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Biomedical subjects

W Pierpaoli

Publications and source records attributed to W Pierpaoli.

7 recordsLinked to original sources
PubMed1979

A new pre-irradiation conditioning regimen which protects against radiation injury and facilitates engraftment of xenogeneic bone marrow.

Administration of a large number of xenogeneic (rat) bone marrow cells before lethal, total body irradiation in mice (preconditioning regimen) results in powerful protection from radiation damage, remarkable prolongation of their survival, facilitation of marrow engraftment and induction of rat chimerism. This protective effect is not exerted by thymus or spleen cells and does not depend on specific immune mechanisms. The preconditioning regimen is more efficient when the bone marrow cells are viable and when the cells are inoculated intravenously a few hours before irradiation.

Animals↗
PubMed1978

Pharmacological control of the hormonally modulated immune response. II. Blockade of antibody production by a combination of drugs acting on neuroendocrine functions. Its prevention by gonadotropins and corticotrophin.

Injection of a combination of three drugs, 5-hydroxytryptophan, the alpha-blocker phentolamine and the neuroleptic drug haloperidol into mice before or together with sheep red blood cells (SRBC) induces a complete and long-lasting inhibition of antibody production to SRBC and leads to specific unresponsiveness. The mice unresponsive to SRBC respond normally to another antigen. Treatment with a combination of luteotropic (LH), follicle stimulating (FSH) and corticotropic hormone (ACTH) before administration of drugs and antigen prevents the immune blockade. Injection of SRBC induces an early elevation of LH in blood. This effect is prevented by previous administration of the three drugs in combination. The hormonal response to a second injection of the same antigen of mice previously made 'unresponsive' is different from that of immunized animals. The suppression of these hormonal changes which follow antigen injection by drugs acting on neuroendocrine regulation and cell membrane adrenergic receptors represents a step forward in efforts aimed at a pharmacological control of acquired immunity.

5-Hydroxytryptophan↗
PubMed1978

Pharmacologic control of the hormonally modulated immune response. III. Prolongation of allogeneic skin graft rejection and prevention of runt disease by a combination of drugs acting on neuroendocrine functions.

A recently developed pharmacologic means for suppressing acquired immunity by drugs acting on neuroendocrine regulation has been applied to transplantation immune reactions. A number of drugs have been tested singly and in combination for their capacity to suppress the immune response of mice grafted with allogeneic skin. Another model involved newborn F1 hybrid recipients inoculated with spleen cells from donors of parental strains that had been made specifically "unresponsive" by drug and alloantigen treatment. These procedures led to the identification of a combination of four drugs that induced a remarkable delay in allograft rejection and a prolonged unresponsiveness to alloantigens. This combination of drugs also abrogated the graft-vs-host-runting syndrome in newborn hybrid recipients.

Animals↗
PubMed1977

Role of host endocrine status in murine leukaemogenesis.

Permanent changes in the endocrine status of female SJL/J and CR mice were induced by masculinization, ablation of endocrine glands, inoculation of hormones, or feeding of the chemical carcinogen DMBA. All these procedures resulted in modification of the host hormonal milieu, as shown by blood hormone determination. Masculinization reduced drastically the onset of lymphosarcoma and increased the incidence of systemic neoplasms respectively in DMBA-treated female SJL/J and CR mice. Continued administration of gonadotrophins increased the incidence of systemic neoplasia in CR mice. A direct correlation is suggested between onset of lymphosarcoma or other tumours in mice and a specific shift to an abnormal hormonal environment.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1975

Inability of thymus cells from newborn donors to restore transplantation immunity in athymic mice.

Passive transfer of thymus cells from congenic donors to athymic mice reconstitutes the recipient's capacity to reject allogeneic skin grafts, provided the donor is immunologically mature and the number of thymus cells from the adult donor is high enough. Passive transfer of thymus cells from adult allogeneic donors induces a mild to severe graft-versus-host disease and the grafts are retained until death. These results are interpreted on the basis of recent findings on the endocrine conditions of congenitally athymic mice and on the previous data on the hormone dependence of thymus cells to acquire immunocompetence. It is proposed that a normal host environment is a prerequisite for the thymus-derived cells to perform in cell-mediated immune reactions.

Animals↗