Biography:

In the past David M. Pinson has collaborated on articles with Marilyn S. Smith and Shakil A. Saghir. One of their most recent publications is Alimentary tractDrug-induced hypergastrinemia: Absence of trophic effects on colonic carcinoma in rats☆. Which was published in journal Gastroenterology.

More information about David M. Pinson research including statistics on their citations can be found on their Copernicus Academic profile page.

David M. Pinson's Articles: (4)

Alimentary tractDrug-induced hypergastrinemia: Absence of trophic effects on colonic carcinoma in rats☆

AbstractBackground/Aims: Published studies suggest that hypergastrinemia stimulates growth of normal or malignant colon tissue. Other studies dispute these findings. This study was designed to test the hypothesis that hypergastrinemia enhances progression or invasiveness of colon cancer. Methods: Colonic carcinomas were induced in male Sprague-Dawley rats by six weekly intraperitoneal injections of methylazoxymethanol. Four weeks after the last injection of carcinogen, the animals were randomized into four treatment groups, including vehicle control, low- and high-dose omeprazole, and ranitidine. After 10 weeks of treatment, the animals were bled, stomach weights were recorded, and colon tumors were mapped, enumerated, measured, and scored histopathologically by Dukes' classification. Crypt and mucosal heights were determined in colonic mucosa unaffected by tumor. Results: Drug administration induced a sustained hypergastrinemia that did not enhance tumor burden or invasiveness or crypt height/mucosal height ratios. Ranitidine-treated rats consumed less food, weighed less, and developed fewer tumors. This group also had lower crypt and mucosal heights than rats in the vehicleor omeprazole-treated rats. Conclusions: The results suggest that endogenous hypergastrinemia induced by these acid-suppressing drugs has no stimulatory effect on colon mucosal growth or progression or biological behavior of experimental rat colon cancer.

Activation-associated marker proteins: Peptide mapping and their expression in macrophage cell lines

SummaryThe activation-associated markers, p47b and p71/73, have been recognized as minor proteins in peritoneal and bone marrow culture-derived macrophages activated for tumor cell killing. Proteins with identical characteristics of migration on 2-dimensional gels and comparable Cleveland peptide maps are described here in macrophage cell lines that could be activated for tumor cell killing (J774A.1, RAW 264, UNC-2). Macrophage cell lines that could not be activated (P388D1 and PU5-1.8) did not express the markers. The expression of these markers in activatable macrophage cell lines strengthens their association with the activation process and provides a bulk source of the proteins for purification studies.

Regular ArticleSystemic Infection and Limited Replication of SHIV Vaccine Virus in Brains of Macaques Inoculated Intracerebrally with Infectious Viral DNA

AbstractSHIV deleted in two accessory genes, ΔvpuΔnef SHIVPPC, functioned well as a vaccine against later challenge with highly pathogenic SHIVKU, and it was able to reach the brain after oral inoculation of live virus. In this study, the proviral genome cloned into a plasmid was inoculated as DNA intracerebrally and spread systemically. Few regions of the brain had detectable proviral DNA by real-time PCR. Two measures of virus replication, detection of viral mRNA expression and circular proviral DNA, were negative for those brain regions, with the exception of the infection site in the right parietal lobe, whereas lymphoid tissues were positive by both measures. Histopathological analyses of all the sampled brain and spinal cord regions did not reveal any abnormalities. Despite intracerebral inoculation of the viral DNA, the brain was not targeted for high levels of virus replication.

Validation of Haber's Rule (dose × time = constant) in rats and mice for monochloroacetic acid and 2,3,7,8-tetrachlorodibenzo-p-dioxin under conditions of kinetic steady state

AbstractHaber's Rule and associated time to coma after monochloroacetic acid (MCA) exposure in male Sprague–Dawley (SD) rats and time to death after 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure in female Sprague–Dawley rats and male A/J mice were investigated at isoeffective or nearly isoeffective doses. Animals exposed to MCA received either single bolus intravenous (iv) doses or a loading dose rate via the iv route followed by a maintenance dose rate through subcutaneously implanted osmotic mini pumps. For TCDD, rats received a loading dose rate via bolus oral gavage followed by maintenance dose rates through iv injection every fourth day until death. Mice received both loading and maintenance (once a week) dose rates via oral gavage. Different dosing regimens were employed to demonstrate that the key to Haber's Rule lies not in the route of administration but in conducting experiments under conditions of kinetic steady state. Single doses of MCA produced inconsistent time responses but a reasonably constant c × t product (7657 ± 391 mg/kg × min) which was not anticipated although it should have been expected because MCA's elimination half-life (2 h) is twice as long as its time to coma (∼1 h). Generation of kinetic steady state by infusion of MCA after iv injection of a loading dose rate resulted in a consistently decreasing time response with increasing dose which diminished the variability in the c × t (dose × time) = k relationship (8032 ± 136 mg/kg × min). Both acute and chronic toxicity of TCDD under conditions of kinetic steady state yielded consistent time responses with inverse proportionality between dose and time leading to robust c × t = k products in both rats (1060 ± 82 μg/kg × day) and mice (80 ± 2 mg/kg × day).

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