Understanding Contrasting Approaches to Nationwide Implementations of Electronic Health Record Systems:England, the USA and Australia

As governments commit to national electronic health record (EHR) systems, there is increasing international interest in identifying effective implementation strategies. We draw on Coiera's typology of national programmes - ‘top-down’, ‘bottom-up’ and ‘middle-out’ - to review EHR implementation strategies in three exemplar countries: England, the USA and Australia. In comparing and contrasting three approaches, we show how different healthcare systems, national policy contexts and anticipated benefits have shaped initial strategies. We reflect on progress and likely developments in the face of continually changing circumstances. Our review shows that irrespective of the initial strategy, over time there is likely to be convergence on the negotiated, devolved middle-out approach, which aims to balance the interests and responsibilities of local healthcare constituencies and national government to achieve national connectivity. We conclude that, accepting the current lack of empirical evidence, the flexibility offered by the middle-out approach may make this the best initial national strategy

Vibrational spectrum of solid picene (C_22H_14)

Recently, Mitsuhashi et al., have observed superconductivity with transition temperature up to 18 K in potassium doped picene (C22H14), a polycyclic aromatic hydrocarbon compound [Nature 464 (2010) 76]. Theoretical analysis indicate the importance of electron-phonon coupling in the superconducting mechanisms of these systems, with different emphasis on inter- and intra-molecular vibrations, depending on the approximations used. Here we present a combined experimental and ab-initio study of the Raman and infrared spectrum of undoped solid picene, which allows us to unanbiguously assign the vibrational modes. This combined study enables the identification of the modes which couple strongly to electrons and hence can play an important role in the superconducting properties of the doped samples

Integrated cardiovascular/respiratory control in type 1 diabetes evidences functional imbalance : Possible role of hypoxia

Background: Cardiovascular (baroreflex) and respiratory (chemoreflex) control mechanisms were studied separately in diabetes, but their reciprocal interaction (well known for diseases like heart failure) had never been comprehensively assessed. We hypothesized that prevalent autonomic neuropathy would depress both reflexes, whereas prevalent autonomic imbalance through sympathetic activation would depress the baroreflex but enhance the chemoreflexes. Methods: In 46 type-1 diabetic subjects (7.0 +/- 0.9 year duration) and 103 age-matched controls we measured the baroreflex (average of 7 methods), and the chemoreflexes, (hypercapnic: ventilation/carbon dioxide slope during hyperoxic progressive hypercapnia; hypoxic: ventilation/oxygen saturation slope during normocapnic progressive hypoxia). Autonomic dysfunction was evaluated by cardiovascular reflex tests. Results: Resting oxygen saturation and baroreflex sensitivity were reduced in the diabetic group, whereas the hypercapnic chemoreflex was significantly increased in the entire diabetic group. Despite lower oxygen saturation the hypoxic chemoreflex showed a trend toward a depression in the diabetic group. Conclusion: Cardio-respiratory control imbalance is a common finding in early type 1 diabetes. A reduced sensitivity to hypoxia seems a primary factor leading to reflex sympathetic activation (enhanced hypercapnic chemoreflex and baroreflex depression), hence suggesting a functional origin of cardio-respiratory control imbalance in initial diabetes. (C) 2017 Elsevier B.V. All rights reserved.Peer reviewe

Enhanced urinary stability of peptide hormones and growth factors by dried urine microsampling

Volumetric absorptive microsampling (VAMS) and dried urine spot (DUS) strategies were applied for the collection of dried microsamples for anti-doping testing of low-stability peptide hormones and growth factors prohibited by the World Anti-Doping Agency (WADA). Drying, storage and transport conditions, as well as pretreatment steps, were optimised before liquid chromatography - tandem mass spectrometry (LC–MS/MS) analysis. The analytical method has been fully validated in terms of sensitivity (limits of quantitation 0.3−10 ng/mL), precision (RSD% < 6.6 %) and extraction yields (78–91 %). Dried microsample stability studies (90 days) have been performed and compared to fluid urine stability. Significantly higher losses have been observed in fluid urine stored at −20 °C (up to 55 %) and −80 °C (up to 29 %) than in dried urine microsamples stored at room temperature (< 19 %). The final microsampling and analysis protocols allow the collection of urine microvolumes, unlikely to be tampered, stably storable and shippable with no particular precautions for possible anti-doping testing of prohibited peptides and hormones

Metformin increases skeletal muscle lactate production in pigs: a microdialysis study

Introduction Lactic acidosis during metformin intoxication is mainly attributed to impaired hepatic lactate clearance [1]. The aim of this present work was to clarify whether metformin at high dose also increases skeletal muscle lactate production. Methods Reverse microdialysis was used in six healthy, sedated and mechanically ventilated pigs, equipped with two skeletal muscle catheters (CMA Microdialysis AB, Sweden). Following a baseline recording, a continuous infusion of saline (control) or metformin diluted in saline (1 mol/l) began. Outfl ow lactate concentration was measured every 3 hours, up to 12 hours. Results Data are presented as the mean and standard deviation in Figure 1. The interaction between infusion (saline vs. metformin) and time was statistically signifi cant (P = 0.02; two-way repeated-measures ANOVA). Conclusions In skeletal muscle, a high dose of metformin increases interstitial lactate levels, a fi nding consistent with local lactate overproduction. Reference 1. Lalau JD: Drug Saf 2010, 33:727-740

Contribution of red blood cells to the compensation for hypocapnic alkalosis through plasmatic strong ion difference variations

Introduction Chloride shift is the movement of chloride between red blood cells (RBC) and plasma (and vice versa) caused by variations in pCO2. The aim of our study was to investigate changes in plasmatic strong ion diff erence (SID) during acute variations in pCO2 and their possible role in the compensation for hypocapnic alkalosis.Methods Patients admitted in this year to our ICU requiring extracorporeal CO2 removal were enrolled. Couples of measurements of gases and electrolytes on blood entering (v) and leaving (a) the respiratory membrane were analyzed. SID was calculated as [Na+] + [K+] + 2[Ca2+] \u2013 [Cl\u2013] \u2013 [Lac\u2013]. Percentage variations in SID (SID%) were calculated as (SIDv \u2013 SIDa) x 100 / SIDv. The same calculation was performed for pCO2 (pCO2%). Comparison between v and a values was performed by paired t test or the signed-rank test, as appropriate. Results Analysis was conducted on 205 sample-couples of six enrolled patients. A signifi cant diff erence (P <0.001) between mean values of v\u2013a samples was observed for pH (7.41 \ub1 0.05 vs. 7.51 \ub1 0.06), pCO2 (48 \ub1 6 vs. 35 \ub1 7 mmHg), [Na+] (136.3 \ub1 4.0 vs. 135.2 \ub1 4.0 mEq/l), [Cl\u2013] (101.5 \ub1 5.3 vs. 102.8 \ub1 5.2 mEq/l) and therefore SID (39.5 \ub1 4.0 vs. 36.9 \ub1 4.1 mEq/l). pCO2% and SID% signifi cantly correlated (r2 = 0.28, P <0.001). Graphical representation by quartiles of pCO2% is shown in Figure 1. Conclusions As a reduction in SID decreases pH, the observed movement of anions and cations probably limited the alkalinization caused by hypocapnia. In this model, the only source of electrolytes are blood cells (that is, no interstitium and no infl uence of the kidney is present); it is therefore conceivable to consider the observed phenomenon as the contribution of RBC for the compensation of acute hypocapnic alkalosi

Left Ventricular Unloading in Extracorporeal Membrane Oxygenation:A Clinical Perspective Derived from Basic Cardiovascular Physiology

Purpose of Review: To present an abridged overview of the literature and pathophysiological background of adjunct interventional left ventricular unloading strategies during veno-arterial extracorporeal membrane oxygenation (V-A ECMO). From a clinical perspective, the mechanistic complexity of such combined mechanical circulatory support often requires in-depth physiological reasoning at the bedside, which remains a cornerstone of daily practice for optimal patient-specific V-A ECMO care. Recent Findings: Recent conventional clinical trials have not convincingly shown the superiority of V-A ECMO in acute myocardial infarction complicated by cardiogenic shock as compared with medical therapy alone. Though, it has repeatedly been reported that the addition of interventional left ventricular unloading to V-A ECMO may improve clinical outcome. Novel approaches such as registry-based adaptive platform trials and computational physiological modeling are now introduced to inform clinicians by aiming to better account for patient-specific variation and complexity inherent to V-A ECMO and have raised a widespread interest. Summary: To provide modern high-quality V-A ECMO care, it remains essential to understand the patient's pathophysiology and the intricate interaction of an individual patient with extracorporeal circulatory support devices. Innovative clinical trial design and computational modeling approaches carry great potential towards advanced clinical decision support in ECMO and related critical care.</p

Strain threshold for ventilator-induced lung injury

Introduction Unphysiological lung strain (tidal volume/functional residual capacity, TV/FRC) may cause ventilator-induced lung injury (VILI) [1]. Whether VILI develops proportionally to the applied strain or only above a critical threshold remains unknown. Methods In 20 healthy, mechanically ventilated pigs, FRC and lung weight were measured by computed tomography. Animals were then ventilated for up to 54 hours with a TV set to produce a predetermined strain. At the end, lung weight was measured with a balance. VILI was defi ned as fi nal lung weight exceeding the initial one. Results Lung weight either did not increase at all (no-VILI group; lung weight change \u201373 \ub1 42 g, n = 9) or markedly augmented (VILI group; 264 \ub1 80 g, n = 11). In the two groups, strain was 1.38 \ub1 0.68 and 2.16 \ub1 0.50 (P <0.01), respectively. VILI occurred only when lung strain reached or exceeded a critical threshold, between 1.5 and 2.1 (Figure 1). Conclusions In animals with healthy lungs VILI only occurs when lung strain exceeds a critical threshold. Reference 1. Gattinoni L, Carlesso E, Cadringher P, et al.: Physical and biological triggers of ventilator-induced lung injury and its prevention [review]. Eur Respir J 2003, 22(Suppl 47):15s-25s