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Biomedical subjects

R P Bolande

Publications and source records attributed to R P Bolande.

12 recordsLinked to original sources
PubMed1978

Thymic epithelial injury in graft-versus-host reactions following adrenalectomy.

In four separate experiments 140 adults A(H-2a) x C57BL/6(H-2b) F1hybrid mice were surgically adrenalectomized and divided into three experimental groups. Seventy-one additional adult F1hybrids (AXC57BL/6) which had not been adrenalectomized were divided into three similar groups. In Group 1 (GvH group), GvH reactions were induced by the injection of 50 x 106 pooled parental lymphoid cells intravenously. The second group (syngeneic group) received 50 x 106 pooled F1 hybrid lymphoid cells intravenously. The third group (uninoculated group) received no lymphoid inoculum. At regular intervals the animals were killed, autopsied, and histologically studied. Visceral alterations of GvH reaction were recorded in the thymus, lymph nodes, spleen, and liver in the GvH groups; none was present in the other groups. The thymuses in the nonadrenalectomized GvH group underwent prompt involution characterized by size reduction and cortical lymphoid cell depletion. These changes were not apparent in the GvH adrenalectomized group. Both GvH groups, however, demonstrated an effacement of the medulla, lymphocyte incursion into the medulla, lymphocyte emperipolesis of medullary epithelial cells, gradual disappearance of Hassall's corpuscles, epithelial cell injury, and an ingress of macrophages laden with nuclear and cellular debris. This study suggests that the stress and corticosteroid response which accompany a GvH reaction account for the reduction in the thymic size and cortical lymphoid cell mass. The medullary alterations, therefore, would appear to be initiated by the GvH reaction per se.

Adrenal Glands↗
PubMed1977

Thymic involution in murine graft-versus-host reaction. Epithelial injury mimicking human thymic dysplasia.

Mild, moderate, and severe graft-versus-host (GVH) reactions were induced in four series of experiments in 71 CBA X A and C57BL/6 X A F1 hybrid mice. At regular intervals post-GVH reaction induction (Days 4-42), the animals were sacrificed, autopsied, and histologically studied. Visceral alterations of GVH reaction were recorded in the spleen, lymph nodes, liver, kidney, gut, and thymus. A spectrum of thymic changes was documented, ranging from obliteration of a definable cortex and medulla with loss of Hassall's corpuscles to marked involution with complete disappearance of the gland. Ultrastructural studies revealed damage to both lymphocytes and epithelial cells along with lymphocyte emperipolesis of epithelial cells, lymphocytolysis within epithelial cells, and accumulation of numerous autophagic vacuoles containing fragments of cellular debris within epithelial cells and histiocytes. The resemblance of these alterations to human thymic dysplasia as observed in primary immunodeficient conditions was striking. The theoretical implications of these studies for the pathogenesis of human congenital immunodeficiency states are considered.

Animals↗
PubMed1976

Neoplasia of early life and its relationships to teratogenesis.

The biologic peculiarities of tumors of early life are elucidated. The oncogenic grace period is emphasized, wherein infantile tumors tend to behave in a relatively benign fashion up until 3-6 months of age. A review of the types of congenital malformations associated with the development of neoplasms is presented. These associations appear to be of fundamental importance in developmental pathobiology. They are illustrated by the tendency for neoplasms to develop in anomalous or dysplastic tissues, such as developmental vestiges, undescended testes, dysgenic gonads and certain hamartoses. There is an increased incidence of tumor occurrence in: (1) specific teratologic disorders: aniridia, hemihypertrophy, Beckwith's syndrome, basal cell nevus syndromes and others; (2) cytogenetic abnormalities: Down's syndrome, 13q- syndrome (D-deletion), trisomy 18; (3) chromosomal instability syndromes: Fanconi's anemia, ataxia-telangiectasia, Bloom's syndrome. Finally, many agents, known to be carcinogenic when administered postnatally to animals, are teratogenic in the fetus. A few agents--urethan, alkylnitrosoureas, estrogens--are both teratogenic and carcinogenic when administered to the fetus transplacentally. It is suggested that the timing of intrauterine insult is important in determining whether the effect on the offspring is teratogenic, oncogenic or both. Teratogenesis appears to be the more primitive response. Other theories explaining the concurrence of tumors and anomalies are offered.

Abnormalities, Drug-Induced↗