Health Analytics as a Service with Artemis Cloud: Service Availability.

Critical care units internationally contain medical devices that generate Big Data in the form of high speed physiological data streams. Great opportunities exist for systemic and reliable approaches for the analysis of high speed physiological data for clinical decision support. This paper presents the instantiation of a Big Data analytics based Health Analytics as-a-Service model.

Adaptive API for Real-Time Streaming Analytics as a Service.

A significant amount of physiological data is generated from bedside monitors and sensors in neonatal intensive units (NICU) every second, however facilitating the ingestion of such data into multiple analytical processes in a real time streaming architecture remains a central challenge for systems that seek effective scaling of real-time data streams. In this paper we demonstrate an adaptive streaming application program interface (API) that provides real time streams of data for consumption by multiple analytics services enabling real-time exploration and knowledge discovery from live data streams. We have designed, developed and evaluated an adaptive API with multiple ingestion of data streamed out of bedside monitors that is passed to a middleware for standardization and structuring and finally distributed as a service for multiple analytical services to consume and perform further processing.

Time and motion study of pharmacist prescribing of oral hormonal contraceptives in Oregon community pharmacies.

Objectives: The aim of this time and motion study was to evaluate the procedural time and steps of performing an oral hormonal contraceptive pharmacist prescribing service in an Oregon community pharmacy.

Methods: A standardized patient seeking oral hormonal contraception visited 13 community pharmacies throughout February 2018 in the tri-county Portland, Oregon, metropolitan area for pharmacist-prescribed hormonal contraception services for a total of 26 patient encounters. An observer was present at each encounter to record the time for each step and the total encounter time.

Advancing the 3Rs in regulatory ecotoxicology: A pragmatic cross-sector approach.

The ecotoxicity testing of chemicals for prospective environmental safety assessment is an area in which a high number of vertebrates are used across a variety of industry sectors. Refining, reducing, and replacing the use of animals such as fish, birds, and amphibians for this purpose addresses the ethical concerns and the increasing legislative requirements to consider alternative test methods. Members of the UK-based National Centre for the Replacement, Refinement and Reduction of Animals in Research (NC3Rs) Ecotoxicology Working Group, consisting of representatives from academia, government organizations, and industry, have worked together over the past 6 y to provide evidence bases to support and advance the application of the 3Rs in regulatory ecotoxicity testing.

Assessing pharmacologic and nonpharmacologic risks in candidates for kidney transplantation.

Purpose: Pharmacotherapy concerns and other factors with a bearing on patient selection for kidney transplantation are discussed.

Summary: The process of selecting appropriate candidates for kidney transplantation involves multidisciplinary assessment to evaluate a patient's mental, social, physical, financial, and medical readiness for successful surgery and good posttransplantation outcomes. Transplantation pharmacists can play important roles in the recognition and stratification of pharmacologic and nonpharmacologic risks in prospective kidney transplant recipients and the identification of issues that require a mitigation strategy.

Pharmacogenomic considerations in the treatment of the pediatric cardiomyopathy called Barth syndrome.

Barth syndrome (BTHS) is a genetic, X-linked, rare but often fatal, pediatric skeletal- and cardiomyopathy occurring due to mutations in the tafazzin gene (TAZ). TAZ encodes a transacylase involved in phospholipid biosynthesis, also called tafazzin, which is responsible for remodeling the inner mitochondrial membrane phospholipid, cardiolipin (CL). Tafazzin mutations lead to compositional alterations in CL molecular species, causing extensive mitochondrial aberrations and ultrastructural muscle damage.

Differential gene expression analysis in human monocyte-derived macrophages: impact of cigarette smoke on host defence.

Alveolar macrophages have been implicated in the pathophysiology of chronic obstructive pulmonary disease (COPD). In this setting they are routinely exposed to cigarette smoke and a range of pathogens including bacteria and viruses. The gene expression changes that result from these challenges may contribute to the initiation and progression of the disease.

Fractional exhaled NO and serum pneumoproteins after swimming in a chlorinated pool.

Purpose: The purpose of this study was to examine whether a swimming session performed in a pool sanitized with chlorine-based agents induces lung inflammation, modifies lung epithelium permeability, and alters lung function.

Methods: Eleven volunteers performed two standardized swimming sessions: one in a nonchlorinated indoor swimming pool and the other one in a chlorinated indoor pool. Lung inflammation was assessed by fractional exhaled nitric oxide (FE(NO)).

Intracellular storage of surfactant and proinflammatory cytokines in co-cultured alveolar epithelium and macrophages in response to increasing CO2 and cyclic cell stretch.

Cell stretch stimulates both surfactant and cytokine production. The authors proposed that stretch, through these effects, modifies the pathogenesis of lipopolysaccharide-induced acute lung injury (ALI), and that this is CO(2) dependent. Rat alveolar type II cells and macrophages were co-cultured with lipopolysaccharide in 5%, 10%, or 20% CO(2) +/- stretch (30%, 60 cycles/min) for 6 hours.

Hypercapnic acidosis modulates inflammation, lung mechanics, and edema in the isolated perfused lung.

Objective: Low tidal volume (V(T)) ventilation strategies may be associated with permissive hypercapnia, which has been shown by ex vivo and in vivo studies to have protective effects. We hypothesized that hypercapnic acidosis may be synergistic with low V(T) ventilation; therefore, we studied the effects of hypercapnia and V(T) on unstimulated and lipopolysaccharide-stimulated isolated perfused lungs.

Materials And Methods: Isolated perfused rat lungs were ventilated for 2 hours with low (7 mL/kg) or moderately high (20 mL/kg) V(T) and 5% or 20% CO(2), with lipopolysaccharide or saline added to the perfusate.

Stretch and CO2 modulate the inflammatory response of alveolar macrophages through independent changes in metabolic activity.

Ventilatory-induced strain can exacerbate acute lung injury (ALI). Current ventilation strategies favour low tidal volumes and high end-expiratory volumes to 'rest' the lung, but can lead to an increase in CO2. Alveolar macrophages (AM) play a pivotal role in ALI through the release of inflammatory mediators.

Circulating surfactant protein-B levels increase acutely in response to exercise-induced left ventricular dysfunction.

1. As a result of its enormous surface area and necessary thinness for gas exchange, the alveolocapillary barrier is vulnerable to mechanical disruption from raised pulmonary microvascular pressure (Pmv). 2.

Effect of CO2 on LPS-induced cytokine responses in rat alveolar macrophages.

Alveolar macrophages (AM) may be exposed to a range of CO(2) and pH levels depending on their location in the alveoli and the health of the lung. Cytokines produced by AM contribute to inflammation in acute lung injury (ALI). Current ventilatory practices for the management of ALI favor low tidal volumes, which can give rise to increases in CO(2) and changes in pH of the alveolar microenvironment.

Plasma surfactant protein-B: a novel biomarker in chronic heart failure.

Background: In chronic heart failure (CHF), elevated pulmonary microvascular pressure (P(mv)) results in pulmonary edema. Because elevated P(mv) may alter the integrity of the alveolocapillary barrier, allowing leakage of surfactant protein-B (SP-B) from the alveoli into the circulation, we aimed to determine plasma levels of SP-B in CHF and their relation to clinical status.

Methods And Results: Fifty-three outpatients with CHF had plasma SP-B and N-terminal proBNP (NT-proBNP) assayed, in addition to a formalized clinical assessment at each clinic review over a period of 18 months.

Determinants of serum levels of surfactant proteins A and B and Clara cell protein CC16.

Increased leakage of surfactant proteins A and B (SP-A and SP-B) and Clara cell secretory protein (CC16) from the air spaces into the circulation occurs in a range of respiratory conditions. However, circulating levels depend not only on the rate of entry into the circulation, but also on the rate of clearance. In order to clarify the role of the kidney in the clearance of these proteins, serum levels were related to markers of glomerular filtration in 54 non-smoking patients with varying degrees of renal dysfunction, none of whom had respiratory disease or were receiving dialysis at the time of sampling.

Lucinactant (Discovery Laboratories).

Discovery Laboratories Inc (formerly Acute Therapeutics Inc (ATI) is developing lucinactant, originally identified at the Scripps Research Institute and sublicensed from Johnson & Johnson, for the potential treatment of respiratory diseases [174059], [357077], [361765], [422819]. The company anticipated filing an NDA for lucinactant in 2002, and by March 2002, lucinactant was in two pivotal phase III international trials for respiratory distress syndrome (RDS) in premature infants, a phase III trial for meconium aspiration syndrome (MAS) in full-term infants, and a phase II trial for acute lung injury/acute respiratory distress syndrome (ALI/ARDS) in adults. The company expected to complete trials by late 2003 [400846], [445166].

Prolonged alveolocapillary barrier damage after acute cardiogenic pulmonary edema.

Objectives: To determine whether acute cardiogenic pulmonary edema is associated with damage to the alveolocapillary barrier, as evidenced by increased leakage of surfactant specific proteins into the circulation, to document the duration of alveolocapillary barrier damage in this setting, and to explore the role of pulmonary parenchymal inflammation by determining if circulating tumor necrosis factor-alpha is increased after acute cardiogenic pulmonary edema.

Design: Prospective, observational study.

Setting: Critical care, cardiac intensive care, and cardiology wards of a tertiary-care university teaching hospital.

Changes in serum pneumoproteins caused by short-term exposures to nitrogen trichloride in indoor chlorinated swimming pools.

Nitrogen trichloride (NCl(3)) is an irritant gas released in the air of indoor pools sanitized with chlorine-based disinfectants. In the present study we investigated the effects of NCl(3) on the pulmonary epithelium of pool attendees by measuring the leakage into serum of three lung-specific proteins (pneumoproteins): the alveolar surfactant-associated proteins A and B (SP-A and SP-B) and the bronchiolar 16 kDa Clara cell protein (CC16). These pneumoproteins were measured in the serum of 29 recreational swimmers (16 children and 13 adults) before and after attending a chlorinated pool with a mean NCl(3) concentration of 490 microg m(-3).

Infarct-induced chronic heart failure increases bidirectional protein movement across the alveolocapillary barrier.

Chronic heart failure (CHF) is associated with adaptive structural changes at the alveolocapillary barrier that may be associated with altered protein permeability. Bidirectional protein movement across the barrier was studied in anesthetized rats with infarct-induced CHF by following (125)I-labeled albumin ((125)I-albumin) flux into the alveoli and the leakage of surfactant protein (SP)-B from the alveoli into the circulation. Three groups were studied: controls [0% left ventricular (LV) infarction], moderate infarct (25-45% LV infarction), and large infarct (>46% LV infarction).

A phase I study of the GM-CSF antagonist E21R.

Purpose: E21R is a competitive inhibitor of GM-CSF. This is the initial clinical study to investigate the safety, toxicity and pharmacokinetics of escalating doses of E21R.

Patients And Methods: Cohorts of three patients received doses of 10, 30, 100, 300, 600 and 1000 micro g/kg per day given subcutaneously daily for 10 days.