bluuebunny/crossref_metadata_2025_split huggingface dataset:
A critical analysis of the implementation of service user involvement in primary care research and health service development using normalization process theory
Authors: Tierney Edel , McEvoy Rachel , O'Reilly‐de Brún Mary , de Brún Tomas , Okonkwo Ekaterina , Rooney Michelle , Dowrick Chris , Rogers Anne , MacFarlane Anne 
Published: July 2014

AbstractBackgroundThere have been recent important advances in conceptualizing and operationalizing involvement in health research and health‐care service development. However, problems persist in the field that impact on the scope for meaningful involvement to become a routine – normalized – way of working in primary care. In this review, we focus on current practice to critically interrogate factors known to be relevant for normalization – definition, enrolment, enactment and appraisal.MethodOurs was a multidisciplinary, interagency team, with community representation. We searched EBSCO host for papers from 2007 to 2011 and engaged in an iterative, reflexive approach to sampling, appraising and analysing the literature following the principles of a critical interpretive synthesis approach and using Normalization Process Theory.FindingsTwenty‐six papers were chosen from 289 papers, as a purposeful sample of work that is reported as service user involvement in the field. Few papers provided a clear working definition of service user involvement. The dominant identified rationale for enrolling service users in primary care projects was linked with policy imperatives for co‐governance and emancipatory ideals. The majority of methodologies employed were standard health services research methods that do not qualify as research with service users. This indicates a lack of congruence between the stated aims and methods. Most studies only reported positive outcomes, raising questions about the balance or completeness of the published appraisals.ConclusionTo improve normalization of meaningful involvement in primary care, it is necessary to encourage explicit reporting of definitions, methodological innovation to enhance co‐governance and dissemination of research processes and findings.
Predictors for chronic pain‐related health care utilization: a cross‐sectional nationwide study in Iceland
Authors: Jonsdottir Thorbjorg , Jonsdottir Helga , Lindal Eirikur , Oskarsson Gudmundur K. , Gunnarsdottir Sigridur 
Published: July 2014

AbstractBackgroundIndividuals with chronic pain are among the most frequent users of health care. Still, a significant percentage does not utilize health care for pain. A range of factors predict chronic pain‐related health care utilization.DesignA cross‐sectional study aimed at identifying predictors of chronic pain‐related health care utilization and comparing predictors between men and women.MethodsA postal questionnaire measuring sociodemographic variables, pain characteristics, health‐related quality of life (HRQoL) and pain‐related health care utilization, was sent to a sample of 4500 individuals randomly drawn from the national population of Iceland. The relationships between sociodemographic and pain‐related factors and pain‐related health care utilization among participants reporting chronic pain (≥3 months) were tested by using bivariate and multivariate statistical analysis.ResultsAmong participants reporting chronic pain, 53.2% had consulted a health care provider for pain during the previous 6 months. Predictors for chronic pain‐related health care utilization differed between men and women. Interference with life and pain pattern was the strongest predictors among women, as compared with interference with life and the physical components of HRQoL for men. Pain‐related health care utilization was not linked to sociodemographic factors.ConclusionsPain‐related variables are better predictors of chronic pain‐related health care utilization than sociodemographic factors. Even though gender does not predict chronic pain‐related health care utilization, there are gender differences in the relationships between pain‐related variables and health care utilization. Men tend to postpone health care consultations for chronic pain longer than women.
Heat shock protein 90 maintains the stability and function of transcription factor Broad Z7 by interacting with its Broad‐Complex‐Tramtrack‐Bric‐a‐brac domain
Authors: Cai M.‐J. , Li X.‐R. , Pei X.‐Y. , Liu W. , Wang J.‐X. , Zhao X.‐F. 
Published: July 2014

AbstractHeat shock protein 90 (Hsp90) is a highly conserved chaperone protein that interacts with various client proteins to mediate their folding and stability. The Broad‐Complex‐Tramtrack‐Bric‐a‐brac (BTB) domain, also known as poxvirus and zinc finger (POZ) domain, exists widely in different proteins and is highly conserved. However, the stability mechanism of BTB domain‐containing proteins has not been fully understood. Co‐immunoprecipitation and a protein pull‐down assay were performed to investigate the interaction between Hsp90 and the transcription factor Broad isoform Z7 (BrZ7) in vivo and in vitro. The middle domain of Hsp90 directly associated with the BTB domain of BrZ7. The Hsp90 inhibitor 17‐(Allylamino)‐17‐demethoxygeldanamycin (17‐AAG) interrupted the interaction between Hsp90 and BrZ7 and decreased the protein level of BrZ7 but did not affect the mRNA level of BrZ7. The addition of the proteasome inhibitor peptide aldehyde Cbz‐leu‐leu leucinal suppressed the 17‐AAG‐induced degradation of BrZ7. BTB domain deletion and 17‐AAG treatment resulted in inhibition of BrZ7 function in gene expression in the 20‐hydroxyecdysone and juvenile hormone pathways. These results reveal that the middle domain of Hsp90 associates with the BTB domain of BrZ7 to prevent BrZ7 degradation and maintain BrZ7 function in gene expression in the lepidopteran insect Helicoverpa armigera.
Technostress: negative effect on performance and possible mitigations
Authors: Tarafdar Monideepa , Pullins Ellen Bolman. , Ragu‐Nathan T. S. 
Published: July 2014

AbstractWe investigate the effect of conditions that create technostress, on technology‐enabled innovation, technology‐enabled performance and overall performance. We further look at the role of technology self‐efficacy, organizational mechanisms that inhibit technostress and technology competence as possible mitigations to the effects of technostress creators. Our findings show a negative association between technostress creators and performance. We find that, while traditional effort‐based mechanisms such as building technology competence reduce the impact of technostress creators on technology‐enabled innovation and performance, more empowering mechanisms such as developing technology self‐efficacy and information systems (IS) literacy enhancement and involvement in IS initiatives are required to counter the decrease in overall performance because of technostress creators. Noting that the professional sales context offers increasingly high expectations for technology‐enabled performance in an inherently interpersonal‐oriented and relationship‐oriented environment with regard to overall performance, and high failure rates for IS acceptance/use, the study uses survey data collected from 237 institutional sales professionals.
Getting evidence‐based pressure ulcer prevention into practice: a multi‐faceted unit‐tailored intervention in a hospital setting
Authors: Sving Eva , Högman Marieann , Mamhidir Anna‐Greta , Gunningberg Lena 
Published: July 2014

AbstractThe aim of the study was to evaluate whether a multi‐faceted, unit‐tailored intervention using evidenced‐based pressure ulcer prevention affects (i) the performance of pressure ulcer prevention, (ii) the prevalence of pressure ulcers and (iii) knowledge and attitudes concerning pressure ulcer prevention among registered and assistant nurses. A quasi‐experimental, clustered pre‐ and post‐test design was used. Five units at a hospital setting were included. The intervention was based on the PARIHS framework and included a multi‐professional team, training and repeated quality measurements. An established methodology was used to evaluate the prevalence and prevention of pressure ulcers. Nurses' knowledge and attitudes were evaluated using a validated questionnaire. A total of 506 patients were included, of whom 105 patients had a risk to develop pressure ulcer. More patients were provided pressure ulcer prevention care (P = 0·001) and more prevention care was given to each patient (P = 0·021) after the intervention. Corresponding results were shown in the group of patients assessed as being at risk for developing pressure ulcers. Nurses' knowledge about pressure ulcer prevention increased (P < 0·001). Positive attitudes towards pressure ulcer prevention remained high between pre‐ and post‐test surveys. This multi‐faceted unit‐tailored intervention affected pressure ulcer prevention. Facilitation and repeated quality measurement together with constructed feedback of results seemed to be the most important factor for pressure ulcer prevention.
Structural interactions between actin, tropomyosin, caldesmon and calcium binding protein and the regulation of smooth muscle thin filaments
Authors: MARSTON S. , BURTON D. , COPELAND O. , FRASER I. , GAO Y. , HODGKINSON J. , HUBER P. , LEVINE B. , EL‐MEZGUELDI M. , NOTARIANNI G. 
Published: July 2014

ABSTRACTThe basic structure and functional properties of smooth muscle thin filaments were established about 10 years ago. Since then we and others have been working on the details of how tropomyosin, caldesmon and the Ca2+‐binding protein regulate actin interaction with myosin. Our work has tended to emphasize the similarities between caldesmon and troponin function whilst others have been more concerned with the differences. The need to resolve the resulting differences has stimulated us to find new and more direct ways of investigating the mechanism of thin filament regulation. In recent years an apparent divergence has opened up between functional measurements, which indicate an allosteric‐cooperative regulatory mechanism in which caldesmon and Ca2+‐binding protein control actin—tropomyosin state in the same way as troponin, and structural measurements which show thin filament structures unlike striated muscle thin filaments. The challenge is to interpret function in terms of structure. We have combined functional studies with expression and mutagenesis of caldesmon and with structural methods including X‐ray crystalography of tropomyosin—caldesmon crystals, electron microscopy and helical reconstruction of actin—tropomyosincaldesmon complexes and high resolution nuclear magnetic resonance spectroscopy of the C‐terminus of caldesmon in interaction with actin and calmodulin. We have used this information to propose a structural mechanism for caldesmon regulation of the smooth muscle thin filament.
A common pathway for regulation of nutritive blood flow to the brain: arterial muscle membrane potential and cytochrome P450 metabolites
Authors: HARDER D.R. , ROMAN R.J. , GEBREMEDHIN D. , BIRKS E.K. , LANGE A.R. 
Published: July 2014

ABSTRACTPerfusion pressure to the brain must remain relatively constant to provide rapid and efficient distribution of blood to metabolically active neurones. Both of these processes are regulated by the level of activation and tone of cerebral arterioles. The active state of cerebral arterial muscle is regulated, to a large extent, by the level of membrane potential. At physiological levels of arterial pressure, cerebral arterial muscle is maintained in an active state owing to membrane depolarization, compared with zero pressure load. As arterial pressure changes, so does membrane potential. The membrane is maintained in a relatively depolarized state because of, in part, inhibition of K+ channel activity. The activity of K+ channels, especially the large conductance Ca2+‐activated K+ channel (KCa) is dependent upon the level of 20‐HETE produced by arterial muscle. As arterial pressure increases, so does cytochrome P450 (P4504A) activity. P4504A enzymes catalyse ω‐hydroxylation of arachidonic acid and formation of 20‐hydroxyeicosatetraenoic acid (20‐HETE). 20‐HETE is a potent inhibitor of KCa which maintains membrane depolarization and muscle cell activation. Astrocytes also metabolize AA via P450 enzymes of the 2C11 gene family to produce epoxyeicosatrienoic acids (EETs). Epoxyeicosatrienoic acids are released from astrocytes by glutamate which ‘spills over’ during neuronal activity. These locally released EETs shunt blood to metabolically active neurones providing substrate to support neuronal function. This short paper will discuss the findings which support the above scenario, the purpose of which is to provide a basis for future studies on the molecular mechanisms through which cerebral blood flow matches metabolism.
The role of phospholamban and SERCA3 in regulation of smooth muscle‐endothelial cell signalling mechanisms: evidence from gene‐ablated mice
Authors: PAUL R.J. 
Published: July 2014

ABSTRACTIt is generally agreed that intracellular Ca2+ stores, the sarco(endo)plasmic‐reticulum (SER), affect Ca2+ homeostasis and thus contractility of vascular smooth muscle. There is, however, no general consensus as to the magnitude of the SER contribution to Ca2+ handling, the basis for isoforms of the SER Ca2+‐ATPases (SERCAs) or the role of an SER‐associated regulatory protein, phospholamban (PLB). Although the biochemical and cell biological roles of the SER have been intensely studied in vitro, the development of gene‐targeted and transgenic mouse models enables one to extend our information to the in vivo levels. A brief review of the role of PLB and SERCA function in vascular and endothelial cell function is presented. Studies on the PLB gene‐ablated mouse indicate that vascular contractility is considerably altered. This is mirrored by changes in intracellular Ca2+. Moreover, differences in contractility of the gene‐ablated tissues are eliminated by treatment with cyclopiazonic acid, which pharmacologically abolishes SER function by inhibiting the Ca2+‐ATPase. Thus PLB modulation of sarcoplasmic reticulum (SR) Ca2+ uptake plays a major role in modulating vascular contractility. It is interesting that endothelium‐dependent relaxation was decreased in the PLB‐deficient aorta. This is surprising in light of the PLB distribution, thought to be limited to cardiac, slow skeletal and smooth muscle. Our data indicate the presence of PLB in endothelial cells and point to an unrecognized pathway for modulation of endothelial cell [Ca2+]i and vascular contractility. Data from smooth muscle tissues of the SERCA3 gene‐ablated mouse demonstrate that this isoform affects endothelium‐dependent function, but not that of smooth muscle, consistent with its known distribution. This isoform appears to perform a modulatory function, rather than the more essential role of SERCA2. Gene‐targeted and transgenic models provide an important avenue for understanding the role of SER in vascular signalling.
Long‐term effects of intracellular calcium and growth factors on excitation and contraction in smooth muscle
Authors: HELLSTRAND P. 
Published: July 2014

ABSTRACTModulation of vascular smooth muscle cells from a contractile to a synthetic phenotype is thought to be important in the development of the atherosclerotic lesion. Such modulation depends on growth factors and is influenced by cell—cell and cell—matrix interactions. Whereas smooth muscle cells in the vessel wall are contractile, dispersed cells in culture rapidly modulate to synthetic phenotype, which complicates long‐term in vitro studies. In contrast, vascular segments or smooth muscle strips in organ culture can maintain contractility for at least a week, sufficient for studies involving altered metabolism or protein expression. Examples are effects of endogenous polyamines on membrane ion channels and excitation—contraction coupling. While smooth muscle tissue is well preserved in serum‐free culture, growth stimulation with fetal calf serum (FCS) causes multiple effects, including decreased contractility, ultrastructural changes, decreased expression of l‐type Ca2+ channels, and increased SR release of Ca2+ via ryanodine receptors. These are all consequences of increased basal [Ca2+]i caused by FCS, as they are reversed by culture with verapamil in a concentration (1 μm) that does not inhibit stimulation of DNA and protein synthesis by FCS. The effects of FCS on contractility and Ca2+ channel expression are mimicked in serum‐free culture with increased [Ca2+]i. Contractile protein patterns, including myosin isoform composition, are unaffected by FCS, suggesting that reversal to synthetic phenotype is limited and not the immediate cause of decreased contractility.
Psychosocial factors related to smoking: The midlife study
Authors: Brook Judith S. , Zhang Chenshu , Brook David W. 
Published: July 2014

BackgroundThere is limited research on the correlates of cigarette smoking in women in late midlife.ObjectivesThe present study examined the associations between risk factors in several psychosocial domains and current cigarette smoking among women in their mid‐60s. These domains included risks in personal attributes, family relationships, negative life events, financial stressors, contextual factors, and problematic alcohol use.MethodsData were from a cohort of women originally living in two upstate New York counties (N = 511) in late midlife (mean age = 65). Bivariate and multivariate logistic regression analyses were conducted.ResultsThe results supported our hypotheses. The cumulative psychosocial risk index was significantly associated with a greater likelihood of cigarette smoking [A.O.R. = 1.53; 95% C.I. (1.3–.181); p < .001] after controlling for age and educational level.Conclusions and Scientific SignificanceIt is important to reduce the number of psychosocial risk factors faced by women in their 60s in order to reduce the likelihood of continued cigarette smoking. (Am J Addict 2014;23:423–428)
Frequency and Temperature‐Independent Electrical Transport Properties of 2BaO–0.5Na2O–2.5Nb2O5–4.5B2O3 Glass‐Ceramics
Authors: Kundu Swarup , Varma Kalidindi B. R. 
Published: July 2014

The temperature (300–973 K) and frequency (100 Hz–10 MHz) response of the dielectric and impedance characteristics of 2BaO‐0.5Na2O–2.5Nb2O5–4.5B2O3 glasses and glass nanocrystal composites were studied. The dielectric constant of the glass was found to be almost independent of frequency (100 Hz–10 MHz) and temperature (300–600 K). The temperature coefficient of dielectric constant was 8 ± 3 ppm/K in the 300–600 K temperature range. The relaxation and conduction phenomena were rationalized using modulus formalism and universal AC conductivity exponential power law, respectively. The observed relaxation behavior was found to be thermally activated. The complex impedance data were fitted using the least square method. Dispersion of Barium Sodium Niobate (BNN) phase at nanoscale in a glass matrix resulted in the formation of space charge around crystal‐glass interface, leading to a high value of effective dielectric constant especially for the samples heat‐treated at higher temperatures. The fabricated glass nanocrystal composites exhibited P versus E hysteresis loops at room temperature and the remnant polarization (Pr) increased with the increase in crystallite size.
Structure Evolution and Enhanced Microwave Dielectric Characteristics of (Sr1−xCax)La2Al2O7Ceramics
Authors: Yi Lei , Li Lei , Liu Xiao Qiang , Chen Xiang Ming 
Published: July 2014

(Sr1−xCax)La2Al2O7(0.1 ≤ x ≤ 0.5) ceramics were prepared by a standard solid‐state reaction method. Their densification behavior and microwave dielectric properties were investigated together with the structural evolution. X‐ray diffraction analysis indicated that the major phase of Ruddlesden–Popper structure withn = 2 was obtained for all the compositions investigated here. PartialCasubstitution improved the sintering behavior ofSrLa2Al2O7ceramics. More importantly, microwave dielectric characteristics were enhanced in (Sr1−xCax)La2Al2O7ceramics with compositions ofx = 0.1~0.3. The stacking fault was confirmed by TEM observation in the present ceramics, and the microwave dielectric loss was influenced by it. The best combination of microwave dielectric characteristics was achieved for the composition ofx = 0.1: εr= 19.9,Qf = 135 400 GHz and τf = −18.5 ppm/°C.
Voluntary Benefits from Wrongdoing
Authors: Pasternak Avia 
Published: July 2014

AbstractThe principle of wrongful benefits prescribes that beneficiaries from wrongdoing incur duties towards the victims of the wrongdoing. The principle focuses on involuntary beneficiaries, demanding that they disgorge their tainted benefit. However, it overlooks the duties of beneficiaries who are not straightforwardly involuntary. The article addresses this gap in the literature. It explores the duties of ‘voluntary beneficiaries’, who could avoid receiving the tainted benefit; and the duties of ‘welcoming beneficiaries’, who cannot avoid receiving the tainted benefit but welcome it. The article demonstrates that in both cases, the duties of the beneficiary towards the victim of the original wrongdoing are not limited to the disgorgement of the benefit. Rather, voluntary and welcoming beneficiaries are themselves involved in the commission of wrongdoing against the victim of the original wrongdoing, and hence may owe the victim compensation that exceeds the level of their own benefit. This argument has various practical implications, e.g. in specifying the duties of companies who benefit from human rights violations down their supply chain.
The Priority of Solidarity to Justice
Authors: Kolers Avery 
Published: July 2014

AbstractRecognising and responding to injustices that benefit us is a pervasive problem of contemporary life, and arguably a mark of moral seriousness in anyone who presumes to take moral stands at all. In response, a number of authors have defended the view that such benefits normally bring with them prima facie obligations of compensation. This ‘wrongful‐benefits’ approach has considerable intuitive plausibility, much of it founded in the financial metaphor that gives it an appearance of precision. Yet while the compensation scenario works reasonably well in one‐off cases such as receiving stolen property, it yields incoherent results when facing ongoing structural injustices. In such cases ‘innocence’ is ambiguous and our status as beneficiaries and victims is complex. In contrast, solidarity — understood as a principle of equity requiring that we side with the least well off — provides a better account of duties to respond to structural injustice. In solidarity the agent follows the lead of organised out‐groups and defers to their judgment about collective actions to overcome injustice. Solidarity leads us to support the organised group that suffers from the greatest inequity. Solidarity does not use a financial metaphor and thus it neither requires full disgorgement, nor absolves us of further action when we reach the point of net‐zero benefit. Rather, solidarity is a principal means for ordinary citizens to promote equity by affirming the equal status of the victims, and to atone for having benefited from injustice, whether they did so willingly or otherwise.