Motor Vehicle Crash Fatalities for Week Ending, January 8, 2010

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Motor Vehicle Crash Fatalities for Week Ending, January 15, 2010

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Motor Vehicle Crash Fatalities for Week Ending, January 22, 2010

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Motor Vehicle Crash Fatalities for Week Ending, January 29, 2010

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Motor Vehicle Crash Fatalities for Week Ending, February 5, 2010

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Motor Vehicle Crash Fatalities for Week Ending, February 12, 2010

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Motor Vehicle Crash Fatalities for Week Ending, February 19, 2010

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Motor Vehicle Crash Fatalities for Week Ending, February 29, 2010

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Somatosensory motor bodily representation cortical thinning in Tourette : effects of tic severity, age and gender

Introduction: Tourette syndrome (TS) implicates the disinhibition of the cortico-striatal-thalamic-cortical circuitry (CSTC). Previous studies used a volumetric approach to investigate this circuitry with inconsistent findings. Cortical thickness may represent a more reliable measure than volume due to the low variability in the cytoarchitectural structure of the grey matter. Methods: 66 magnetic resonance imaging scans were acquired from 34 TS (age range 10-25, mean 17.19±4.1) and 32 normal controls (NC) (age range 10-20, mean 16.33±3.56). Brain morphology was assessed using the fully automated Civet pipeline at the Montreal Neurological Institute. Results: We report (1) significant cortical thinning in the fronto-parietal and somatosensory-motor cortices in TS relative to NC (p<0.05); (2) TS boys showed thinner cortex relative to TS girls in the fronto-parietal cortical regions (p<0.05); (3) significant decrease in the fronto-parietal mean cortical thickness in TS with age relative to NC and in the pre-central cortex in TS boys relative to TS girls; (4) significant negative correlations between tic severity and the somatosensory-motor cortical thickness. Conclusions: TS revealed important thinning in brain regions particularly involved in the somatosensory/motor bodily representations which may play an important role in tics. Our findings are in agreement with Leckman et al. (1991) hypothesis stating that facial tics would be associated with dysfunction in an orofacial subset of the motor circuit, eye blinking with the occulo-motor circuit, whereas lack of inhibition to a dysfunction in the prefrontal cortex. Gender and age differences may reflect differential etiological factors, which have significant clinical relevance in TS and should be considered in developing and using diagnostic and therapeutic interventions.

Motor Vehicle Crash Fatalities for Week Ending, March 5, 2010

Motor Vehicle Crash Fatalities

Brain dynamics underlying training-induced improvement in suppressing inappropriate action.

Inhibitory control, a core component of executive functions, refers to our ability to suppress intended or ongoing cognitive or motor processes. Mostly based on Go/NoGo paradigms, a considerable amount of literature reports that inhibitory control of responses to "NoGo" stimuli is mediated by top-down mechanisms manifesting ∼200 ms after stimulus onset within frontoparietal networks. However, whether inhibitory functions in humans can be trained and the supporting neurophysiological mechanisms remain unresolved. We addressed these issues by contrasting auditory evoked potentials (AEPs) to left-lateralized "Go" and right NoGo stimuli recorded at the beginning versus the end of 30 min of active auditory spatial Go/NoGo training, as well as during passive listening of the same stimuli before versus after the training session, generating two separate 2 × 2 within-subject designs. Training improved Go/NoGo proficiency. Response times to Go stimuli decreased. During active training, AEPs to NoGo, but not Go, stimuli modulated topographically with training 61-104 ms after stimulus onset, indicative of changes in the underlying brain network. Source estimations revealed that this modulation followed from decreased activity within left parietal cortices, which in turn predicted the extent of behavioral improvement. During passive listening, in contrast, effects were limited to topographic modulations of AEPs in response to Go stimuli over the 31-81 ms interval, mediated by decreased right anterior temporoparietal activity. We discuss our results in terms of the development of an automatic and bottom-up form of inhibitory control with training and a differential effect of Go/NoGo training during active executive control versus passive listening conditions.

Reactivation of protein aggregates by mortalin and Tid1-the human mitochondrial Hsp70 chaperone system.

The mitochondrial 70-kDa heat shock protein (mtHsp70), also known in humans as mortalin, is a central component of the mitochondrial protein import motor and plays a key role in the folding of matrix-localized mitochondrial proteins. MtHsp70 is assisted by a member of the 40-kDa heat shock protein co-chaperone family named Tid1 and a nucleotide exchange factor. Whereas, yeast mtHsp70 has been extensively studied in the context of protein import in the mitochondria, and the bacterial 70-kDa heat shock protein was recently shown to act as an ATP-fuelled unfolding enzyme capable of detoxifying stably misfolded polypeptides into harmless natively refolded proteins, little is known about the molecular functions of the human mortalin in protein homeostasis. Here, we developed novel and efficient purification protocols for mortalin and the two spliced versions of Tid1, Tid1-S, and Tid1-L and showed that mortalin can mediate the in vitro ATP-dependent reactivation of stable-preformed heat-denatured model aggregates, with the assistance of Mge1 and either Tid1-L or Tid1-S co-chaperones or yeast Mdj1. Thus, in addition of being a central component of the protein import machinery, human mortalin together with Tid1, may serve as a protein disaggregating machine which, for lack of Hsp100/ClpB disaggregating co-chaperones, may carry alone the scavenging of toxic protein aggregates in stressed, diseased, or aging human mitochondria.

Motor Vehicle Crash Fatalities for Week Ending, March 12, 2010

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Motor Vehicle Crash Fatalities for Week Ending, March 19, 2010

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Motor Vehicle Crash Fatalities for Week Ending, March 26, 2010

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