TAROT: A status report

TAROT-1 is an automatic, autonomous ground based observatory whose primary goal is the rapid detection of the optical counterparts of cosmic gamma-ray burst sources. It will be able to begin imaging any GRB localization 8 seconds after receipt of an alert from CGRO/BATSE or HETE-2. TAROT-1 will reach the 17th V magnitude in 10 seconds, at a 10$\sigma$ confidence level. TAROT will be able to observe GRB positions given by Beppo-SAX or RXTE, EUV transients from ALEXIS alerts, etc. TAROT will also study a wide range of secondary objectives and will feature a complete automatic data analysis system, and a powerful scheduling software. TAROT will be installed this fall on the Plateau du Calern, 1200m above sea level. We report on the status of the project.Comment: 5 pages. To appear in the proceedings of the 4th Huntsville Gamma-Ray Burst Symposium, eds C.A. Meegan and P. Cushma

Involvement of pholcodine in the cause of death in 127 forensic cases in France

Date du colloque&nbsp;: 2008</p

Primerjava toksičnosti etanola in acetaldehida za podganje astrocite v primarni kulturi

This study compared the effects of toxicity of ethanol and its first metabolite acetaldehyde in rat astrocytes through cell viability and cell proliferation. The cells were treated with different concentrations of ethanol in the presence or absence of a catalase inhibitor 2-amino-1,2,4 triazole (AMT) or with different concentrations of acetaldehyde. Cell viability was assessed using the trypan blue test. Cell proliferation was assessed after 24 hours and after seven days of exposure to either ethanol or acetaldehyde. We showed that both ethanol and acetaldehyde decreased cell viability in a dose-dependent manner. In proliferation studies, after seven days of exposure to either ethanol or acetaldehyde, we observed a significant dose-dependent decrease in cell number. The protein content study showed biphasic dose-response curves, after 24 hours and seven days of exposure to either ethanol or acetaldehyde. Co-incubation in the presence of AMT significantly reduced the inhibitory effect of ethanol on cell proliferation. We concluded that long-term exposure of astrocytes to ethanol is more toxic than acute exposure. Acetaldehyde is a much more potent toxin than ethanol, and at least a part of ethanol toxicity is due to ethanol’s first metabolite acetaldehyde.V študiji smo primerjali toksičnost etanola in njegovega prvega metabolita acetaldehida za podganje astrocite z določitvijo celične viabilnosti in proliferacije. Celične kulture smo tretirali z različnimi koncentracijami etanola, etanola v prisotnosti inhibitorja katalaze 2-amino-1,2,4 triazol-a (AMT) ali z različnimi koncentracijami acetaldehida. Celično viabilnost smo vrednotili s pomočjo testa s tripanskim modrilom, celično proliferacijo pa s štetjem celic in določitvijo koncentracije proteinov po 24-urni, kot tudi 7-dnevni izpostavljenosti. S študijo smo pokazali, da tako etanol kot tudi acetaldehid v odvisnosti od njune koncentracije zmanjšata celično viabilnost. V študiji proliferacije sta etanol in acetaldehid, v odvisnosti od njunih koncentracij, značilno zmanjšala število celic po 7-dnevni izpostavljenosti. Pri ugotavljanju vsebnosti proteinov smo dobili bifazno krivuljo tako po 24-urni, kot tudi po 7-dnevni izpostavljenosti različnim koncentracijam etanola oziroma acetaldehida. Prisotnost AMT je signifi kantno zmanjšala učinek etanola na celično proliferacijo. Zaključimo lahko, da je dolgotrajna izpostavljenost astrocitov etanolu bolj toksična kot akutna. Acetaldehid je močnejši toksin kot etanol in vsaj del toksičnosti etanola je posledica delovanja njegovega prvega metabolita, acetaldehida

Rupture of the left ventricle due to blunt trauma – A pediatric case study and literature review

International audienc

Gas Chromatographic Quantitation of Dextropropoxyphene and Norpropoxyphene in Urine after Solid-Phase Extraction

A gas chromatographic technique with flame ionization detection, which is based on a solid-phase extraction (SPE) procedure using mixed-mode SPE columns, for the simultaneous quantitation of dextropropoxyphene and norpropoxyphene in urine is presented. Urine is treated with sodium hydroxide in order to rearrange, by base catalysis, norpropoxyphene to norpropoxyphene amide, which is then extracted with these columns and chromatographed. The method is specific, linear over the range 0-2000 ng/mL, sensitive, and reproducible. The extracts are cleaner than those obtained with traditional liquid-liquid extraction procedure, which is an important feature in view of further mass spectrometric confirmation of narcotics and other drugs