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Biomedical subjects

J A Falk

Publications and source records attributed to J A Falk.

At least 19 recordsLinked to original sources
PubMed1979

Early diagnosis of relapse in acute myeloblastic leukemia: Serologic detection of leukemia-associated antigens in human marrow.

We tested serial bone-marrow samples from 47 adults with acute myeloblastic leukemia in remission for reactivity with heteroantiserums to leukemia-associated antigens, to determine whether imminent relapse could be detected in patients with acute leukemia. Of 26 patients who relapsed by standard morphologic criteria, 21 had increased immunoreactivity of bone marrow for one to six months (mean, 3.7 months) before relapse. High concordance was observed between a positive test and relapse during the period of study (chi-square = 27.53, P less than 0.001). The median time to relapse after a positive test was four months, as compared with the median remission duration of 19 months for the whole group (P less than 0.02, Peto's log-rank analysis). Serologic detection of leukemia-associated antigens in marrow may be a reliable indicator of imminent relapse in acute myeloblastic leukemia.

Animals↗
PubMed1979

Modulation of the immune response and control of tumour spread by a new synthetic compound.

A small molecular weight biofunctional polymer, NED 137, has been investigated for its anti-neoplastic effect. Through its effect on the immune system, particularly the induction of B cell differentiation to antibody producing cells, this synthetic compound can retard tumour growth and prevent the development of distant metastases. Reactivity to tumour developed following administration of the NED 137. No toxicity has been observed. The polymer NED 137 is now being tested in phase I and phase II clinical trials.

Adjuvants, Immunologic↗
PubMed1978

Effective antitumor immunity following elimination of suppressor T cell function.

An increased resistance to a transplantable tumor was demonstrable in Fischer (F344) strain rats after thymectomy and high doses of total body irradiation, followed by bone marrow cell repopulation if the animals were allowed to recover for 6 to 8 weeks. Further experiments demonstrated that removal of a subpopulation of T cells by lower doses of radiation plus thymectomy could (1) reduce recurrences after surgical excision, and (2) prolong survival of animals with established pulmonary metastases. It was found that thymectomy + 50 leads to 100 R total body irradiation could eliminate a T cell-mediated suppression of effective antitumor immunity. The removal of the suppressor cell component by lower doses of irradiation was dependent on pre-exposure of the animals to tumor antigen. These experiments indicate the specificity of suppressor T cells to tumor antigen and their exquisite sensitivity to radiation in appropriate circumstances.

Animals↗
PubMed1978

Severe combined immunodeficiency disease: a model of T-cell dysfunction.

Studies in three patients with severe combined immunodeficiency disease (SCID) and normal adenosine deaminase demonstrated that the combined defect of both T- and B-lymphocyte function may reflect the lack of normal maturation of thymic epithelial cells. This results in the failure of initiation of T-cell differentiation and consequent failure of T-cell dependent maturation of B-lymphocytes to an antibody-secreting stage. SCID B lymphocytes were shown to be capable of generating a specific IgM-antibody response to two T-cell-dependent antigens in vitro under either of the following conditions: (a) provision of autologous T-helper cells which were induced following incubation of precursor cells on monolayers of cultured human thymic epithelium or (b) in the presence of allogeneic T-helper cells. Specific IgM anti-ovalbumin (OA) responses were also generated in the absence of provided T-helper cells when the antigen was insolubilized (Sepharose-OA). The antibody-secreting cells and their circulating precursors carried surface IgM, HLA and Ia-like determinants and proliferated in response to antigen. Identification of this form of SCID may be important when considering therapy and provides an excellent model for the study of the T-cell-dependent acquisition and expression of B-cell immunity.

Antibody Formation↗
PubMed1977

Intensive plasma exchange, complement dependent microcytotoxicity and renal transplant rejection.

Intensive plasma exchange (IPE) was used to treat 13 rejection episodes in eight renal transplant recipients with biopsy evidence of humoral rejection. Prior to IPE, each patients had several rejection episodes treated with high dose steroids. The IPE-treated rejections had not responded to conventional anti-rejection therapy and all patients appeared likely to lose their grafts. IPE reversed 7 of the 13 rejections (5 of 8 patients responded). Two of the 8 grafts continue to have adequate function 6 and 8 months after IPE. IPE temporarily reverses rejection but not increase long term graft survival.

Blood Transfusion↗
PubMed1976

Nonspecific complement activation by streptococcal structures. I. Re-evaluation of HLA cytotoxicity inhibition.

A number of experiments have suggested that there is an antigenic relationship between the HLA complex and streptococcal bacterial structures. Using inhibition of cytotoxicity of HLA antisera as our assay system, it was demonstrated that the inhibitory effect on HLA cytotoxicity by streptococcal antigens is, in reality, due to activation and consumption of components of the alternate complement pathway. In addition, antisera prepared against streptococcal membrane antigens had no cytotoxic effect on a large panel of human lymphocytes, nor did these antisera exhibit immunofluorescent staining of lymphocytes directly. These experiments are compatible with our concept that the HLA complex may have evolved through selective evolutionary pressure as a means of escaping bacterial mimicry.

Antibodies, Bacterial↗
PubMed1975

A surface antigen marker for human monocytes.

Antisera have been raised in rabbits aginst human peritoneal macrophages. After absorption with tonsil cells the sera reacted, by direct and indirect immunfluorescence, with phagocytic mononuclear cells from a variety of tissues and, in addition, stained a small population of nonphagocytic non-T, non-B mononuclear cells present in blood, spleen, and marrow but absent or very rare in tonsil and thymus. The antisera may define a human monocyte-macrophage cell surface differentiation antigen (HuMA) and can be used to deplete or enrich reactive cell population.

Animals↗