6,141 research outputs found

    A High-Mass Protobinary System in the Hot Core W3(H2O)

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    We have observed a high-mass protobinary system in the hot core W3(H2O) with the BIMA Array. Our continuum maps at wavelengths of 1.4mm and 2.8mm both achieve sub-arcsecond angular resolutions and show a double-peaked morphology. The angular separation of the two sources is 1.19" corresponding to 2.43X10^3 AU at the source distance of 2.04 kpc. The flux densities of the two sources at 1.4mm and 2.8mm have a spectral index of 3, translating to an opacity law of kappa ~ nu. The small spectral indices suggest that grain growth has begun in the hot core. We have also observed 5 K components of the CH3CN (12-11) transitions. A radial velocity difference of 2.81 km/s is found towards the two continuum peaks. Interpreting these two sources as binary components in orbit about one another, we find a minimum mass of 22 Msun for the system. Radiative transfer models are constructed to explain both the continuum and methyl cyanide line observations of each source. Power-law distributions of both density and temperature are derived. Density distributions close to the free-fall value, r^-1.5, are found for both components, suggesting continuing accretion. The derived luminosities suggest the two sources have equivalent zero-age main sequence (ZAMS) spectral type B0.5 - B0. The nebular masses derived from the continuum observations are about 5 Msun for source A and 4 Msun for source C. A velocity gradient previously detected may be explained by unresolved binary rotation with a small velocity difference.Comment: 38 pages, 9 figures, accepted by The Astrophysical Journa

    Language control and parallel recovery of language in individuals with aphasia

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    Background: The causal basis of the different patterns of language recovery following stroke in bilingual speakers is not well understood. Our approach distinguishes the representation of language from the mechanisms involved in its control. Previous studies have suggested that difficulties in language control can explain selective aphasia in one language as well as pathological switching between languages. Here we test the hypothesis that difficulties in managing and resolving competition will also be observed in those who are equally impaired in both their languages even in the absence of pathological switching. Aims: To examine difficulties in language control in bilingual individuals with parallel recovery in aphasia and to compare their performance on different types of conflict task. Methods & procedures: Two right-handed, non-native English-speaking participants who showed parallel recovery of two languages after stroke and a group of non-native English-speaking, bilingual controls described a scene in English and in their first language and completed three explicit conflict tasks. Two of these were verbal conflict tasks: a lexical decision task in English, in which individuals distinguished English words from non-words, and a Stroop task, in English and in their first language. The third conflict task was a non-verbal flanker task. Outcomes & Results: Both participants with aphasia were impaired in the picture description task in English and in their first language but showed different patterns of impairment on the conflict tasks. For the participant with left subcortical damage, conflict was abnormally high during the verbal tasks (lexical decision and Stroop) but not during the non-verbal flanker task. In contrast, for the participant with extensive left parietal damage, conflict was less abnormal during the Stroop task than the flanker or lexical decision task. Conclusions: Our data reveal two distinct control impairments associated with parallel recovery. We stress the need to explore the precise nature of control problems and how control is implemented in order to develop fuller causal accounts of language recovery patterns in bilingual aphasia

    Open-target sparse sensing of biological agents using DNA microarray

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    Background Current biosensors are designed to target and react to specific nucleic acid sequences or structural epitopes. These 'target-specific' platforms require creation of new physical capture reagents when new organisms are targeted. An 'open-target' approach to DNA microarray biosensing is proposed and substantiated using laboratory generated data. The microarray consisted of 12,900 25 bp oligonucleotide capture probes derived from a statistical model trained on randomly selected genomic segments of pathogenic prokaryotic organisms. Open-target detection of organisms was accomplished using a reference library of hybridization patterns for three test organisms whose DNA sequences were not included in the design of the microarray probes. Results A multivariate mathematical model based on the partial least squares regression (PLSR) was developed to detect the presence of three test organisms in mixed samples. When all 12,900 probes were used, the model correctly detected the signature of three test organisms in all mixed samples (mean(R2)) = 0.76, CI = 0.95), with a 6% false positive rate. A sampling algorithm was then developed to sparsely sample the probe space for a minimal number of probes required to capture the hybridization imprints of the test organisms. The PLSR detection model was capable of correctly identifying the presence of the three test organisms in all mixed samples using only 47 probes (mean(R2)) = 0.77, CI = 0.95) with nearly 100% specificity. Conclusions We conceived an 'open-target' approach to biosensing, and hypothesized that a relatively small, non-specifically designed, DNA microarray is capable of identifying the presence of multiple organisms in mixed samples. Coupled with a mathematical model applied to laboratory generated data, and sparse sampling of capture probes, the prototype microarray platform was able to capture the signature of each organism in all mixed samples with high sensitivity and specificity. It was demonstrated that this new approach to biosensing closely follows the principles of sparse sensing.Mitre Corporatio

    Caffeine protects against experimental acute pancreatitis by inhibition of inositol 1,4,5-trisphosphate receptor-mediated Ca 2+ release

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    Objective Caffeine reduces toxic Ca2+ signals in pancreatic acinar cells via inhibition of inositol 1,4,5-trisphosphate receptor (IP3R)-mediated signalling, but effects of other xanthines have not been evaluated, nor effects of xanthines on experimental acute pancreatitis (AP). We have determined effects of caffeine and its xanthine metabolites on pancreatic acinar IP3R-mediated Ca2+ signalling and experimental AP. Design Isolated pancreatic acinar cells were exposed to secretagogues, uncaged IP3 or toxins that induce AP and effects of xanthines, non-xanthine phosphodiesterase (PDE) inhibitors and cyclic adenosine monophosphate and cyclic guanosine monophosphate (cAMP/cGMP) determined. The intracellular cytosolic calcium concentration ([Ca2+]C), mitochondrial depolarisation and necrosis were assessed by confocal microscopy. Effects of xanthines were evaluated in caerulein-induced AP (CER-AP), taurolithocholic acid 3-sulfate-induced AP (TLCS-AP) or palmitoleic acid plus ethanol-induced AP (fatty acid ethyl ester AP (FAEE-AP)). Serum xanthines were measured by liquid chromatography-mass spectrometry. Results Caffeine, dimethylxanthines and non-xanthine PDE inhibitors blocked IP3-mediated Ca2+ oscillations, while monomethylxanthines had little effect. Caffeine and dimethylxanthines inhibited uncaged IP3-induced Ca2+ rises, toxin-induced Ca2+ release, mitochondrial depolarisation and necrotic cell death pathway activation; cAMP/cGMP did not inhibit toxin-induced Ca2+ rises. Caffeine significantly ameliorated CER-AP with most effect at 25 mg/kg (seven injections hourly); paraxanthine or theophylline did not. Caffeine at 25 mg/kg significantly ameliorated TLCS-AP and FAEE-AP. Mean total serum levels of dimethylxanthines and trimethylxanthines peaked at >2 mM with 25 mg/kg caffeine but at <100 µM with 25 mg/kg paraxanthine or theophylline. Conclusions Caffeine and its dimethylxanthine metabolites reduced pathological IP3R-mediated pancreatic acinar Ca2+ signals but only caffeine ameliorated experimental AP. Caffeine is a suitable starting point for medicinal chemistr
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