Plos One
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Behavioral models of cold responses are important tools for exploring the molecular mechanisms of cold sensation. To complement the currently cold behavioral assays and allow further studies of these mechanisms, we have developed a new technique to measure the cold response threshold, the cold plantar assay. ⋯ The latency to withdrawal from the cooled glass is used as a measure of the cold response threshold of the rodents, and the dry ice pellet provides a ramping cold stimulus on the glass that allows the correlation of withdrawal latency values to rough estimates of the cold response threshold temperature. The assay is highly sensitive to manipulations including morphine-induced analgesia, Complete Freund's Adjuvant-induced inflammatory allodynia, and Spinal Nerve Ligation-induced neuropathic allodynia.
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Emergency department (ED) utilization has dramatically increased in developed countries over the last twenty years. Because it has been associated with adverse outcomes, increased costs, and an overload on the hospital organization, several policies have tried to curb this growing trend. The aim of this study is to systematically review the effectiveness of organizational interventions designed to reduce ED utilization. ⋯ The evidence suggests that interventions aimed at increasing primary care accessibility and ED cost-sharing are effective in reducing ED use. However, the rest of the interventions aimed at decreasing ED utilization showed contradictory results. Changes in health care policies require rigorous evaluation before being implemented since these can have a high impact on individual health and use of health care resources. Systematic review registration: http://www.crd.york.ac.uk/PROSPERO. Identifier: CRD420111253.
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Excessive use of computed tomography (CT) in emergency departments (EDs) has become a concern due to its expense and the potential risks associated with radiation exposure. Although studies have shown a steady increase in the number of CT scans requested by ED physicians in developed countries like the United States and Australia, few empirical data are available regarding China. ⋯ CT utilization was associated with higher ED cost, longer ED length of stay and more likely to receive emergency operations, but did not correlate with a significant change in the admission rate.
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Voltage-gated sodium channels (VGSCs) play a key role in the initiation and propagation of action potentials in neurons. Na(V)1.8 is a tetrodotoxin (TTX) resistant VGSC expressed in nociceptors, peripheral small-diameter neurons able to detect noxious stimuli. Na(V)1.8 underlies the vast majority of sodium currents during action potentials. ⋯ Moreover, treatments with methyl-β-cyclodextrin (MβCD) and 7-ketocholesterol (7KC) led to the dissociation between rafts and Na(V)1.8. By calcium imaging we demonstrated that the lack of association between rafts and Na(V)1.8 correlated with impaired neuronal excitability, highlighted by a reduction in the number of neurons able to conduct mechanically- and chemically-evoked depolarisations. These findings reveal the sub-cellular localisation of Na(V)1.8 in nociceptors and highlight the importance of the association between Na(V)1.8 and lipid rafts in the control of nociceptor excitability.
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Oxidative stress is known to play an important role in the pathology of traumatic brain injury. Mitochondria are thought to be the major source of the damaging reactive oxygen species (ROS) following TBI. However, recent work has revealed that the membrane, via the enzyme NADPH oxidase can also generate the superoxide radical (O(2)(-)), and thereby potentially contribute to the oxidative stress following TBI. The current study thus addressed the potential role of NADPH oxidase in TBI. ⋯ As a whole, the study demonstrates that NADPH oxidase activity and superoxide production exhibit a biphasic elevation in the hippocampus and cortex following TBI, which contributes significantly to the pathology of TBI via mediation of oxidative stress damage, microglial activation, and AD protein induction in the brain following TBI.