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Biomedical subjects

R A Good

Publications and source records attributed to R A Good.

At least 775 records · Page 43Linked to original sources
PubMed1975

Biosynthesis and secretion of immunoglobulins by peripheral blood lymphocytes in severe hypogammaglobulinemia and by cultured lymphoblast cells.

Peripheral blood lymphocytes of two patients with infantile X-linked agammaglobulinemia could neither synthesize nor secrete immunoglobulins in detectable amounts. Peripheral blood lymphocytes of patients with common variable type of hypogammaglobulinemia synthesize but do not secrete immunoglobulins. Serologic precipitation with antiimmunoglobulin serum and acrylamide-gel analysis of immunoglobulins synthesized by lymphocytes of these patients showed predominant mu-chain, as compared to immunoglobulins synthesized by normal lymphocytes. Biosynthesis and secretion of immunoglobulins by cultured lymphoblast cells from normal persons was very much analogous to that of lymphocytes of hypogammaglobulinemic patients. These findings suggest that lymphocytes of patients with common variable type of hypogammaglobulinemia are immature B cells like cultured lymphoblast cells, and that a block in cytodifferentiation of IgM to IgG-producing cells is present in their B cells.

Adult↗
PubMed1975

Complement inhibitor(s) released by leukocytes. I. Pretreatment of sheep erythrocytes with supernatants of mouse spleen and thymus cells inhibit whole complement activity and C2 utilization.

Sheep erythrocytes pretreated with supernatants of mouse spleen or thymus cells become resistant to lysis by guinea pig complement. The inhibitory activity (IA) reduces the utilization of C2 by EAC14. Because IA binds to the surface of sheep erythrocytes and does not inhibit C1 irreversibly, it is probably a hitherto undescribed inhibitor of complement.

Animals↗
PubMed1975

Chronic mucocutaneous candidiasis with macrophage dysfunction, a plasma inhibitor, and co-existent aplastic anemia.

A 56-year-old man developed chronic mucocutaneous candidiasis (MCC) and pernicious anemia. Nine years later he developed aplastic anemia which ultimately was fatal. A small thymoma was found at autopsy. He was anergic and his mononuclear leukocytes (MNL) failed to undergo a proliferative response in culture to soluble antigens. His monocytes did not mediate a proliferative response by lymphocytes from sensitized control donors when stimulated with Monilia albicans antigen but did mediate a mixed leukocyte reaction normally. His plasma contained a poten inhibitor of -3H-thymidine incorporation by sensitized control MNL when stimulated with soluble antigens but was not inhibitory of the mixed leukocyte reaction, lymphoproliferative responses to plant mitogens, and was not shown either in vivo or in vitro to depress hematopoiesis. Patient lymphocytes were responsive to plant mitogens, Monilia antigen, in the mixed leukocyte reaction, and produced macrophage migration inhibitory factor in response to Monilia antigen. After plasmapheresis, delayed hypersensitivity and lymphoproliferative responses to soluble antigens were temporarily restored. This case implicates the macrophage in the pathogenesis of MCC and demonstrates some consequences of chronic monocyte dysfunction. The inhibitor of some expressions of cell-mediated immunity was removed by plasmapheresis.

Aged↗
PubMed1975

Transfer factor therapy: evidence for nonspecificity.

Four patients were treated with multiple doses of dialyzed transfer factor in which one Wiskott-Aldrich patient with abnormal IgG monocyte receptors obtained benefit. All patients converted skin reactivity, and had improved in vitro lymphocyte responses to varying degrees. Three patients developed positive reactivity to allogeneic cells in MLC, and one patient developed DNCB reactivity. These latter two findings suggest transfer factor may act by inducing a nonspecific maturation of lymphocyte function. A possible mechanism for the action of transfer factor is discussed.

Antibody Formation↗
PubMed1975

Congenital and experimentally induced complement deficiency in rabbits.

Deficiency of the sixth component of complement in rabbits is an autosomal recessive defect which also renders C7-9 functionally unavailable. The function of C6-9 appears to be that of amplification of immunologic processes. Defective animals are associated with a subtle disadvantage. Normal rabbits injected with cobra-venom-anticomplementary-factor show primary C3-9 and secondary polymorphonuclear leukocyte and platelet functional deficiency. Animals treated with cobra venom showed striking deficits in manifestations of some immunologic functions. Thus the complement system plays a vital role in maintaining integrity of immunologic mechanisms.

Animals↗
PubMed1975

The effects of protein deprivation on cell-mediated immunity.

The effect of protein insufficiency on immune responsiveness was investigated in inbred mice fed isocaloric diets low and normal in protein. Mice were tested for aberrations of cell-mediated and humoral immunities. Protein insufficiency enhances cell-mediated immunity while depressing or not affecting humoral immunity. Cell-mediated immunity was enhanced in testing: allogeneic skin graft rejection, spleen cell responsiveness to phytohemagglutinin, the graft-vs-host reaction, macrophage function, and resistance to viral and bacterial infections.

Animals↗
PubMed1975

Primary immunodeficiency and malignancy.

Evidence indicating an essential relationship between immunologic deviation and cancer has accumulated rapidly over the past 15 years. Following a brief review of the enormous body of literature linking experimental immunodeficiency and cancer, this discussion will center on humans with primary immunodeficiency disorders and the inordinate number of malignancies which develop in these patients.

Agammaglobulinemia↗
PubMed1975

Fetal thymus transplantation: experimental and clinical observations.

The murine fetal thymus obtained early in gestation was found to develop normally in a syngeneic host. In contrast to the adult thymus grafts, the fetal thymus did not undergo the early and marked necrosis following transplantation into syngeneic hosts. Indeed, the fetal thymus was as effective as the adult thymus in achieving immunologic reconstitution of neonatally thymectomized syngeneic mice, and superior to adult thymus, when transplanted into allogeneic hosts. Furthermore, the fetal thymus, unlike the adult thymus, did not induce graft-vs-host disease (GVH) in genetically susceptible neonatally thymectomized mice. These observations seem relevant to thymus transplantation in children with a congenital absence of the thymus. Transplantation of fetal thymus in a child with DiGeorge syndrome corrected the T-cell immunodeficiency, and led to a reduction toward normal of the B-cell population.

Animals↗
PubMed1975

Transplantation of incompatible bone marrow in infants with severe combined immunodeficiency disease.

Our efforts to overcome the fatal GVH disease following transplantation of incompatible bone marrow have been: 1) isolation of patient in sterile laminar flow room, 2) elimination of bacterial flora from GI tract, 3) repeated infusions of plasma containing blocking antibodies, 4) selection of HL-A identical but unrelated donor from general population, 5) use of stem-cell fraction of bone marrow and 6) gradual transplantation of marrow (less than 0.01 ml) carefully aspirated, free of immunocompetent T-cell contamination. A mild form of GVH disease, partial reconstitution of immune function and hematologic chimera were noted in 2 patients, who survived 67 days and 125 days after transplantation. More recently, an infant with severe combined immunodeficiency disease (SCID) has been reconstituted immunologically using marrow from HL-A mismatched, mixed leukocytes culture (MLC) non-reactive donor. The gradual transplantation method may be a useful means of transplanting incompatible marrow in infants with SCID.

Antibody Formation↗
PubMed1975

Compatible bone marrow transplantation and immunologic reconstitution of combined immunodeficiency disease.

To date, bone marrow transplantation affords the only successful means of achieving full immunologic reconstitution of patients with severe combined immunodeficiency disease (SCID). We have achieved immunologic reconstitution in 6 of 7 SCID patients using marrow transplants from compatible sib donors. One child died of Pneumocystis carinii pneumonia following early immunologic reconstitution. A second child died of sepsis without evidence of engraftment, despite 3 marrow grafts, and a third died unexpectedly from massive aspiration pneumonia following complete immunologic reconstititon. Thus, in 4 of 7 children with SCID full and long-lasting immunologic reconstitution has been achieved by transplantation of marrow from matched sib donors. From these initial efforts, much has been learned, and it is clear that several factors, some of which remain poorly understood, may influence the outcome of marrow grafting. However, despite the difficulties encountered, bone marrow transplantation continues to hold real promise for correction of this otherwise fatal disease.

Antibody Formation↗
PubMed1975

An autopsy study of human axillary lymph node histology.

This is a histologic study of axillary lymph nodes removed from 487 random autopsies. Histologic features such as germinal centers, deep cortical regions, sinus histiocytosis, hyalin deposition, fibrosis and overall cellularity were evaluated in each case. Results were correlated with the age of the deceased and cause of death. The results a) support the general opinion that germinal centers are more frequently found in children and young adults than in the old, b) showed that hyaline deposits increase with age, c) showed that lymphocyte depletion associated with fibrosis and hyaline deposits was found in patients dying of chronic disease, particularly cancer, d) pointed out a selective depletion of the deep cortical regions in patients dying of hemorrhage, and e) contributed to knowledge of the morphology of axillary lymph nodes in neonates. (Am J Pathol 78:7-22, 1975)

Adolescent↗