Models of quintessence coupled to the electromagnetic field and the cosmological evolution of alpha

We study the change of the effective fine structure constant in the cosmological models of a scalar field with a non-vanishing coupling to the electromagnetic field. Combining cosmological data and terrestrial observations we place empirical constraints on the size of the possible coupling and explore a large class of models that exhibit tracking behavior. The change of the fine structure constant implied by the quasar absorption spectra together with the requirement of tracking behavior impose a lower bound of the size of this coupling. Furthermore, the transition to the quintessence regime implies a narrow window for this coupling around $10^{-5}$ in units of the inverse Planck mass. We also propose a non-minimal coupling between electromagnetism and quintessence which has the effect of leading only to changes of alpha determined from atomic physics phenomena, but leaving no observable consequences through nuclear physics effects. In doing so we are able to reconcile the claimed cosmological evidence for a changing fine structure constant with the tight constraints emerging from the Oklo natural nuclear reactor.Comment: 13 pages, 10 figures, RevTex, new references adde

The HIV-1 envelope protein, gp120, causes neuronal apoptosis in the neocortex of the adult rat:a useful experimental model to study neuroAIDS

The viral protein gp120 causes apoptosis in rat cortex. The effects of the HIV-1 coat protein gp120 given into one lateral cerebral ventricle (i.c.v.) on the expression of cyclooxygenase type 2 (COX-2) and PGE(2) levels, studied using Western blotting and ELISA techniques is described. Enhanced COX-2 expression is implicated in the mechanisms of apoptosis evoked by gp120 because the latter is prevented by NS398 (10 mg/kg i.p.), a selective inhibitor of COX-2 activity. Protection is also afforded by NMDA receptor antagonists, such as MK801 (0.3 mg/kg i.p.) and CGP040116 (10 mg/kg i.p.), and by the free radical scavenger, U-74389G (10 mg/kg i.p.), supporting a glutamate-mediated, excitotoxic, mechanism of apoptotic death induced by gp120. The products of the arachidonic cascade may be responsible for elevation of synaptic glutamate leading neocortical cells to oxidative stress and excitotoxic apoptosis

Identification of transglutaminase 3 splicing isoforms [9]

[No abstract available

Neuroprotection by the caspase-1 inhibitor Ac-YVAD-(acyloxy)mk in experimental neuroAIDS is independent from IL-1β generation

[No abstract available

Modulation of the endocannabinoid system by focal brain ischemia in the rat is involved in neuroprotection afforded by 17 beta-estradiol

Endogenous levels of the endocannabinoid anandamide, and the activities of the synthesizing and hydrolyzing enzymes, i.e. N-acylphosphatidylethanolamine-hydrolyzing phospholipase D and fatty acid amide hydrolase, respectively, were determined in the cortex and the striatum of rats subjected to transient middle cerebral artery occlusion. Anandamide content was markedly increased (similar to 3-fold over controls; P < 0.01) in the ischemic striatum after 2 h of middle cerebral artery occlusion, but not in the cortex, and this elevation was paralleled by increased activity of N-acylphosphatidylethanolamine-hydrolyzing phospholipase D (similar to 1.7-fold; P < 0.01), and reduced activity (similar to 0.6-fold; P < 0.01) and expression (similar to 0.7-fold; P < 0.05) of fatty acid amide hydrolase. These effects of middle cerebral artery occlusion were further potentiated by 1 h of reperfusion, whereas anandamide binding to type 1 cannabinoid and type 1 vanilloid receptors was not affected significantly by the ischemic insult. Additionally, the cannabinoid type 1 receptor antagonist SR141716, but not the receptor agonist R-(+)-WIN55,212-2, significantly reduced (33%; P < 0.05) cerebral infarct volume detected 22 h after the beginning of reperfusion. A neuroprotective intraperitoneal dose of 17 beta-estradiol (0.20 mg.kg(-1)) that reduced infarct size by 43% also minimized the effect of brain ischemia on the endocannabinoid system, in an estrogen receptor-dependent manner. In conclusion, we show that the endocannabinoid system is implicated in the pathophysiology of transient middle cerebral artery occlusion-induced brain damage, and that neuroprotection afforded by estrogen is coincident with a re-establishment of anandamide levels in the ischemic striatum through a mechanism that needs to be investigated further