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Biomedical subjects

J G Gartner

Publications and source records attributed to J G Gartner.

31 records · Page 2Linked to original sources
PubMed1984

Precocious thymic involution manifest by epithelial injury in the acquired immune deficiency syndrome.

Thymuses from six heterosexual Haitian patients with the acquired immune deficiency syndrome (AIDS) were studied by light microscopy and the findings were compared with those from three control groups. The control groups included 1) five age-matched Haitian hospital patients; 2) ten age- and sex-matched Montreal patients who had died suddenly or had had brief illnesses; and 3) 20 middle-elderly Montreal patients who had experienced chronic, wasting illnesses or prolonged hospitalization. Thymuses from patients with AIDS demonstrated pronounced involution, effacement of the cortex and medulla, marked thymocyte depletion, variable degrees of plasma cell infiltration and fibrosis, and, above all, absence of Hassall's corpuscles. Thymuses from Haitian and Montreal control subjects who had died suddenly or had brief illnesses demonstrated minimal involution and abundant Hassall's corpuscles. Although thymuses from 12 of the chronically ill control subjects demonstrated marked involution, architectural effacement, and absence of Hassall's corpuscles, partial architectural preservation and variable numbers of Hassall's corpuscles were observed in eight of these subjects. Thus, the extent of thymic involution observed in patients with AIDS antedates that incurred with aging and supersedes that induced by sustained stress and inanition. The loss of Hassall's corpuscles in patients with AIDS suggests that the thymic epithelium either incurs a form of injury or undergoes precocious involution during the illness. Whether this lesion is central to the pathogenesis of AIDS or merely a reflection of intense, sustained stress coupled with accelerated physiologic involution is unknown. It is possible that the disappearance of Hassall's corpuscles may indicate important, although as yet cryptic events within the thymic microenvironment in this syndrome.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Mammary carcinoma arising in mice undergoing a chronic graft-versus-host reaction.

A graft-versus-host reaction (GVHR) was induced in 30 (CBA X A)F1 mice by the iv injection of 50 X 10(6) parental strain A lymphoid cells. Solid tumors emerged in 5 of 10 experimental animals that survived beyond 14 months after the GVHR was initiated. The neoplasms were judged to be mammary carcinomas by light and electron microscopic examinations. C-type RNA viral structures were observed in some tumor cells. The neoplasms were successfully transplanted into syngeneic animals by either sc or ip injections of tumor cell suspensions. Tumor transfer to syngeneic mice was not possible if only spleen cells from tumor-bearing animals were transferred. No tumors developed in an age-matched control group that received no treatment.

Animals↗
PubMed1981

Epstein-Barr virus in a malignant lymphoproliferative disorder of B-cells occurring after thymic epithelial transplantation for combined immunodeficiency.

A fatal disseminated polyclonal malignant lymphoproliferative disorder of B-cells (immunoblastic sarcoma) developed shortly after a second thymic epithelial peritoneal implant in a 5-yr-old girl with combined immunodeficiency. The immunodeficiency was characterized by low T-cell numbers and function, very low levels of thymic hormone, dysgammaglobulinemia, and an inability to mount a primary antibody or cell-mediated response to new antigens. At necropsy, the thymus fulfilled morphological criteria for thymic dysplasia. Epstein-Barr virus (EBV) antigen and DNA were identified in neoplastic infiltrates in the lymph nodes and thymus by immunofluorescence for the EBV nuclear antigen and by EBV-specific complementary RNA/DNA hybridization. No antibodies to nuclear antigen, early antigen, or viral capsid antigen of EBV were identified in the serum. The concurrence of these events suggests that the thymic epithelial implant itself may have been instrumental in the pathogenesis of this neoplasm. It is proposed that the thymus may have provided factors which indirectly potentiated the proliferation of EBV-infected B-cells, possibly by induction of nonspecific T-helper cells and perhaps through other thymic humoral factors. It is suggested that some forms of immunoblastic sarcoma, even when polyclonal, and especially those which arise in immunocompromised hosts, may, in some instances, represent an opportunistic form of EBV-induced B-cell neoplasia.

Antibodies, Viral↗
PubMed1981

Ultrastructural changes in the glomerular basement membrane of patients with Laurence-Moon-Biedl-Bardet syndrome.

Renal disease, although not a cardinal feature of the Laurence-Moon-Biedl-Bardet syndrome (LMBBS), occurs in more than 70% of patients and is an important cause of morbidity and mortality. Renal ultrastructural changes have not been well delineated. We have studied glomeruli from three patients with LMBBS and have found similar ultrastructural changes in glomerular basement membrane (GBM). Two patients had decreased renal function, hypertension, and markedly abnormal intravenous urograms with reduced concentration of dye and abnormal pelvicalyceal systems; one patient had normal renal function and minimal distortion of the pelvicalyceal system of one kidney. Ligh microscopy revealed varying degrees of increase in mesangial cellularity and matrix. These changes involved almost all glomeruli and were segmental. The abnormalities ranged from mild mesangial cell proliferation to complete sclerosis of the glomerular tuft. Ultrastructural study revealed marked alterations of the glomerular basement membrane: effacement of the trilaminar architecture, segmental and irregular thickening alternating with thinning and rarefaction, accumulation of granular and fibrillary material within the inner third of the GBM. These ultrastructural changes may be the earliest and primary glomerular abnormality seen in LMBBS because they were seen in a patient who had minimal changes on light microscopy.

Adolescent↗
PubMedDate not supplied

Thymic involution with loss of Hassall's corpuscles mimicking thymic dysplasia in a child with transfusion-associated graft-versus-host disease.

A 7-year-old leukemic girl developed pancytopenia following chemotherapy and was given several transfusions of nonirradiated blood. Within 2 weeks she developed a maculopapular rash, fever, abnormal liver function, diarrhea, and wasting. She became septic and died 6 weeks later. Transfusion-associated graft-versus-host disease (GVHD) was suspected clinically. At autopsy, changes diagnostic of GVHD were present in the skin and liver. The remarkable feature of the case was the histopathology of the thymus, which was morphologically "dysplastic," i.e., minute, lymphoid depleted, devoid of a corticomedullary demarcation, and completely lacking in Hassall's corpuscles. These changes were virtually identical to those seen in the thymus of children with severe combined immunodeficiency disease (SCID). There was no evidence of preexisting immune deficiency. There is compelling experimental evidence that GVHD can produce changes in the thymus that are identical to those of "thymic dysplasia." These observations have led to the hypothesis that immunodeficiency associated with GVHD may stem, in part, from injury to thymic epithelium resulting in defective T cell maturation. As a corollary of this hypothesis, it has been suggested that the pathogenesis of some forms of SCID may involve GVHD-associated injury to the thymus by a maternal allograft acquired in utero. This report further documents thymic pathology in human GVHD and discusses these changes in the light of these ideas.

Acute Disease↗