نتایج جستجو برای: ada recommendation

تعداد نتایج: 54271  

Journal: :The Journal of clinical investigation 2001
S G Apasov M R Blackburn R E Kellems P T Smith M V Sitkovsky

Adenosine deaminase (ADA) deficiency in humans results in a severe combined immunodeficiency (SCID). This immunodeficiency is associated with severe disturbances in purine metabolism that are thought to mediate lymphotoxicity. The recent generation of ADA-deficient (ADA(-/-)) mice has enabled the in vivo examination of mechanisms that may underlie the SCID resulting from ADA deficiency. We demo...

2017
Jenny Link Ryan Ramanujam Michael Auer Malin Ryner Signe Hässler Delphine Bachelet Cyprien Mbogning Clemens Warnke Dorothea Buck Poul Erik Hyldgaard Jensen Claudia Sievers Kathleen Ingenhoven Nicolas Fissolo Raija Lindberg Verena Grummel Naoimh Donnellan Manuel Comabella Xavier Montalban Bernd Kieseier Per Soelberg Sørensen Hans-Peter Hartung Tobias Derfuss Andy Lawton Dan Sikkema Marc Pallardy Bernhard Hemmer Florian Deisenhammer Philippe Broët Pierre Dönnes Julie Davidson Anna Fogdell-Hahn

Antibodies against biopharmaceuticals (anti-drug antibodies, ADA) have been a well-integrated part of the clinical care of multiple sclerosis (MS) in several European countries. ADA data generated in Europe during the more than 10 years of ADA monitoring in MS patients treated with interferon beta (IFNβ) and natalizumab have been pooled and characterized through collaboration within a European ...

Journal: :Nucleic acids research 1987
T M Berkvens E J Gerritsen M Oldenburg C Breukel J T Wijnen H van Ormondt J M Vossen A J van der Eb P Meera Khan

We have investigated the structural gene for adenosine deaminase (ADA) in a female infant with ADA deficiency associated severe combined immune deficiency (ADA-SCID) disease and her family by DNA restriction-fragment-length analysis. In this family a new ADA-specific restriction-fragment-length variant was detected, which involves a 3.2-kb deletion spanning the ADA promoter as well as the first...

Journal: :The Journal of allergy and clinical immunology 2014
Jonathan J Lyons Guangping Sun Kelly D Stone Celeste Nelson Laura Wisch Michelle O'Brien Nina Jones Andrew Lindsley Hirsh D Komarow Yun Bai Linda M Scott Daly Cantave Irina Maric J Pablo Abonia Marc E Rothenberg Lawrence B Schwartz Joshua D Milner Todd M Wilson

also suggest that early initiation of PEG-ADA should be considered for ADA-deficient patients suffering from PAP, particularly when rapid hematopoietic stem cell transplantation cannot be performed. Our study also has several significant limitations. While we focused on AMs, future studies are needed to assess the role of pneumocytes and other lung cell abnormalities in the development of PAP i...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 1985
R L Friedman

Human adenosine deaminase (ADA; adenosine aminohydrolase, EC 3.5.4.4) was expressed at high levels in cultured mouse cells using a transmissable murine retrovirus vector system. A cDNA clone encoding ADA has been inserted into a plasmid vector containing retroviral transcription and packaging signals as well as a selectable gene for G418 resistance. The constructions were transfected into psi 2...

Journal: :Blood 2012
Aisha V Sauer Immacolata Brigida Nicola Carriglio Raisa Jofra Hernandez Samantha Scaramuzza Daniela Clavenna Francesca Sanvito Pietro L Poliani Nicola Gagliani Filippo Carlucci Antonella Tabucchi Maria Grazia Roncarolo Elisabetta Traggiai Anna Villa Alessandro Aiuti

Adenosine acts as anti-inflammatory mediator on the immune system and has been described in regulatory T cell (Treg)-mediated suppression. In the absence of adenosine deaminase (ADA), adenosine and other purine metabolites accumulate, leading to severe immunodeficiency with recurrent infections (ADA-SCID). Particularly ADA-deficient patients with late-onset forms and after enzyme replacement th...

Journal: :Blood 2006
Holger K Eltzschig Marion Faigle Simone Knapp Jorn Karhausen Juan Ibla Peter Rosenberger Kirsten C Odegard Peter C Laussen Linda F Thompson Sean P Colgan

Extracellular levels of adenosine increase during hypoxia. While acute increases in adenosine are important to counterbalance excessive inflammation or vascular leakage, chronically elevated adenosine levels may be toxic. Thus, we reasoned that clearance mechanisms might exist to offset deleterious influences of chronically elevated adenosine. Guided by microarray results revealing induction of...

Journal: :Neuroscience letters 1984
J I Nagy M Buss L A LaBella P E Daddona

Adenosine deaminase (ADA) was detected immunohistochemically in neuronal cell bodies of dorsal root ganglia (DRG) of the rat. ADA-immunoreactivity was confined exclusively to small type B ganglion neurons in cervical, thoracic and lumbar sensory ganglia; large type A neurons in sensory ganglia were devoid of immunostaining for ADA. It was consistently found that only a small proportion of type ...

Journal: :The Biochemical journal 2002
Silvia Ginés Marta Mariño Josefa Mallol Enric I Canela Chikao Morimoto Christian Callebaut Ara Hovanessian Vicent Casadó Carmen Lluis Rafael Franco

The extra-enzymic function of cell-surface adenosine deaminase (ADA), an enzyme mainly localized in the cytosol but also found on the cell surface of monocytes, B cells and T cells, has lately been the subject of numerous studies. Cell-surface ADA is able to transduce co-stimulatory signals in T cells via its interaction with CD26, an integral membrane protein that acts as ADA-binding protein. ...

Journal: :American journal of human genetics 1974
S H Chen R Scott E R Giblett

Genetic polymorphism of erythrocyte adenosine deaminase (ADA) was first described by Spencer et al. in 1968 [1]. Its three phenotypes, ADA 1, ADA 2, and ADA 2-1, were found to represent the homozygous or heterozygous expression of two allelic genes at the ADA autosomal locus. Subsequent studies revealed several rare phenotypes representing heterozygosity for either the ADA1 or ADA2 allele and a...

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