bluuebunny/crossref_metadata_2025_split huggingface dataset:
Can a purchaser be a partner? nursing education in the English universities
Authors: Meerabeau E. 
Published: January 2005

AbstractSince the early 1990s, public sector management in England has been exhorted to follow the example of the private sector, and ‘quasi‐markets’ have been established, for example in the health service. A quasi‐market also exists between the NHS and higher education for the purchasing (or procurement) of nursing education. This paper uses policy documents such as the National Health Service Executive Circular (March 1999) on ‘Good Contracting Guidelines’ for Non‐Medical Education and Training, plus other relevant literature on the commodification of higher education, quasi‐markets and contract theory to examine this market, and the confusion of two rhetorics, those of competition and partnership. Nursing occupies a marginal place in higher education in England, having only recently become part of it. The emphasis of the quasi‐market on the output of a trained ‘fit for purpose’ labour force combines with professional attempts to create an academic discipline, in complex ways which are as yet underanalysed. Copyright © 2001 John Wiley & Sons, Ltd.
Clinical guidelines: attitudes, information processes and culture in English primary care
Authors: Dowswell George , Harrison Stephen , Wright John 
Published: January 2005

AbstractThe application to clinical medicine of evidence‐based clinical guidelines is an increasingly international policy prescription, yet research on how such guidelines might be implemented has tended to focus on change initiatives without seeking to understand change processes. This paper reports an empirical study of guideline implementation in UK general practice. Most GPs welcome guidelines as a means of improving care, though have reservations about their authority, relevance and effect on professional autonomy. ‘Clan’ organizational culture predominates and general practices do not generally have well‐functioning internal arrangements for the management of clinical evidence and related information. We found no coherent relationships between these variables and practices' actual uptake of guidelines. Copyright © 2001 John Wiley & Sons, Ltd.
The practice characterization model: the importance of organizational life cycles and targeted interventions in general medical practice
Authors: Atkins E. M. , Duffy M. C. , Bain D. J. 
Published: January 2005

AbstractIn response to a climate of constant change and increasing demand for services, general practice in the UK has undergone significant modification over the last 10 years. It has become a multi‐disciplinary organisation encouraged by funding bodies to plan for service delivery using a more structured team based approach.In Tayside in 1996, practices were charged with producing formal Practice Development Plans (PDPs) which would focus on priority areas aligned with the Health Boards own strategic plan–those were teamwork, information management and technology, and clinical service delivery.The University of Dundee's Department of General Practice successfully applied for funding to develop ways of facilitating practices so that they could a) identify their own development priorities, and b) plan and implement action and learning to see these priorities through.Using action research methodology, the project attempted to create a climate for change, provide support and training to see the changes implemented, and ensure commitment to the changes from all members of the practice team. The Facilitator adopted a flexible style varying her role between expert, guide and support.Analysis of progress made by different practices, coupled with the Facilitator's in depth knowledge of them, suggested the importance of certain key aspects of practice organisation and culture. A practice characterisation model identified practices which were stable, currently coping, proactive and ready to face the challenge of change as best placed to engage in a full scale development programme. Other profiles suggested a range of alternative interventions as more likely to be acceptable and productive.
On a hiding to nothing? assessing the corporate governance of hospital and health services in New Zealand 1993–1998
Authors: Barnett Pauline , Perkins Rod , Powell Michael 
Published: January 2005

AbstractIn New Zealand the governance of public sector hospital and health services has changed significantly over the past decade. For most of the century hospitals had been funded by central government grants but run by locally elected boards. In 1989 a reforming Labour government restructured health services along managerialist lines, including changing governance structures so that some area health board members were government appointments, with the balance elected by the community. More market oriented reform under a new National government abolished this arrangement and introduced (1993) a corporate approach to the management of hospitals and related services. The hospitals were established as limited liability companies under the Companies Act. This was an explicitly corporate model and, although there was some modification of arrangements following the election of a more politically moderate centre‐right coalition government in 1996, the corporate model was largely retained. Although significant changes occurred again after the election of a Labour government in 1999, the corporate governance experience in New Zealand health services is one from which lessons can, nevertheless, be learnt. This paper examines aspects of the performance and process of corporate governance arrangements for public sector health services in New Zealand, 1993–1998. Copyright © 2001 John Wiley & Sons, Ltd.
Regulation effects on the lower Peace River, Canada
Authors: Peters Daniel L. , Prowse Terry D. 
Published: January 2005

AbstractThe headwaters of the Peace River, Canada became regulated in 1968 by a major hydroelectric facility and associated reservoir located in the Rocky Mountains. This paper examines the change to the downstream hydrographs that have resulted from regulation. To facilitate the comparison, a naturalized (without regulation effects) flow regime (1972–1996) was generated using a combination of hydrologic and hydraulic flow models. The results showed that even some 1100 km downstream, there have been significant changes to the hydrograph. Specifically, average winter flows were 250% higher, annual peaks (1‐day, 15‐day, 30‐day highs) were in the order of 35–39% lower, and overall variability in daily flows decreased. Despite the reduction in peaks and variability, however, the downstream hydrograph is far from flat and has retained the basic shape of the pre‐regulation hydrograph. This is primarily due to the strong influence of tributary inflow below the point of regulation. Recommendation for improvements to the model and future application of these data are also discussed. Copyright © 2001 John Wiley & Sons, Ltd.
Job access at labour market entry and occupational achievement in the life course
Authors: van Ham Maarten 
Published: January 2005

AbstractThis paper addresses the question of the extent to which job access at labour market entry influences socio‐economic status later in life. Multivariate models of workers' socio‐economic status at the ages of 30, 40 and 50 were estimated using longitudinal data. The results show that job access at labour market entry is indeed instrumental in career advancement over the life course. The importance of job access at labour market entry increases significantly with age. Good job access at the beginning of the labour career evidently gives workers an advantage over others who start in less favourable labour markets. Copyright © 2003 John Wiley & Sons, Ltd.
Protection of endotoxin‐induced oxidative renal tissue damage of rats by vitamin E or/and EGb 761 treatment
Authors: Coskun Omer , Armutcu Ferah , Kanter Mehmet , Kuzey Gamze Mocan 
Published: January 2005

AbstractThe aim of the present study was to evaluate the possible protective effects of vitamin E and EGb 761 treatments, alone or in combination, against oxidative renal tissue damage in experimentally induced endotoxaemic rats. Fifty healthy male Wistar albino rats, weighing 150–250 g and averaging 12 weeks old, were allotted randomly into one of ﬁve experimental groups: A (untreated), B (endotoxaemic), C (endotoxaemic + vitamin E treated), D (endotoaxemic + EGb 761 treated) and E (endotoxaemic + vitamin E and EGb 761 treated), each containing ten animals. Group A received only an intraperitoneal (i.p.) injection of 2 ml of normal saline solution and served as the control. Groups B, C, D and E were administrated a single i.p. injection of 0.5 ml of endotoxin solution. In addition, groups C, D and E received i.p. injections of 600 mg kg−1 body mt. of vitamin E and oral extract of 50 mg kg−1 body wt. of EGb 761, alone or in combination, immediately after the endotoxin injection. The experiment lasted for 24 h. At the end of the experiment blood and tissue samples were obtained for biochemical and histopathological investigation. Endotoxin injection produced renal damage, increased lipid peroxidation and decreased antioxidant enzyme activity. Vitamin E or/and EGb 761 treatment decreased lipid peroxidation, increased antioxidant enzyme activity and also prevented renal tissue damage in experimentally induced endotoxaemic rats. In conclusion, vitamin E and EGb 761 treatment, alone or in combination, appears to be beneﬁcial in preventing endotoxin‐induced oxidative renal tissue damage and therefore shows potential for clinical use. Copyright © 2005 John Wiley & Sons, Ltd.
Segmentary effects on the renal proximal tubule due to hexachloro‐1,3‐butadiene in rats: biomarkers related to gender
Authors: Trevisan Andrea , Cristofori Patrizia , Beggio Michela , Venturini Matteo Borella , Marco Livio Di , Zanetti Edoardo 
Published: January 2005

AbstractRenal tissue biomarkers (glutamine synthetase and p‐aminohippuric acid uptake) were studied in male and female rats after treatment with hexachloro‐1,3‐butadiene. Reduced glutathione content also was also determined in liver and kidney. Histopathological examination (light microscopy) was then performed. The aim was to deﬁne sex differences in nephrotoxic effects caused by the solvent injected i.p. at 50, 100 and 200 mg kg−1 dose. The rats were sacriﬁced 24 and 48 h after treatment; after 24 h a signiﬁcant (P < 0.05) dose‐dependent depletion of liver reduced glutathione was observed in male rats only; after 48 h male and female rats showed a signiﬁcant (P < 0.05) increase at 50 and 100 mg kg−1 doses. Reduced glutathione in the kidney was increased in male but not in female rats 24 and 48 h after treatment. Glutamine synthetase activity in renal tissue showed a signiﬁcant (P < 0.05) dose‐dependent decrease 24 and 48 h after treatment in both sexes, but is was signiﬁcantly (P < 0.05) greater in female rats after 48 h. p‐Aminohippuric acid uptake in renal cortical slices appeared signiﬁcantly (P < 0.05) decreased in both sexes at the higher dose 24 h after treatment but this was signiﬁcantly (P < 0.05) greater in female rats. A further signiﬁcant (P < 0.05) impairment was observed after 48 h in males treated with a 200 mg kg−1 dose. In addition, a slight but signiﬁcant (P < 0.05) loss of p‐aminohippuric acid uptake was observed 48 h after treatment with a 100 mg kg−1 dose in both sexes. Light microscopy showed that the pars recta of the proximal tubule was mainly affected and tubular damage increased according to dose and time, involving the inner medulla and cortex. In conclusion, female rats show a signiﬁcantly earlier and higher susceptibility of the kidney to toxic effects of hexachloro‐1,3‐butadiene. Copyright © 2005 John Wiley & Sons, Ltd.
Protective effects of MESNA (2‐mercaptoethane sulphonate) against acetaminophen‐induced hepatorenal oxidative damage in mice
Authors: Şener Göksel , Sehirli Özer , Cetinel Şule , Yeğen Berrak G. , Gedik Nursal , Ayanoğlu‐Dülger Gül 
Published: January 2005

AbstractAcetaminophen, a widely used analgesic and antipyretic, is known to cause hepatic and renal injury in humans and experimental animals when administered in high doses. It was reported that these toxic effects of acetaminophen are due to oxidative reactions that take place during its metabolism. In this study we aimed to investigate the possible beneﬁcial effect of 2‐mercaptoethane sulphonate (MESNA), an antioxidant agent, against acetaminophen toxicity in mice.Balb‐c mice were injected i.p. with: vehicle (the control group); a single dose of 150 mg kg−1 MESNA (MES group); a single dose of 900 mg kg−1 i.p. acetaminophen (AA4h and AA24h groups); and MESNA, at a dose of 150 mg kg−1 after acetaminophen injection (AA4h‐MES and AA24h‐MES groups). The MESNA injection was repeated once more 12 h after the ﬁrst injection in the AA24h‐MES group. Blood urea nitrogen, serum creatinine, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels in blood and glutathione (GSH) and malondialdehyde (MDA) levels, myeloperoxidase (MPO) activity and collagen contents in liver and kidney tissues were measured. Tissues also were examined microscopically.Blood urea nitrogen and serum creatinine, which were increased signiﬁcantly (P < 0.001) following acetaminophen treatment were decreased signiﬁcantly (P < 0.05–0.001) after treatment with MESNA. The ALT and AST levels were also increased signiﬁcantly (P < 0.001) after acetaminophen treatment but were not reduced with MESNA. Acetaminophen treatment caused a signiﬁcant (P < 0.05–0.001) decrease in GSH levels whereas MDA levels and MPO activity were increased in both tissues. These changes were reversed by MESNA treatment. Collagen contents of the liver and kidney tissues were increased by acetaminophen treatment (P < 0.001) and reversed back to the control levels with MESNA. Our results imply that acetaminophen causes oxidative damage in hepatic and renal tissues and that MESNA, via its antioxidant effects, protects these tissues. Therefore, its therapeutic role as a ‘tissue injury‐limiting agent’ must be elucidated further in drug‐induced oxidative damage. Copyright © 2005 John Wiley & Sons, Ltd.
Characterization of the binding of cholera toxin to ganglioside GM1 immobilized onto microtitre plates
Authors: Dawson R. M. 
Published: January 2005

AbstractGanglioside GM1 is the receptor for cholera toxin on cell surfaces, and the binding of cholera toxin to GM1 immobilized on microtitre plates has been reported previously by several authors as an assay for the toxin (GM1‐ELISA). This assay has been examined in detail. Results were independent of the adsorption solvent for GM1 (methanol or phosphate‐buffered saline), the pH of aqueous solvents (7.4–10.2) and the temperature (4–37 °C). High and near‐maximal rates of absorbance change in the assay were found for lower concentrations of GM1 (100 ng ml−1) and for shorter incubation times (a few hours) than reported in the literature. A method was devised to provide a semi‐quantitative estimate of the amount of GM1 bound to the plate; this was found to be in the low nanogram range. Binding of cholera toxin to the immobilized GM1 required ≥1.5 h for maximal assay results. The failure of free GM1 in solution to displace cholera toxin once bound to immobilized GM1 indicated that binding to immobilized GM1 is irreversible in the time frame of the experiment. Data from the literature support the very slow dissociation rates of the toxin–GM1 complex. Copyright © 2005 John Wiley & Sons, Ltd.
Role of molecular geometry, valence charge distribution and vibrational modes in bioactivity of cyclodiene insecticides
Authors: Saxena P. N. , Gupta V. D. 
Published: January 2005

AbstractFourier transform infrared spectral measurement and complete normal mode calculations have been carried out for heptachlor and wedge modes have been identiﬁed. In addition, valence charge distributions have been obtained for aldrin, endrin, heptachlor, beta‐endosulfan, cis‐chlordane, trans‐chlordane, photo‐cis‐chlordane and photo‐trans‐chlordane using CNDO/2 (complete neglect of differential overlap) molecular orbital calculations. A toxicity parameter has been deﬁned as the product of the charge distribution and surface area of the corresponding active wedges, depending on the interacting structural features. The variation of this toxicity parameter is generally in order and in agreement with the reported measurements based on the corresponding order of observed ld50 values. Because of the structural features, the toxicity in these cases is a surface phenomenon rather than a volume effect as in the case of Gammexane, wherein the insecticide binds itself to membrane channels. Because the biological activity is a dynamic rather than a static phenomenon, it is expected that the normal modes involving the wedge atoms play an important role. Copyright © 2005 John Wiley & Sons, Ltd.
Effects of a single intratracheal administration of phenanthraquinone on murine lung
Authors: Hiyoshi Kyoko , Takano Hirohisa , Inoue Ken‐ichiro , Ichinose Takamichi , Yanagisawa Rie , Tomura Shigeo , Cho Arthur K. , Froines John R. , Kumagai Yoshito 
Published: January 2005

AbstractAlthough several studies have reported that diesel exhaust particles (DEP) affect cardiorespiratory health in animals and humans, the responsible components in DEP for the effects remain to be deﬁned. Diesel exhaust particles contain quinones that can catalyse the generation of reactive oxygen species, resulting in the induction of oxidative stress. Oxidative stress can correlate with a variety of diseases and health effects. In the present study, we investigated the effects of phenanthraquinone — a relatively abundant quinone in DEP — on lung inﬂammation and the local expression of cytokine proteins in mice as a measure of oxidative damage. The animals were randomized into two experimental groups that received vehicle or phenanthraquinone by intratracheal instillation. The cellular proﬁles of bronchoalveolar lavage ﬂuid (BALF) and local expression of cytokines were evaluated 24 and 48 h after the instillation. Phenanthraquinone challenge revealed an increase in the numbers of neutrophils and eosinophils in BALF as compared to vehicle challenge (P < 0.05 at 48 h post‐instillation). Phenanthraquinone induced the lung expression of interleukin (IL)‐5 and eotaxin 48 h and 24 h after the challenge, respectively. These results indicate that intratracheal exposure to phenanthraquinone induces recruitment of inﬂammatory cells, at least partly, through the local expression of IL‐5 and eotaxin. Copyright © 2005 John Wiley & Sons, Ltd.
Weak inhibitors protect cholinesterases from strong inhibitors (paraoxon): in vitro effect of ranitidine
Authors: Petroianu G. A. , Arafat K. , Schmitt A. , Hasan M. Y. 
Published: January 2005

AbstractMetoclopramide (MCP) is a dopamine receptor antagonist and serotonin receptor agonist widely used as an antiemetic and gastric prokinetic drug. In addition MCP is a weak and reversible inhibitor of cholinesterases. We have shown that MCP has a cholinesterase protective effect against inhibition by organophosphates. The putative mode of protective action of MCP is competition for the active site of the enzyme with the more potent organophosphate. In the present paper we present our results using another weak inhibitor of cholinesterases: ranitidine (RAN).The purpose of the study was to quantify in vitro the extent of RAN‐conferred protection, using paraoxon (POX) as an inhibitor. Paraoxon is a non‐neuropathic organophosphate responsible for a large number of accidental or suicidal exposures.Red blood cell (RBC) acetylcholinesterase (AChE) activities in whole blood and butyrylcholinesterase (BChE) activities in human plasma were measured photometrically in the presence of different POX and RAN concentrations and the ic50 was calculated. Determinations were repeated in the presence of increasing RAN concentrations. The ic50 shift induced by the presence of RAN increases with the RAN concentration in a linear manner. The shift was more pronounced with RBC‐AChE.The protective effect of RAN on cholinesterase could be of practical relevance in the treatment of POX poisoning. We conclude that in vivo testing of RAN as an organophosphate protective agent is warranted. Copyright © 2005 John Wiley & Sons, Ltd.
Protective agents in acute high‐dose organophosphate exposure: comparison of ranitidine with pralidoxime in rats
Authors: Petroianu G. A. , Hasan M. Y. , Nurulain S. M. , Arafat K. , Shaﬁullah M. , Naseer O. 
Published: January 2005

AbstractWeak and reversible inhibitors of cholinesterase, when coadministred in excess with a more potent inhibitor such as organophosphates, can act in a protective manner. Ranitidine (RAN) is a clinically widely used histamine type 2 (H2) receptor blocker. Ranitidine is also the most potent inhibitor of acetylcholinesterase among H2 blockers (inhibitory constant K in the low micromolar range) but roughly three orders of magnitude less potent than paraoxon. This study evaluates RAN‐conferred protection in acute high‐dose organophosphate (paraoxon, POX) exposure in rats in direct comparison with the therapeutic gold‐standard pralidoxime (PRX).Group 1 received 1 µM POX, group 2 received 50 µM RAN, group 3 received 50 µM PRX, group 4 received 1 µM POX + 50 µM RAN and group 5 received 1 µM POX + 50 µM PRX. All substances were applied intraperitoneally. The animals were monitored for 48 h and mortality was recorded at 30 min and 1, 2, 3, 4, 24 and 48 h. Blood was taken for red blood cell acetylcholinesterase (RBC‐AChE) measurements at baseline, 30 min and 24 and 48 h. Mortality occurred mainly in the ﬁrst 30 min after POX administration, with minimal changes occurring thereafter. Mortality (in %) at 30 min in groups 1, 4 and 5 was 52 ± 18, 37 ± 20 and 17 ± 18, respectively, and mortality at 48 h was 59 ± 12, 39 ± 20 and 28 ± 20, respectively. The RBC‐AChE activities (in % of baseline values) at 30 min in groups 1, 4 and 5 were 18 ± 16, 47 ± 23 and 48 ± 20, respectively. At 24 h the values were 46 ± 16, 65 ± 24 and 86 ± 17, respectively, and at 48 h the values were 71 ± 19, 78 ± 21 and 110 ± 27, respectively.Coadministration of PRX signiﬁcantly decreases mortality in the described model at all points in time. Coadministration of RAN statistically signiﬁcantly decreases mortality at 24 and 48 h. The extent of protection conferred by RAN is less (but not statistically signiﬁcantly so) than that conferred by the gold‐standard PRX. Coadministration of PRX statistically signiﬁcantly increases RBC‐AChE activities in the described model at all points in time. Ranitidine confers a statistically signiﬁcant protection for the enzyme at 30 min only.We conclude that RAN is potentially of clinical use in reducing mortality in acute high‐dose organophosphate exposure. Further studies involving different organophosphates and dosages, as well as different animal species, will be needed both to conﬁrm these initial ﬁndings and to address the issue of the optimal timing for RAN preadministration. Copyright © 2005 John Wiley & Sons, Ltd.