Search PubMed⌕ Search

Biomedical subjects

D T Purtilo

Publications and source records attributed to D T Purtilo.

At least 109 records · Page 6Linked to original sources
PubMed1985

A method for determination of antibody-dependent cellular cytotoxicity (ADCC) of human peripheral mononuclear cells.

A method is described for measuring antibody-dependent cellular cytotoxicity (ADCC) of mononuclear cells from human peripheral blood using an established murine cell line and commercially prepared antisera. The test utilizes a standard 51Cr release technique. The ADCC activity of mononuclear cells obtained from 10 healthy human volunteers was measured at 4 different effector: target cell ratios. A linear relationship between %51Cr release (ADCC) and the number of effector cells was observed.

Animals↗
PubMed1985

Role of Epstein-Barr virus in acquired immune deficiency syndrome.

We have reviewed the biologic characteristics, immune responses, and diverse array of diseases occurring from Epstein-Barr virus infections in immune deficient patients. We have summarized possible roles of the virus in the risk groups for AIDS. Data is convincing that EBV is responsible for some of the cases of lymphadenomegaly and Burkitt-like, non-Hodgkin's lymphomas in patients with pre-AIDS and AIDS. A hypothesis has been proposed wherein EBV and other stimulants of B and T cells allow productive infection by the retrovirus and spread of HTLV-III throughout the helper T cell populations.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Catalogue of Epstein-Barr virus (EBV) receptors on human malignant and non-malignant hematopoietic cell lines.

Epstein-Barr virus (EBV) can induce a broad spectrum of hematological diseases, especially in immune deficient patients. We assayed for receptor for EBV (EBVR) using fluoresceinated viral particles on 44 human hematopoietic cell lines derived from patients with T, B, and non-T, non-B acute lymphocytic leukemia (ALL), non-lymphoid leukemia, Burkitt lymphoma, myeloma and several unique lines we and others have recently developed. All 31 EBV nuclear-associated antigen (EBNA) negative cell lines were of neoplastic origin. Seven of 13 EBNA-positive cell lines were of normal cell origin. Four of 25 non-B (surface immunoglobulin negative) EBNA-negative neoplastic cell lines were EBVR-positive. Three of six EBNA-negative B-cell (surface immunoglobulin positive) lines were EBVR-positive. Nine of 13 EBNA-positive Burkitt and non-Burkitt cell lines strongly expressed EBVR. Four EBNA-positive Burkitt lymphoma cell lines exhibited EBVR only to a limited degree. Studies of the cell lines for EBVR, complement receptors (CR) and surface immunoglobulin (SIg) revealed that presence of SIg does not obligate the presence of EBVR. Functional EBVR accompanied SIg among EBNA-negative cell lines. SIg-negative cell lines can possess EBVR. Fourteen of 16 EBVR-positive lines were also positive for CR. The EBVR assay is a useful tool for assessing the potential role of EBV in the induction of hematopoietic disorders.

Antigens, Surface↗
PubMed1985

Chromosome aberrations in peripheral lymphocytes of male homosexuals.

Karyotypes of peripheral lymphocytes of 19 male homosexuals showed increased hypodiploidy. Chromosomes #19 and #20 were most frequently lost. Also, structural chromosome aberrations frequently occurred consisting chiefly of translocations and simple chromosome breaks. Terminal deletions, inversions, and isochromosomes occurred less commonly. In three of the cases, 100% of the cells were involved in a pericentric inversion of a chromosome #9. Chromosomes #3 in p21.1 and 1 in p32.3 were repeatedly affected. Structural aberrations were seen less frequently in men with acquired immunodeficiency syndrome(AIDS) and AIDS-related complex than in asymptomatic homosexuals. The hypodiploidy with preferential loss of chromosomes was constantly present. The marker chromosomes and simple breaks at repeated sites are another manifestation of damage to the immune system in these male homosexuals from Greenwich Village in New York City. The chromosomal damage was potentially the result of exposure to amyl and butyl nitrites, viral infections, or immunologic reactions to sperm, which crossreact with lymphocytes.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Diet, nutrition, and cancer. An update on a controversial relationship.

The multiple-step model of carcinogenesis discussed here identifies the two major stages of initiation and promotion. A more recent research development proposes that oncogenes present in chromosomes are activated by viral, chemical, or physical agents and cause cancer. A great variety of natural mutagens and carcinogens find their way into the modern US diet. Excessive fat and alcohol consumption have been studied in relation to many kinds of malignancies. Dietary anticarcinogens include vitamins A, C, and E, although under certain conditions some generally inhibitive substances can actually enhance carcinogenesis. A provocative hypothesis argues that a high-fiber diet can substantially reduce the likelihood of carcinoma of the colon.

Aflatoxins↗
PubMed1985

Necrotizing lymphoid vasculitis in X-linked lymphoproliferative syndrome.

An 8-year-old maternally related relative of three boys who had developed agammaglobulinemia associated with Epstein-Barr virus (EBV)-induced infectious mononucleosis was studied for X-linked lymphoproliferative syndrome (XLP) in 1979. At that time, he demonstrated no striking immunologic aberrations and was seronegative for EBV. Subsequently, immunologic abnormalities including failure to switch from IgM to IgG antibody synthesis after secondary immunization with bacteriophage phi X174 were detected. In 1983, he experienced episodic intracerebral hemorrhages, with the second being fatal. At autopsy, necrotizing vasculitis and aneurysms involving arteries of the central nervous system were observed. Studies of blood obtained immediately before and after death failed to show antibodies to EBV. However, EBV genome was demonstrated in tissues obtained at autopsy by DNA hybridization studies. Fatal lymphoid vasculitis in this patient is unique among boys with XLP in the registry. These findings probably extend the phenotypic expressions of XLP.

Antibodies, Viral↗
PubMed1985

Epstein-Barr virus-induced diseases in the X-linked lymphoproliferative syndrome and related disorders.

Information regarding the development of diverse diseases associated with EBV virus in immune deficient patients has been gained by studying males with XLP, and their families. Multiple immune defenses normally protect against the ubiquitous EBV. Depending on the type and degree of inherited or acquired immunodeficiency, EBV may more or less be capable of inducing a variety of diseases. Multiple methods may be needed to document EBV in the immune deficient individual. Rational approaches to prevention and intervention in EBV-induced diseases in immune compromised individuals are being developed.

Animals↗
PubMed1985

Role of Epstein-Barr virus in the etiology of Burkitt's lymphoma.

Although Epstein-Barr virus (EBV) was discovered in cultured Burkitt's lymphoma (BL) cells, its exact role remains unclear. Viral genome is found in 95-98% of endemic BL and 15-20% of non-endemic BL. Children destined to develop BL in Africa show elevated titres of viral capsid antibodies one to two years preceding emergence of BL. A multistep process follows early EBV infection during early childhood. Immune deficiency probably permits continuation of the infections, with smouldering polyclonal B-cell proliferation proceeding. Final steps in the pathogenesis consist of cytogenetic and molecular conversion to monoclonal BL. Reciprocal chromosomal translocations involve breakpoints containing c-myc, heavy- and light-chain Ig loci. Activation of oncogenes, c-myc and B-lym, may be essential in the molecular pathogenesis of BL. A spectrum of EBV-induced pathological entities is found in individuals with X-linked lymphoproliferative and acquired immune deficiency syndromes. Lymphoma identical to endemic BL occurs in these immune-deficient patients. Non-endemic BL is possibly due to immune defects, initiators and promoters of B-cell proliferation, which may not be identical to factors in endemic BL; however, cytogenetic events and activation of oncogenes may be pathways of both endemic and non-endemic BL.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Inherited partial trisomy #15 complicated by neuroblastoma.

The proband in this study had multiple congenital malformations and a constitutional 46,XY,-13, + der(13),t(13;15)(q34;q23)mat chromosome complement. A bone marrow aspirate revealed neuroblastoma, and cytogenetic studies on tumor cells revealed, in addition to the partial trisomy #15 and probable partial monosomy #13, hypotetraploidy with a mean chromosome number of 82-84, including 3 or 4 copies of each autosome, 2 X chromosomes, no Y chromosome, and a marker. Translocations involving chromosomes #1, #2, #3, #7, and #14 were present, along with multiple double minutes. The possibility that the inherited partial trisomy #15 (and/or partial chromosome #13 monosomy) predisposed to neuroblastoma and additional chromosome changes in this tumor is discussed.

Chromosome Aberrations↗