A 'dry' condensation origin for circumstellar carbonates

The signature of carbonate minerals has long been suspected in the mid-infrared spectra of various astrophysical environments such as protostars. Abiogenic carbonates are considered as indicators of aqueous mineral alteration in the presence of CO2-rich liquid water. The recent claimed detection of calcite associated with amorphous silicates in two planetary nebulae and protostars devoid of planetary bodies questions the relevance of this indicator; but in the absence of an alternative mode of formation under circumstellar conditions, this detection remains controversial. The main dust component observed in circumstellar envelopes is amorphous silicates, which are thought to have formed by non-equilibrium condensation. Here we report experiments demonstrating that carbonates can be formed with amorphous silicates during the non-equilibrium condensation of a silicate gas in a H2O-CO2-rich vapour. We propose that the observed astrophysical carbonates have condensed in H2O(g)-CO2(g)-rich, high-temperature and high-density regions such as evolved stellar winds, or those induced by grain sputtering upon shocks in protostellar outflows.     

Mutations in genes in the renin-angiotensin system are associated with autosomal recessive renal tubular dysgenesis

Autosomal recessive renal tubular dysgenesis is a severe disorder of renal tubular development characterized by persistent fetal anuria and perinatal death, probably due to pulmonary hypoplasia from early-onset oligohydramnios (Potter phenotype). Absence or paucity of differentiated proximal tubules is the histopathological hallmark of the disease and may be associated with skull ossification defects. We studied 11 individuals with renal tubular dysgenesis, belonging to nine families, and found that they had homozygous or compound heterozygous mutations in the genes encoding renin, angiotensinogen, angiotensin converting enzyme or angiotensin II receptor type 1. We propose that renal lesions and early anuria result from chronic low perfusion pressure of the fetal kidney, a consequence of renin-angiotensin system inactivity. This is the first identification to our knowledge of a renal mendelian disorder linked to genetic defects in the renin-angiotensin system, highlighting the crucial role of the renin-angiotensin system in human kidney development.     

Low dose oral cannabinoid therapy reduces progression of atherosclerosis in mice

Atherosclerosis is a chronic inflammatory disease, and is the primary cause of heart disease and stroke in Western countries. Derivatives of cannabinoids such as delta-9-tetrahydrocannabinol (THC) modulate immune functions and therefore have potential for the treatment of inflammatory diseases. We investigated the effects of THC in a murine model of established atherosclerosis. Oral administration of THC (1 mg kg(-1) per day) resulted in significant inhibition of disease progression. This effective dose is lower than the dose usually associated with psychotropic effects of THC. Furthermore, we detected the CB2 receptor (the main cannabinoid receptor expressed on immune cells) in both human and mouse atherosclerotic plaques. Lymphoid cells isolated from THC-treated mice showed diminished proliferation capacity and decreased interferon-gamma secretion. Macrophage chemotaxis, which is a crucial step for the development of atherosclerosis, was also inhibited in vitro by THC. All these effects were completely blocked by a specific CB2 receptor antagonist. Our data demonstrate that oral treatment with a low dose of THC inhibits atherosclerosis progression in the apolipoprotein E knockout mouse model, through pleiotropic immunomodulatory effects on lymphoid and myeloid cells. Thus, THC or cannabinoids with activity at the CB2 receptor may be valuable targets for treating atherosclerosis.     

Effect of glucagon on ethanol oxidation in isolated rat liver cells

Summary Addition of glucagon 5 min after ethanol was found to stimulate the rate of ethanol oxidation in hepatocytes isolated from starved rats. This stimulation is of the same order of magnitude as that mediated by asparagine. The glucagon effect is suppressed by antiproteolytic agents such as insulin or NH₄Cl. The stimulatingeffect of glucagon on ethanol oxidation is probably liked to enhanced proteolysis andan elevated glutamate level in the hepatocytes.Acknowledgments. this investigation was supported by grants from the Institut de la Santé de la Recherche Médicale, the Scientific Council of the Faculté de Médecine Paris-Ouest and the Ecole Pratique des Hautes Etudes (3rd section).     

Longitudinal stress relaxation in the canine aorta

Résumé On a mesuré chez le chien la relaxation de la tension longitudinale en fonction de la déformation dans l'aorte, l'artère rénale et l'artère mésentérique supérieure. Dans les déformations équivalent à celles du vaisseau in vivo, la relaxation de la tension longitudinale est mise en relation avec les effets combinés de la teneur en collagène et des muscles lisses.

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This work was supported by Program Project Research Grant No. HL 07762 from the Public Health Service.     

Wnt and lithium: a common destiny in the therapy of nervous system pathologies?

Wnt signaling is required for neurogenesis, the fate of neural progenitors, the formation of neuronal circuits during development, neuron positioning and polarization, axon and dendrite development and finally for synaptogenesis. This signaling pathway is also implicated in the generation and differentiation of glial cells. In this review, we describe the mechanisms of action of Wnt signaling pathways and their implication in the development and correct functioning of the nervous system. We also illustrate how a dysregulated Wnt pathway could lead to psychiatric, neurodegenerative and demyelinating pathologies. Lithium, used for the treatment of bipolar disease, inhibits GSK3β, a central enzyme of the Wnt/β-catenin pathway. Thus, lithium could, to some extent, mimic Wnt pathway. We highlight the possible dialogue between lithium therapy and modulation of Wnt pathway in the treatment of the diseases of the nervous system.