10 research outputs found
Psychology and BAPCPA: Enhanced Disclosure and Emotion
This article describes a program of research that applies social analytic jurisprudence to test some of the assumptions in consumer bankruptcy law and policy.4 Our work first seeks to describe selected provisions from the newly enacted bankruptcy amendments that pertain to enhanced disclosure requirements, and then to locate some of the behavioral assumptions implicit in these provisions. 5 Next, we assess the accuracy of these assumptions based on an experiment that we conducted looking at a simulated online shopping trip that we constructed specifically to test the effects of enhanced disclosur
Interaction and Modulation of Two Antagonistic Cell Wall Enzymes of Mycobacteria
Bacterial cell growth and division require coordinated cell wall hydrolysis and synthesis, allowing for the removal and expansion of cell wall material. Without proper coordination, unchecked hydrolysis can result in cell lysis. How these opposing activities are simultaneously regulated is poorly understood. In Mycobacterium tuberculosis, the resuscitation-promoting factor B (RpfB), a lytic transglycosylase, interacts and synergizes with Rpf-interacting protein A (RipA), an endopeptidase, to hydrolyze peptidoglycan. However, it remains unclear what governs this synergy and how it is coordinated with cell wall synthesis. Here we identify the bifunctional peptidoglycan-synthesizing enzyme, penicillin binding protein 1 (PBP1), as a RipA-interacting protein. PBP1, like RipA, localizes both at the poles and septa of dividing cells. Depletion of the ponA1 gene, encoding PBP1 in M. smegmatis, results in a severe growth defect and abnormally shaped cells, indicating that PBP1 is necessary for viability and cell wall stability. Finally, PBP1 inhibits the synergistic hydrolysis of peptidoglycan by the RipA-RpfB complex in vitro. These data reveal a post-translational mechanism for regulating cell wall hydrolysis and synthesis through protein–protein interactions between enzymes with antagonistic functions
Motivation & Loss Aversion in the Health Savings Account Paradigm
This investigation examined the role of “loss aversion” and consumers’ motivational orientations in the context of healthcare purchasing under the individual account paradigm and the defined benefit (insurance) paradigm. Specifically, this dissertation investigated (1) whether Health Savings Accounts (HSAs) encourage more prudent health care spending compared to traditional health insurance plans and (2) the impact of individuals\u27 motivational preferences (either towards “gains” or towards “losses”) between decision tasks under each type of health plan.
Three experiments varied the type of healthcare plan that consumers had and the manner in which they received information (either as a “gain” or “loss”). The experiments examined (a) intentions to obtain skin cancer screening and willingness to pay for cancer screening, (b) intentions to obtain an immunization injection and willingness to pay for it, and (c) preferred treatment option in the face of an imagined lung cancer and willingness to pay for each of the two possible treatments.
The results reveal several interesting findings. Individuals’ knowledge about their healthcare plans was consistently a significant factor. Individuals with a high degree of knowledge would spend less money on healthcare services than would individuals with less knowledge.
Individuals’ motivational orientations were also consistently influential. A persistent motivational tendency towards “promotion” concerns increased the likelihood that individuals would obtain certain healthcare services and enhanced the amount of money participants would spend on other services. Conversely, a persistent motivational tendency towards “prevention” concerns decreased the likelihood that individuals would obtain certain healthcare services and decreased the amount of money individuals would spend on other services.
Moreover, the experiments yielded some evidence of loss aversion, albeit inconsistently. The findings support the conclusion that the framing of healthcare information can impact the choice-behaviors of healthcare consumers.
As a whole, this investigation helps advance our understanding of how the individual account paradigm interfaces with decision making errors and how “loss aversion” may impact healthcare choices. The results have implications for both psychological theories of decision making and healthcare policy.
Adviser: Richard Wiene
Motivation & loss aversion in the health savings account paradigm
This investigation examined the role of “loss aversion” and consumers\u27 motivational orientations in the context of healthcare purchasing under the individual account paradigm and the defined benefit (insurance) paradigm. Specifically, this dissertation investigated (1) whether Health Savings Accounts (HSAs) encourage more prudent health care spending compared to traditional health insurance plans and (2) the impact of individuals\u27 motivational preferences (either towards “gains” or towards “losses”) between decision tasks under each type of health plan. Three experiments varied the type of healthcare plan that consumers had and the manner in which they received information (either as a “gain” or “loss”). The experiments examined (a) intentions to obtain skin cancer screening and willingness to pay for cancer screening, (b) intentions to obtain an immunization injection and willingness to pay for it, and (c) preferred treatment option in the face of an imagined lung cancer and willingness to pay for each of the two possible treatments. The results reveal several interesting findings. Individuals\u27 knowledge about their healthcare plans was consistently a significant factor. Individuals with a high degree of knowledge would spend less money on healthcare services than would individuals with less knowledge. Individuals\u27 motivational orientations were also consistently influential. A persistent motivational tendency towards “promotion” concerns increased the likelihood that individuals would obtain certain healthcare services and enhanced the amount of money participants would spend on other services. Conversely, a persistent motivational tendency towards “prevention” concerns decreased the likelihood that individuals would obtain certain healthcare services and decreased the amount of money individuals would spend on other services. Moreover, the experiments yielded some evidence of loss aversion, albeit inconsistently. The findings support the conclusion that the framing of healthcare information can impact the choice-behaviors of healthcare consumers. As a whole, this investigation helps advance our understanding of how the individual account paradigm interfaces with decision making errors and how “loss aversion” may impact healthcare choices. The results have implications for both psychological theories of decision making and healthcare policy
Serotonylation of small GTPases is a signal transduction pathway that triggers platelet alpha-granule release
Serotonin is a neurotransmitter in the central nervous system. In the periphery, serotonin functions as a ubiquitous hormone involved in vasoconstriction and platelet function. Serotonin is synthesized independently in peripheral tissues and neurons by two different rate-limiting tryptophan hydroxylase (TPH) isoenzymes. Here, we show that mice selectively deficient in peripheral TPH and serotonin exhibit impaired hemostasis, resulting in a reduced risk of thrombosis and thromboembolism, although the ultrastructure of the platelets is not affected. While the aggregation of serotonin-deficient platelets in vitro is apparently normal, their adhesion in vivo is reduced due to a blunted secretion of adhesive -granular proteins. In elucidating the mechanism further, we demonstrate that serotonin is transamidated to small GTPases by transglutaminases during activation and aggregation of platelets, rendering these GTPases constitutively active. Our data provides evidence for a receptor-independent signaling mechanism, termed herein as "serotonylation," which leads to -granule exocytosis from platelets