Sensory sensitivity as a link between concussive traumatic brain injury and PTSD.

Traumatic brain injury (TBI) is one of the most common injuries to military personnel, a population often exposed to stressful stimuli and emotional trauma. Changes in sensory processing after TBI might contribute to TBI-post traumatic stress disorder (PTSD) comorbidity. Combining an animal model of TBI with an animal model of emotional trauma, we reveal an interaction between auditory sensitivity after TBI and fear conditioning where 75 dB white noise alone evokes a phonophobia-like phenotype and when paired with footshocks, fear is robustly enhanced. TBI reduced neuronal activity in the hippocampus but increased activity in the ipsilateral lateral amygdala (LA) when exposed to white noise. The white noise effect in LA was driven by increased activity in neurons projecting from ipsilateral auditory thalamus (medial geniculate nucleus). These data suggest that altered sensory processing within subcortical sensory-emotional circuitry after TBI results in neutral stimuli adopting aversive properties with a corresponding impact on facilitating trauma memories and may contribute to TBI-PTSD comorbidity

Impact of Nutrition on Pollutant Toxicity: An Update with New Insights Into Epigenetic Regulation

Exposure to environmental pollutants is a global health problem and is associated with the development of many chronic diseases, including cardiovascular disease, diabetes and metabolic syndrome. There is a growing body of evidence that nutrition can both positively and negatively modulate the toxic effects of pollutant exposure. Diets high in proinflammatory fats, such as linoleic acid, can exacerbate pollutant toxicity, whereas diets rich in bioactive and anti-inflammatory food components, including omega-3 fatty acids and polyphenols, can attenuate toxicant-associated inflammation. Previously, researchers have elucidated direct mechanisms of nutritional modulation, including alteration of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling, but recently, increased focus has been given to the ways in which nutrition and pollutants affect epigenetics. Nutrition has been demonstrated to modulate epigenetic markers that have been linked either to increased disease risks or to protection against diseases. Overnutrition (i.e. obesity) and undernutrition (i.e. famine) have been observed to alter prenatal epigenetic tags that may increase the risk of offspring developing disease later in life. Conversely, bioactive food components, including curcumin, have been shown to alter epigenetic markers that suppress the activation of NF-κB, thus reducing inflammatory responses. Exposure to pollutants also alters epigenetic markers and may contribute to inflammation and disease. It has been demonstrated that pollutants, via epigenetic modulations, can increase the activation of NF-κB and upregulate microRNAs associated with inflammation, cardiac injury and oxidative damage. Importantly, recent evidence suggests that nutritional components, including epigallocatechin gallate (EGCG), can protect against pollutant-induced inflammation through epigenetic regulation of proinflammatory target genes of NF-κB. Further research is needed to better understand how nutrition can modulate pollutant toxicity through epigenetic regulation. Therefore, the objective of this review is to elucidate the current evidence linking epigenetic changes to pollutant-induced diseases and how this regulation may be modulated by nutrients allowing for the development of future personalized lifestyle interventions

Self-Reported Emergency Medicine Residency Applicant Attitudes Towards a Procedural Cadaver Laboratory Curriculum

Objective: Residency applicants consider a variety of factors when ranking emergency medicine (EM) programs for their NRMP match list. A human cadaver emergency procedure lab curriculum is uncommon. We hypothesized that the presence this curriculum would positively impact the ranking of an EM residency program.Methods: The EM residency at Nebraska Medical Center is an urban, university-based program with a PGY I-III format. Residency applicants during the interview for a position in the PGY I class of 2006 were surveyed by three weekly electronic mailings. The survey was distributed in March 2006 after the final NRMP match results were released. The survey explored learner preferences and methodological commonality of models of emergency procedural training, as well as the impact of a procedural cadaver lab curriculum on residency ranking. ANOVA of ranks was used to compare responses to ranking questions.Results: Of the 73 potential subjects, 54 (74%) completed the survey. Respondents ranked methods of procedural instruction from 1 (most preferred or most common technique) to 4 (least preferred or least common technique). Response averages and 95% confidence intervals for the preferred means of learning a new procedure are as follows: textbook (3.69; 3.51-3.87), mannequin (2.83; 2.64-3.02), human cadaver (1.93; 1.72-2.14), and living patient (1.56; 1.33-1.79). Response averages for the commonality of means used to teach a new procedure are as follows: human cadaver (3.63; 3.46-3.80), mannequin (2.70; 2.50-2.90), living patient (2.09; 1.85-2.33), and textbook (1.57; 1.32-1.82). When asked if the University of Nebraska Medical Center residency ranked higher in the individual’s match list because of its procedural cadaver lab, 14.8% strongly disagreed, 14.8% disagreed, 40.7% were neutral, 14.8% agreed, and 14.8% strongly agreed.Conclusion: We conclude that, although cadaveric procedural training is viewed by senior medical student learners as a desirable means of learning a procedure, its use is uncommon during medical school, and its presence as part of a residency curriculum does not influence ranking of the residency program.[WestJEM. 2008;9:141-145.

Long-range energy-state maneuvers for minimum time to specified terminal conditions.

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/76474/1/AIAA-1973-229-104.pd

Specificity and Actions of an Arylaspartate Inhibitor of Glutamate Transport at the Schaffer Collateral-CA1 Pyramidal Cell Synapse

In this study we characterized the pharmacological selectivity and physiological actions of a new arylaspartate glutamate transporter blocker, L-threo-ß-benzylaspartate (L-TBA). At concentrations up to 100 µM, L-TBA did not act as an AMPA receptor (AMPAR) or NMDA receptor (NMDAR) agonist or antagonist when applied to outside-out patches from mouse hippocampal CA1 pyramidal neurons. L-TBA had no effect on the amplitude of field excitatory postsynaptic potentials (fEPSPs) recorded at the Schaffer collateral-CA1 pyramidal cell synapse. Excitatory postsynaptic currents (EPSCs) in CA1 pyramidal neurons were unaffected by L-TBA in the presence of physiological extracellular Mg2+ concentrations, but in Mg2+-free solution, EPSCs were significantly prolonged as a consequence of increased NMDAR activity. Although L-TBA exhibited approximately four-fold selectivity for neuronal EAAT3 over glial EAAT1/EAAT2 transporter subtypes expressed in Xenopus oocytes, the L-TBA concentration-dependence of the EPSC charge transfer increase in the absence of Mg2+ was the same in hippocampal slices from EAAT3 +/+ and EAAT3 −/− mice, suggesting that TBA effects were primarily due to block of glial transporters. Consistent with this, L-TBA blocked synaptically evoked transporter currents in CA1 astrocytes with a potency in accord with its block of heterologously expressed glial transporters. Extracellular recording in the presence of physiological Mg2+ revealed that L-TBA prolonged fEPSPs in a frequency-dependent manner by selectively increasing the NMDAR-mediated component of the fEPSP during short bursts of activity. The data indicate that glial glutamate transporters play a dominant role in limiting extrasynaptic transmitter diffusion and binding to NMDARs. Furthermore, NMDAR signaling is primarily limited by voltage-dependent Mg2+ block during low-frequency activity, while the relative contribution of transport increases during short bursts of higher frequency signaling

Health Professionals and Public Awareness of Carbon Monoxide Poisoning in Vermont

Introduction. Carbon monoxide (CO) is the second leading cause of non-medical poisoning death in the United States. Between 1999 and 2012, Vermont saw the highest rates of CO poisoning deaths in New England. Public education and the use of CO alarms have been identified as important prevention strategies. We developed and distributed a survey to assess public and health professional knowledge of CO. Methods. A 21-question survey was designed, based on the validated Chicago Lead Knowledge Test, to assess knowledge about sources of CO exposure and symptoms and treatment of poisoning. Fifteen additional questions collected occupational and demographic information and preferred sources of educational information. Surveys were distributed over two months to the public, healthcare professionals, and emergency responders within Chittenden County, as well as physicians throughout Vermont. Survey responses were analyzed using SPSS. Results. There were 256 respondents. Healthcare professionals performed better than public respondents overall (public: mean correct=15.69, SD= 2.83, N=104; healthcare provider and emergency responder: mean correct= 17.5, SD= 2.23, N= 152). The survey questions which were most frequently answered incorrectly related to treatment and sources of exposure, as well as the similarity of CO poisoning to symptoms of influenza. Respondents preferred to receive information from printed and internet sources. Discussion. Medical professionals are more knowledgeable about carbon mon- oxide than the general public. Public education should include printed and online for- mats, focusing on important sources of exposure (particularly ice rinks), seeking treatment following symptoms, and similarity to flu symptoms.https://scholarworks.uvm.edu/comphp_gallery/1267/thumbnail.jp

Emerging Roles of Xenobiotic Detoxification Enzymes in Metabolic Diseases

Mammalian systems have developed extensive molecular mechanisms to protect against the toxicity of many exogenous xenobiotic compounds. Interestingly, many detoxification enzymes, including cytochrome P450s and flavin-containing monooxygenases, and their associated transcriptional activators [e.g. the aryl hydrocarbon receptor (AhR)], have now been shown to have endogenous roles in normal physiology and the pathology of metabolic diseases. This mini-review will focus on two such instances: the role of flavin-containing monooxygenase 3 (FMO3) in the formation of the cardiometabolic disease biomarker trimethylamine-N-oxide (TMAO) and the role of AhR as a sensor of endogenous ligands such as those generated by the gut microbiota. Understanding the roles of xenobiotic sensing pathways in endogenous metabolism will undoubtedly lead to a better understanding of how exposure to environmental pollutants can perturb these physiological processes

System and Method for Generating Psuedo-Noise Sequences

Disclosed is a method for generating psuedo-noise (PN) sequences utilizing a system comprised of a quantizer, and N directly quantized output/input map containing chaotic map cells, each in functional combination with combiner means and an m-bit shift register