bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of phencyclidine (PCP) and MK 801 on the EEGq in the prefrontal cortex of conscious rats; antagonism by clozapine, and antagonists of AMPA‐, α1‐ and 5‐HT2A‐receptors
Authors: Sebban Claude , Tesolin‐Decros Brigitte , Ciprian‐Ollivier Jorge , Perret Laurent , Spedding Michael 
Published: June 2006

The electroencephalographic (EEG) effects of the propsychotic agent phencyclidine (PCP), were studied in conscious rats using power spectra (0 – 30 Hz), from the prefrontal cortex or sensorimotor cortex. PCP (0.1 – 3 mg kg−1s.c.) caused a marked dose‐dependent increase in EEG power in the frontal cortex at 1 – 3 Hz with decreases in power at higher frequencies (9 – 30 Hz). At high doses (3 mg kg−1s.c.) the entire spectrum shifted to more positive values, indicating an increase in cortical synchronization. MK 801 (0.05 – 0.1 mg kg−1i.p.) caused similar effects but with lesser changes in power.In contrast, the non‐competitive AMPA antagonists GYKI 52466 and GYKI 53655 increased EEG power over the whole power spectrum (1 – 10 mg kg−1i.p.) The atypical antipsychotic clozapine (0.2 mg kg−1s.c.) synchronized the EEG (peak 8 Hz). The 5‐HT2A‐antagonist, M100907, specifically increased EEG power at 2 – 3 Hz at low doses (10 and 50 μg kg÷1s.c.), whereas at higher doses (0.1 mg kg−1s.c.) the profile resembled that of clozapine.Clozapine (0.2 mg kg−1s.c.), GYKI 53655 (5 mg kg−1i.p.), prazosin (0.05 and 0.1 mg kg−1i.p.), and M100907 (0.01 and 0.05 mg kg−1s.c.) antagonized the decrease in power between 5 and 30 Hz caused by PCP (1 mg kg−1s.c.), but not the increase in power at 1 – 3 Hz in prefrontal cortex.British Journal of Pharmacology(2002)135, 65–78; doi:10.1038/sj.bjp.0704451
Expression of mRNA and functional alpha1‐adrenoceptors that suppress the GIRK conductance in adult rat locus coeruleus neurons
Authors: Osborne Peregrine B , Vidovic Maria , Chieng Billy , Hill Caryl E , Christie MacDonald J 
Published: June 2006

Locus coeruleus neurons in adult rats express binding sites and mRNA for α1‐adrenoceptors even though the depolarizing effect of α1‐adrenoceptor agonists on neonatal neurons disappears during development.
In this study intracellular microelectrodes were used to record from locus coeruleus neurons in brain slices of adult rats and reverse transcription‐polymerase chain reaction (RT – PCR) was used to investigate the mRNA expression of α1‐ and α2‐adrenoceptors in juvenile and adult rats.
The α1‐adrenoceptor agonist phenylephrine had no effect on the membrane conductance of locus coeruleus neurons (Vhold −60 mV) but decreased the G protein coupled, inward rectifier potassium (GIRK) conductance induced by α2‐adrenoceptor or μ‐opioid agonists. The GIRK conductance induced by noradrenaline was increased in amplitude when α1‐adrenoceptors were blocked with prazosin.
RT – PCR of total cellular RNA isolated from microdissected locus coeruleus tissue demonstrated strong mRNA expression of α1a‐, α1b‐ and α1d‐adrenoceptors in both juvenile and adult rats. However, only mRNA transcripts for the α1b‐adrenoceptors were consistently detected in cytoplasmic samples taken from single locus coeruleus neurons of juvenile rats, suggesting that this subtype may be responsible for the physiological effects seen in juvenile rats.
Juvenile and adult locus coeruleus tissue expressed mRNA for the α2a‐ and α2c‐adrenoceptors while the α2b‐adrenoceptor was only weakly expressed in juveniles and was not detected in adults.
The results of this study show that α1‐adrenoceptors expressed in adult locus coeruleus neurons function to suppress the GIRK conductance that is activated by μ‐opioid and α2‐adrenoceptors.

British Journal of Pharmacology (2002) 135, 226–232; doi:10.1038/sj.bjp.0704453
Capacitative Ca2+ entry in vascular endothelial cells is mediated via pathways sensitive to 2 aminoethoxydiphenyl borate and xestospongin C
Authors: Bishara Nour B , Murphy Timothy V , Hill Michael A 
Published: June 2006

Agonists increase endothelial cell intracellular Ca2+, in part, by capacitative entry, which is triggered by the filling state of intracellular Ca2+ stores. It has been suggested that depletion of endoplasmic reticulum (ER) Ca2+ stores either leads to a physical coupling between the ER and a plasma membrane channel, or results in production of an intracellular messenger which affects the gating of membrane channels. As an axis involving the IP3 receptor has been implicated in a physical coupling mechanism the aim of this study was to examine the effects of the putative IP3 receptor antagonists/modulators, 2 aminoethoxydiphenyl borate (2APB) and xestospongin C, on endothelial cell Ca2+ entry.
Studies were conducted in fura 2 loaded cultured bovine aortic endothelial cells and endothelial cells isolated from rat heart.
2APB (30 – 300 μM) inhibited Ca2+ entry induced by both agonists (ATP 1 μM, bradykinin 0.1 μM) and receptor‐independent mechanisms (thapsigargin 1 μM, ionomycin 0.5 and 5 μM). 2APB did not diminish endothelial cell ATP‐induced production of IP3 nor effect in vitro binding of [3H]‐IP3 to an adrenal cortex binding protein. Capacitative Ca2+ entry was also blocked by disruption of the actin cytoskeleton with cytochalasin (100 nM) while the initial Ca2+ release phase was unaffected.
Similarly to 2APB, xestospongin C (3 – 10 μM) inhibited ATP‐induced Ca2+ release and capacitative Ca2+ entry. Further, xestospongin C inhibited capacitative Ca2+ entry induced by thapsigargin (1 μM) and ionomycin (0.5 μM).
The data are consistent with a mechanism of capacitative Ca2+ entry in vascular endothelial cells which requires (a) IP3 receptor binding and/or an event distal to the activation of the ER receptor and (b) a spatial relationship, dictated by the cytoskeleton, between Ca2+ release and entry pathways.

British Journal of Pharmacology (2002) 135, 119–128; doi:10.1038/sj.bjp.0704465
The developing relationship between receptor‐operated and store‐operated calcium channels in smooth muscle
Authors: McFadzean Ian , Gibson Alan 
Published: June 2006

Contraction of smooth muscle is initiated, and to a lesser extent maintained, by a rise in the concentration of free calcium in the cell cytoplasm ([Ca2+]i). This activator calcium can originate from two intimately linked sources – the extracellular space and intracellular stores, most notably the sarcoplasmic reticulum. Smooth muscle contraction activated by excitatory neurotransmitters or hormones usually involves a combination of calcium release and calcium entry. The latter occurs through a variety of calcium permeable ion channels in the sarcolemma membrane. The best‐characterized calcium entry pathway utilizes voltage‐operated calcium channels (VOCCs). However, also present are several types of calcium‐permeable channels which are non‐voltage‐gated, including the so‐called receptor‐operated calcium channels (ROCCs), activated by agonists acting on a range of G‐protein‐coupled receptors, and store‐operated calcium channels (SOCCs), activated by depletion of the calcium stores within the sarcoplasmic reticulum. In this article we will review the electrophysiological, functional and pharmacological properties of ROCCs and SOCCs in smooth muscle and highlight emerging evidence that suggests that the two channel types may be closely related, being formed from proteins of the Transient Receptor Potential Channel (TRPC) family.British Journal of Pharmacology(2002)135, 1–13; doi:10.1038/sj.bjp.0704468
Agmatine is transported into liver mitochondria by a specific electrophoretic mechanism
Authors: Salvi Mauro , Battaglia Valentina , Mancon Mario , Colombatto Sebastiano , Cravanzola Carlo , Calheiros Rita , Marques Maria P. M. , Grillo Maria A. , Toninello Antonio 
Published: June 2006

Agmatine, a divalent diamine with two positive charges at physiological pH, is transported into the matrix of liver mitochondria by an energy-dependent mechanism the driving force of which is ΔΨ (electrical membrane potential). Although this process showed strict electrophoretic behaviour, qualitatively similar to that of polyamines, agmatine is most probably transported by a specific uniporter. Shared transport with polyamines by means of their transporter is excluded, as divalent putrescine and cadaverine are ineffective in inhibiting agmatine uptake. Indeed, the use of the electroneutral transporter of basic amino acids can also be discarded as ornithine, arginine and lysine are completely ineffective at inducing the inhibition of agmatine uptake. The involvement of the monoamine transporter or the existence of a leak pathway are also unlikely. Flux-voltage analysis and the determination of activation enthalpy, which is dependent upon the valence of agmatine, are consistent with the hypothesis that the mitochondrial agmatine transporter is a channel or a single-binding centre-gated pore. The transport of agmatine was non-competitively inhibited by propargylamines, in particular clorgilyne, that are known to be inhibitors of MAO (monoamine oxidase). However, agmatine is normally transported in mitoplasts, thus excluding the involvement of MAO in this process. The I2 imidazoline receptor, which binds agmatine to the mitochondrial membrane, can also be excluded as a possible transporter since its inhibitor, idazoxan, was ineffective at inducing the inhibition of agmatine uptake. Scatchard analysis of membrane binding revealed two types of binding site, S1 and S2, both with mono-co-ordination, and exhibiting high-capacity and low-affinity binding for agmatine compared with polyamines.Agmatine transport in liver mitochondria may be of physiological importance as an indirect regulatory system of cytochrome c oxidase activity and as an inducer mechanism of mitochondrial-mediated apoptosis.
Regulation of prokaryotic adenylyl cyclases by CO2
Authors: Hammer Arne , Hodgson David R. W. , Cann Martin J. 
Published: June 2006

The Slr1991 adenylyl cyclase of the model prokaroyte Synechocystis PCC 6803 was stimulated 2-fold at 20 mM total Ci (inorganic carbon) at pH 7.5 through an increase in kcat. A dose response demonstrated an EC50 of 52.7 mM total Ci at pH 6.5. Slr1991 adenylyl cyclase was activated by CO2, but not by HCO3−. CO2 regulation of adenylyl cyclase was conserved in the CyaB1 adenylyl cyclase of Anabaena PCC 7120. These adenylyl cyclases represent the only identified signalling enzymes directly activated by CO2. The findings prompt an urgent reassessment of the activating carbon species for proposed HCO3−-activated adenylyl cyclases.
Digestive and metabolic effects of altering feeding frequency in athletic horses
Authors: Jansson A , Sandin A , Lindberg JE 
Published: June 2006

AbstractThe aim of this study was to investigate the effect of feeding frequency on total tract digestibility and plasma glucose, insulin, urea, gastrin and cortisol concentrations at rest and following exercise in seven Standardbred horses in race training. The horses were fed every 12 h (twice a day, 2TD) and every 4 h (six times a day, 6TD) for 25 days, in a cross-over design. The diet (64% grass hay, 36% concentrates on weight basis) was fed at twice the maintenance energy requirement. Blood samples were taken every hour for 24 h on day 17, total collection of urine and faeces was made on days 19–21 and an intensive exercise test was performed on day 25. Altering feeding frequency caused small variations in diurnal plasma glucose, urea, gastrin and cortisol concentrations and did not affect total tract nutrient digestibility. There was an increase in the mean diurnal plasma urea concentration on the 2TD regime and low levels of plasma insulin were observed 7 h after feeding 2TD. The response to intensive exercise on heart rate, plasma lactate and plasma glucose was similar on both treatments but the plasma insulin concentration was higher following exercise in the 2TD regime, indicating that post-exercise glucose metabolism was altered. In conclusion, this study shows that feeding athletic horses only 2TD caused metabolic signs resembling those observed during feed deprivation (low levels of plasma insulin and an increased diurnal plasma urea concentration) and an altered post-exercise glucose metabolism, but did not affect the digestive response.
The freestyle dressage competition as a test of the horse's performance
Authors: Stachurska A , Pięta M , Niewczas J , Markowski W 
Published: June 2006

AbstractThe objective of the study has been to examine whether the freestyle dressage classes are judged reliably and to elaborate a method assessing the consistency of judging. The data contained 13 000 marks of the ten best-ranked horses at nine Grand Prix classes and four Intermediate I classes from ten international competitions. The marks concerned 119 horses in total and were given by 37 judges. A method for evaluating the consistency of judging has been proposed. The index of disagreement (ID) assesses the disagreement of ranking by an individual judge relative to the general ranking based on the sum of marks awarded by five judges. The results show that the mean ID of individual judges is highly differentiated. The ID is influenced by the judge's position in the arena. The consistency of judging was lower in Intermediate I Freestyle Tests than in Grand Prix Freestyle Tests and it varied in different competitions. The conclusion of the study is that the results of the freestyle dressage classes are often biased. The present system of judging should be permanently checked. The offered method of evaluating agreement between judges' rankings may help to improve the consistency of judging and the reliability of the horses' scores.
Risk Factors for Nosocomial Primary Bloodstream Infection in Pediatric Intensive Care Unit Patients: A 2-Year Prospective Cohort Study
Authors: Elward Alexis M. , Fraser Victoria J. 
Published: June 2006

Objective.The primary objective was to determine the rate of and risk factors for nosocomial primary bloodstream infection (BSI) in pediatric intensive care unit (PICU) patients in order to determine the validity of our previously published findings. The secondary objective was to analyze whether risk factors for primary BSI differed by organism type, particularly whether device use was more strongly associated with BSI due to gram-positive organisms.Design.Prospective cohort study.Settings.St. Louis Children's Hospital, a 235-bed academic tertiary care center with a 28-bed combined medical and surgical PICU.Patients.PICU patients admitted between September 1, 1999, and September 1, 2001.Outcome Measures.Nosocomial primary BSIs.Results.Of 2,310 patients, 55% were male, and 73% were white. There were 124 episodes of primary BSI in 87 patients (3.8%). Coagulase-negative Staphylococcus organisms were the leading cause of BSI (42 of 124 episodes). The rate of BSI was 9 BSIs/1,000 central venous catheter–days. Multiple logistic regression analysis showed that independent predictors of nosocomial primary BSI included higher number of arterial catheter–days (adjusted odds ratio [aOR], 5.7 per day of arterial catheterization; 95% confidence interval [CI], 3.4-9.8), higher number of packed red blood cell transfusions (aOR, 1.2; 95% CI, 1.1-1.4), and genetic syndrome (aOR, 4.7; 95% CI, 1.8-12). Severity of illness, underlying illnesses, and medications were not independently associated with increased risk of nosocomial BSI.Conclusion.Arterial catheter use and packed red blood cell transfusion are potentially modifiable risk factors for nosocomial primary BSI in PICU patients. Genetic syndromes may be markers for unrecognized immune defects that impair host defense against microorganisms.
Outbreak of Pertussis Among Healthcare Workers in a Hospital Surgical Unit
Authors: Pascual F. Brian , McCall Candace L. , McMurtray Aaron , Payton Tony , Smith Forrest , Bisgard Kristine M. 
Published: June 2006

Background.In September 1999, a pertussis outbreak was detected among surgical staff of a 138-bed community hospital. Patients were exposed toBordetella pertussisduring the 3-month outbreak period.Objective.To describe the outbreak among surgical staff, to evaluate implemented control measures, and to determine whether nosocomial transmission occurred.Methods.Clinical pertussis was defined as acute cough illness with a duration of 14 days or more without another apparent cause; persons with positive culture, PCR, or serologic test results were defined as having laboratory-confirmed pertussis. Surgical healthcare workers (HCWs) were interviewed regarding pertussis symptoms, and specimens were obtained for laboratory analysis. Patients exposed toB. pertussisduring an ill staff member's 3-week infectious period were interviewed by phone to determine the extent of nosocomial spread.Participants.A total of 53 HCWs assigned to the surgical unit and 146 exposed patients. HCWs with pertussis were defined as case subjects; HCWs without pertussis were defined as non-case subjects.Results.Twelve (23%) of 53 HCWs had clinical pertussis; 6 cases were laboratory confirmed. The median cough duration in the 12 case subjects was 27 days (range, 20-120 days); 10 (83%) had paroxysms. Eleven (92%) of 12 case subjects and 28 (86%) of 41 non-case subjects received antibiotic treatment or prophylaxis. Seven case subjects (58%) reported they always wore a mask when near patients. Of 146 patients potentially exposed to pertussis from the 12 case subjects, 120 (82%) were interviewed; none reported a pertussis-like illness.Conclusions.Surgical staff transmittedB. pertussisamong themselves; self-reported data suggests that these HCWs did not transmitB. pertussisto their patients, likely because of mask use, cough etiquette, and limited face-to-face contact. Control measures might have helped limit the outbreak once pertussis was recognized.
Analyzing Oppression
Authors: Cudd Ann E. 
Published: June 2006

AbstractThis book presents a new, integrated theory of social oppression, which tackles the fundamental question that no theory of oppression has satisfactorily answered: if there is no natural hierarchy among humans, why are some cases of oppression so persistent? The book argues that the explanation lies in the coercive co-opting of the oppressed to join in their own oppression. This answer sets the stage for analysis throughout the book, as it explores the questions of how and why the oppressed join in their oppression. The book argues that oppression is an institutionally structured harm perpetrated on social groups by other groups using direct and indirect material, economic, and psychological force. Among the most important and insidious of the indirect forces is an economic force that operates through oppressed persons' own rational choices. This force constitutes the central feature of analysis, and the book argues that this force is especially insidious because it conceals the fact of oppression from the oppressed and from others who would be sympathetic to their plight. The oppressed come to believe that they suffer personal failings and this belief appears to absolve society from responsibility. While in the book's view oppression is grounded in material exploitation and physical deprivation, it cannot be long sustained without corresponding psychological forces. The book examines the direct and indirect psychological forces that generate and sustain oppression. It discusses strategies that groups have used to resist oppression and argues that all persons have a moral responsibility to resist in some way. The concluding chapter proposes a concept of freedom that would be possible for humans in a world that is actively opposing oppression, arguing that freedom for each individual is only possible when we achieve freedom for all others.
Social Groups and Institutional Constraints
Authors: Cudd Ann E. 
Published: June 2006

AbstractThis chapter characterizes social groups and institutions in a way that meets the plausible objections of individualists, yet allows a social explanation of oppression. Topics discussed include explaining human behavior, social groups, institutionally structured constraints, oppression and social groups, social groups and group harm. It is argued that any account of oppression that distinguishes it from other types of harm that can come to individuals and locates it as a social injustice requires an account of social groups. Further, harms that accrue to members of voluntary and nonvoluntary groups must be treated separately in moral arguments.
Psychological Mechanisms of Oppression
Authors: Cudd Ann E. 
Published: June 2006

AbstractThis chapter is concerned with explaining how our cognitive psychology equips us for oppression, that is, what psychological mechanisms we have that allow and motivate us to oppress or suffer oppression. It addresses the question: what psychological mechanisms account for our tendency to form social groups and to invidiously discriminate among those groups? It argues that there are two main types of material forces of oppression — violence and economic deprivation — and that oppression cannot survive without being enforced by at least one of these material ways of harming persons. Violence is separated from economic deprivation to illustrate how different cases of oppression involve different kinds of reinforcements and argue that they will require different strategies of resistance.
Economic Forces of Oppression
Authors: Cudd Ann E. 
Published: June 2006

AbstractThis chapter discusses three main forces of economic oppression: oppressive economic systems (capitalism and socialism), direct forces of economic oppression, and indirect forces of economic oppression. It is argued that while capitalism and socialism are not intrinsically oppressive, both systems lend themselves to oppression in characteristic ways, and therefore each sort of system must take certain steps to guard against their respective characteristic oppressions. Direct forces of economic oppression are restrictions on opportunities that are applied from the outside on the oppressed, including enslavement, segregation, employment discrimination, group-based harassment, opportunity inequality, neocolonialism, and governmental corruption. Direct forces may not always be clearly visible, either because they happen far from the reach of legal authorities or from the view of consumers, or because they are diffused in a large society, and only apparent from a statistical analysis and comparison among social groups. In indirect forces, or oppression by choice, the oppressed are co-opted into making individual choices that add to their own oppression. When this force is at work the oppressed are faced with options that rationally induce them to choose against the collective good of their social group, and in the long run, against their own good as well. But choosing otherwise requires choosing against their own immediate interests, and changing their beliefs or preferences in ways that they may resent.
Psychological Harms of Oppression
Authors: Cudd Ann E. 
Published: June 2006

AbstractThis chapter discusses the direct and indirect psychological harms of oppression. Direct psychological harms are intentionally inflicted by dominant on subordinate groups. These include terror and psychological trauma, humiliation and degradation, objectification, religion, ideology, and cultural domination. Indirect psychological harms occur when the beliefs and values of the privileged or oppressor groups are subconsciously accepted by the subordinate and assimilated into their self-concept or value/belief scheme. Indirect forces thus work through the psychology of the oppressed to mold them and co-opt them to result in choices and decisions that harm the oppressed while benefiting the privileged. These include shame and low self-esteem, false consciousness, and deformed desire.