Impact of an Expeditor on Emergency Department Patient Throughput

Objective: Our hypothesis was that an individual whose primary role was to assist with patient throughput would decrease emergency department (ED) length of stay (LOS), elopements and ambulance diversion. The objective of this study was to measure how the use of an expeditor affected these throughput metrics.Methods: This pre- and post-intervention study analyzed ED patients > 21-years-old between June 2008 and June 2009, at a level one trauma center in an academic medical center with an annual ED census of 40,000 patients. We created the expeditor position as our study intervention in December 2008, by modifying the job responsibilities of an existing paramedic position. An expeditor was on duty from 1PM-1AM daily. The pre-intervention period was June to November 2008, and the post-intervention period was January to June 2009. We used multivariable to assess the impact of the expeditor on throughput metrics after adjusting for confounding variables.Results: We included a total of 13,680 visits in the analysis. There was a significant decrease in LOS after expeditor implementation by 0.4 hours, despite an increased average daily census (109 vs. 121, p<0.001). The expeditor had no impact on elopements. The probability that the ED experienced complete ambulance diversion during a 24-hour period decreased from 55.2% to 16.0% (OR:0.17, 95%CI:0.05-0.67).Conclusion: The use of an expeditor was associated with a decreased LOS and ambulance diversion. These findings suggest that EDs may be able to improve patient flow by using expeditors. This tool is under the control of the ED and does not require larger buy-in, resources, or overall hospital changes. [West J Emerg Med. 2011;12(2):198-203.

As a critical behavior to improve quality and patient safety in health care: Speaking up!

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Experimental Implementation of Optical Clockwork without Carrier-Envelope Phase Control

We demonstrate an optical clockwork without camer-envelope phase control using sum-frequency generation between a CW optical parametric oscillator at 3.39 μm and a modelocked Tisapphire laser with dominant spectral peaks at 834 and 670 nm

Optical Clockwork without Carrier-Envelope Phase Control

We demonstrate optical clockwork without carrier-envelope phase control using sum-frequency generation between a cw optical parametric oscillator at 3.39 μm and a mode-locked Ti:sapphire laser with dominant spectral peaks at 834 nm and 670 nm

MANP Activation Of The cGMP Inhibits Aldosterone Via PDE2 And CYP11B2 In H295R Cells And In Mice

Background: Aldosterone is a critical pathological driver for cardiac and renal diseases. We recently discovered that mutant atrial natriuretic peptide (MANP), a novel atrial natriuretic peptide (ANP) analog, possessed more potent aldosterone inhibitory action than ANP in vivo. MANP and natriuretic peptide (NP)-augmenting therapy sacubitril/valsartan are under investigations for human hypertension treatment. Understanding the elusive mechanism of aldosterone inhibition by NPs remains to be a priority. Conflicting results were reported on the roles of the pGC-A (particulate guanylyl cyclase A receptor) and NP clearance receptor in aldosterone inhibition. Furthermore, the function of PKG (protein kinase G) and PDEs (phosphodiesterases) on aldosterone regulation are not clear. Methods: In the present study, we investigated the molecular mechanism of aldosterone regulation in a human adrenocortical cell line H295R and in mice. Results: We first provided evidence to show that pGC-A, not NP clearance receptor, mediates aldosterone inhibition. Next, we confirmed that MANP inhibits aldosterone via PDE2 (phosphodiesterase 2) not PKG, with specific agonists, antagonists, siRNA silencing, and fluorescence resonance energy transfer experiments. Further, the inhibitory effect is mediated by a reduction of intracellular Ca2+ levels. We then illustrated that MANP directly reduces aldosterone synthase CYP11B2 (cytochrome p450 family 11 subfamily b member 2) expression via PDE2. Last, in PDE2 knockout mice, consistent with in vitro findings, embryonic adrenal CYP11B2 is markedly increased. Conclusions: Our results innovatively explore and expand the NP/pGC-A/3',5', cyclic guanosine monophosphate (cGMP)/PDE2 pathway for aldosterone inhibition by MANP in vitro and in vivo. In addition, our data also support the development of MANP as a novel ANP analog drug for aldosterone excess treatment

Phase I study of TP300 in patients with advanced solid tumors with pharmacokinetic, pharmacogenetic and pharmacodynamic analyses

Background: A Phase I dose escalation first in man study assessed maximum tolerated dose (MTD), dose-limiting toxicity (DLT) and recommended Phase II dose of TP300, a water soluble prodrug of the Topo-1 inhibitor TP3076, and active metabolite, TP3011. &lt;p/&gt;Methods: Eligible patients with refractory advanced solid tumors, adequate performance status, haematologic, renal, and hepatic function. TP300 was given as a 1-hour i.v. infusion 3-weekly and pharmacokinetic (PK) profiles of TP300, TP3076 and TP3011 were analysed. Polymorphisms in CYP2D6, AOX1 and UGT1A1 were studied and DNA strand-breaks measured in peripheral blood mononuclear cells (PBMCs). &lt;p/&gt;Results: 32 patients received TP300 at 1, 2, 4, 6, 8, 10, 12 mg/m2. MTD was 10 mg/m2; DLTs at 12 (2/4 patients) and 10 mg/m2 (3/12) included thrombocytopenia and febrile neutropenia; diarrhea was uncommon. Six patients (five had received irinotecan), had stable disease for 1.5-5 months. TP3076 showed dose proportionality in AUC and Cmax from 1--10 mg/m2. Genetic polymorphisms had no apparent influence on exposure. DNA strand-breaks were detected after TP300 infusion. &lt;p/&gt;Conclusions: TP300 had predictable hematologic toxicity, and diarrhea was uncommon. AUC at MTD is substantially greater than for SN38. TP3076 and TP3011 are equi-potent with SN38, suggesting a PK advantage

Les Albinos Face Au Développement Economique Du Territoire De Bumba « Cas De La Cité De Bumba »

l’albinisme est une affection autosomique récessive due à l’absence de mélanine dans  la peau, les  cheveux et les jeux. Les gens qui souffrent   de cette affection sont des albinos, souvent victimes des sacrifices humains d’assassinat voire d’enlèvement pour des fins magiques.  Etant marginalisés, leurs capacités restent inexploitées dans le menu du développement leur identification intégration  et leur promotion éducative seraient  des pistes de sortie du comportement  discriminatoire  leur affiché  afin d’atteindre  les  objectifs  du  millénaire  pour le développement  qui stipule « amélioration  de la santé  sous toutes ces formes  et  réduire par  conséquent ; l’extrême pauvreté »

Pressure-Induced Magnetic Crossover Driven by Hydrogen Bonding in CuF2(H2O)2(3-chloropyridine)

Hydrogen bonding plays a foundational role in the life, earth, and chemical sciences, with its richness and strength depending on the situation. In molecular materials, these interactions determine assembly mechanisms, control superconductivity, and even permit magnetic exchange. In spite of its long-standing importance, exquisite control of hydrogen bonding in molecule-based magnets has only been realized in limited form and remains as one of the major challenges. Here, we report the discovery that pressure can tune the dimensionality of hydrogen bonding networks in CuF2(H2O)2(3-chloropyridine) to induce magnetic switching. Specifically, we reveal how the development of exchange pathways under compression combined with an enhanced ab-plane hydrogen bonding network yields a three dimensional superexchange web between copper centers that triggers a reversible magnetic crossover. Similar pressure- and strain-driven crossover mechanisms involving coordinated motion of hydrogen bond networks may play out in other quantum magnets

Chemotaxis: a feedback-based computational model robustly predicts multiple aspects of real cell behaviour

The mechanism of eukaryotic chemotaxis remains unclear despite intensive study. The most frequently described mechanism acts through attractants causing actin polymerization, in turn leading to pseudopod formation and cell movement. We recently proposed an alternative mechanism, supported by several lines of data, in which pseudopods are made by a self-generated cycle. If chemoattractants are present, they modulate the cycle rather than directly causing actin polymerization. The aim of this work is to test the explanatory and predictive powers of such pseudopod-based models to predict the complex behaviour of cells in chemotaxis. We have now tested the effectiveness of this mechanism using a computational model of cell movement and chemotaxis based on pseudopod autocatalysis. The model reproduces a surprisingly wide range of existing data about cell movement and chemotaxis. It simulates cell polarization and persistence without stimuli and selection of accurate pseudopods when chemoattractant gradients are present. It predicts both bias of pseudopod position in low chemoattractant gradients and-unexpectedly-lateral pseudopod initiation in high gradients. To test the predictive ability of the model, we looked for untested and novel predictions. One prediction from the model is that the angle between successive pseudopods at the front of the cell will increase in proportion to the difference between the cell's direction and the direction of the gradient. We measured the angles between pseudopods in chemotaxing Dictyostelium cells under different conditions and found the results agreed with the model extremely well. Our model and data together suggest that in rapidly moving cells like Dictyostelium and neutrophils an intrinsic pseudopod cycle lies at the heart of cell motility. This implies that the mechanism behind chemotaxis relies on modification of intrinsic pseudopod behaviour, more than generation of new pseudopods or actin polymerization by chemoattractant

Rhomboid family member 2 regulates cytoskeletal stress-associated Keratin 16.

Keratin 16 (K16) is a cytoskeletal scaffolding protein highly expressed at pressure-bearing sites of the mammalian footpad. It can be induced in hyperproliferative states such as wound healing, inflammation and cancer. Here we show that the inactive rhomboid protease RHBDF2 (iRHOM2) regulates thickening of the footpad epidermis through its interaction with K16. K16 expression is absent in the thinned footpads of irhom2-/- mice compared with irhom2+/+mice, due to reduced keratinocyte proliferation. Gain-of-function mutations in iRHOM2 underlie Tylosis with oesophageal cancer (TOC), characterized by palmoplantar thickening, upregulate K16 with robust downregulation of its type II keratin binding partner, K6. By orchestrating the remodelling and turnover of K16, and uncoupling it from K6, iRHOM2 regulates the epithelial response to physical stress. These findings contribute to our understanding of the molecular mechanisms underlying hyperproliferation of the palmoplantar epidermis in both physiological and disease states, and how this 'stress' keratin is regulated