Dexamethasone Improves Wound Healing by Decreased Inflammation and Increased Vasculogenesis in Mouse Skin Frostbite Model.

INTRODUCTION: Frostbite is thought to result from initial vasoconstriction, ischemia, intracellular ice crystal formation, and inflammation caused by reperfusion injury. Corticosteroids have demonstrated beneficial anti-inflammatory effects in the treatment of other ischemia/reperfusion clinical conditions. The objective of this study was to determine the effect of dexamethasone (dex) on wound healing, inflammatory response, and vasculogenesis in a mouse skin frostbite model. METHODS: Treatment and control groups of C57/BL6 mice were subjected to frostbite using a previously described model. Treatment with intraperitoneal dex (1 mg·kg-1·d-1) began on the day of frostbite induction and lasted for 7 d. Over 4 wk, we compared wound diameter; morphology by visual inspection, hematoxylin-eosin staining, and Masson's trichrome staining; density of inflammatory cytokines IL-1ß and TNFα using Western blot analysis; and formation of microvasculature using immunofluorescence staining. Data were analyzed using 1-way or 1-way repeated-measures analysis of variance. RESULTS: After frostbite injury, morphological images demonstrated epidermal necrosis and loss in the frostbitten skin as well as infiltration of inflammation-related leukocytes. Increased production of inflammatory cytokines and disappearance of the microvasculature also occurred in the frostbitten skin. In comparison to the control group, treatment with dex promoted wound healing as demonstrated by decreased wound diameter; decreased levels of inflammatory cytokines, and accelerated formation of mature microvasculature. CONCLUSIONS: In this animal model, dex improved wound healing in frostbitten skin and demonstrated both anti-inflammatory effects and stimulation of vasculogenesis. This study suggests that the use of potent anti-inflammatory agents may be an effective strategy for mitigating frostbite injury.

American Board of Emergency Medicine Report on Residency and Fellowship Training Information (2018-2019).

The American Board of Emergency Medicine (ABEM) gathers extensive background information on emergency medicine-sponsored residency and fellowship programs, residents and fellows training in those programs, and all fellows for whom ABEM issues subspecialty certifications. We present the 2019 annual report on the status of US emergency medicine training programs.

American Board of Emergency Medicine Report on Residency and Fellowship Training Information (2017-2018).

The American Board of Emergency Medicine (ABEM) gathers extensive background information on emergency medicine-sponsored residency and fellowship programs, as well as the residents and fellows training in those programs. We present the 2018 annual report on the status of US emergency medicine training programs.

American Board of Emergency Medicine Report on Residency and Fellowship Training Information (2016-2017).

The American Board of Emergency Medicine (ABEM) gathers extensive background information on emergency medicine residency programs and the residents training in those programs. We present the 2017 annual report on the status of US emergency medicine training programs.

American Board of Emergency Medicine Report on Residency Training Information (2015-2016).

The American Board of Emergency Medicine (ABEM) gathers extensive background information on emergency medicine residency programs and the residents training in those programs. We present the 2016 annual report on the status of US emergency medicine training programs.

American Board of Emergency Medicine report on residency training information (2014-2015).

The American Board of Emergency Medicine (ABEM) gathers extensive background information on emergency medicine residency programs and the residents in those programs. We present the 2015 annual report on the status of US emergency medicine training programs.

Emergency Department Processes for the Evaluation and Management of Persons Under Investigation for Ebola Virus Disease.

INTRODUCTION: Due to the recent Ebola virus outbreak in West Africa, patients with epidemiologic risk for Ebola virus disease and symptoms consistent with Ebola virus disease are presenting to emergency departments (EDs) and clinics in the United States. These individuals, identified as a person under investigation for Ebola virus disease, are initially screened using a molecular assay for Ebola virus. If this initial test is negative and the person under investigation has been symptomatic for < 3 days, a repeat test is required after 3 days of symptoms to verify the negative result. In the time interval before the second test result is available, manifestations of the underlying disease process for the person under investigation, whether due to Ebola virus disease or some other etiology, may require further investigation to direct appropriate therapy. MATERIALS AND METHODS: ED administrators, physicians, and nurses proposed processes to provide care that is consistent with other ED patients. Biocontainment unit administrators, industrial hygienists, laboratory directors, physicians, and other medical personnel examined the ED processes and offered biocontainment unit personal protective equipment and process strategies designed to ensure safety for providers and patients. CONCLUSION: ED processes for the safe and timely evaluation and management of the person under investigation for Ebola virus disease are presented with the ultimate goals of protecting providers and ensuring a consistent level of care while confirmatory testing is pending.

Heart failure-induced changes of voltage-gated Ca2+ channels and cell excitability in rat cardiac postganglionic neurons.

Chronic heart failure (CHF) is characterized by decreased cardiac parasympathetic and increased cardiac sympathetic nerve activity. This autonomic imbalance increases the risk of arrhythmias and sudden death in patients with CHF. We hypothesized that the molecular and cellular alterations of cardiac postganglionic parasympathetic (CPP) neurons located in the intracardiac ganglia and sympathetic (CPS) neurons located in the stellate ganglia (SG) possibly link to the cardiac autonomic imbalance in CHF. Rat CHF was induced by left coronary artery ligation. Single-cell real-time PCR and immunofluorescent data showed that L (Ca(v)1.2 and Ca(v)1.3), P/Q (Ca(v)2.1), N (Ca(v)2.2), and R (Ca(v)2.3) types of Ca2+ channels were expressed in CPP and CPS neurons, but CHF decreased the mRNA and protein expression of only the N-type Ca2+ channels in CPP neurons, and it did not affect mRNA and protein expression of all Ca2+ channel subtypes in the CPS neurons. Patch-clamp recording confirmed that CHF reduced N-type Ca2+ currents and cell excitability in the CPP neurons and enhanced N-type Ca2+ currents and cell excitability in the CPS neurons. N-type Ca2+ channel blocker (1 µM ω-conotoxin GVIA) lowered Ca2+ currents and cell excitability in the CPP and CPS neurons from sham-operated and CHF rats. These results suggest that CHF reduces the N-type Ca2+ channel currents and cell excitability in the CPP neurons and enhances the N-type Ca2+ currents and cell excitability in the CPS neurons, which may contribute to the cardiac autonomic imbalance in CHF.

American Board of Emergency Medicine report on residency training information (2013-2014), American Board of Emergency Medicine.

The American Board of Emergency Medicine gathers extensive background information on emergency medicine residency programs and the residents in them. We present the 2014 annual report on the status of US emergency medicine training programs.

Using Google Flu Trends data in forecasting influenza-like-illness related ED visits in Omaha, Nebraska.

INTRODUCTION: Emergency department (ED) visits increase during the influenza seasons. It is essential to identify statistically significant correlates in order to develop an accurate forecasting model for ED visits. Forecasting influenza-like-illness (ILI)-related ED visits can significantly help in developing robust resource management strategies at the EDs. METHODS: We first performed correlation analyses to understand temporal correlations between several predictors of ILI-related ED visits. We used the data available for Douglas County, the biggest county in Nebraska, for Omaha, the biggest city in the state, and for a major hospital in Omaha. The data set included total and positive influenza test results from the hospital (ie, Antigen rapid (Ag) and Respiratory Syncytial Virus Infection (RSV) tests); an Internet-based influenza surveillance system data, that is, Google Flu Trends, for both Nebraska and Omaha; total ED visits in Douglas County attributable to ILI; and ILI surveillance network data for Douglas County and Nebraska as the predictors and data for the hospital's ILI-related ED visits as the dependent variable. We used Seasonal Autoregressive Integrated Moving Average and Holt Winters methods with3 linear regression models to forecast ILI-related ED visits at the hospital and evaluated model performances by comparing the root means square errors (RMSEs). RESULTS: Because of strong positive correlations with ILI-related ED visits between 2008 and 2012, we validated the use of Google Flu Trends data as a predictor in an ED influenza surveillance tool. Of the 5 forecasting models we have tested, linear regression models performed significantly better when Google Flu Trends data were included as a predictor. Regression models including Google Flu Trends data as a predictor variable have lower RMSE, and the lowest is achieved when all other variables are also included in the model in our forecasting experiments for the first 5 weeks of 2013 (with RMSE = 57.61). CONCLUSIONS: Google Flu Trends data statistically improve the performance of predicting ILI-related ED visits in Douglas County, and this result can be generalized to other communities. Timely and accurate estimates of ED volume during the influenza season, as well as during pandemic outbreaks, can help hospitals plan their ED resources accordingly and lower their costs by optimizing supplies and staffing and can improve service quality by decreasing ED wait times and overcrowding.

American Board of Emergency Medicine report on residency training information (2012-2013), American Board of Emergency Medicine.

The American Board of Emergency Medicine (ABEM) gathers extensive background information on emergency medicine residency programs and the residents in those programs. We present the 2013 annual report on the status of US emergency medicine training programs.

Alterations of calcium channels and cell excitability in intracardiac ganglion neurons from type 2 diabetic rats.

Clinical study has demonstrated that patients with type 2 diabetes with attenuated arterial baroreflex have higher mortality rate compared with those without arterial baroreflex dysfunction. As a final pathway for the neural control of the cardiac function, functional changes of intracardiac ganglion (ICG) neurons might be involved in the attenuated arterial baroreflex in the type 2 diabetes mellitus (T2DM). Therefore, we measured the ICG neuron excitability and Ca(2+) channels in the sham and T2DM rats. T2DM was induced by a combination of both high-fat diet and low-dose streptozotocin (STZ, 30 mg/kg ip) injection. After 12-14 wk of the above treatment, the T2DM rats presented hyperglycemia, hyperlipidemia, and insulin resistance but no hyperinsulinemia, which closely mimicked the clinical features of the patients with T2DM. Data from immunofluorescence staining showed that L, N, P/Q, and R types of Ca(2+) channels were expressed in the ICG neurons, but only protein expression of N-type Ca(2+) channels was decreased in the ICG neurons from T2DM rats. Using whole cell patch-clamp technique, we found that T2DM significantly reduced the Ca(2+) currents and cell excitability in the ICG neurons. ω-Conotoxin GVIA (a specific N-type Ca(2+) channel blocker, 1 µM) lowered the Ca(2+) currents and cell excitability toward the same level in sham and T2DM rats. These results indicate that the decreased N-type Ca(2+) channels contribute to the suppressed ICG neuron excitability in T2DM rats. From this study, we think high-fat diet/STZ injection-induced T2DM might be an appropriate animal model to test the cellular and molecular mechanisms of cardiovascular autonomic dysfunction.

Report on residency training information (2011-2012), American Board of Emergency Medicine.

The American Board of Emergency Medicine (ABEM) gathers extensive background information on emergency medicine residency training programs and the residents in those programs. We present the 2012 annual report on the status of US emergency medicine training programs.

Inhibition of N-type calcium channels in cardiac sympathetic neurons attenuates ventricular arrhythmogenesis in heart failure.

AIMS: Cardiac sympathetic overactivation is an important trigger of ventricular arrhythmias in patients with chronic heart failure (CHF). Our previous study demonstrated that N-type calcium (Cav2.2) currents in cardiac sympathetic post-ganglionic (CSP) neurons were increased in CHF. This study investigated the contribution of Cav2.2 channels in cardiac sympathetic overactivation and ventricular arrhythmogenesis in CHF. METHODS AND RESULTS: Rat CHF was induced by surgical ligation of the left coronary artery. Lentiviral Cav2.2-α shRNA or scrambled shRNA was transfected in vivo into stellate ganglia (SG) in CHF rats. Final experiments were performed at 14 weeks after coronary artery ligation. Real-time polymerase chain reaction and western blot data showed that in vivo transfection of Cav2.2-α shRNA reduced the expression of Cav2.2-α mRNA and protein in the SG in CHF rats. Cav2.2-α shRNA also reduced Cav2.2 currents and cell excitability of CSP neurons and attenuated cardiac sympathetic nerve activities (CSNA) in CHF rats. The power spectral analysis of heart rate variability (HRV) further revealed that transfection of Cav2.2-α shRNA in the SG normalized CHF-caused cardiac sympathetic overactivation in conscious rats. Twenty-four-hour continuous telemetry electrocardiogram recording revealed that this Cav2.2-α shRNA not only decreased incidence and duration of ventricular tachycardia/ventricular fibrillation but also improved CHF-induced heterogeneity of ventricular electrical activity in conscious CHF rats. Cav2.2-α shRNA also decreased susceptibility to ventricular arrhythmias in anaesthetized CHF rats. However, Cav2.2-α shRNA failed to improve CHF-induced cardiac contractile dysfunction. Scrambled shRNA did not affect Cav2.2 currents and cell excitability of CSP neurons, CSNA, HRV, and ventricular arrhythmogenesis in CHF rats. CONCLUSIONS: Overactivation of Cav2.2 channels in CSP neurons contributes to cardiac sympathetic hyperactivation and ventricular arrhythmogenesis in CHF. This suggests that discovering purely selective and potent small-molecule Cav2.2 channel blockers could be a potential therapeutic strategy to decrease fatal ventricular arrhythmias in CHF.

Reduced expression and activation of voltage-gated sodium channels contributes to blunted baroreflex sensitivity in heart failure rats.

Voltage-gated sodium (Na(v)) channels are responsible for initiation and propagation of action potential in the neurons. To explore the mechanisms of chronic heart failure (CHF)-induced baroreflex dysfunction, we measured the expression and current density of Na(v) channel subunits (Na(v)1.7, Na(v)1.8, and Na(v)1.9) in the aortic baroreceptor neurons and investigated the role of Na(v) channels in aortic baroreceptor neuron excitability and baroreflex sensitivity in sham and CHF rats. CHF was induced by left coronary artery ligation. The development of CHF (6-8 weeks after the coronary ligation) was confirmed by hemodynamic and morphological characteristics. Immunofluorescent data indicated that Na(v)1.7 was expressed in A-type (myelinated) and C-type (unmyelinated) nodose neurons, but Na(v)1.8 and Na(v)1.9 were expressed only in C-type nodose neurons. Real-time RT-PCR and Western blot data showed that CHF reduced mRNA and protein expression levels of Na(v) channels in nodose neurons. In addition, using the whole-cell patch-clamp technique, we found that Na(v) current density and cell excitability of the aortic baroreceptor neurons were lower in CHF rats than that in sham rats. Aortic baroreflex sensitivity was blunted in anesthetized CHF rats, compared with that in sham rats. Furthermore, Na(v) channel activator (rATX II, 100 nM) significantly enhanced Na(v) current density and cell excitability of aortic baroreceptor neurons and improved aortic baroreflex sensitivity in CHF rats. These results suggest that reduced expression and activation of the Na(v) channels are involved in the attenuation of baroreceptor neuron excitability, which subsequently contributes to the impairment of baroreflex in CHF state.

The future of emergency medicine.

BACKGROUND: The specialty of emergency medicine (EM) continues to experience a significant workforce shortage in the face of increasing demand for emergency care. SUMMARY: In July 2009, representatives of the leading EM organizations met in Dallas for the Future of Emergency Medicine Summit. Attendees at the Future of Emergency Medicine Summit agreed on the following: 1) Emergency medical care is an essential community service that should be available to all; 2) An insufficient emergency physician workforce also represents a potential threat to patient safety; 3) Accreditation Council for Graduate Medical Education/American Osteopathic Association (AOA)-accredited EM residency training and American Board of Medical Specialties/AOA EM board certification is the recognized standard for physician providers currently entering a career in emergency care; 4) Physician supply shortages in all fields contribute to-and will continue to contribute to-a situation in which providers with other levels of training may be a necessary part of the workforce for the foreseeable future; 5) A maldistribution of EM residency-trained physicians persists, with few pursuing practice in small hospital or rural settings; 6) Assuring that the public receives high quality emergency care while continuing to produce highly skilled EM specialists through EM training programs is the challenge for EM's future; 7) It is important that all providers of emergency care receive continuing postgraduate education.

The future of emergency medicine.

Physician shortages are being projected for most medical specialties. The specialty of emergency medicine continues to experience a significant workforce shortage in the face of increasing demand for emergency care. The limited supply of emergency physicians, emergency nurses, and other resources is creating an urgent, untenable patient care problem. In July 2009, representatives of the leading emergency medicine organizations met in Dallas, TX, for the Future of Emergency Medicine Summit. This consensus document, agreed to and cowritten by all participating organizations, describes the substantive issues discussed and provides a foundation for the future of the specialty.

A comparison of emergency medicine resident clinical experience in a rural versus urban emergency department.

INTRODUCTION: Strategies for increasing the numbers of American Board of Emergency Medicine certified/emergency medicine (EM) residency trained physicians practicing in rural emergency departments (EDs) include providing rural EM experiences during residency training. However, no studies to date describe the clinical work of EM residents rotating in a rural ED. The objective of the study was to compare the clinical experience of EM residents participating in a rural ED rotation with that on an urban university-based ED rotation. METHODS: Second-year EM residents completing both urban and rural clinical ED rotations self-reported the number of patients evaluated, number of patients admitted and admitting bed type, and the number and type of procedures performed over a 6 month period. Total admission rates, telemetry admission rates, and intensive care unit (ICU) admission rates were calculated and compared by z-test for two proportions. Total numbers for central venous access, conscious sedation, dislocation or fracture relocation/reduction endotracheal intubation, laceration repair, lumbar puncture, tube thoracostomy adult medical resuscitation, adult trauma resuscitation, pediatric medical resuscitation, pediatric trauma resuscitation, and the total number of ED hours completed at each clinical site were collected and procedure/resuscitation numbers calculated per 100 resident-hours in the ED. RESULTS: Five of six residents completed the patient data forms requested. Patients evaluated per hour in the rural versus urban EDs were 1.22 and 1.21, respectively. Rural versus urban ED total admission rates were 21.74% (95% CI, 28.19.01-24.47) versus 33.35% (31.50-35.20), telemetry admission rates were 3.40% (2.28-4.52) versus 14.24% (12.87-15.61), and ICU admission rates were 0.9% (0.31-1.49) versus 4.38% (3.58-5.18), with the differences in all admission rates determined to be statistically significant. Rural versus urban procedures/100 resident-hours in the ED were 0 versus 0.6 for central venous access (p = 0.087), 0.8 versus 0.3 for conscious sedation (p = 0.170), 1.3 versus 0.2 for dislocation or fracture relocation/reduction (p = 0.001), 0 versus 0.9 for endotracheal intubation (p = 0.026), 6.1 versus 2.7 for laceration repair (p < 0.001), 1.0 versus 1.0 for lumbar puncture (p = 0.845), 0.4 versus 0.2 for tube thoracostomy (p = 0.720), 2.4 versus 3.6 for adult medical resuscitation (p = 0.135), 0.7 versus 2.1 for adult trauma resuscitation (p = 0.023), 0.6 versus 0.3 for pediatric medical resuscitation (p = 0.642), and 0.8 versus 0.2 for pediatric trauma resuscitation (p = 0.034). The higher frequency of endotracheal intubations and adult trauma resuscitations per 100 resident-hours in the urban versus rural EDs was statistically significant by z-test, while laceration repair, dislocation/fracture relocation/reduction, and pediatric trauma resuscitations occurred more frequently in the rural ED by statistically significant margins. No other procedure or resuscitation type differed significantly. CONCLUSION: A rural ED rotation provides an active clinical experience, with patients per hour and most procedure frequencies being similar to those at urban sites, but with lower patient acuity as determined by admission rates.

Reduced N-Type Ca2+ Channels in Atrioventricular Ganglion Neurons Are Involved in Ventricular Arrhythmogenesis.

BACKGROUND: Attenuated cardiac vagal activity is associated with ventricular arrhythmogenesis and related mortality in patients with chronic heart failure. Our recent study has shown that expression of N-type Ca2+ channel α-subunits (Cav2.2-α) and N-type Ca2+ currents are reduced in intracardiac ganglion neurons from rats with chronic heart failure. Rat intracardiac ganglia are divided into the atrioventricular ganglion (AVG) and sinoatrial ganglion. Ventricular myocardium receives projection of neuronal terminals only from the AVG. In this study we tested whether a decrease in N-type Ca2+ channels in AVG neurons contributes to ventricular arrhythmogenesis. METHODS AND RESULTS: Lentiviral Cav2.2-α shRNA (2 µL, 2×107 pfu/mL) or scrambled shRNA was in vivo transfected into rat AVG neurons. Nontransfected sham rats served as controls. Using real-time single-cell polymerase chain reaction and reverse-phase protein array, we found that in vivo transfection of Cav2.2-α shRNA decreased expression of Cav2.2-α mRNA and protein in rat AVG neurons. Whole-cell patch-clamp data showed that Cav2.2-α shRNA reduced N-type Ca2+ currents and cell excitability in AVG neurons. The data from telemetry electrocardiographic recording demonstrated that 83% (5 out of 6) of conscious rats with Cav2.2-α shRNA transfection had premature ventricular contractions (P<0.05 versus 0% of nontransfected sham rats or scrambled shRNA-transfected rats). Additionally, an index of susceptibility to ventricular arrhythmias, inducibility of ventricular arrhythmias evoked by programmed electrical stimulation, was higher in rats with Cav2.2-α shRNA transfection compared with nontransfected sham rats and scrambled shRNA-transfected rats. CONCLUSIONS: A decrease in N-type Ca2+ channels in AVG neurons attenuates vagal control of ventricular myocardium, thereby initiating ventricular arrhythmias.

Dexamethasone Protects Against Tourniquet-Induced Acute Ischemia-Reperfusion Injury in Mouse Hindlimb.

Extremity injuries with hemorrhage have been a significant cause of death in civilian medicine and on the battlefield. The use of a tourniquet as an intervention is necessary for treatment to an injured limb; however, the tourniquet and subsequent release results in serious acute ischemia-reperfusion (IR) injury in the skeletal muscle and neuromuscular junction (NMJ). Much evidence demonstrates that inflammation is an important factor to cause acute IR injury. To find effective therapeutic interventions for tourniquet-induced acute IR injuries, our current study investigated effect of dexamethasone, an anti-inflammatory drug, on tourniquet-induced acute IR injury in mouse hindlimb. In C57/BL6 mice, a tourniquet was placed on unilateral hindlimb (left hindlimb) at the hip joint for 3 h, and then released for 24 h to induce IR. Three hours of tourniquet and 24 h of release (24-h IR) caused gastrocnemius muscle injuries including rupture of the muscle sarcolemma and necrosis (42.8 ± 2.3% for infarct size of the gastrocnemius muscle). In the NMJ, motor nerve terminals disappeared, and endplate potentials were undetectable in 24-h IR mice. There was no gastrocnemius muscle contraction in 24-h IR mice. Western blot data showed that inflammatory cytokines (TNFα and IL-1ß) were increased in the gastrocnemius muscle after 24-h IR. Treatment with dexamethasone at the beginning of reperfusion (1 mg/kg, i.p.) significantly inhibited expression of TNFα and IL-1ß, reduced rupture of the muscle sarcolemma and infarct size (24.8 ± 2.0%), and improved direct muscle stimulation-induced gastrocnemius muscle contraction in 24-h IR mice. However, this anti-inflammatory drug did not improve NMJ morphology and function, and sciatic nerve-stimulated skeletal muscle contraction in 24-h IR mice. The data suggest that one-time treatment with dexamethasone at the beginning of reperfusion only reduced structural and functional impairments of the skeletal muscle but not the NMJ through inhibiting inflammatory cytokines.