Globalizing the Ethics of Care: Policy, Transformation, and Judgment

his thesis argues that the ethics of care is an important lens through which to view complex international moral and political contexts. Specifically, I argue care ethics offers a different perspective than human rights discourses, because the relational perspective care ethics offers generates different questions, and thus different answers, about the moral and political landscape than the traditionally individualist perspective of mainstream human rights theories. This thesis does not deny the usefulness of human rights analysis, but instead questions their assumed pride of place, especially when assessing and addressing contexts such as severe poverty, gender and race oppression, and the activity of care work itself. Further, this thesis argues that the ethics of care is, in some situations, the better philosophical tool for the task at hand.«br /» Fiona Robinson’s body of work on a global ethic of care is central to this project. She claims that global institutional relations structure our lives and our relationships with others, and as such, are a prime target for a critical care analysis, revealing the ways in which governments, corporations, and social norms shape our lives. In particular, her focus is on how such institutions perpetuate harmful relations of power, which continue to marginalize women and the work of care itself from public consideration. This critical care analysis prioritizes understanding the root causes of such moral and political contexts in order to transform the way in which we approach and judge these contexts, which in turn would allow us to craft longer lasting and more holistic solutions. «br /» The global care ethic, however, has faced sharp criticism about its ability to be a prescriptive theory because of its contextual flexibility. I engage with the work of Daniel Engster and Kimberly Hutchings, who each critique the global, critical ethic of care. Engster argues that critical care ethics is too flexible to be practicable, especially where public policy is concerned, and as such he argues a ‘care based’ human rights theory provides better action guidance. Conversely, Hutchings’ critique of care ethics criticises the universalization of the standpoint of care, which then negates its usefulness in making intelligible moral judgments across cultures.«br /» I reject Engster’s ‘caring’ human rights and argue that care ethics can be a substantive guide for public policy. I do so by critiquing Engster’s version of care theory, and then using care ethics to examine real world case studies of public policy to demonstrate its practical applications. I also reject Hutchings’ final claim, arguing we need not relinquish the standpoint of care as an important moral point of view. Instead, I argue that the critical ethic of care is, in fact, able to outline a means by which we can reach moral and political judgments across cultures, spurring the transformation of our moral and political landscape

Marked Suppression of Ghrelin Concentration by Insulin in Prader-Willi Syndrome

The plasma ghrelin has been reported to be elevated in Prader-Willi syndrome (PWS) and modulated by insulin. It was hypothesized that insulin might have a more pronounced effect on reducing plasma ghrelin in PWS patients, which would influence appetite. This study investigated the degree of ghrelin suppression using an euglycemic hyperinsulinemic clamp in children with PWS (n=6) and normal children (n=6). After a 90-min infusion of insulin, the plasma ghrelin level decreased from a basal value of 0.86±0.15 to 0.58±0.12 ng/mL in the controls, and from 2.38±0.76 to 1.12±0.29 ng/mL in children with PWS (p=0.011). The area under the curve below the baseline level over the 90 min insulin infusion was larger in children with PWS than in controls (-92.82±44.4 vs. -10.41±2.87 ng/mL/90 min) (p=0.011). The insulin sensitivity measured as the glucose infusion rate at steady state was similar in the two groups (p=0.088). The decrease in the ghrelin levels in response to insulin was more pronounced in the children with PWS than in the controls. However, the level of ghrelin was always higher in the children with PWS during the clamp study. This suggests that even though insulin sensitivity to ghrelin is well maintained, an increase in the baseline ghrelin levels is characteristic of PWS

Structure And Enzymology Of The Chemotaxis Histidine Kinase, Chea

Bacterial chemotaxis enables changes in motility via response to the surrounding chemical environment and is noted for its high signal gain, range, and sensitivity. The efficacy of the bacterial chemotaxis signaling pathway is highly dependent on the propagation of the extracellular chemical signal through a hexagonal array comprised of: methyl-accepting chemotaxis protein receptors, histidine kinase CheA, and coupling protein CheW. CheA is the principal enzyme in the chemotaxis pathway and is composed of five domains (P1-5). Initiation of the phospho-relay by CheA ends in rotational switching of the flagellar rotor. CheA only achieves a broad range of autophosphorylation activity when associated with chemoreceptors. This dissertation focuses on the structural and biochemical changes during the CheA autophosphorylation event. The propensity of Thermotoga maritima CheA to naturally undergo trans autophosphorylation was elucidated and strategic mutations enabled generation of disulfide-locked CheA variants to further probe protein dynamics. Employing small-angle x-ray scattering (SAXS), the resting state of CheA was determined to be globular. Where upon nucleotide addition the protein transitioned to a dynamic state as a result of the movement of P1 and P4 domains to facilitate transfer of the [gamma]-phosphate. Coupling crystallographic and biochemical data, a model was generated of CheA that is able to account for variances in enzymatic activity, incorporating key structural features to the functional response of signal transduction. To further the understanding the influence the receptors impart to CheA, chemoreceptor cytoplasmic kinase-control modules based on the E. coli aspartate receptor, Tar, were covalently fused into a dimer and trimerized by a foldon domain (TarFO). SAXS, multiangle light scattering, and pulsed-dipolar electron paramagnetic resonance spectroscopy of spinlabeled proteins indicate that the TarFO is soluble, monodisperse, and assembles into homogenous trimers wherein the protein interaction regions closely associate at the opposite ends of the foldon domain. The TarFO activates CheA autophosphorylation to the same degree as membrane integrated receptors and stabilizes a planar conformation of the kinase consistent with current array models for the assembly state of the ternary complex. Overall, these studies illuminate a planar CheA active structure and provide a more in depth investigation of the CheA autophosphorylation event