158 research outputs found

    Called to Safety? Individual and Combined Effects of Safety Climate and Occupational Callings on Aviator Safety Performance

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    This study examined the individual and combined effects of two potential antecedents to aviation-related safety performance: safety climate and occupational callings. Research exploring the importance of occupational callings to the safety domain is in its nascent stages. The extent that someone is living a calling may explain variance in actual safety performance above that which can be explained by safety climate alone. Survey data from aviators in a flight training program were analyzed to evaluate the ability of occupational calling assessments to inform the potential for safety mishaps within the aviation industry. Results indicate that both safety climate and occupational callings may inform the potential for safety mishaps better than either alone. Occupational callings may be used to augment safety climate assessments in monitoring and improving aviation safety performance

    Primary somatosensory cortex in chronic low back pain – a 1H-MRS study

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    The goal of this study was to investigate whether certain metabolites, specific to neurons, glial cells, and the neuronal-glial neurotransmission system, in the primary somatosensory cortex (SSC), are altered and correlated with clinical characteristics of pain in patients with chronic low back pain (LBP). Eleven LBP patients and eleven age-matched healthy controls were included. N-acetylaspartate (NAA), choline (Cho), myo-inositol (mI), and glutamine/glutamate (Glx) were measured with proton magnetic resonance spectroscopy (1H-MRS) in left and right SSC. Differences in metabolite concentrations relative to those of controls were evaluated as well as analyses of metabolite correlations within and between SSCs. Relationships between metabolite concentrations and pain characteristics were also evaluated. We found decreased NAA in the left SSC (P = 0.001) and decreased Cho (P = 0.04) along with lower correlations between all metabolites in right SSC (P = 0.007) in LBP compared to controls. In addition, we found higher and significant correlations between left and right mI (P < 0.001 in LBP vs P = 0.1 in controls) and between left mI and right Cho (P = 0.048 vs P = 0.6). Left and right NAA levels were negatively correlated with pain duration (P = 0.04 and P = 0.02 respectively) while right Glx was positively correlated with pain severity (P = 0.04). Our preliminary results demonstrated significant altered neuronal-glial interactions in SSC, with left neural alterations related to pain duration and right neuronal-glial alterations to pain severity. Thus, the 1H-MRS approach proposed here can be used to quantify relevant cerebral metabolite changes in chronic pain, and consequently increase our knowledge of the factors leading from these changes to clinical outcomes

    Dopamine receptor alterations in female rats with diet-induced decreased brain docosahexaenoic acid (DHA): interactions with reproductive status

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    Decreased tissue levels of n-3 (omega-3) fatty acids, particularly docosahexaenoic acid (DHA), are implicated in the etiologies of non-puerperal and postpartum depression. This study examined the effects of a diet-induced loss of brain DHA content and concurrent reproductive status on dopaminergic parameters in adult female Long–Evans rats. An α-linolenic acid-deficient diet and breeding protocols were used to produce virgin and parous female rats with cortical phospholipid DHA levels 20–22% lower than those fed a control diet containing adequate α-linolenic acid. Decreased brain DHA produced a significant main effect of decreased density of ventral striatal D2-like receptors. Virgin females with decreased DHA also exhibited higher density of D1-like receptors in the caudate nucleus than virgin females with normal DHA. These receptor alterations are similar to those found in several rodent models of depression, and are consistent with the proposed hypodopaminergic basis for anhedonia and motivational deficits in depression

    Rats bred for low and high running capacity display alterations in peripheral tissues and nerves relevant to neuropathy and pain

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    IntroductionDiet and activity are recognized as modulators of nervous system disease, including pain. Studies of exercise consistently reveal a benefit on pain. This study focused on female rats to understand differences related to metabolic status and peripheral nerve function in females.MethodsHere, we investigated parameters of peripheral nerve function relevant to pain in rats selectively bred for high (high‐capacity runners; HCR) or low endurance exercise capacity (low‐capacity runners; LCR) resulting in divergent intrinsic aerobic capacities and susceptibility for metabolic conditions.ResultsLCR female rats have reduced mechanical sensitivity, higher intraepidermal nerve fiber density and TrkA‐positive epidermal axons, increased numbers of Langerhans and mast cells in cutaneous tissues, and a higher fat content despite similar overall body weights compared to female HCR rats. Sensory and motor nerve conduction velocities, thermal sensitivity, and mRNA expression of selected genes relevant to peripheral sensation were not different.ConclusionsThese results suggest that aerobic capacity and metabolic status influence sensory sensitivity and aspects of inflammation in peripheral tissues that could lead to poor responses to tissue damage and painful stimuli. The LCR and HCR rats should prove useful as models to assess how the metabolic status impacts pain.These results suggest that aerobic capacity and metabolic status influence sensory sensitivity and aspects of inflammation in peripheral tissues that could lead to poor responses to tissue damage and painful stimuli. The LCR and HCR rats should prove useful as models to assess how the metabolic status impacts pain.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/139060/1/brb3780.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/139060/2/brb3780_am.pd

    New Paramagnetic Susceptibility Thermometers for Fundamental Physics Measurements

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    New paramagnetic susceptibility thermometers have been developed for use in fundamental physics missions in earth orbit. These devices use a SQUID magnetometer to measure the variation in the dc magnetization of a thermometric element that consists of a dilute concentration of manganese in a palladium matrix. Near 2.2 K these new PdMn thermometers have demonstrated a temperature resolution of better than 100 pK/√Hz and a time constant of 50 ms when operated with a 50 K/W thermal resistance to the liquid helium sample. These thermometers have been observed to be remarkably stable, with a drift of less than 10 fK/s. The observed power spectral density of the noise from these thermometers is consistent with separate measurements of the device’s time constant and thermal standoff from the bath. Recently these PdMn materials have been made into thin films and microstructures for use in future studies of quantum liquids, and for possible use in a new class of bolometers and radiometers. These thermometers have been integrated into an experimental cell and thermal isolation network that are adequate to keep stray heats stable to within a few picowatts, with no systematic temperature errors greater than 60 pK, over the course of a planned fundamental physics experiment on Earth orbit

    Intrathecal reboxetine suppresses evoked and ongoing neuropathic pain behaviours by restoring spinal noradrenergic inhibitory tone.

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    The descending noradrenergic (NAergic) projection to the spinal cord forms part of an endogenous analgesic system. After nerve injury, a localised failure in this compensatory system has been implicated as a permissive factor in the development of neuropathic sensitisation. We investigated whether restoring descending NAergic tone with intrathecal reboxetine can oppose the development of the neuropathic pain phenotype after tibial nerve transection (TNT). Rats had a lumbar intrathecal catheter implanted at the time of nerve injury for administration of reboxetine (10 μg) in both acute and chronic dosing experiments. In acute dosing experiments, both intrathecal and systemic (30 mg/kg) reboxetine partially reversed mechanical allodynia. This antiallodynic effect of intrathecal reboxetine was blocked by prior administration of yohimbine (α2-adrenoceptor antagonist, 30 μg) but not by prazosin (α1-adrenoceptor antagonist, 30 μg) or propranolol (β-adrenoceptor antagonist, 100 μg). Chronic intrathecal reboxetine (10 μg, intrathecally, twice daily for 2 weeks) suppressed the development of cold and mechanical allodynia. Nerve-injured animals demonstrated a place preference for intrathecal reboxetine, suggesting that it also reduced spontaneous pain. In contrast, an equivalent antiallodynic dose of systemic reboxetine (30 mg/kg) was aversive in both naive and TNT rats. On cessation of chronic intrathecal reboxetine, there was a gradual development of allodynic sensitisation that was indistinguishable from control TNT animals by 7 days after the end of dosing. Our results suggest that pharmacological restoration of spinal NAergic tone with intrathecal reboxetine can suppress both allodynia and spontaneous pain in the TNT model

    The role of substance P in secondary pathophysiology after traumatic brain injury

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    It has recently been shown that substance P (SP) plays a major role in the secondary injury process following traumatic brain injury (TBI), particularly with respect to neuroinflammation, increased blood-brain barrier (BBB) permeability, and edema formation. Edema formation is associated with the development of increased intracranial pressure (ICP) that has been widely associated with increased mortality and morbidity after neurotrauma. However, a pharmacological intervention to specifically reduce ICP is yet to be developed, with current interventions limited to osmotic therapy rather than addressing the cause of increased ICP. Given that previous publications have shown that SP, NK1 receptor antagonists reduce edema after TBI, more recent studies have examined whether these compounds might also reduce ICP and improve brain oxygenation after TBI. We discuss the results of these studies, which demonstrate that NK1 antagonists reduce posttraumatic ICP to near normal levels within 4 h of drug administration, as well as restoring brain oxygenation to near normal levels in the same time frame. The improvements in these parameters occurred in association with an improvement in BBB integrity to serum proteins, suggesting that SP-mediated increases in vascular permeability significantly contribute to the development of increased ICP after acute brain injury. NK1 antagonists may therefore provide a novel, mechanistically targeted approach to the management of increased ICP.Robert Vink, Levon Gabrielian and Emma Thornto
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