Simulation of Alternative Marketing Strategies for U.S. Cotton

Three marketing strategies (selling a put option, cash sale at harvest, and cash sale in June) are simulated based on historical values and ranked based on certainty equivalents for a representative irrigated and dryland cotton farm Scenario analysis is also used to compare varying yield values.Simulation, Marketing, Cotton, Risk, Marketing, Research Methods/ Statistical Methods,

Kierkegaard: Poet Penitent

Kierkegaard: Poet Peniten

Kierkegaard on Self and Society

Kierkegaard on Self and Societ

HYDROGEN SULFIDE THERAPY ATTENUATES ISCHEMIA-INDUCED HEART FAILURE VIA NRF2 AND NRF1 SIGNALING

Codi d'Art Públic: 9008-1 (Cavalls desbocats)Ros Sabaté, Joaquim (Escultura); Batlle, Enric; Roig, Joa

Troglitazone, a PPAR-γ activator prevents endothelial cell adhesion molecule expression and lymphocyte adhesion mediated by TNF-α

BACKGROUND: Cytokine mediated induction of the mucosal addressin cell adhesion molecule-1(MAdCAM-1) expression is associated with the onset and progression of inflammatory bowel disease (IBD). RESULTS: Using western blotting and cell-based ELISA, we show in this study that troglitazone, an activator of the peroxisome proliferator-activated receptor-γ (PPAR-γ), widely used in the treatment of diabetes, has as well recently been highlighted as protective in models of inflammation and cancer. We found that troglitazone (10–40 μM), significantly reduced the TNF-α (1 ng/ml) mediated induction of endothelial MAdCAM-1 in a dose-dependent manner, achieving a 34.7% to 98.4% reduction in induced MAdCAM-1. Trogliazone (20μM) reduced TNF-α induced VCAM-1, ICAM-1 and E-selectin expression. Moreover, troglitazone significantly reduced α4β7-integrin dependent lymphocyte adhesion to TNF-α cultured endothelial cells. CONCLUSIONS: These results suggest that PPAR-γ agonists like troglitazone may be useful in the clinical treatment of IBD

Many-body interactions among adsorbed atoms and molecules within carbon nanotubes and in free space

This paper assesses the importance of three-body triple dipole interactions for quasi-one dimensional phases of He, Ne, H_2, Ar, Kr and Xe confined within interstitial channels or on the external surfaces of nanotube bundles. We find the substrate-mediated contribution to be substantial: for interstitial H_2 the well depth of the effective pair potential is reduced to approximately one half of its value in free space. We carry out ab initio calculations on linear and equilateral configurations of H_2 trimer and find that overlap interactions do not greatly change the DDD interaction in the linear configuration when the spacing is greater than about 3 A. However, the DDD interaction alone is clearly insufficient for the triangular configurations studied.Comment: 11 pages, 5 figure

Bax and Bak function as the outer membrane component of the mitochondrial permeability pore in regulating necrotic cell death in mice

A critical event in ischemia-based cell death is the opening of the mitochondrial permeability transition pore (MPTP). However, the molecular identity of the components of the MPTP remains unknown. Here, we determined that the Bcl-2 family members Bax and Bak, which are central regulators of apoptotic cell death, are also required for mitochondrial pore-dependent necrotic cell death by facilitating outer membrane permeability of the MPTP. Loss of Bax/Bak reduced outer mitochondrial membrane permeability and conductance without altering inner membrane MPTP function, resulting in resistance to mitochondrial calcium overload and necrotic cell death. Reconstitution with mutants of Bax that cannot oligomerize and form apoptotic pores, but still enhance outer membrane permeability, permitted MPTP-dependent mitochondrial swelling and restored necrotic cell death. Our data predict that the MPTP is an inner membrane regulated process, although in the absence of Bax/Bak the outer membrane resists swelling and prevents organelle rupture to prevent cell death

Mitochondrial calcium exchange links metabolism with the epigenome to control cellular differentiation.

Fibroblast to myofibroblast differentiation is crucial for the initial healing response but excessive myofibroblast activation leads to pathological fibrosis. Therefore, it is imperative to understand the mechanisms underlying myofibroblast formation. Here we report that mitochondrial calcium (mCa2+) signaling is a regulatory mechanism in myofibroblast differentiation and fibrosis. We demonstrate that fibrotic signaling alters gating of the mitochondrial calcium uniporter (mtCU) in a MICU1-dependent fashion to reduce mCa2+ uptake and induce coordinated changes in metabolism, i.e., increased glycolysis feeding anabolic pathways and glutaminolysis yielding increased α-ketoglutarate (αKG) bioavailability. mCa2+-dependent metabolic reprogramming leads to the activation of αKG-dependent histone demethylases, enhancing chromatin accessibility in loci specific to the myofibroblast gene program, resulting in differentiation. Our results uncover an important role for the mtCU beyond metabolic regulation and cell death and demonstrate that mCa2+ signaling regulates the epigenome to influence cellular differentiation