Costs of Measuring Outcomes of Acute Hospital Care in a Longitudinal Outcomes Measurement System

It is widely acknowledged that the measurement of outcomes of care and the comparison of outcomes over time within health care providers and risk-adjusted comparisons among providers are important parts of improving quality and cost-effectiveness of care. However, few studies have assessed the costs of measuring outcomes of care. We sought to evaluate the personnel and financial resources spent for a prospective assessment of outcomes of acute hospital care by health professionals in internal medicine. The study included 15 primary care hospitals participating in a longitudinal outcomes measurement program and 2005 patients over an assessment period with an average duration of 6 months. Each hospital project manager participated in a previously-tested structured 30-minute telephone interview. Outcome measures include time spent by the individual job titles in implementing and running the outcomes measurement program. Job-title-specific times were used to calculate costs from the hospitals' perspective. One-time costs (C2132 + 1352) and administrative costs (95 97 per week) varied substantially. Costs per patient were fairly stable at around 20. We estimated that the total cost for each hospital to assess outcomes of care for accreditation (10 tracer diagnoses over 6 months) would be 9700 and that continuous monitoring of outcomes (5 tracer diagnoses) would cost 12,400 per year. This study suggests that outcomes of acute hospital care can be assessed with limited resources and that standardized training programs would reduce variability in overall costs. This study should help hospital decision makers to estimate the necessary funding for outcomes measurement initiatives

Neuronal Actin Dynamics, Spine Density and Neuronal Dendritic Complexity Are Regulated by CAP2

Actin remodeling is crucial for dendritic spine development, morphology and density. CAP2 is a regulator of actin dynamics through sequestering G-actin and severing F-actin. In a mouse model, ablation of CAP2 leads to cardiovascular defects and delayed wound healing. This report investigates the role of CAP2 in the brain using Cap2(gt)/(gt) mice. Dendritic complexity, the number and morphology of dendritic spines were altered in Cap2(gt)/(gt) with increased number of excitatory synapses. This was accompanied by increased F-actin content and F-actin accumulation in cultured Cap2(gt)/(gt) neurons. Moreover, reduced surface GluA1 was observed in mutant neurons under basal condition and after induction of chemical LTP. Additionally, we show an interaction between CAP2 and n-cofilin, presumably mediated through the C-terminal domain of CAP2 and dependent on cofilin Ser3 phosphorylation. In vivo, the consequences of this interaction were altered phosphorylated cofilin levels and formation of cofilin aggregates in the neurons. Thus, our studies identify a novel role of CAP2 in neuronal development and neuronal actin dynamics

Energy imbalance alters Ca2+ handling and excitability of POMC neurons

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AgRP innervation onto POMC neurons increases with age and is accelerated with chronic high-fat feeding in male mice

Copyright © 2013 by The Endocrine Society

Integer equal flows

The integer equal flow problem is an NP-hard network flow problem, in which all arcs in given sets R1,…,R[subscript ℓ] must carry equal flow. We show that this problem is effectively inapproximable, even if the cardinality of each set R[subscript k] is two. When ℓ is fixed, it is solvable in polynomial time

K-ATP-Channel-Dependent Regulation of Catecholaminergic Neurons Controls BAT Sympathetic Nerve Activity and Energy Homeostasis

Brown adipose tissue (BAT) is a critical regulator of glucose, lipid, and energy homeostasis, and its activity is tightly controlled by the sympathetic nervous system. However, the mechanisms underlying CNS-dependent control of BAT sympathetic nerve activity (SNA) are only partly understood. Here, we demonstrate that catecholaminergic neurons in the locus coeruleus (LC) adapt their firing frequency to extracellular glucose concentrations in a K-ATP-channel-dependent manner. Inhibiting K-ATP-channel-dependent control of neuronal activity via the expression of a variant K-ATP channel in tyrosine-hydroxylase-expressing neurons and in neurons of the LC enhances diet-induced obesity in mice. Obesity results from decreased energy expenditure, lower steady-state BAT SNA, and an attenuated ability of centrally applied glucose to activate BAT SNA. This impairs the thermogenic transcriptional program of BAT. Collectively, our data reveal a role of K-ATP-channel-dependent neuronal excitability in catecholaminergic neurons in maintaining thermogenic BAT sympathetic tone and energy homeostasis

High-fat feeding promotes obesity via insulin receptor/PI3k-dependent inhibition of SF-1 VMH neurons

© 2011 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved

PNOCARC neurons promote hyperphagia and obesity upon high-fat-diet feeding

Calorie-rich diets induce hyperphagia and promote obesity, although the underlying mechanisms remain poorly defined. We find that short-term high-fat-diet (HFD) feeding of mice activates prepronociceptin (PNOC)-expressing neurons in the arcuate nucleus of the hypothalamus (ARC). PNOCARC neurons represent a previously unrecognized GABAergic population of ARC neurons distinct from well-defined feeding regulatory AgRP or POMC neurons. PNOCARC neurons arborize densely in the ARC and provide inhibitory synaptic input to nearby anorexigenic POMC neurons. Optogenetic activation of PNOCARC neurons in the ARC and their projections to the bed nucleus of the stria terminalis promotes feeding. Selective ablation of these cells promotes the activation of POMC neurons upon HFD exposure, reduces feeding, and protects from obesity, but it does not affect food intake or body weight under normal chow consumption. We characterize PNOCARC neurons as a novel ARC neuron population activated upon palatable food consumption to promote hyperphagia

Neonatal Insulin Action Impairs Hypothalamic Neurocircuit Formation in Response to Maternal High-Fat Feeding

Maternal metabolic homeostasis exerts long-term effects on the offspring's health outcomes. Here, we demonstrate that maternal high-fat diet (HFD) feeding during lactation predisposes the offspring for obesity and impaired glucose homeostasis in mice, which is associated with an impairment of the hypothalamic melanocortin circuitry. Whereas the number and neuropeptide expression of anorexigenic proopiomelanocortin (POMC) and orexigenic agouti-related peptide (AgRP) neurons, electrophysiological properties of POMC neurons, and posttranslational processing of POMC remain unaffected in response to maternal HFD feeding during lactation, the formation of POMC and AgRP projections to hypothalamic target sites is severely impaired. Abrogating insulin action in POMC neurons of the offspring prevents altered POMCprojections to the preautonomic paraventricular nucleus of the hypothalamus (PVH), pancreatic parasympathetic innervation, and impaired glucosestimulated insulin secretion in response to maternal overnutrition. These experiments reveal a critical timing, when altered maternal metabolism disrupts metabolic homeostasis in the offspring via impairing neuronal projections, and show that abnormal insulin signaling contributes to this effect