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OBJECTIVES: To evaluate the quality of pain assessment by emergency medical services (EMS) in out-of-hospital emergencies. METHODS: A prospective study was conducted on a convenience sample of patients during a one-year observation period. Pain ratings assessed by emergency patients were documented at three different intervals during the emergency call, and compared with concomitant assessments by EMS providers. A visual analog scale (VAS) and a verbal pain scale (VPS) were used for pain assessment. Repeated-measures ANOVA and Dunnett's t-test were used for data analysis. RESULTS: Fifty-one out of 70 eligible patients met inclusion criteria. In most emergency patients the intensity of pain was underestimated by EMS, especially when pain was severe (p = 0.0001). During the course of transport, both pain and pain assessment by EMS improved significantly (p = 0.0001). The VAS and VPS were significantly correlated (p = 0.0001). CONCLUSIONS: EMS providers significantly underestimate their patients' pain severity. EMS providers should be more attentive to their patients' complaints and comfort.  相似文献   
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The Ca2+ release channel ryanodine receptor 2 (RyR2) is required for excitation-contraction coupling in the heart and is also present in the brain. Mutations in RyR2 have been linked to exercise-induced sudden cardiac death (catecholaminergic polymorphic ventricular tachycardia [CPVT]). CPVT-associated RyR2 mutations result in "leaky" RyR2 channels due to the decreased binding of the calstabin2 (FKBP12.6) subunit, which stabilizes the closed state of the channel. We found that mice heterozygous for the R2474S mutation in Ryr2 (Ryr2-R2474S mice) exhibited spontaneous generalized tonic-clonic seizures (which occurred in the absence of cardiac arrhythmias), exercise-induced ventricular arrhythmias, and sudden cardiac death. Treatment with a novel RyR2-specific compound (S107) that enhances the binding of calstabin2 to the mutant Ryr2-R2474S channel inhibited the channel leak and prevented cardiac arrhythmias and raised the seizure threshold. Thus, CPVT-associated mutant leaky Ryr2-R2474S channels in the brain can cause seizures in mice, independent of cardiac arrhythmias. Based on these data, we propose that CPVT is a combined neurocardiac disorder in which leaky RyR2 channels in the brain cause epilepsy, and the same leaky channels in the heart cause exercise-induced sudden cardiac death.  相似文献   
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Both AVP and dDAVP effect a transient increase in cytosolic free calcium (iCa2+) in cortical collecting tubule (CCT) cells. To investigate the physiological role of this increase in iCa2+, we examined the effect of TMB-8, a putative inhibitor of iCa2+ release, on the initial and sustained phase of AVP- and dDAVP-stimulated water permeability (Pf) in isolated, perfused CCTs. Pretreatment of tubules with TMB-8, 50 microM, suppressed the increase in osmotic water permeability (Pf) induced by 10 microU/ml AVP and dDAVP, but had no effect on the sustained phase of the response. When increased to 100 microM. TMB-8 inhibited the sustained phase of AVP action. A similar pattern was observed on AVP-stimulated adenyly cyclase activity in rabbit renal membranes. Pretreatment of tubules with 50 microM TMB-8 attenuated the initial increase in Pf in response to cholera toxin but not to 8-Br-cAMP or forskolin. There was no effect of this concentration of TMB-8 on the sustained phase of these agonists. These studies suggest that, in lower concentrations, TMB-8 inhibits the mobilization of iCa2+, which is important for the interaction of Gs with the catalytic unit of adenylyl cyclase and the initial increase in AVP-stimulated Pf. In higher concentrations, TMB-8 inhibits adenylyl cyclase activity directly.  相似文献   
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Carpal bone is an uncommon location for metastases, and diagnostic problems can occur when a solitary metastasis mimics acute arthritis or osteomyelitis clinically as well as radiologically.  相似文献   
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