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aids-related complex/adenosine
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Enhancement of erythrocytic adenosine deaminase following treatment of AIDS-related complex/AIDS patients with zidovudine.
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The levels of adenosine deaminase (ADA) were determined in the erythrocytes of 10 patients with sexually transmitted HIV-1 infection [five cases with AIDS-related complex (ARC) and five with AIDS] before and after therapy with zidovudine (azidothymidine; AZT). A linear increase in ADA activity was
Adenosine deaminase activity in cats infected with feline immunodeficiency virus.
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Adenosine deaminase (ADA), an enzyme involved in purine metabolism, has been shown to be of clinical importance in several diseases in humans. To investigate whether ADA is of any clinical significance in cats, plasma adenosine deaminase (P-ADA) and T cell adenosine deaminase (T-ADA) activities were
Decreased 5'-nucleotidase activity in suppressor (OKT8) T lymphocytes from homosexuals with AIDS-related complex: nonassociation with enhanced deoxynucleoside toxicity.
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The purine metabolic enzymes adenosine deaminase (ADA), purine nucleoside phosphorylase (PNP), and 5'nucleotidase (5NT) have been shown to be important for normal lymphocyte maturation. Abnormalities of these enzymes have been associated with hereditary as well as acquired immunodeficiency states.
Prognostic significance of adenosine deaminase determinations in subjects with the lymphoadenopathy syndrome.
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The association between human immunodeficiency virus type I (HIV-I) infection and high levels of erythrocyte adenosine deaminase (ADA) has been suggested by Cowan et al [1986]. We have analyzed the specific activities of the same enzyme during different stages of acquired immunodeficiency syndrome
Decreased B lymphocyte ecto-5'nucleotidase and increased adenosine deaminase in mononuclear cells from patients infected with human immunodeficiency virus.
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The levels of purine enzyme activities were studied in 10 patients with acquired immunodeficiency syndrome (AIDS) or AIDS related complex (ARC) and in 6 healthy individuals with antibodies against human immunodeficiency virus (HIV). All AIDS/ARC patients studied had ecto-5'nucleotidase (ecto-5'NUC)
Sudden infant death syndrome (SIDS): T-cell immunodeficiency--Part 1.
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It is hypothesized that SIDS mimics AIDS and atopic eczema in that defective T lymphocytes and overactive B cells overstimulate pro-inflammatory cytokines in the mucosal immune system. Virally infected cells are unable to convert linoleic acid (LA) into gamma-linolenic acid (GLA) which eventually
[In vitro synergic lymphocyte stimulation in HIV-1 infected patients using inosine derivatives and radio-detoxified endotoxin].
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Restoration of immune functions through promoting cell cycle might delay acquired immunodeficiency syndrome development. Therefore, stimulation of peripheral lymphocytes of human immunodeficiency virus-1 infected patients in successive clinical stages was studied by phytohaemagglutinin and other
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