SN 2008S: an electron capture SN from a super-AGB progenitor?

We present comprehensive photometric and spectroscopic observations of the faint transient SN 2008S discovered in NGC 6946. SN 2008S exhibited slow photometric evolution and almost no spectral variability during the first nine months, implying a high density CS medium. The light curve is similar in shape to that of SN 1998S and SN 1979C, although significantly fainter at maximum light. Our quasi-bolometric lightcurve extends to 300 days and shows a tail phase decay rate consistent with that of ^{56}Co. We propose that this is evidence for an explosion and formation of ^{56}Ni (0.0015 +/- 0.0004 M_Sun). The large MIR flux detected shortly after explosion can be explained by a light echo from pre-exisiting dust. The late NIR flux excess is plausibly due to a combination of warm newly-formed ejecta dust together with shock-heated dust in the CS environment. We reassess the progenitor object detected previously in Spitzer archive images, supplementing this discussion with a model of the MIR spectral energy distribution. This supports the idea of a dusty, optically thick shell around SN 2008S with an inner radius of nearly 90AU and outer radius of 450AU, and an inferred heating source of 3000 K and luminosity of L ~ 10^{4.6} L_Sun. The combination of our monitoring data and the evidence from the progenitor analysis leads us to support the scenario of a weak electron capture supernova explosion in a super-AGB progenitor star (of initial mass 6-8 M_sun) embedded within a thick CS gaseous envelope. We suggest that all of main properties of the electron capture SN phenomenon are observed in SN 2008S and future observations may allow a definitive answer.Comment: accepted for publication in MNRAS (2009 May 7

Methamphetamine Preconditioning Alters Midbrain Transcriptional Responses to Methamphetamine-Induced Injury in the Rat Striatum

Methamphetamine (METH) is an illicit drug which is neurotoxic to the mammalian brain. Numerous studies have revealed significant decreases in dopamine and serotonin levels in the brains of animals exposed to moderate-to-large METH doses given within short intervals of time. In contrast, repeated injections of small nontoxic doses of the drug followed by a challenge with toxic METH doses afford significant protection against monoamine depletion. The present study was undertaken to test the possibility that repeated injections of the drug might be accompanied by transcriptional changes involved in rendering the nigrostriatal dopaminergic system refractory to METH toxicity. Our results confirm that METH preconditioning can provide significant protection against METH-induced striatal dopamine depletion. In addition, the presence and absence of METH preconditioning were associated with substantial differences in the identity of the genes whose expression was affected by a toxic METH challenge. Quantitative PCR confirmed METH-induced changes in genes of interest and identified additional genes that were differentially impacted by the toxic METH challenge in the presence of METH preconditioning. These genes include small heat shock 27 kD 27 protein 2 (HspB2), thyrotropin-releasing hormone (TRH), brain derived neurotrophic factor (BDNF), c-fos, and some encoding antioxidant proteins including CuZn superoxide dismutase (CuZnSOD), glutathione peroxidase (GPx)-1, and heme oxygenase-1 (Hmox-1). These observations are consistent, in part, with the transcriptional alterations reported in models of lethal ischemic injuries which are preceded by ischemic or pharmacological preconditioning. Our findings suggest that multiple molecular pathways might work in tandem to protect the nigrostriatal dopaminergic pathway against the deleterious effects of the toxic psychostimulant. Further analysis of the molecular and cellular pathways regulated by these genes should help to provide some insight into the neuroadaptive potentials of the brain when repeatedly exposed to drugs of abuse

Optical Coherence Tomography as a Tool for In Vivo Staging and Grading of Upper Urinary Tract Urothelial Carcinoma: A Study of Diagnostic Accuracy

Purpose: Biopsies and cytology are cornerstones in the diagnosis of upper urinary tract urothelial carcinoma. However, a high rate of nondiagnostic biopsies, tumor upgrading and tumor up staging after nephroureterectomy has been observed. In this prospective in vivo study we evaluated the diagnostic accuracy of optical coherence tomography for the grading and staging of upper tract urothelial carcinoma. Materials and Methods: A total of 26 patients underwent diagnostic ureterorenoscopy including biopsies and optical coherence tomography, followed by nephroureterectomy or segmental ureter resection. The sensitivity, specificity, negative predictive value and positive predictive value of upper tract urothelial carcinoma grading and staging by optical coherence tomography were evaluated according to the STARD (Standards for Reporting of Diagnostic Accuracy) initiative and the second stage (2a and 2b) of the IDEAL model. For tumor staging a 2 x 2 table for sensitivity and specificity was calculated. For tumor grading the Wilcoxon rank sum test was used to test mu(oct) in low and high grade lesions followed by ROC analysis for sensitivity and specificity. Results: In 83% the staging of lesions was in accordance with final histopathology. Sensitivity and specificity analysis for tumor invasion was 100% and 92%, respectively. Tumor size greater than 2 mm and inflammation were risks for false-positives. For low and high grade lesions median moct was 2.1 and 3.0 mm(-1), respectively (p <0.01). ROC analysis showed a sensitivity of 87% and a specificity of 90% using a mu(oct) cutoff of 2.4 mm(-1). Conclusions: This report describes optical coherence tomography as a real-time, intraoperatively diagnostic modality in the diagnostic evaluation of upper tract urothelial carcinoma. We confirmed the ability of optical coherence tomography to visualize, grade and stage urothelial carcinoma in the upper urinary trac