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Despite decades of effort to drive quality improvement, many health care organizations still struggle to optimize their performance on quality metrics. The advent of publicly reported quality rankings and ratings allows for greater visibility of overall organizational performance, but has not provided a roadmap for sustained improvement in these assessments. Most quality training programs have focused on developing knowledge and skills in pursuit of individual and project-level improvements. To date, no training program has been associated with improvements in overall organization-level, publicly reported measures. In 2012, the Institute for Health care Quality, Safety, and Efficiency was launched, which is an integrated set of quality and safety training programs, with a focus on leadership development and support of performance improvement through data analytics and intensive coaching. This effort has trained nearly 2000 individuals and has been associated with significant improvement in organization-level quality rankings and ratings, offering a framework for organizations seeking systematic, long-term improvement. [ABSTRACT FROM AUTHOR]

Cold stress severity is routinely described in terms of core temperature (Tc) and heat loss, both of which are dependent upon vascular response, subcutaneous fat, body surface area, muscular composition, and metabolic rate. When exposed to cold stress, variations in each of these can contribute to large differences in heat loss among individuals, wherein some are able to preserve Tc while others are not. The impact of such Tc variations on psychomotor performance is poorly understood. Identifying underlying mechanisms that contribute to impaired performance is important so that strategies can be developed to counteract psychomotor impairments caused by cold stress. PURPOSE: Determine the influence of Tc on psychomotor performance during cold water immersion. METHODS: Thirty-six military personnel (mean ± SD; age: 26 ± 4 yr, ht: 175 ± 8 cm, wt: 79.1 ± 11.1 kg) completed a 10-min whole-body cold water immersion (1°C). Participants' simple reaction time (SRT) was evaluated using a psychomotor vigilance task administered prior to, during, and immediately after immersion, and at three time points (0, 15, 60 min) during a 60-min rewarming activity (entering sleeping bags with dry clothing). For analysis, participants were divided into groups based on their lowest recorded Tc (which occurred immediately after immersion or early in rewarming). Groups were classified as < 35°C (n = 7), between 35-36°C (n = 12), and > 36°C (n = 17). SRT, as well as mean skin temperature (Tsk), hand temperature (Thand), thermal sensation (TS), and shivering sensation (SS), were then compared between groups. Significance was set at p < 0.05. RESULTS: Cold water immersion increased response times for SRT (mean ± SE; pre: 235 ± 12, immersion: 315 ± 14, post: 366 ± 30 ms; p < 0.001). However, no differences were observed between Tc groups for SRT (mean ± SE; < 35°C: 298 ± 31, 35-36°C: 313 ± 18, > 36°C: 326 ± 15 ms; p = 0.677). Additionally, no differences were observed between groups for Tsk (p = 0.409), Thand (p = 0.843), or SS (p = 0.663). CONCLUSIONS: Current findings suggest that psychomotor performance is not greatly influenced by Tc, even in the presence of mild hypothermia. Future work should evaluate other possible contributing physiological factors that impact performance, which will improve understanding of psychomotor performance during cold stress. [ABSTRACT FROM AUTHOR]

Objective: To examine the use of surgical procedures for Crohn's disease since the introduction of infliximab., Summary Background Data: Prior studies have shown that the overall rate of surgery for Crohn's disease has not changed significantly since the introduction of infliximab, an immunomodulator considered particularly effective in treating Crohn's fistulas. How infliximab has affected individual rates of specific types of procedures, particularly surgery for intestinal fistulas, is unknown., Methods: We used the Nationwide Inpatient Sample to identify all hospital admissions for Crohn's disease for each year from 1993 through 2004. Cases of Crohn's disease and relevant surgical interventions were identified using International Classification of Diseases, 9th Revision, Clinical Modification (ICD-9-CM) codes. Using US Census data to establish population denominators, trends in population-based rates of use of these procedures were examined over time. Trends were tested for significance with Spearman rank correlation tests., Results: From 1993 to 2004, there was no statistically significant change in population-based rates of small bowel and right colon resection, while rates of left colon resection, other colon resection, and rectal resection declined moderately. However, rates of surgical repair of fistulas of the small intestine, the most commonly performed fistula operation, increased by 60%, from 1.5 per 1,000,000 in 1993 to 2.4 per 1,000,000 in 2004 (P = 0.04)., Conclusions: During the period of adoption of infliximab as a novel treatment for Crohn's disease, overall rates of bowel resections have either remained relatively stable or decreased moderately, while rates of small bowel fistula repair have increased significantly. These findings call into question the effectiveness of infliximab in preventing the need for surgery for Crohn's disease at the population level.

Background: Atrial fibrillation (AF) is the most common sustained arrhythmia observed in otherwise healthy individuals. Most lone AF cases are nonfamilial, leading to the assumption that a primary genetic origin is unlikely. In this study, we provide data supporting a novel paradigm that atrial tissue-specific genetic defects may be associated with sporadic cases of lone AF., Methods and Results: We sequenced the entire coding region of the connexin 43 (Cx43) gene (GJA1) from atrial tissue and lymphocytes of 10 unrelated subjects with nonfamilial, lone AF who had undergone surgical pulmonary vein isolation. In the atrial tissue of 1 patient, we identified a novel frameshift mutation caused by a single nucleotide deletion (c.932delC) that predicted 36 aberrant amino acids followed by a premature stop codon, leading to truncation of the C-terminal domain of Cx43. The mutation was absent from the lymphocyte DNA of the patient, indicating genetic mosaicism. Protein trafficking studies demonstrated intracellular retention of the mutant protein and a dominant-negative effect on gap junction formation of both wild-type Cx43 and Cx40. Electrophysiological studies revealed no electrical coupling of cells expressing the mutant protein alone and significant reductions in coupling when coexpressed with wild-type connexins., Conclusions: This study reports atrial tissue genetic mosaicism of a novel loss-of-function Cx43 mutation associated with lone AF. These findings implicate somatic genetic defects of Cx43 as a potential cause of AF and support the paradigm that sporadic, nonfamilial cases of lone AF may arise from genetic mosaicism that creates heterogeneous coupling patterns, predisposing the tissue to reentrant arrhythmias.

Background: Neuronal nitric oxide synthase (nNOS) is expressed in cardiomyocytes and plays a role in regulating cardiac function and Ca2+ homeostasis. However, the role of nNOS in cardiac electrophysiology after myocardial infarction (MI) is unclear. We hypothesized that nNOS deficiency increases ventricular arrhythmia and mortality after MI., Methods and Results: MI was induced in wild-type (WT) or nNOS(-/-) mice by ligation of the left coronary artery. Thirty-day mortality was significantly higher in nNOS(-/-) compared with WT mice. Additionally, nNOS(-/-) mice had impaired cardiac function 2 days after MI. Telemetric ECG monitoring showed that compared with WT, nNOS(-/-) mice had significantly more ventricular arrhythmias and were more likely to develop ventricular fibrillation after MI. Treatment with the L-type Ca2+ channel blocker verapamil reduced the incidence of arrhythmia and ventricular fibrillation in nNOS(-/-) mice after MI. To assess the role of nNOS in Ca2+ handling, patch-clamp and Ca2+ fluorescence techniques were used. Ca2+ transients and L-type Ca2+ currents were higher in nNOS(-/-) compared with WT cardiomyocytes. Additionally, nNOS(-/-) cardiomyocytes exhibited significantly higher systolic and diastolic Ca2+ over a range of pacing frequencies. Treatment with the NO donor S-nitroso N-acetyl-penicillamine decreased Ca2+ transients and L-type Ca2+ current in both nNOS(-/-) and WT cardiomyocytes. Furthermore, S-nitrosylation of Ca2+ handling proteins was significantly decreased in nNOS(-/-) myocardium after MI., Conclusions: Deficiency in nNOS increases ventricular arrhythmia and mortality after MI in mice. The antiarrhythmic effect of nNOS involves inhibition of L-type Ca2+ channel activity and regulation of Ca2+ handling proteins via S-nitrosylation.

Purpose of Review: The loss of skeletal muscle with injury or critical illness can be dramatic. This review emphasizes the importance of skeletal muscle as a metabolic reserve. Changes in protein metabolism with bed rest alone and during physiological stress are discussed. Nutritional and hormonal interventions that ameliorate the loss of skeletal muscle are highlighted., Recent Findings: The loss of skeletal muscle that occurs with inactivity alone can be prevented by nutritional supplementation with an essential amino acid formula. Bed rest with accompanying hypercortisolemia produces a threefold greater loss of skeletal muscle than bed rest alone. Essential amino acids stimulate muscle anabolism during acute hypercortisolemia; however, their effects during chronic hypercortisolemia must be explored., Summary: Skeletal muscle loss with trauma or critical illness is due in great part to the interaction of bed rest (muscular inactivity) and stress (hypercortisolemia). Younger individuals respond to nutritional and pharmacological interventions during bed rest alone. Given a lower relative lean mass in the elderly and the importance of skeletal muscle as a metabolic reserve during stress, it is understandable that clinical outcomes are worse in older patients. Countermeasures to the loss of skeletal muscle, especially in the stressed patient, must be developed.

3,4-Methylenedioxyamphetamine (MDA) and 3,4-methylenedioxymethamphetamine (MDMA, ecstasy) are ring-substituted amphetamine derivatives with stimulant and hallucinogenic properties. The recreational use of these amphetamines, especially MDMA, is prevalent despite warnings of irreversible damage to the central nervous system. MDA and MDMA are primarily serotonergic neurotoxicants. Because (1) neither MDA nor MDMA produces neurotoxicity when injected directly into brain, (2) intracerebroventricular (i.c.v.) administration of some major metabolites of MDA and MDMA fails to reproduce their neurotoxicity, (3) alpha-methyldopamine (alpha-MeDA) and N-methyl-alpha-MeDA are metabolites of both MDA and MDMA, (4) alpha-MeDA and N-methyl-alpha-MeDA are readily oxidized to the corresponding ortho-quinones, which can undergo conjugation with glutathione (GSH), and (5) quinone thioethers exhibit a variety of toxicologic activities, we initiated studies on the potential role of thioether metabolites of alpha-MeDA and N-methyl-alpha-MeDA in the neurotoxicity of MDA and MDMA. Our studies have revealed that the thioether conjugates stimulate the acute release of serotonin, dopamine, and norepinephrine and produce a behavioral response commensurate with the "serotonin syndrome." Direct injection of the conjugates into rat brain also produces long-term depletions in serotonin (5-HT) concentrations, elevations in GFAP expression, and activation of microglial cells. The data are consistent with the view that thioether metabolites of alpha-MeDA and N-methyl-alpha-MeDA contribute to the neurotoxicity of the parent amphetamines.