<p> The development of new medical treatments for patients is limited by the challenges of recruiting clinical-research participants. In the United States, the Food and Drug Administration regulates the multidimensional approval process for new drugs, biologics, and medical devices to ensure consumer safety. The regulatory approval processes includes complex clinical trials that necessitate either healthy volunteers or patients who are willing to participate. The low enrollment rates of volunteers and patients willing to participate in clinical trials are resulting in significant delays in bringing new treatments to the market and substantially increasing development costs, for which consumers ultimately pay. The available research indicates that young adults and adolescents represent two of the lowest participating groups in clinical trials. Even though they are the next generation of consumers and patients, little to no research has examined the adolescent and young adult populations and their knowledge and perceptions of clinical research or their willingness to participate in clinical trials. Understanding these populations' perspectives and knowledge of the drug-development process and providing education regarding on this issue may have a profound, positive trickle-down effect on medicine, their personal well-being, and the well-being of the general public. </p><p> This study used a simple experimental design consisting of an intervention group and a control group. The intervention was a 10-minute educational video on participation in clinical research. Adolescents and young adults (<i> n</i> = 527) were randomly distributed into the two groups. The knowledge, perceptions, and willingness to participate in clinical research were measured in both groups utilizing a 31-question survey instrument. The findings from this study may be used by educators, health care providers, patient advocacy groups, payers, and the pharmaceutical research and development industry to determine the best methods for educating adolescents and young adults on clinical research and trial participation. </p><p> The study concluded with a discussion of the importance of the role of leadership in social change and the process of igniting and sustaining such change. This process includes how, historically, public and private interests have come together to positively influence important public-health initiatives and, in turn, social change that holistically benefited all of society. Moving forward, leadership for social change could potentially deliver new and improved medical treatments in a timelier manner.</p>

Thesis (Ph.D.)--Arizona State University, 2005. / (UnM)AAI3194930. Source: Dissertation Abstracts International, Volume: 66-11, Section: B, page: 5749. Adviser: William (Dennis) Clark.

Thesis (Ed.D.)--Teachers College, Columbia University, 1992. / Includes tables. Typescript; issued also on microfilm. Sponsor: Carmine Paul Gibaldi. Dissertation Committee: L. Lee Knefelkamp. Includes bibliographical references (leaves 164-168).

Thesis (Ph.D.)--Fairleigh Dickinson University, 1998. / Source: Dissertation Abstracts International, Volume: 59-10, Section: B, page: 5592. Chairperson: Neil A. Massoth. Includes bibliographical references (leaves [99]-111).

Introduction. Adverse drug events (ADEs) caused by medication errors occur regularly in hospitals. Research questions. (1) How effective are in-hospital drug-distribution technologies at improving medication safety? (2) How prevalent are such technologies in Canada's acute-care hospitals? Methods. A systematic review synthesized publications from 1985 to 2002 about the effectiveness of inpatient drug-distribution technologies. A cross-sectional survey of pharmacy directors at Canada's 100 largest acute-care hospitals described technology use, plans for change, and pharmacy-directors' attitudes to technology use and medication error. Results. The systematic review categorized 154 technology comparisons into 23 technology groupings. The evidence consistently favoured the new technologies but its strength was limited. The survey response rate was 78%. Clinical pharmacy services, computerized decision support for pharmacists, and unit-dose system were common; bar-coding and computerized physician order entry were not. Conclusion. This thesis offers a unique compilation of evidence to guide decision-makers in their uptake of technologies intended to improve medication safety.

The presence of pharmaceuticals in the aquatic environment is a growing area of concern. The objective of this thesis was to examine the effects of statin drugs, a class of pharmaceuticals prescribed to lower endogenous cholesterol production by inhibiting 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCoAR), in the rainbow trout Oncorhynchus mykiss. The study also aimed to provide some insight into mechanisms governing the control of HMGCoAR in fish. Two statin drugs were used in this study, cerivastatin (CVT) and atorvastatin (AVT). Cerivastatin inhibited hepatic microsomal and brain homogenate HMGCoAR activities when incubated in vitro and following an in vivo intra-peritoneal injection. Atorvastatin reduced HMGCoAR activity in vitro following incubation with liver microsomes and brain homogenates. Fasting trout for 14 days resulted in a significant decrease in plasma cholesterol and glucose levels compared with the fed-controls. A significant decrease was observed in brain homogenates prepared from fish fasted for 14 days and re-fed for 7 days. Phosphorylation is an important regulator of mammalian HMGCoAR activities. In trout a significant decrease in HMGCoAR activity was observed when liver microsomes were incubated in a buffer that should stimulate AMPK. Two HMGCoAR subtypes were found in rainbow trout. HMGCoAR-1 mRNA is present in higher quantities than HMGCoAR-2 however HMGCoAR-1 is located in a limited number of tissues. HMGCoAR-2 mRNA appeared in all tissues assessed. The results of this thesis indicate that HMGCoAR shares some similar control mechanisms with mammals. These results also demonstrate that statin drugs in the aquatic environment have the potential to disrupt HMGCoAR in fish.

Le brain-derived neurotrophic factor (BDNF) est une protéine de la famille des neurotrophines ayant été initialement découverte au système nerveux central, où elle est impliquée dans la mémoire et l‘apprentissage par la régulation de la croissance et de la survie neuronale. Les effets du BDNF sont médiés par le tropomyosin receptor kinase B (TrkB) et le récepteur pan-neurotrophique de 75 kDa (p75NTR). Le BDNF est le résultat du clivage d’une protéine précurseur, le proBDNF, laquelle a plutôt des effets pro-apoptotiques sur les neurones. Malgré sa découverte au cerveau, le BDNF est retrouvé en concentrations beaucoup plus importantes dans la circulation sanguine, où il est majoritairement contenu dans les plaquettes. Il est rapporté que ces cellules peuvent contenir des concentrations de BDNF allant de 100 à 1000 fois celles retrouvées au cerveau et que celles-ci peuvent être altérées par certaines maladies neurologiques. Malgré les importantes concentrations de BDNF qu’elles contiennent, très peu d’études ont investigué la présence du proBDNF ainsi que des récepteurs TrkB et p75NTR dans les plaquettes. Dans ces études, l’identification de ces protéines au niveau plaquettaire ne représentait pas un objectif primaire et les résultats obtenus ne sont souvent pas présentés. Jusqu’à présent, le proBDNF et les récepteurs TrkB et p75NTR n’ont pas été répertoriés dans les plaquettes. L’objectif principal de ce mémoire était d’investiguer la présence du proBDNF ainsi que des récepteurs TrkB et p75NTR dans les plaquettes de volontaires sains humains et de caractériser ces protéines dans le cas où elles seraient présentes. Les résultats obtenus suggèrent que les plaquettes expriment chacune de ces trois protéines, mais que les isoformes retrouvées au niveau plaquettaire diffèrent de celles retrouvées au cerveau. Les résultats proposent également que ces différences ne résident pas dans le profil de N-glycosylation des protéines. L’identité exacte des protéines étudiées n’a pas pu être confirmée par séquençage et leur nature demeure donc à confirmer. La présence plaquettaire du proBDNF et des récepteurs TrkB et p75NTR pourrait s’avérer intéressante au niveau des biomarqueurs périphériques de certaines maladies neuronales et psychiatriques. Leur présence pourrait aussi permettre la progression des connaissances dans le domaine de la biologie plaquettaire. / The brain-derived neurotrophic factor (BDNF) is a protein that was initially identified in the central nervous system, where it is involved in learning and memory by promoting neuronal growth and survival. These effects of BDNF are mediated through its binding to the tropomyosin receptor kinase B (TrkB) and the 75 kDa pan-neurotrophic receptor (p75NTR). Mature BDNF results from the cleavage of its precursor protein proBDNF, which rather has a proapoptotic effect on neurons. While discovered in the brain, BDNF is found in much higher abundance in the blood circulation, where it is mostly contained within platelets. It has been shown that BDNF concentration in platelets can reach up to 1000 times those of the brain, and that peripheral BDNF levels are altered in certain neurological and psychiatric diseases. Despite these important BDNF concentrations in platelets, very few studies assessed the presence of proBDNF, TrkB and p75NTR in these cells. Furthermore, identification of these proteins in platelets was not a main objective of the studies that did assess that question. Consequently, methodology is not always described, and the results are mostly reported as data not shown. Until now, proBDNF, TrkB and p75NTR have not been reported in platelets. The main objective of this master’s thesis was to investigate the presence of proBDNF as well as receptors TrkB and p75NTR in healthy human platelets, and to characterize them if they were found in these cells. The results suggest that platelets express all three proteins, but that the isoforms found in platelets differ from the ones found in the brain. Also, the results show that these differences are not explained by differential N-glycosylation patterns. The identity of the proteins of interest could not be verified by protein sequencing, and their exact nature is yet to be confirmed. The presence of proBDNF as well as the TrkB and p75NTR receptors in platelets could be of interest in the search of peripheral biomarkers for neurological diseases. In addition, presence of these proteins at the platelet level could pave the way for further studies investigating their functions in platelets, and possibly result in advances in our knowledge of platelet biology.

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