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Biomedical subjects

P Dore-Duffy

Publications and source records attributed to P Dore-Duffy.

50 records · Page 3Linked to original sources
PubMed1982

Elevation of serum prostaglandin E levels following electrical stimulation of the midbrain.

Serum prostaglandin E (PGE) levels were measured in rats immediately following electrical stimulation of the mesencephalic periaqueductal gray (PAG) region and the nucleus raphe magnus (NRM) and compared to controls. An additional group received aspirin prior to PAG stimulation. A significant increase in serum PGE levels was found after stimulation of the PAG, but not the NRM. Aspirin inhibited the stimulation-induced increases in PGE.

Animals↗
PubMed1982

Differential effect of prostaglandins and other products of arachidonic acid metabolism on measles virus replication in Vero cells.

The influence of cyclic adenosine 3', 5'-monophosphate (cAMP) and prostaglandin (PG), E1, E2, F2 alpha, A2 and thromboxane B2 (TxB2) and measles virus infection was investigated. Addition of PGE1, E2 and cAMP (10(-3)-10(-)8M) inhibited measles virus replication in Vero cells. TxB2 and PGA2 enhanced replication. Cytotoxic effects were not observed. Inhibition of infectious titers (98%) was most pronounced when agents were present throughout replication. Treated cells exhibited hemadsorbing antigen, but the size and number of cytoplasmic inclusions was decreased by cAMP. Pre-treatment of cells with PGE1 or presence of PGE1 during virus adsorption enhanced infectious titers (30%). Results suggest that cAMP and PGE1 inhibit measles virus production infection. That both enhancing and inhibiting effects of PGs were seen suggest that measles virus may require PG at specific times during the replicative cycle.

Animals↗
PubMed1981

Adherence of human peripheral blood lymphocytes to virus infected cells: role of the cytoskeleton and prostaglandin E.

Human peripheral blood lymphocytes from patients with multiple sclerosis (MS) form significantly greater numbers of rosettes with virus infected cells than healthy controls. Because increased lymphocyte adherence in MS may be important to the disease process, we have investigated the mechanisms governing lymphocyte adherence in healthy control volunteers. We have previously shown that prostaglandins E1, E2 (PGE2), and dibutyryl cyclic AMP (db cAMP) increase control lymphocyte adherence to MS levels. We now report that colchicine (10(-7) M) and nocodazole (10(-7) M) significantly increased control lymphocyte adherence to measles virus infected human epithelial (HEp-2) cells. Lumicolchicine had no effect. Cytochalasins A, B, C, and D also had no effect on lymphocyte adherence. Colchicine (10(-5) + 10(-7) M) treatment of mononuclear cells enhanced PGE synthesis in tissue culture. Cytochalasins had no effect on PGE synthesis. Thus, microtubules appear important to adherence of lymphocytes to virus infected cells perhaps by virtue of their involvement and/or control of PG biosynthesis.

Cells, Cultured↗
PubMed1980

Lymphocyte adherence to myelinated tissue in multiple sclerosis.

A small subpopulation of human peripheral blood T lymphocytes has the capacity to adhere selectively to myelinated sections of human and nonhuman brain tissue. Adherence of lymphocytes from patients with multiple sclerosis is significantly greater than adherence of control lymphocytes. Monocytes inhibit binding in controls. This function appears to be lost by multiple sclerosis monocytes.

Cell Adhesion↗
PubMed1979

Lymphocyte adherence in multiple sclerosis: effect of aspirin.

Peripheral blood lymphocytes from multiple sclerosis (MS) patients form substantially greater numbers of rosettes with measles virus-infected human epithelial cells than do lymphocytes from healthy controls or from patients with other diseases. We have previously shown that prostaglandin E(1)-treated normal lymphocytes exhibit increased lymphocyte adherence, and thus behave like MS lymphocytes in this in vitro system. In this study we describe the effect of prostaglandin synthesis inhibition on lymphocyte adherence in both MS and control patients. Direct addition of aspirin or indomethacin to peripheral blood mononuclear cells from MS patients in vitro reduced lymphocyte adherence to control levels. Ingestion of therapeutic (anti-inflammatory) doses of aspirin (1 g, 4 times daily for 2 d) by MS patients resulted in reduction of lymphocyte adherence to levels seen in healthy controls. A single 325-mg dose of aspirin did not reduce lymphocyte adherence. A dose-dependent reduction in lymphocyte adherence was observed after single doses ranging from 650 mg to 1.3 g; duration of the effect was directly related to the aspirin dose. These observations indicate that treatment of MS patients with aspirin profoundly influences adherence of their lymphocytes to measles virus-infected cells and suggest that the altered cellular response, which results in increased lymphocyte adherence in MS patients, may be mediated by a prostaglandin-sensitive mechanism.

Aspirin↗
PubMed1979

Lymphocyte adherence in multiple sclerosis.

It has been reported that peripheral blood lymphocytes from patients with multiple sclerosis (MS) adhere to measles-infected human epithelial cells in significantly greater numbers than do lymphocytes from healthy volunteers or patients with other neurologic diseases. We have confirmed this observation in three separate studies, and have investigated the relationship of lymphocyte adherence to the clinical state. Lymphocyte adherence determination values correlated with the degree of certainty of the clinical diagnosis of MS, and lymphocyte adherence values in individual patients increased during clinical exacerbations. Judicious use of this test may facilitate the diagnosis of MS.

Epithelium↗
PubMed1977

Adherence of human peripheral blood lymphocytes to measles-infected cells. Enhancement by prostaglandin E1.

We studied the effect of prostaglandins in vitro on an immune reaction mediated by T cells; adherence of lymphocytes to measles-virus-infected human epithelial cells. Normal human lymphocytes adhered to a mean +/- S.D. 20.1 +/- 5.2 per cent of these HEp-2 cells. The percentage positive cells increased to 50.3 +/- 5.7 when lymphocytes were incubated with 10(-6) M prostaglandin E1 (P less than 0.01 vs. untreated lymphocytes); 10(-8) M and 10(-10) M were as effective. Prostaglandin F2alpha had no effect on lymphocyte adherence. Prostaglandin E1 increased lymphocyte cyclic AMP five to 10 times whereas prostagladin F2alpha did not affect cellular levels of this nucleotide. Dibutyryl cyclic AMP (10(-8) M) increased lymphocyte adherence: positive human epithelial cells increased from 16.0 +/- 2.4 to 38.7 +/- 1.1 per cent (P less than 0.01). Prostagladin E1 also increased adherence of lymphocytes from patients with systemic lupus erythematosus from 21.8 +/- 5.8 to 52.5 +/- 9.2 per cent (P less than 0.01). These results indicate that prostagladin E1 and cyclic AMP may serve to stimulate T-cell function and cell-mediated immunity.

Antigens, Viral↗
PubMedDate not supplied

Endothelial cell activation following moderate traumatic brain injury.

Traumatic brain injury (TBI) initiates a cascade of acute and chronic injury responses which include disturbances in the cerebrovasculature that may result in the activation of the microvascular endothelial development of a dysfunction endothelium. The present study examines endothelial cell (EC) activation in a percussion model of moderate TBI. The criteria for endothelial activation used in these studies was surface expression of a number of markers collectively termed endothelial activation antigens. Temporal induction of the major histocompatibility (MHC) class II molecules, E-selectin (CD62E), vascular cell adhesion molecule (VACM-1) (CD106) as well as altered expression of constitutively expressed intercellular adhesion molecule-1 (ICAM-1) (CD54), the glucose transporter protein (glut-1), the transferrin receptor (tfR) (CD71), and MHC class I molecules was examined at various times following impact. Induction of E-selectin and increased expression of ICAM-1 was seen by 2 h post-impact (PI) and was sustained through 24 h PI. Decreased expression of immunologically reactive glut-1 and tfR was observed by 2-4 h PI and remained low up to 24 h PI. No induction of VCAM-1, MHC class II molecules or altered constitutive expression or MHC class I molecules was seen. Changes in EC activation were observed predominantly at the site of impact and were diminished temporarily. These results indicate that mild concussive injury to the brain results in activation of the endothelium.

ATP-Binding Cassette Transporters↗
PubMedDate not supplied

Zinc profiles in rheumatoid arthritis.

Evidence has accumulated which suggests that zinc may play an important role in immune function and inflammation. In this study we examined the zinc status in patients with rheumatoid arthritis (RA), osteoarthritis, other rheumatic diseases and healthy controls. Results indicate that serum and plasma zinc levels are decreased significantly in patients with RA. Reduced zinc values may be due to decreased albumin-bound and micromolecular protein-bound zinc.

Adult↗