The concentration of selenium in soil, water, or minerals is site specific. World or regional averages are of little practical value. In one report from the front range area of Colorado, average selenium concentrations in bodies of standing water were from 0.3 to 15.8 micrograms Se per liter of water. In some aquatic organisms there is a strong correlation between the Se content of the water ant that of the body tissues; in others no such correlation obtains. Some organisms bioaccumulate Se by factors as high as 1300 to 3800. In most fish the amount of Se in the flesh seems to depend on the amount in the food taken in; there are exceptions, however. Aquatic organisms from seleniferous regions bioconcentrate selenium so as to reach total body levels of 60 micrograms Se per gram or up to 100 micrograms Se per gram of liver. There seems to be no evidence for "biomagnification" of selenium by aquatic organisms. Selenium exerts a strong protective action against the poisoning effects of many heavy metals (lead, cadmium, arsenic, and mercury, for example) and of some organic toxicants (paraquat, for example) in birds, mammals, and man. Data on man are sketchy. Selenium is released into the environment from the burning of coal. No identifiable hazard to man or to plants and animals useful to man can, at this time, be attributed to this source. Selenium is poisonous to man and animal in large amounts. It is a necessary micronutrient for many animals in small amounts; it may also be a needed micronutrient for man, but the data are sparse. The usual American diet contains adequate selenium for human health. Occupational selenium poisoning is mostly accidental and rare.

One approach for developing targeted stroke therapies is to identify the neuronal protective and destructive signaling pathways and gene expression that follow ischemic insult. In some neural injury models, the transforming growth factor-beta family member activin can provide neuroprotective effects in vivo and promote neuronal survival. This study tests if activin supports cortical neurons after ischemic challenge in vitro and if signals after cerebral ischemia involve activin in vivo. In a defined cell culture model that uses hydrogen peroxide (H2O2)-free radical stress, activin addition maintained neuronal survival. H2O2 treatment increased activin mRNA twofold in surviving cortical neurons, and inhibition of activin with neutralizing antibodies caused neuronal death. These data identify activin gene changes as a rapid response to oxidative stress, and indicate that endogenous activin acts as a protective factor for cortical neurons in vitro. Similarly, after transient focal cerebral ischemia in adult mice, activin mRNA increased at 1 and 4 h ipsilateral to the infarct but returned to control values at 24 h after reperfusion. Intracellular activated smad signals were detected in neurons adjacent to the infarct. Activin was also increased after 2 h of 11% hypoxia. Activin mRNA increased at 1 h but not 4 or 24 h after hypoxia, similar to the time course of erythropoietin and vascular endothelial growth factor induction. These findings identify activin as an early-regulated gene response to transient ischemia and hypoxia, and its function in cortical neuron survival during oxidative challenge provides a basis to test activin as a potential therapeutic in stroke injury.

Background US nationwide estimates indicate 50–80% of prisoners have a history of substance abuse or dependence. Tailoring substance abuse treatment to specific needs of incarcerated individuals could improve effectiveness of treating substance dependence and preventing drug abuse relapse. The purpose of the present study was to test the hypothesis that pre-treatment neural measures of a Go/NoGo task would predict which individuals would or would not complete a 12-week cognitive behavioral substance abuse treatment program. Methods Adult incarcerated participants (N=89; Females=55) who volunteered for substance abuse treatment performed a response inhibition (Go/NoGo) task while event-related potentials (ERP) were recorded. Stimulus- and response-locked ERPs were compared between individuals who completed (N=68; Females=45) and discontinued (N=21; Females=10) treatment. Results As predicted, stimulus-locked P2, response-locked error-related negativity (ERN/Ne), and response-locked error positivity (Pe), measured with windowed time-domain and principal component analysis, differed between groups. Using logistic regression and support-vector machine (i.e., pattern classifiers) models, P2 and Pe predicted treatment completion above and beyond other measures (i.e., N2, P300, ERN/Ne, age, sex, IQ, impulsivity, and self-reported depression, anxiety, motivation for change, and years of drug abuse). Conclusions We conclude individuals who discontinue treatment exhibited deficiencies in sensory gating, as indexed by smaller P2, error-monitoring, as indexed by smaller ERN/Ne, and adjusting response strategy post-error, as indexed by larger Pe. However, the combination of P2 and Pe reliably predicted 83.33% of individuals who discontinued treatment. These results may help in the development of individualized therapies, which could lead to more favorable, long-term outcomes.

The Buffalo Concussion Treadmill Test (BCTT) identifies the heart rate threshold (HRt) of exercise tolerance in concussed patients. A previous study found that an absolute HRt of < 135 bpm was associated with prolonged recovery (>30 days) from sport-related concussion (SRC). In this study, we assessed the relationship of ΔHR (difference between resting HR and HRt) and recovery from SRC. Using a retrospective cohort design, we compared acutely (<10 days since injury) concussed adolescents who were prescribed either (1) relative rest (RG, n = 27, 15.2 ± 1 years, 33% female, median 17 days to recovery, ΔHR = 69.6 ± 28 bpm), (2) a placebo-stretching program (PG, n = 51, 15.4 ± 2 years, 49% female, median 17 days to recovery, ΔHR = 60.9 ± 22 bpm), or (3) sub-threshold aerobic exercise (AG, n = 52, 15.3 ± 2 years, 46% female, median 13 days to recovery, ΔHR = 62.4 ± 26 bpm). Linear regression showed that ΔHR significantly correlated with duration of clinical recovery for RG ( p = 0.012, R 2 = 0.228) and PG ( p = 0.011, R 2 = 0.126) but not for AG ( p = 0.084, R 2 = 0.059). ΔHR values were significantly lower in participants with prolonged recovery (>30 days) in RG ( p = 0.01) and PG ( p = 0.04). A ΔHR of ≤50 bpm on the BCTT is 73% sensitive and 78% specific for predicting prolonged recovery in concussed adolescents who were prescribed the current standard of care (i.e., cognitive and physical rest).

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Peer-led group interventions may be more effective in reducing family self-stigma than clinician-led education, at least for persons reporting experiencing low to moderate anxiety levels on a standard questionnaire

Purpose of review:Recent studies are challenging the utility of prolonged rest as treatment for concussion and post-concussion syndrome (PCS). The purpose of this paper is to review the evidence for active recovery from concussion and PCS. Recent findings:Emerging data identify the central role of autonomic nervous system (ANS) dysfunction in concussion pathophysiology. The exercise intolerance demonstrated by athletes after sport-related concussion (SRC) may be related to abnormal ANS regulation of cerebral blood flow (CBF). Since aerobic exercise training improves ANS function, sub-threshold exercise treatment is potentially therapeutic for concussion. A systematic assessment of exercise tolerance using the Buffalo Concussion Treadmill Test (BCTT) has been safely employed to prescribe a progressive, individualized sub-threshold aerobic exercise treatment program that can return patients to sport and work. Multiple studies are demonstrating the efficacy of an active approach to concussion management. Summary: Sustained rest from all activities after concussion, so called "cocoon therapy", is not beneficial to recovery. Evidence supports the safety, tolerability, and efficacy of controlled subthreshold aerobic exercise treatment for PCS patients. Further study should determine the efficacy and optimal timing, dose, and duration of sub-threshold aerobic exercise treatment acutely after concussion because early intervention has potential to prevent PCS.

Introduction: Blunted cardiac autonomic nervous system (ANS) responses, quantified using heart rate variability (HRV), have been reported after sport-related concussion (SRC). Research suggests this persists beyond clinical recovery. This study compared cardiac parasympathetic responses in student athletes with a remote history of SRC (> 1-year ago, Concussion History: CH) with those who reported no lifetime history of SRC (Concussion Naïve: CN). Design: Retrospective nested case-control. Setting: University laboratory. Patients or Other Participants: CH (n = 9, 18.3 ± 2 years, 44% male, median 2 years since injury) were student athletes with a remote history of concussion(s) from more than 1 year ago. CN (n = 21, 16.7 ± 3 years, 67% male) were student athletes with no lifetime history of concussion. Exclusion criteria included taking medications that could affect ANS function, history of concussion within the past year, persistent concussion symptoms, lifetime history of moderate to severe brain injury, and lifetime history of more than 3 concussions. Material and Methods: Participants performed the Face Cooling (FC) test for 3-min after 10-min of supine rest while wearing a 3-lead electrocardiogram in a controlled environment. Outcome Measures: Heart rate (HR), R-R interval (RRI), root mean square of the successive differences (RMSSD) of RRI, high frequency (HF) and low frequency to HF (LF:HF) ratios. Haider et al. Persistent ANS Dysfunction After Concussion Results: At baseline, CH had a lower resting HR than CN (62.3 ± 11 bpm vs. 72.9 ± 12, p = 0.034). CH had a different HR response to FC than CN (+8.9% change from baseline in CH vs. −7.5% in CN, p = 0.010). CH also had a smaller RMSSD increase to FC than CN (+31.8% change from baseline in CH vs. +121.8% in CN, p = 0.048). There were no significant group differences over time in RRI (p = 0.106), HF (p = 0.550) or LF:HF ratio (p = 0.053). Conclusion: Asymptomatic student athletes with a remote history of concussion had a blunted cardiac parasympathetic response to FC when compared with athletes with no lifetime history of concussion. These data suggest that an impaired autonomic response to a physiological stressor persists after clinical recovery from SRC for longer than previously reported.