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For thesis abstract select View Thesis Title, Contents and Abstract

For thesis abstract select View Thesis Title, Contents and Abstract

Graduation date: 1999

Bacterial cultures enriched from sheep rumen fluid have demonstrated the ability to detoxify pyrrolizidine alkaloids (seneciphylline and jacobine) in tansy ragwort (Senecio jacobaea). The microbes are difficult to isolate using classical anaerobic techniques, therefore, microbes from two different enrichment cultures demonstrating similar degradation activity were identified using their 16S ribosomal RNA genes. Gene sequences from a rich medium enrichment were matched to Clostridium bifermentans, Prevotella ruminicola, Escherichia coif, and from a minimal medium enrichment to, C. clostridiiforme, C. aminophilum, Streptococcus bovis, and Butyrivibrio fibrosolvens. There were no identical organisms between the two libraries, but the common genus was Clostridium. / Graduation date: 1998

Thesis (Ph. D.)--Rutgers University, 2009. / "Graduate Program in Toxicology." Includes bibliographical references (p. 62-72).

A dose related carcinogenic response was established for dimethylnitrosamine administered in the diet of rainbow trout (Salmo gairdneri). An equation was derived for the relationship between dose and hepatocellular carcinoma incidence. From a published dose response study using Porton rats as a test animal, a second equation was derived for comparison. The rat and the trout were approximately equivalent in their sensitivity to dimethylnitrosamine carcinogenesis. The histological nature of the carcinogenic response in trout was similar to to that of mammalian species. Apart from carcinogenesis, no indications of chronic toxicity were observed after a one year feeding experiment. The median lethal dose after intraperitoneal injection of dimethylnitrosamine was 1,770 mg/kg body weight in rainbow trout. Relative to the range of 15 to 50 mg/kg body weight reported for several mammalian species, trout were resistant to the acutely toxic effects of dimethylnitrosamine. / Graduation date: 1977

Capsaicin, the primary pungent component of hot peppers, produced chemogenic and thermal antinociception within two hours after administration to adult guinea pigs (2-8 mg/kg). Antinociception lasted in excess of 10 days. In addition, in somewhat higher doses (4-25 mg/kg s.c.) capsaicin also depleted the putative peptide neurotransmitter, substance P, from primary afferent neurons. Depletion of substance P by capsaicin did not occur until at least one day after capsaicin treatment and the onset of antinociception. Antinociception produced by capsaicin appeared to be a result of bioactivation and covalent binding of capsaicin to the distal ends of sensory neurons. Capsaicin depleted substance P from sensory nerves by inhibiting the rate of substance P synthesis by 48 percent. Inhibition of substance P synthesis by capsaicin occurred with some degree of specificity as the rate at which total protein was synthesized was unchanged. The biochemical mechanism by which capsaicin altered substance P synthesis involved alterations in the retrograde axoplasmic transport of nerve growth factor. Doses of capsaicin which depleted substance P also inhibited the retrograde axoplasmic transport of nerve growth factor. Inhibition of the retrograde transport of nerve growth factor by capsaicin preceded substance P depletion. Supplementation of guinea pigs with mouse nerve growth factor completely prevented capsaicin-induced substance P depletion. It is concluded that capsaicin depletes substance P from primary afferent neurons of the adult guinea pig by altering the availability of NGF. The data support a role for NGF in the normal maintenance of neuropeptide levels in some sensory neurons in the adult animal.

No description available.

<p> Radiation is a ubiquitous health risk. Contemporary populations are exposed to several hundred milliSieverts per person over their lifetimes from both natural and human made sources such as radon, cosmic rays, CT-scans, etc. Risk estimates based on studies of atomic bomb survivors suggest that these exposures induce excess cancer mortality at a rate of several percent per Sievert. </p><p> To develop accurate risk estimates, it is important to recognize that contemporary exposures are different than atomic bomb survivor exposures. Instead of a single acute high dose rate exposure from an atomic explosion, populations today experience many small, protracted exposures accumulating to moderate total doses over their lifetimes. Therefore, in order to estimate the risk of contemporary exposures using atomic bomb survivor data, it is important to determine the differences in radiation dose response following acute vs. protracted exposures. </p><p> The committee to estimate the biological effects of ionizing radiation exposure in humans (BEIR) is one of the central authorities in the United States tasked with estimating radiation risk. Their seventh and most recent report (BEIR VII) written in 2006 estimated that contemporary protracted exposures induce 1.5 fold less risk than atomic bomb survivor exposures. </p><p> The work presented in this dissertation leverages a large body of historical animal mortality data to argue that BEIR VII overestimates the risk of protracted exposures. Concretely, evidence is presented from animal exposures that support the concept that contemporary protracted exposures induce about 2 fold less risk than atomic bomb survivor exposures.</p>