This document only includes an excerpt of the corresponding thesis or dissertation. To request a digital scan of the full text, please contact the Ruth Lilly Medical Library's Interlibrary Loan Department (rlmlill@iu.edu).

This document only includes an excerpt of the corresponding thesis or dissertation. To request a digital scan of the full text, please contact the Ruth Lilly Medical Library's Interlibrary Loan Department (rlmlill@iu.edu).

A subcutaneous injection of sodium selenite (30 umol/kg body weight) in 10â day old rats produced a cataract within 72 hours. Lens opacification was preceded by a 15% decrease in ATP content. Lens ATP did not fully recover to control concentrations by 11 days post-injection. A moderate correlation existed between lens weight and total ATP content in control lenses <r=O.509, n=153), but this relationship disappeared with selenite treatment <r=0.023, n=153). There was a significant inhibition by selenite on lens growth from 4 through 11 days after an injection. / Master of Science

Thesis (Ph. D.)--University of Virginia, 2008. / Title from title page. Includes bibliographical references. Also available online through Digital Dissertations.

A series of laboratory experiments and a field investigation were conducted to closely define the application of the ATP assay and ATP as a planktonic biomass estimator for routine use in reservoir limnology. The laboratory experiments verified the published range of C:ATP ratios (i.e. 250:1) as a conversion factor for ATP to biomass in cultured selected genera of freshwater algae, except for the species of blue-green algae examined. The field investigation conducted at Moss Reservoir included organic carbon measurements with ATP biomass in size classes on a depth basis. The ATP biomass varied seasonally and with depth; the best significant mtltiple correlation was between organic carbon and the smallest size class (.45 to 10 um) and total net plankton biomass (.45 to 165 um). Daily monitoring of biomass in size classes demonstrated the sensitivity of the technique.

Thesis (Ph. D.)--University of Missouri--Columbia, 1998. / Typescript. Vita. Includes bibliographical references (l. 140-148). Also available on the Internet.

published_or_final_version / Physiology / Doctoral / Doctor of Philosophy

N^6,O^2' -Dibutyryl cyclic adenosine 3',5'-monophosphate (Bt_2cAMP) was investigated for its effects on various tissue culture cells infected with temperature-sensitive (ts) mutant, LA31 and Bratislava 77 (B77), a wild-type Rous sarcoma virus. Specifically, known parameters of transformation were investigated and a possible site of action has been tenably proposed. The drug Bt_2cAMP was found to have little effect on the transformation related properties of primary chick embryo fibroblasts (CEF) infected with either virus or normal rat kidney fibroblasts (NRK) infected with the wild-type B77-RSV. However, significant inhibition of the transforming properties in NRK infected with the ts mutant LA31 (LA31-NRK) were reported at the permissive temperature 33 degrees centigrade (33 C).

Bladder pain syndrome (BPS)/interstitial cystitis (IC) is a chronic pain disorder characterized by at least six weeks of lower urinary tract symptoms and unpleasant sensations (pain, pressure and discomfort) thought to be related to the urinary bladder and not meeting exclusion criteria. While the etiology is not known, BPS/IC may involve a "vicious circle" of uroepithelial dysfunction, inflammation and peripheral and central sensitization. We propose that the urinary bladder inflammatory insult partly mediates voiding dysfunction and visceral neurogenic pain characteristic of BPS/IC. Several studies from our laboratory have already demonstrated the role(s) of cytokines and their downstream targets in the functional alterations in micturition reflex pathways following chemically (cyclophosphamide, CYP)-induced cystitis. More recently, the pleiotropic protein, TGF-β, has been implicated in the pathogenesis of CYP-induced cystitis. TGF-β is activated locally at the initial site of injury by protease-dependent or protease-independent mechanisms to initiate a proinflammatory milieu. Depending on its contextual cues, TGF-β may then aid in resolving the primary immune response and support tissue repair. Though TGF-β is necessary to maintain normal immunological function, its aberrant expression and activation may have detrimental effects on responding tissues and cell types. A sustained increase in peripheral TGF-β reactivity, such as what may be observed in chronic inflammatory bladder conditions, may influence bladder afferent excitability to amplify nociceptive transmission and CNS input. The subsequent sensitization of peripheral afferent nociceptors at the level of the DRG or urothelium may promote spinal cord "wind-up" and cascade into visceral hyperalgesia and allodynia. In the first aim of this dissertation we investigated the functional profile of TGF-β isoforms and receptor (TβR) variants in the normal and inflamed (CYP-induced cystitis) urinary bladder with qRT-PCR, ELISA, IHC and in vivo cystometry. Our studies determined (i) the involvement of TGF-β in lower urinary tract neuroplasticity following urinary bladder inflammation, (ii) a functional role for TGF-β signaling in the afferent limb of the micturition reflex and (iii) urinary bladder TβR-1 as a viable target to reduce voiding frequency with cystitis. In the second aim of this dissertation we investigated the sensory components of the urinary bladder that may underlie the pathophysiology of aberrant TGF-β activation with bladder-pelvic nerve electrophysiology and luciferin-luciferase assays for ATP measurement. Our studies determined that TGF-β1 increased bladder afferent nerve excitability by stimulating ATP release from the urothelium via vesicular exocytosis mechanisms with minimal contribution from pannexin-1 channels. Furthermore, blocking aberrant TGF-β signaling in CYP-induced cystitis with TβR-1 inhibition decreased afferent nerve excitability with an equivalent decrease in ATP release. Taken together, these results establish a causal link between an inflammatory mediator, TGF-β, and intrinsic signaling mechanisms of the urothelium that may contribute to the altered sensory processing of bladder filling to facilitate increased voiding frequency. The distinct interactions of multiple mediators underscore the challenges for single target therapies and support the development of combinatory therapeutics for bladder dysfunction. Ultimately, these studies have increased our understanding of functional disorders and visceral pain and have the potential to improve the health of those suffering from inflammation-associated bladder syndromes.

While coffee culture has long since been positively associated with intellectual and working life, the health and safety of its primary stimulant, caffeine, has recently fallen under scrutiny by the FDA. This medical anthropology thesis provides a biocultural synthesis of caffeine culture, health effects, and biological variation in adverse effects related to pharmacodynamics and pharmacokinetics. Supporting evidence for variation in responses to caffeine was found through surveying 100 participants, investigating caffeine consumption levels, perceptions and health beliefs, adverse effects experienced, and medical encounters. Increased rates of adverse effects were found for students, pharmaceutical and over-the-counter drug users, and for participants reporting negative or ambivalent perceptions of caffeine, intolerance, or sensitivity to caffeine. Variation in rates of adverse effects suggests biocultural interactions account not only for patterns in pharmacological data, but are also clinically significant in constructing risk of caffeine intoxication. / Includes bibliography. / Thesis (M.A.)--Florida Atlantic University, 2014. / FAU Electronic Theses and Dissertations Collection