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Biomedical subjects

R E Falk

Publications and source records attributed to R E Falk.

At least 127 records · Page 7Linked to original sources
PubMed1976

Detection of monocyte specific antigen on human acute leukaemia cells.

Heteroantisera with specificity for human monocyte and macrophage antigens (HuMa) have been tested for activity against peripheral blood cells from patients with acute leukaemia. Using indirect immunofluorescence, blast cells from 25/27 patients with acute myelomonocytic leukaemia were reactive with anti-HuMa antisera, whereas blasts from 19/20 patients with acute myeloblastic leukaemia and 13/13 patients with acute lymphoblastic leukaemia were not reactive. The F(ab1)2 fragment of the antibody retained specific activity. Activity of whole serum against myelomonocytic blast cells was specifically removed by absorption with macrophages. These observations indicate that circulating blast cells from patients with acute myelomonocytic leukaemia may carry differentiation antigens characteristic of monocytes and macrophages.

Animals↗
PubMed1976

Immunostimulation with intraperitoneally administered bacille Calmette Guérin for advanced malignant tumors of the gastrointestinal tract.

Thirty-five patients with advanced malignant tumors of the stomach, pancreas, biliary tract or colon were treated intraperitoneally with bacille Calmette Guérin and, subsequently, were given orally booster doses of bacille Calmette Guérin and one of two schedules of cytotoxic drugs. Patients with all types of tumors responded, but this was most marked in patients with metastases to the liver from primary carcinoma of the colon.

Adult↗
PubMed1976

Redistribution of the Fc receptor on human blood monocytes and peritoneal macrophages induced by immunoglobulin G-sensitized erythrocytes.

The Fc receptor is a plasma membrane component exhibiting an affinity for the C gamma 3 domain of certain subclasses of immunoglobulin G. Using anti-Rho (D)-sensitized red cells (EA) in a slide rosette technique, we have demonstrated a translational mobility and polar redistribution of this receptor on the human blood monocyte and peritoneal macrophage. These cells, isolated from venous blood and malignant ascites and identified histochemically, showed a time- and temperature-dependent receptor capping defined by binding six or more EA confined to the cell half-perimeter. Caps formed in serum were mainly extreme caps in which bound EA appeared as a morula contiguous with the adherent cell. At 21 degrees C and 37 degrees C in serum 80% live rosettes formed caps; virtually none formed at 4 degrees C and about 25% were seen in PBS at 21 degrees C. Similarly, 10% extreme caps in PBS and 60 and 70% in serum were seen at room temperature and 37 degrees C, respectively, suggesting a serum factor(s) was important in promoting live rosette capping. Capping was reversibly inhibited by sodium azide although inhibition was incomplete even at 0.1 M, a concentration 10-fold higher than that giving complete inhibition of lymphocyte antigen-receptor capping. Azide also induced reversion of capped rosettes to diffuse, noncapped rosettes, and to levels comparable to those seen in inhibition studies. Re-exposure to EA after rosette capping failed to increase either the proportion of cells forming rosettes or the fullness of such rosettes indicating a critical number of receptors had been capped. Live rosettes induced a spherocytosis in bound EA irrespective of capping status; such changes appeared early in PBS where capping was minimal. Dead cells bore EA as normal biconcave discs. Some rosetting EA were ultimately hemolyzed upon prolonged incubation, and erythrophagocytosis was seen in about 15% of capped rosettes at 37 degrees C.

Binding Sites, Antibody↗
PubMed1976

Ketonic diet in the management of pyruvate dehydrogenase deficiency.

Two brothers, aged 11 years 6 months and 2 years 3 months, with psychomotor and growth retardation, episodes of weakness, ataxia, ophthalmoplegia, and elevated levels of blood pyruvate were shown to have a deficiency in the pyruvate dehydrogenase complex (PDH). When they ate a diet high enough in fats to cause ketonemia but not acidosis, there was a fall in blood pyruvate levels, a decrease in the frequency and severity of the episodes of neurological deterioration, an increased rate of growth and development in the younger brother, and increased strength and endurance in the older one. The possibility of dietary treatment makes the early diagnosis of PDH deficiency more important. Determination of blood pyruvate and lactate levels following a standard glucose meal (glucose-pyruvate test) appears to be the most reliable screening test for this condition.

Alanine↗
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↗
PubMed1975

Oral bacille Calmette Guérin immunostimulation in malignant melanoma.

Forty-seven patients representing all stages of malignant melanoma have been treated orally with bacille Calmette Guérin as an adjunct to standard treatment regimens. This is a preliminary study, but it appears that orally administered bacille Calmette Guérin in localized disease may delay the development of local recurrence and distant spread. In patients with disseminated melanoma but without intracranial metastases, the survival time is increased from 4.0 to 12.7 months. It has no effect on the progress of disease in patients with intracranial metastases or in those with hepatic metastases from intraocular melanoma.

Administration, Oral↗
PubMed1974

Cellular reactivity studies to streptococcal antigens. Migration inhibition studies in patients with streptococcal infections and rheumatic fever.

The question of whether hypersensitivity to streptococcal antigens plays a role in the pathogenesis of the nonsuppurative sequelae of streptococcal infections remains at present unclear. As a first step in the approach to this question, the degree of cellular reactivity of peripheral blood leucocytes to streptococcal antigens was investigated in a number of rheumatic fever patients, patients with uncomplicated streptococcal infections, as well as normal healthy subjects. Using the in vitro technique for the inhibition of capillary migration of peripheral blood leucocytes as an index of the degree of sensitivity to streptococcal antigens, the results indicate that patients with acute rheumatic fever exhibit an exaggerated cellular reactivity to these antigens and in particular to streptococcal cell membrane antigens. This abnormal response to streptococcal membrane antigens appears to persist in rheumatic subjects for at least 5 yr after the initial attack of rheumatic fever. Only Group A streptococcal membrane antigens elicited this unusual response in rheumatic subjects, since the cellular reactivity to Group C and D streptococcal membranes was the same in all groups. Patients with evidence of valvular disease exhibited the same degree of cellular reactivity to these antigens as did patients without clinical evidence of rheumatic heart disease. The nature of the antigens responsible for the observed cellular response remains unknown. Enzymatic treatment of streptococcal cell walls and membranes designed to remove type-specific M proteins did not alter the observed cellular reactivity to the streptococcal antigens. The finding that an abnormal cellular response to certain streptococcal antigens is present only in rheumatic patients suggests that cell-mediated factors may play an important role in the disease process.

Animals↗