bluuebunny/crossref_metadata_2025_split huggingface dataset:
Review of Chemical, Medication, and Anesthesia Toxicity in the OR
Authors: Fiedler Michael A. , Biddle Chuck 
Published: August 2006

ABSTRACTA host of toxic substances exist in the OR. The toxicity of prep‐solutions, cleaning chemicals, common medications, and trace anesthetic gases varies greatly. Nurses use, direct others in the use of, or administer potential toxins while breathing air that may be contaminated to some degree with anesthetic vapors. Often, the OR nurse is the neighborhood resource when questions about the toxicity of common chemicals and drugs arise. A general knowledge of the toxicity of these substances improves the nurse's ability to assess the risk from trace anesthetic gases, prevent injury to patients, provide first aid when potentially dangerous exposure occurs, and direct others in the safe use of OR chemicals. AORN J 67 (Feb 1998) 398–411.
How to Thrive in Merger Mania
Authors: McConnell Edwina A. 
Published: August 2006

ABSTRACTMergers, consolidations, and amalgamations are common in today's health care environment. Such changes and transitions affect everyone and threaten organizational cultures and beliefs. To help you thrive, this article differentiates change from transition, reviews the phases of planned change, and explains the emotional components of the transition stages. Equally important, this article offers strategies, tips, and interventions for both staff member nurses and managers to facilitate the transition process and help themselves emerge victorious. AORN J 67 (Feb 1998) 412–419.
Perioperative Assistants Are a New Resource
Authors: Speers Alice T. , Ziolkowski Linda 
Published: August 2006

ABSTRACTIn the current health care environment, buzzwords such as redesign, reengineering, restructuring, right‐sizing, customer service, diversity, quality, multiskilled workers, and unlicensed assistive personnel conjure up many notions about how perioperative nurses can meet the needs and wants of their patients. Unlicensed assistive personnel are becoming commonplace in our hospitals and have assumed a variety of positions and functions. This article describes a project that one hospital undertook to create unlicensed, multi‐skilled workers in the perioperative area. AORN J 67 (Feb 1998) 420–427.
Incidence of schizophrenia and other psychoses in ethnic minority groups: results from the MRC AESOP Study
Authors: FEARON PAUL , KIRKBRIDE JAMES B. , MORGAN CRAIG , DAZZAN PAOLA , MORGAN KEVIN , LLOYD TUHINA , HUTCHINSON GERARD , TARRANT JANE , LUN ALAN FUNG WAI , HOLLOWAY JOHN , MALLETT ROSEMARIE , HARRISON GLYNN , LEFF JULIAN , JONES PETER B. , MURRAY ROBIN M. 
Published: August 2006

Background. The incidence of schizophrenia in the African-Caribbean population in England is reported to be raised. We sought to clarify whether (a) the rates of other psychotic disorders are increased, (b) whether psychosis is increased in other ethnic minority groups, and (c) whether particular age or gender groups are especially at risk.Method. We identified all people (n=568) aged 16–64 years presenting to secondary services with their first psychotic symptoms in three well-defined English areas (over a 2-year period in Southeast London and Nottingham and a 9-month period in Bristol). Standardized incidence rates and incidence rate ratios (IRR) for all major psychosis syndromes for all main ethnic groups were calculated.Results. We found remarkably high IRRs for both schizophrenia and manic psychosis in both African-Caribbeans (schizophrenia 9·1, manic psychosis 8·0) and Black Africans (schizophrenia 5·8, manic psychosis 6·2) in men and women. IRRs in other ethnic minority groups were modestly increased as were rates for depressive psychosis and other psychoses in all minority groups. These raised rates were evident in all age groups in our study.Conclusions. Ethnic minority groups are at increased risk for all psychotic illnesses but African-Caribbeans and Black Africans appear to be at especially high risk for both schizophrenia and mania. These findings suggest that (a) either additional risk factors are operating in African-Caribbeans and Black Africans or that these factors are particularly prevalent in these groups, and that (b) such factors increase risk for schizophrenia and mania in these groups.
A risk index for 12-month suicide attempts in the National Comorbidity Survey Replication (NCS-R)
Authors: BORGES GUILHERME , ANGST JULES , NOCK MATTHEW K. , RUSCIO AYELET MERON , WALTERS ELLEN E. , KESSLER RONALD C. 
Published: August 2006

Background. Clinical judgments about the likelihood of suicide attempt would be aided by an index of risk factors that could be quickly assessed in diverse settings. We sought to develop such a risk index for 12-month suicide attempts among suicide ideators.Method. The National Comorbidity Survey Replication (NCS-R), a household survey of adults aged 18+, assessed the 12-month occurrence of suicide ideation, plans and attempts in a subsample of 5692 respondents. Retrospectively assessed correlates include history of prior suicidality, sociodemographics, parental psychopathology and 12-month DSM-IV disorders.Results. Twelve-month prevalence estimates of suicide ideation, plans and attempts are 2·6, 0·7 and 0·4% respectively. Although ideators with a plan are more likely to make an attempt (31·9%) than those without a plan (9·6%), 43% of attempts were described as unplanned. History of prior attempts is the strongest correlate of 12-month attempts. Other significant correlates include shorter duration of ideation, presence of a suicide plan, and several sociodemographic and parental psychopathology variables. Twelve-month disorders are not powerful correlates. A four-category summary index of correlates is strongly related to attempts among ideators [area under the receiver operator characteristic curve (AUC)=0·88]. The distribution (conditional probability of attempt) of the risk index is: 19·0% very low (0·0%), 51·1% low (3·5%), 16·2% intermediate (21·3%), and 13·7% high (78·1%). Two-thirds (67·1%) of attempts were made by ideators in the high-risk category.Conclusions. A short, preliminary risk index based on retrospectively reported responses to fully structured questions is strongly correlated with 12-month suicide attempts among ideators, with a high concentration of attempts among high-risk ideators.
Autobiographical memory in non-amnesic alcohol-dependent patients
Authors: D'ARGEMBEAU ARNAUD , VAN DER LINDEN MARTIAL , VERBANCK PAUL , NOËL XAVIER 
Published: August 2006

Background. Chronic alcohol abuse is associated with a wide range of cognitive deficits. However, little is known about memory for real-life events (autobiographical memory) in non-amnesic alcoholic patients. The purpose of this study was to investigate (a) non-amnesic alcoholics' ability to recall specific autobiographical memories and (b) their subjective experience when they access specific memories.Method. Twenty non-amnesic (without Korsakoff syndrome) recently detoxified alcoholics and 20 healthy controls completed the Autobiographical Memory Test (AMT), which assesses the frequency of specific (versus general) memories recalled in response to cue words, and the Memory Characteristics Questionnaire (MCQ), which assesses subjective experience (e.g. the amount of sensory and contextual details experienced) when remembering specific events.Results. Alcoholic patients recalled specific memories less frequently and general memories more frequently than healthy controls. Nevertheless, when a specific past event was accessed, alcoholic patients subjectively experienced as many sensory and contextual details as controls.Conclusions. These findings suggest that non-amnesic alcoholics have difficulties strategically accessing event-specific autobiographical knowledge, which might result from changes in frontal lobe function that are associated with alcoholism.
Antidepressant‐like activity of CGP 36742 and CGP 51176, selective GABAB receptor antagonists, in rodents
Authors: Nowak G , Partyka A , Pałucha A , Szewczyk B , Wierońska J M , Dybała M , Metz M , Librowski T , Froestl W , Papp M , Pilc A 
Published: August 2006

Background and purpose:A crucial role for the GABAB receptor in depression was proposed several years ago, but there are limited data to support this proposition. Therefore we decided to investigate the antidepressant‐like activity of the selective GABAB receptor antagonists CGP 36742 and CGP 51176, and a selective agonist CGP 44532 in models of depression in rats and mice.Experimental approach:Effects of CGP 36742 and CGP 51176 as well as the agonist CGP 44532 were assessed in the forced swim test in mice. Both antagonists were also investigated in an olfactory bulbectomy (OB) model of depression in rats, while CGP 51176 was also investigated in the chronic mild stress (CMS) rat model of depression. The density of GABAB receptors in the mouse hippocampus after chronic administration of CGP 51176 was also investigated.Key results:The GABAB receptor antagonists CGP 36742 and CGP 51176 exhibited antidepressant‐like activity in the forced swim test in mice. The GABAB receptor agonist CGP 44532 was not effective in this test, however, it counteracted the antidepressant‐like effects of CGP 51176. The antagonists CGP 36742 and CGP 51176 were effective in an OB model of depression in rats. CGP 51176 was also effective in the CMS rat model of depression. Administration of CGP 51176 increased the density of GABAB receptors in the mouse hippocampus.Conclusions and Implications:These data suggest that selective GABAB receptor antagonists may be useful in treatment of depression, and support an important role for GABA‐ergic transmission in this disorder.British Journal of Pharmacology (2006) 149, 581–590. doi:10.1038/sj.bjp.0706845
Nupafant, a PAF‐antagonist prototype for suppression of ventricular fibrillation without liability for QT prolongation?
Authors: Baker K E , Wood L M , Whittaker M , Curtis M J 
Published: August 2006

Background and purpose:PAF antagonists inhibit ischaemia‐induced ventricular fibrillation (VF) in animals. However, unfavourable ancillary actions (on QT interval and coronary flow) have been reported with the PAF antagonist, BN‐50739. If these are class actions, they would preclude development of PAF antagonists as novel anti‐VF drugs. Our purpose was to examine this proposition using the hitherto untested PAF antagonist, nupafant.Experimental approach:Two rat heart preparations (Langendorff and ‘dual coronary’ perfusion) were used to assay nupafant's effects on ischaemia‐induced VF, coronary flow and QT interval, and to test for the site‐selectivity necessary if any effects on VF are caused by PAF antagonism.Key results:Global (whole‐heart) delivery of 10 μM nupafant, reduced the incidence of ischaemia‐induced VF and widened QT interval without affecting coronary flow. Importantly, lower concentrations (0.1 and 1 μM) had no effect on VF, yet widened QT almost identically to 10 μM nupafant. When nupafant was delivered selectively to (and entrapped within) the involved region it partially protected against VF (P<0.05). This occurred without change in QT interval. Selective nupafant delivery to the uninvolved region was without effect.Conclusions and implications:Nupafant protects against ischaemia‐induced VF primarily by site‐selective actions in the ischaemic region but, unlike BN‐50739, the effect is unrelated to its QT widening action, and is not compromised by any effect on coronary flow. This establishes proof of concept that VF suppression by PAF antagonism need not invariably be associated with QT prolongation or vasodilatation, justifying further development of this drug class.British Journal of Pharmacology (2006) 149, 269–276. doi:10.1038/sj.bjp.0706846
Effect of a nitric oxide releasing derivative of paracetamol in a rat model of endotoxaemia
Authors: Marshall M , Keeble J , Moore P K 
Published: August 2006

Background and purpose:Nitroparacetamol is a nitric oxide‐releasing paracetamol with novel anti‐inflammatory properties compared to the parent compound. This study has investigated the anti‐inflammatory activity of nitroparacetamol in a model of endotoxaemia in rats to probe the mechanisms underlying this effect.Experimental approach:Nitroparacetamol (92 mg kg−1), paracetamol (50 mg kg−1) or vehicle were administered to male, Wistar rats 15 min prior to or 3 h after lipopolysaccharide (0.5 mg kg−1, serotype 0127:B8). Mean arterial pressure and heart rate were measured for 5 h and plasma and organs were then obtained to determine organ dysfunction, inducible nitric oxide synthase and cyclooxygenase‐2 expression (lung, liver and kidney tissue) and plasma nitrate/nitrite. In separate experiments, nitroparacetamol, paracetamol or vehicle was administered 1 h before acetylcholine (0.1 μg kg−1) or sodium nitroprusside (0.25 μg kg−1) to determine if nitroparacetamol desensitizes responses to exogenous/endogenous nitric oxide.Key results:Nitroparacetamol prevented but did not reverse the lipopolysaccharide‐induced hypotension. There was no effect on heart rate or plasma markers of organ dysfunction. Nitroparacetamol prevented the increased plasma nitrate/nitrite and expression of COX‐2 and iNOS, whereas paracetamol exerted partial inhibition of COX‐2 in lung alone. Nitroparacetamol also reduced responses to acetylcholine and sodium nitroprusside.Conclusions and implications:NO is the active component of nitroparacetamol in this model of endotoxaemia. Pro‐inflammatory processes targeted by nitroparacetamol have been shown to include iNOS/COX‐2 induction and possibly vascular soluble guanylyl cyclase. Precise mechanisms underlying the NO effect are unclear but inhbition of cytokine formation may be important.British Journal of Pharmacology (2006) 149, 516–522. doi:10.1038/sj.bjp.0706855
KATPchannel openers of the benzopyran type reach their binding site via the cytosol
Authors: Stephan D , Salamon E , Weber H , Russ U , Lemoine H , Quast U 
Published: August 2006

Background and purpose:ATP‐sensitive K+(KATP) channels are composed of pore‐forming subunits (Kir6.x) and of sulphonylurea receptors (SUR). Both sulphonylureas and KATPchannel openers act by binding to SUR. Sulphonylureas reach their binding site from the cytosol but it remains unknown whether this holds for openers too.Experimental approach:A poorly membrane‐permeant sulphonic acid derivative of the benzopyran‐type opener, bimakalim, was synthesized, descyano‐bimakalim‐6‐sulphonic acid (BMSA). Binding of BMSA and bimakalim was compared in membranes and intact cells expressing the Kir6.2/SUR2B channel and channel opening was compared in inside‐out patches and whole cells.Key results:In membranes, bimakalim and BMSA bound to Kir6.2/SUR2B withKivalues of 61 nMand 4.3 μM, showing that the negative charge decreased affinity 69‐fold. In intact cells, however, binding of BMSA was much weaker than in membranes (75‐fold) whereas that of bimakalim was unchanged. TheKivalue of BMSA decreased with increasing incubation time. In inside‐out patches, bimakalim (1 μM) and BMSA (100 μM) opened the Kir6.2/SUR2B channel closed by MgATP to a similar degree whereas in whole‐cell experiments, only bimakalim was effective.Conclusions and implications:Despite its negative charge, BMSA is an effective channel opener. The fact that BMSA binds and acts more effectively when applied to the inner side of the cell membrane shows that benzopyran openers reach their binding site at SUR from the cytosol. This suggests that the binding pocket of SUR is only open on the cytoplasmic side.British Journal of Pharmacology(2006)149, 199–205. doi:10.1038/sj.bjp.0706858
Rapid desensitization of somatodendritic 5‐HT1Areceptors by chronic administration of the high‐efficacy 5‐HT1Aagonist, F13714: a microdialysis study in the rat
Authors: Assié M‐B , Lomenech H , Ravailhe V , Faucillon V , Newman‐Tancredi A 
Published: August 2006

Background and purpose:Desensitization of somatodendritic 5‐HT1Areceptors is involved in the mechanism of action of several antidepressants, but the rapidity of this effect and the amount of agonist stimulation needed are unclear. We evaluated the capacity of the high‐efficacy 5‐HT1Aagonist, F13714 (3‐chloro‐4‐fluorophenyl‐(4‐fluoro‐4‐{[(5‐methyl‐6‐methylamino‐pyridin‐2‐ylmethyl)‐amino]‐methyl}‐piperidin‐1‐yl‐methanone) and of the partial agonist, flesinoxan, to desensitize somatodendritic 5‐HT1Areceptors involved in the control of 5‐HT release.Experimental approach:Intracerebral microdialysis in the hippocampus of freely moving rats was used to examine the acute and chronic effects of the two compounds (administered by osmotic pumps for 3, 7 or 14 days) on extracellular 5‐HT levels, measured by HPLC with electrochemical detection.Key results:When given acutely, F13714, flesinoxan and the low‐efficacy 5‐HT1Aagonist, buspirone, dose‐dependently decreased extracellular 5‐HT concentrations (ED50values: 0.04, 0.77 and 5.6 mg kg−1, respectively). The selective 5‐HT1Aantagonist WAY100635 inhibited the effects of the three compounds. F13714 (2.5 mg kg−1per day for 3, 7 or 14 days and 0.63 mg kg−1for 7 days) significantly attenuated the inhibition of 5‐HT release induced by buspirone (10 mg kg−1). In contrast, flesinoxan (10 mg kg−1per day) failed to alter the response to buspirone at any of the treatment durations.Conclusions and implications:Rat somatodendritic 5‐HT1Areceptors controlling hippocampal 5‐HT release were rapidly desensitized by chronic activation with a high‐efficacy 5‐HT1Aagonist, but not by chronic activation with a partial agonist. Thus, rapid 5‐HT1Aautoreceptor desensitization by high‐efficacy agonists may accelerate the onset of the therapeutic effects of antidepressants.British Journal of Pharmacology(2006)149, 170–178. doi:10.1038/sj.bjp.0706859
Comparative studies of AJG049, a novel Ca2+ channel antagonist, on voltage‐dependent L‐type Ca2+ currents in intestinal and vascular smooth muscle
Authors: Hashimoto M , Teramoto N , Zhu H‐L , Takahashi K , Ito Y 
Published: August 2006

Background and purpose:Antagonists of Ca2+ channels reduce contraction of intestinal smooth muscle but also affect vascular smooth muscle. We have therefore examined the effects of AJG049, a newly synthesized antagonist for regulation of gut motility, on voltage‐dependent L‐type Ca2+ channels, in vascular and intestinal smooth muscle, comparing AJG049 with two other Ca2+ channel antagonists, verapamil and diltiazem.Experimental approach:Affinities of AJG049 for various types of voltage‐dependent Ca2+ channels were examined by binding studies. Effects of AJG049 on voltage‐dependent inward Ca2+ (or Ba2+) currents (ICa or IBa) in dispersed smooth muscle cells from guinea‐pig ileum, colon and mesenteric artery were measured using conventional whole‐cell configurations.Key results:In binding studies, AJG049 showed a high affinity for the diltiazem‐binding site of L‐type Ca2+ channels. In whole‐cell configuration, AJG049 suppressed ICa in ileal myocytes, with concentration‐, voltage‐and use‐dependencies. AJG049 shifted the steady‐state inactivation curve of ICa to the left. The order of potency to inhibit ICa in ileal myocytes was AJG049>verapamil>diltiazem. AJG049 also suppressed IBa in guinea‐pig mesenteric arterial myocytes, showing concentration‐ and voltage‐dependencies and the potency order for this action was also AJG049>verapamil>diltiazem. For the relative ratio of Ki values between ileal and mesenteric arterial myocytes, the order was AJG049>diltiazem≫verapamil.Conclusions and implications:These results show that AJG049 inhibits L‐type Ca2+ channels mainly through the diltiazem‐binding site(s). From our results, AJG049 showed a little selectivity for these Ca2+ channels in intestinal smooth muscle.British Journal of Pharmacology (2006) 149, 155–162. doi:10.1038/sj.bjp.0706861
Assays for enhanced activity of low efficacy partial agonists at the D2 dopamine receptor
Authors: Lin H , Saisch S G N , Strange P G 
Published: August 2006

Background and purpose:Low efficacy partial agonists at the D2 dopamine receptor may be useful for treating schizophrenia. In this report we describe a method for assessing the efficacy of these compounds based on stimulation of [35S]GTPγS binding.Experimental approach:Agonist efficacy was assessed from [35S]GTPγS binding to membranes of CHO cells expressing D2 dopamine receptors in buffers with and without Na+. Effects of Na+ on receptor/G protein coupling were assessed using agonist/[3H]spiperone competition binding assays.Key results:When [35S]GTPγS binding assays were performed in buffers containing Na+, some agonists (aripiprazole, AJ‐76, UH‐232) exhibited very low efficacy whereas other agonists exhibited measurable efficacy. When Na+ was substituted by N‐methyl D‐glucamine, the efficacy of all agonists increased (relative to that of dopamine) but particularly for aripiprazole, aplindore, AJ‐76, (−)‐3‐PPP and UH‐232. In ligand binding assays, substitution of Na+ by N‐methyl D‐glucamine increased receptor/G protein coupling for some agonists ‐. aplindore, dopamine and (−)‐3‐PPP – but for aripiprazole, AJ‐76 and UH‐232 there was little effect on receptor/G protein coupling.Conclusions and implications:Substitution of Na+ by NMDG increases sensitivity in [35S]GTPγS binding assays so that very low efficacy agonists were detected clearly. For some agonists the effect seems to be mediated via enhanced receptor/G protein coupling whereas for others the effect is mediated at another point in the G protein activation cycle. AJ‐76, aripiprazole and UH‐232 seem particularly sensitive to this change in assay conditions. This work provides a new method to discover these very low efficacy agonists.British Journal of Pharmacology (2006) 149, 291–299. doi:10.1038/sj.bjp.0706866
BML‐241 fails to display selective antagonism at the sphingosine‐1‐phosphate receptor, S1P3
Authors: Jongsma M , Hendriks‐Balk M C , Michel M C , Peters S L M , Alewijnse A E 
Published: August 2006

Background and purpose:The thiazolidine carboxylic acid, BML‐241, has been proposed as a lead compound in development of selective antagonists at the sphingosine‐1‐phosphate receptor (S1P3), based on its inhibition of the rise in intracellular calcium concentrations ([Ca2+]i) in HeLa cells overexpressing S1P receptors. We have studied the antagonistic properties of BML‐241 for the S1P3 receptor in more detail.Experimental approach:Chinese hamster ovary (CHO) cells stably transfected with the S1P3, S1P2 or α1A‐adrenoceptors were used to investigate the effect of BML‐241 on increases in [Ca2+]i mediated via different receptors. CHO‐K1 cells were used to study ATP‐induced [Ca2+]i elevations. Effects on S1P3‐mediated inhibition of forskolin‐induced cAMP accumulation and on binding to α1A‐adrenoceptors were also investigated. In addition, the effect of BML‐241 on contractions of rat mesenteric artery induced by phenylephrine was studied in an organ bath.Key results:High concentrations of BML‐241 (10 μM) inhibited the rise in [Ca2+]i induced by S1P3 and S1P2 receptor stimulation; lower concentrations were ineffective. This high concentration of BML‐241 also inhibited [Ca2+]i increases via P2 (nucleotide) receptor or α1A‐adrenoceptor stimulation. Moreover, BML‐241 (10 μM) inhibited α1‐adrenoceptor‐mediated contraction of rat mesenteric artery but did not displace [3H]‐prazosin from α1A‐adrenoceptors in concentrations up to 100 μM. BML‐241 (10 μM) did not affect the S1P3‐mediated decrease of forskolin‐induced cAMP accumulation.Conclusions and Implications:We conclude that BML‐241 is a low potency, non‐selective inhibitor of increases in [Ca2+]i, rather than a specific antagonist at the S1P3 receptor.British Journal of Pharmacology (2006) 149, 277–282. doi:10.1038/sj.bjp.0706872