Sea Contributions to Spin 1/2 Baryon Structure, Magnetic Moments, and Spin Distribution

We treat the baryon as a composite system made out of a \lq\lq core" of three quarks (as in the standard quark model) surrounded by a \lq\lq sea" (of gluons and $q\bar{q}$-pairs) which is specified by its total quantum numbers like flavor, spin and color. Specifically, we assume the sea to be a flavor octet with spin 0 or 1 but no color. The general wavefunction for spin 1/2 baryons with such a sea component is given. Application to the magnetic moments is considered. Numerical analysis shows that a scalar (spin 0) sea with an admixture of a vector (spin 1) sea can provide very good fits to the magnetic moment data {\em using experimental errors}. Our best fit automatically gives $g_A/g_V$ for neutron beta decay in agreement with data. This fit also gives reasonable values for the spin distributions of the proton and neutron.Comment: 24 pages, REVTEX. References modifie

A priori mixed hadrons, hyperon non-leptonic decays, and the |\Delta I|=1/2 rule

The |\Delta I|=1/2 rule in non-leptonic decays of hyperons can be naturally understood by postulating a priori mixed physical hadrons, along with the isospin invariance of the responsible transition operator. It is shown that this operator can be identified with the strong interaction Yukawa hamiltonian.Comment: Workshops on Particles and Fields and Phenomenology of Fundamental Interactions. J. C. D'Olivo, A. Fernandez, and M. A. Perez, Ed

Endoplasmic reticulum stress, degeneration of pancreatic islet β-cells, and therapeutic modulation of the unfolded protein response in diabetes.

BackgroundMyriad challenges to the proper folding and structural maturation of secretory pathway client proteins in the endoplasmic reticulum (ER) - a condition referred to as "ER stress" - activate intracellular signaling pathways termed the unfolded protein response (UPR).Scope of reviewThrough executing transcriptional and translational programs the UPR restores homeostasis in those cells experiencing manageable levels of ER stress. But the UPR also actively triggers cell degeneration and apoptosis in those cells that are encountering ER stress levels that exceed irremediable thresholds. Thus, UPR outputs are "double-edged". In pancreatic islet β-cells, numerous genetic mutations affecting the balance between these opposing UPR functions cause diabetes mellitus in both rodents and humans, amply demonstrating the principle that the UPR is critical for the proper functioning and survival of the cell.Major conclusionsSpecifically, we have found that the UPR master regulator IRE1α kinase/endoribonuclease (RNase) triggers apoptosis, β-cell degeneration, and diabetes, when ER stress reaches critical levels. Based on these mechanistic findings, we find that novel small molecule compounds that inhibit IRE1α during such "terminal" UPR signaling can spare ER stressed β-cells from death, perhaps affording future opportunities to test new drug candidates for disease modification in patients suffering from diabetes

Religious Groups and Climate Change - Drivers, Barriers and Religious Engagement on Climate Change

This thesis looks at the drivers and barriers religious groups within the United States face on the climate change issue as well as the actions religious groups have taken on the issue as a means for encouraging social and individual changes in behavior to address it. It examines the role of religion in shaping values, investigates the drivers and barriers identified through academic literature sources and then compares those drivers and barriers against the statements issued by religious groups and through a survey conducted by the author. Case studies on two religious groups are also presented to offer further detail regarding the types of programs and activities undertaken by religious groups to promote positive change on the climate change issue