Communicating moral legitimacy in controversial industries: the trade in human tissue

Globally active companies are involved in the discursive construction of moral legitimacy. Establishing normative conformance is problematic given the plurality of norms and values worldwide, and is particularly difficult for companies operating in morally controversial industries. In this paper, we investigate how organizations publicly legitimize the trade of human tissue for private profit when this practice runs counter to deep-seated and widespread moral beliefs. To do so, we use inductive, qualitative methods to analyze the website discourse of three types of organizations that trade in human tissue and are associated with different degrees of moral controversy with respect to tissue procurement and use. Our analysis reveals an object-oriented approach to moral legitimizing centered on the human tissue as a morally disputed good. We find that the website discourse translates human tissue into technology, constructs normative meaning around a dominant instrumental value associated with human-tissue-as-technology, and reproduces and stabilizes this meaning by six discursive mechanisms that amplify and anchor it. Moreover, the use of amplifying and anchoring discourse was greater in organizations associated with greater controversy. The results are consistent with an object-oriented sociality

Hypothesis Generation Using Network Structures on Community Health Center Cancer-Screening Performance

RESEARCH OBJECTIVES: Nationally sponsored cancer-care quality-improvement efforts have been deployed in community health centers to increase breast, cervical, and colorectal cancer-screening rates among vulnerable populations. Despite several immediate and short-term gains, screening rates remain below national benchmark objectives. Overall improvement has been both difficult to sustain over time in some organizational settings and/or challenging to diffuse to other settings as repeatable best practices. Reasons for this include facility-level changes, which typically occur in dynamic organizational environments that are complex, adaptive, and unpredictable. This study seeks to understand the factors that shape community health center facility-level cancer-screening performance over time. This study applies a computational-modeling approach, combining principles of health-services research, health informatics, network theory, and systems science. METHODS: To investigate the roles of knowledge acquisition, retention, and sharing within the setting of the community health center and to examine their effects on the relationship between clinical decision support capabilities and improvement in cancer-screening rate improvement, we employed Construct-TM to create simulated community health centers using previously collected point-in-time survey data. Construct-TM is a multi-agent model of network evolution. Because social, knowledge, and belief networks co-evolve, groups and organizations are treated as complex systems to capture the variability of human and organizational factors. In Construct-TM, individuals and groups interact by communicating, learning, and making decisions in a continuous cycle. Data from the survey was used to differentiate high-performing simulated community health centers from low-performing ones based on computer-based decision support usage and self-reported cancer-screening improvement. RESULTS: This virtual experiment revealed that patterns of overall network symmetry, agent cohesion, and connectedness varied by community health center performance level. Visual assessment of both the agent-to-agent knowledge sharing network and agent-to-resource knowledge use network diagrams demonstrated that community health centers labeled as high performers typically showed higher levels of collaboration and cohesiveness among agent classes, faster knowledge-absorption rates, and fewer agents that were unconnected to key knowledge resources. Conclusions and research implications: Using the point-in-time survey data outlining community health center cancer-screening practices, our computational model successfully distinguished between high and low performers. Results indicated that high-performance environments displayed distinctive network characteristics in patterns of interaction among agents, as well as in the access and utilization of key knowledge resources. Our study demonstrated how non-network-specific data obtained from a point-in-time survey can be employed to forecast community health center performance over time, thereby enhancing the sustainability of long-term strategic-improvement efforts. Our results revealed a strategic profile for community health center cancer-screening improvement via simulation over a projected 10-year period. The use of computational modeling allows additional inferential knowledge to be drawn from existing data when examining organizational performance in increasingly complex environments

Zirconium-catalyzed alkene hydrophosphination and dehydrocoupling with an air-stable, fluorescent primary phosphine

Zirconium-catalyzed alkene hydrophosphination and dehydrocoupling with an air-stable, fluorescent primary phosphine 8-[(4-phosphino)phenyl]-4,4-dimethyl-1,3,5,7-tetramethyl-2,6-diethyl- 4-bora-3a,4a-diaza-s-indacene furnishes fluorescent phosphine products. Hydrophosphination of the fluorescent phosphine produces products with a complete selectivity for the secondary product. A key intermediate in catalysis, a zirconium phosphido compound, was isolated

Numerical Simulation of a Scanning Illumination System for Deep Tissue Fluorescence Imaging

he spatial resolution and light detected in fluorescence imaging for small animals are limited by light scattering, absorption and autofluorescence. To address this, novel near-infrared fluorescent contrast agents and imaging configurations have been investigated. In this paper, the influence of the light wavelength and imaging configurations (full-field illumination system and scanning system) on fluorescence imaging are compared quantitatively. The surface radiance for both systems is calculated by modifying the simulation tool Near-Infrared Fluorescence and Spectral Tomography. Fluorescent targets are embedded within a scattering medium at different positions. The surface radiance and spatial resolution are obtained for emission wavelengths between 620 nm and 1000 nm. It was found that the spatial resolution of the scanning system is independent of the tissue optical properties, whereas for full-field illumination, the spatial resolution degrades at longer wavelength. The full width at half maximum obtained by the scanning system is 25% lower than that obtained by the full-field illumination system when the targets are located in the middle of the phantom. The results indicate that although imaging at near-infrared wavelength can achieve a higher surface radiance, it may produce worse spatial resolution

Role of Fas and Treg Cells in Fracture Healing as Characterized in the Fas-Deficient (lpr) Mouse Model of Lupus

Previous studies showed that loss of tumor necrosis factor α (TNFα) signaling delayed fracture healing by delaying chondrocyte apoptosis and cartilage resorption. Mechanistic studies showed that TNFα induced Fas expression within chondrocytes; however, the degree to which chondrocyte apoptosis is mediated by TNFα alone or dependent on the induction of Fas is unclear. This question was addressed by assessing fracture healing in Fas-deficient B6.MRL/Faslpr/J mice. Loss of Fas delayed cartilage resorption but also lowered bone fraction in the calluses. The reduced bone fraction was related to elevated rates of coupled bone turnover in the B6.MRL/Faslpr/J calluses, as evidenced by higher osteoclast numbers and increased osteogenesis. Analysis of the apoptotic marker caspase 3 showed fewer positive chondrocytes and osteoclasts in calluses of B6.MRL/Faslpr/J mice. To determine if an active autoimmune state contributed to increased bone turnover, the levels of activated T cells and Treg cells were assessed. B6.MRL/Faslpr/J mice had elevated Treg cells in both spleens and bones of B6.MRL/Faslpr/J but decreased percentage of activated T cells in bone tissues. Fracture led to ∼30% to 60% systemic increase in Treg cells in both wild-type and B6.MRL/Faslpr/J bone tissues during the period of cartilage formation and resorption but either decreased (wild type) or left unchanged (B6.MRL/Faslpr/J) the numbers of activated T cells in bone. These results show that an active autoimmune state is inhibited during the period of cartilage resorption and suggest that iTreg cells play a functional role in this process. These data show that loss of Fas activity specifically in chondrocytes prolonged the life span of chondrocytes and that Fas synergized with TNFα signaling to mediate chondrocyte apoptosis. Conversely, loss of Fas systemically led to increased osteoclast numbers during later periods of fracture healing and increased osteogenesis. These findings suggest that retention of viable chondrocytes locally inhibits osteoclast activity or matrix proteolysis during cartilage resorption

SCAMP:standardised, concentrated, additional macronutrients, parenteral nutrition in very preterm infants: a phase IV randomised, controlled exploratory study of macronutrient intake, growth and other aspects of neonatal care

<p>Abstract</p> <p>Background</p> <p>Infants born <29 weeks gestation are at high risk of neurocognitive disability. Early postnatal growth failure, particularly head growth, is an important and potentially reversible risk factor for impaired neurodevelopmental outcome. Inadequate nutrition is a major factor in this postnatal growth failure, optimal protein and calorie (macronutrient) intakes are rarely achieved, especially in the first week. Infants <29 weeks are dependent on parenteral nutrition for the bulk of their nutrient needs for the first 2-3 weeks of life to allow gut adaptation to milk digestion. The prescription, formulation and administration of neonatal parenteral nutrition is critical to achieving optimal protein and calorie intake but has received little scientific evaluation. Current neonatal parenteral nutrition regimens often rely on individualised prescription to manage the labile, unpredictable biochemical and metabolic control characteristic of the early neonatal period. Individualised prescription frequently fails to translate into optimal macronutrient delivery. We have previously shown that a standardised, concentrated neonatal parenteral nutrition regimen can optimise macronutrient intake.</p> <p>Methods</p> <p>We propose a single centre, randomised controlled exploratory trial of two standardised, concentrated neonatal parenteral nutrition regimens comparing a standard macronutrient content (maximum protein 2.8 g/kg/day; lipid 2.8 g/kg/day, dextrose 10%) with a higher macronutrient content (maximum protein 3.8 g/kg/day; lipid 3.8 g/kg/day, dextrose 12%) over the first 28 days of life. 150 infants 24-28 completed weeks gestation and birthweight <1200 g will be recruited. The primary outcome will be head growth velocity in the first 28 days of life. Secondary outcomes will include a) auxological data between birth and 36 weeks corrected gestational age b) actual macronutrient intake in first 28 days c) biomarkers of biochemical and metabolic tolerance d) infection biomarkers and other intravascular line complications e) incidence of major complications of prematurity including mortality f) neurodevelopmental outcome at 2 years corrected gestational age</p> <p>Trial registration</p> <p>Current controlled trials: <a href="http://www.controlled-trials.com/ISRCTN76597892">ISRCTN76597892</a>; EudraCT Number: 2008-008899-14</p

Characterization of the insulin sensitivity of ghrelin receptor KO mice using glycemic clamps

<p>Abstract</p> <p>Background</p> <p>We and others have demonstrated previously that ghrelin receptor (<it>GhrR</it>) knock out (KO) mice fed a high fat diet (HFD) have increased insulin sensitivity and metabolic flexibility relative to WT littermates. A striking feature of the HFD-fed <it>GhrR </it>KO mouse is the dramatic decrease in hepatic steatosis. To characterize further the underlying mechanisms of glucose homeostasis in <it>GhrR </it>KO mice, we conducted both hyperglycemic (HG) and hyperinsulinemic-euglycemic (HI-E) clamps. Additionally, we investigated tissue glucose uptake and specifically examined liver insulin sensitivity.</p> <p>Results</p> <p>Consistent with glucose tolerance-test data, in HG clamp experiments, <it>GhrR </it>KO mice showed a reduction in glucose-stimulated insulin release relative to WT littermates. Nevertheless, a robust 1^stphase insulin secretion was still achieved, indicating that a healthy β-cell response is maintained. Additionally, <it>GhrR </it>KO mice demonstrated both a significantly increased glucose infusion rate and significantly reduced insulin requirement for maintenance of the HG clamp, consistent with their relative insulin sensitivity. In HI-E clamps, both LFD-fed and HFD-fed <it>GhrR </it>KO mice showed higher peripheral insulin sensitivity relative to WT littermates as indicated by a significant increase in insulin-stimulated glucose disposal (Rd), and decreased hepatic glucose production (HGP). HFD-fed <it>GhrR </it>KO mice showed a marked increase in peripheral tissue glucose uptake in a variety of tissues, including skeletal muscle, brown adipose tissue and white adipose tissue. <it>GhrR </it>KO mice fed a HFD also showed a modest, but significant decrease in conversion of pyruvate to glucose, as would be anticipated if these mice displayed increased liver insulin sensitivity. Additionally, the levels of UCP2 and UCP1 were reduced in the liver and BAT, respectively, in <it>GhrR </it>KO mice relative to WT mice.</p> <p>Conclusions</p> <p>These results indicate that improved glucose homeostasis of <it>GhrR </it>KO mice is characterized by robust improvements of glucose disposal in both normal and metabolically challenged states, relative to WT controls. <it>GhrR </it>KO mice have an intact 1^stphase insulin response but require significantly less insulin for glucose disposal. Our experiments reveal that the insulin sensitivity of <it>GhrR </it>KO mice is due to both BW independent and dependent factors. We also provide several lines of evidence that a key feature of the <it>GhrR </it>KO mouse is maintenance of hepatic insulin sensitivity during metabolic challenge.</p