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Biomedical subjects

W Davis

Publications and source records attributed to W Davis.

At least 19 recordsLinked to original sources
PubMed1992

Calcitonin gene-related peptide in inflammatory bowel disease and experimentally induced colitis.

Pronounced changes in gut neuropeptide content have been observed in colonic tissues from animals with acute experimental colitis and in some patients with inflammatory bowel disease. The early decrease of CGRP in the colon during colitis in the animal studies suggest that CGRP is released during the inflammatory process. No data are available showing the biological action of released CGRP during inflammation. The sensory neurotoxin capsaicin was used in animal studies to examine the effect of sensory nerves on inflammation and healing in experimental animal models. The severity of colitis was enhanced after capsaicin pretreatment in acute and chronic animal models of colitis. These data support the hypothesis that sensory nerves exert a protective and healing-promoting function in the gut. CGRP is a good candidate for this action of sensory nerves because it is a major component in sensory nerve fibers. How CGRP exerts its protective function in the intestine is unknown. Data from gastric ulcer models support the hypothesis that a main action of CGRP is regulation of mesenteric and mucosal blood flow resulting in enhanced protection and tissue healing. Other effector roles of CGRP afferent nerve endings could also be considered.

Animals↗
PubMed1992

Bird antigen persistence in the home environment after removal of the bird.

Hypersensitivity pneumonitis (HP) secondary to bird exposure is treated with glucocorticosteroids and avoidance. Despite therapy, symptoms may persist for a prolonged time. Just as cat antigen, Fel d 1, may persist for greater than 20 weeks after cat removal, there may be persistent bird antigen to explain prolonged symptoms in bird HP. It was the intent of this study to determine household distribution and persistence of bird antigen after removal of the bird from the patient's home. The homes of patients with birds were followed serially after bird removal with multiple samples collected using a hand-held vacuum cleaner. Bird antigen levels were determined by an inhibition enzyme-linked immunoassay. In five homes the antigen declined gradually despite extensive environmental control measures, with high levels still detectable at 18 months in one home. This data suggests that high levels of bird antigen can be detected for prolonged periods of time after bird removal and environmental cleanup. The antigen may account for the persistence of disease in some patients with HP. In severe HP, the preferred therapy may be temporary relocation of the patient away from the room in which the bird was housed, in addition to corticosteroids, until the patient's environment is demonstrated to be relatively bird antigen-free.

Air Pollution↗
PubMed1991

A sensitive reverse passive haemagglutination immunoassay for hepatic caeruloplasmin.

A reverse passive haemagglutination assay for the measurement of caeruloplasmin in homogenates and organelle fractions prepared from needle biopsies of human liver tissue is described. Use of serial dilutions over a narrow range of concentrations permits accurate quantitation of caeruloplasmin down to 10 ng/ml, sufficient to detect the protein in needle biopsies with as little as 5 mg wet weight of tissue. Applied to the measurement of caeruloplasmin in human sera, the assay gives values which correlate well with those obtained by the standard radial immunodiffusion technique.

Biopsy, Needle↗
PubMed1991

Calcitonin gene-related peptide and substance P decrease in the rabbit colon during colitis. A time study.

The sensory neuropeptides, substance P and calcitonin gene-related peptide, have been implicated in inflammatory reactions in several tissues. An immune-complex model of colitis was used in rabbits to determine the colonic content (nmol/g protein) of immunoreactive substance P and calcitonin gene-related peptide at various times after induction of inflammation to assess changes in these neuropeptides during the inflammatory response. Calcitonin gene-related peptide content was decreased by 66% 4 hours after induction of inflammation and reached a maximum of 80% at 48 hours. The substance P content was decreased at 8 hours, with a maximum decrease of 64% at 48 hours. Substance P decrease was detected in the muscle layer. The amounts of substance P in the mucosal/submucosal layer extracts were too low to allow accurate measurements. Calcitonin gene-related peptide decreased both in the muscle and the mucosal-submucosal layers. Immunohistochemical analysis showed that calcitonin gene-related peptide and substance P innervation patterns were comparable in normal and inflamed colon, even though there appeared to be a decrease in density and intensity of the staining, particularly for calcitonin gene-related peptide at 48 hours. The early decrease of calcitonin gene-related peptide and substance P during the time course of colitis might be due to release from nerve terminals of the gut during the inflammatory response. The profound changes in colonic calcitonin gene-related peptide and substance P content during colitis may have important implications during inflammation and subsequent tissue repair and may also lead to disturbances in gut motility.

Animals↗
PubMed1990

Activation of human T cell clones through the UM4D4/CDw60 surface antigen.

UM4D4 is a recently defined antigen that is expressed on approximately 25% of peripheral blood T cells, but on the majority of T cells in inflammatory synovial fluid. Anti-UM4D4 activates peripheral blood T cells in the presence of accessory cells and/or phorbol ester. UM4D4 has been assigned to a new antigen cluster termed CDw60. The present study examined the ability of anti-UM4D4 to activate T cell clones derived from the synovial fluid of patients with rheumatoid arthritis. UM4D4 was expressed at varying levels on both lectin-generated and antigen-specific clones, including clones of CD4+, CD8+, and CD4-CD8- phenotypes. Anti-UM4D4 used in soluble form as a single stimulus was typically mitogenic for the CD4+ and some of the CD8+ clones, but not for the CD4-CD8- clones. Phorbol ester boosted the response to anti-UM4D4 in some clones, had no effect in others, and diminished the responses in some cases. In contrast to anti-UM4D4, anti-CD3 was generally not mitogenic in soluble form, although it was mitogenic when conjugated to beads. The data show that T cell clones derived from an inflammatory T cell infiltrate can be readily activated through the UM4D4/CDw60 antigen.

Antibodies, Monoclonal↗
PubMed1990

Trends in the geographic inequality of cardiovascular disease mortality in the United States, 1962-1982.

Substantial geographic variation of cardiovascular disease (CVD) mortality within the U.S. has been recognized for decades. Analyses reported here address the question of whether relative geographic inequality has increased or decreased during the period of rapidly declining CVD mortality 1962-1982. Trends in geographic inequality, as measured by the weighted coefficient of variation of State Economic Area rates, are analyzed for whites and blacks by sex for 10-year age groups 35-44 to 85 and over. The average annual percent change in the coefficient of variation for each demographic group is presented for all cause mortality, all CVD, stroke and ischemic heart disease. In general, geographic inequalities declined in total mortality for all except the youngest age group. This is consistent with reports of a strong convergence of age-adjusted cancer mortality in U.S. counties. By contrast, increasing geographic inequality dominates in the CVD categories, especially for whites in heart disease and stroke. At younger ages, increases in the coefficient of variation for all race-sex groups exceeded 1% per year in stroke and 2% per year in heart disease. These results suggest that factors influencing the percent decline of CVD mortality are not reaching communities of the U.S. equally. Since increases in relative inequality are strongest in the younger age groups, the pattern of inequality may be accentuated as these cohorts move into ages of higher mortality.

Adult↗
PubMed1990

Activation pathways of synovial T lymphocytes. Expression and function of the UM4D4/CDw60 antigen.

Accumulating evidence implicates a central role for synovial T cells in the pathogenesis of rheumatoid arthritis, but the activation pathways that drive proliferation and effector function of these cells are not known. We have recently generated a novel monoclonal antibody against a rheumatoid synovial T cell line that recognizes an antigen termed UM4D4 (CDw60). This antigen is expressed on a minority of peripheral blood T cells, and represents the surface component of a distinct pathway of human T cell activation. The current studies were performed to examine the expression and function of UM4D4 on T cells obtained from synovial fluid and synovial membranes of patients with rheumatoid arthritis and other forms of inflammatory joint disease. The UM4D4 antigen is expressed at high surface density on about three-fourths of synovial fluid T cells and on a small subset of synovial fluid natural killer cells; in synovial tissue it is present on more than 90% of T cells in lymphoid aggregates, and on approximately 50% of T cells in stromal infiltrates In addition, UM4D4 is expressed in synovial tissue on a previously undescribed population of HLA-DR/DP-negative non-T cells with a dendritic morphology. Anti-UM4D4 was co-mitogenic for both RA and non-RA synovial fluid mononuclear cells, and induced IL-2 receptor expression. The UM4D4/CDw60 antigen may represent a functional activation pathway for synovial compartment T cells, which could play an important role in the pathogenesis of inflammatory arthritis.

Adult↗
PubMed1988

Zombification.

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Ceremonial Behavior↗