Publications by authors named "Fudenberg H"

Transfer factor (TF) is a low-molecular-weight lymphocyte extract capable of transferring antigen-specific cell-mediated immunity (CMI) to T lymphocytes. It has been used successfully as an adjuvant or primary therapy for viral, parasitic, fungal, and some bacterial infections, as well as immunodeficiencies, neoplasias, allergies and autoimmune diseases. From the list of infections that seem to respond noticeably to transfer factor, those due to viruses of the herpes family are particularly remarkable.

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Ubiquinones (coenzyme Qs (CoQ)) are essential for oxidative phosphorylation in yeasts and humans, although the isomers present in each are different. The human coenzyme Q, CoQ10, is administered orally for the treatment of heart disease and other disorders. Some patients, however, require much higher doses than others to attain a therapeutic CoQ10 blood level.

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40 infantile autistic patients were studied. They ranged from 6 years to 15 years of age at entry. 22 were cases of classical infantile autism; whereas 18 lacked one or more clinical defects associated with infantile autism ("pseudo-autism").

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Transfer Factor (TF) was used in a placebo controlled pilot study of 20 patients with chronic fatigue syndrome (CFS). Efficacy of the treatment was evaluated by clinical monitoring and testing for antibodies to Epstein-Barr virus (EBV) and human herpes virus-6 (HHV-6). Of the 20 patients in the placebo-controlled trial, improvement was observed in 12 patients, generally within 3-6 weeks of beginning treatment.

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Twenty five HIV-1-infected patients, at various stages (CDC II, III and IV) were treated orally with HIV-1-specific transfer factor (TF) for periods varying from 60 to 1870 days. All patients were receiving antiviral treatments in association with TF. The number of lymphocytes, CD4 and CD8 subsets were followed and showed no statistically significant variations.

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The proportions of IgG subclasses (G1, G2, G3 and G4) were quantified in sera from Alzheimer's disease (AD) patients, older Down's syndrome (DS) patients and age-matched controls. The levels of IgG1, IgG2 and IgG4 were normal in AD patients, but the proportions of IgG3 were significantly elevated in 9 of 20 (45%) patients (0.803 +/- 0.

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The binding of [125I]iodine-labelled corticotropin releasing factor (CRF) was studied using peripheral blood lymphocytes from normal donors and Alzheimer's disease (AD) patients. The high affinity binding of [125I]CRF was found in the membranes of various immunocytes. Monocytes and T cells displayed binding which was several times greater than the binding of brain (cortical) cells.

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By fusion of C3H/HeJ splenic adherent mononuclear cells enriched for macrophages with HPRT-deficient C57L/J HH- hepatoma cells, we have generated six macrophage-hepatoma hybrid clones. The hybrid nature of isolated clones was demonstrated by karyotypic analysis. The hybrid clones were screened for macrophage properties by assaying the presence of two enzymes: nonspecific esterase and lysozyme.

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A glycoprotein termed alpha 1-acid glycoprotein (alpha 1-AGP) is a component of normal human serum; its concentration is often increased in several pathological disorders, including acute inflammation and cancer. Inhibitory effects of alpha 1-AGP on some in vitro T and B cell function assays have been reported but our recent data indicated that alpha 1-AGP is indeed a T cell mitogen at physiological concentrations. The present study was designed to investigate: (a) the relationship between this glycoprotein and two other glycoproteins of the T and B cell membrane, i.

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The effects of human osteosarcoma (OS)-specific dialyzable leukocyte extracts (DLE) in hamsters bearing human OS were investigated. The DLE used in this investigation was prepared from rabbits immunized with human osteosarcoma-associated antigens (DLE-OSAA). Tuberculin (DLE-PPD) and control DLE were prepared from rabbits injected with tuberculin or 0.

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Eighteen patients affected by itching, urticaria, eczema, angioedema, and asthma related to food-stuff intake were studied and classified in two groups (true food allergy and pseudoallergy) on the basis of clinical data, skin prick tests, total and specific IgE levels (PRIST and RAST) and double-blind challenge test. Autologous mixed lymphocyte reaction (AMLR) and T cell activation markers were thought to be tests possibly useful to discriminate between 'true' food allergy and 'pseudoallergy'. The present study failed to show either a significant increase in T cell activation markers (MLR4, Ia) or a significant decrease in AMLR proliferation in such subjects as compared to normal controls.

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The evidence that demonstrates a structural and functional interrelationship between the immune system and central nervous system is reviewed. Based on striking analogies between these two systems, the proposal was made that at least some neuropsychiatric diseases can be evaluated by functional studies of peripheral blood immunocytes. This hypothesis was supported by the results of immunologic function studies of various subpopulations of immunocytes obtained from patients with Alzheimer's disease and retinitis pigmentosa.

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Mitogenesis of human peripheral blood lymphocytes as measured by the uptake of [3H]thymidine was stimulated in vitro by pure orosomucoid glycoprotein when used at concentrations that are considerably lower than the physiological plasma level. The lymphocyte cultures stimulated with PHA or PWM were not affected by low concentration (67 micrograms/ml), but they were mildly suppressed by high concentration (1 mg/ml) of this glycoprotein. The stimulatory response was relatively greater with fractionated T cells than the non-T cells (B cells and monocytes).

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The action of an anti-alpha 1-AGP antibody on AMLR, anti-T3 and PHA T-lymphocyte proliferative response was evaluated. We observed a strong dose-dependent inhibition on T-lymphocyte proliferative responsiveness to autologous non-T cells and to anti-T3 stimulus, whereas PHA activation was unaffected. A lower degree of inhibition of the proliferative response was also observed on pretreating both T and non-T cells with the antibody; the addition of anti-alpha 1-AGP in the culture containing cells pretreated with the antibody showed a further inhibition of thymidine incorporation.

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PHA stimulation assay was the first in vitro method for evaluating the T-cell function, and this T-cell proliferative response has been routinely used to discriminate between normal subjects and patients with deficiency in cell-mediated immunity. However, [3H]thymidine incorporation into lymphocyte DNA can be studied by using additional in vitro assay methods since they measure different lymphocyte activation pathways. In the present study we selected three different tests to investigate the reliability of this single approach: PHA induced lymphocyte DNA synthesis; T lymphocyte DNA synthesis to anti-T3 monoclonal antibody (OKT3); autologous mixed lymphocyte reaction (AMLR).

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