates increased concentrations of tyrosine and 4-hydroxyphenylpyruvic acid, mimicking the human HT3 phenotype.

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