bluuebunny/crossref_metadata_2025_split huggingface dataset:
HETEROGENEOUS EXPRESSION OF TANDEM‐PORE K+ CHANNEL GENES IN ADULT AND EMBRYONIC RAT HEART QUANTIFIED BY REAL‐TIME POLYMERASE CHAIN REACTION
Authors: Liu W , Saint DA 
Published: February 2004

SUMMARY1. Many members of the tandem‐pore K+ channel gene family have been reported to be present in cardiac cells. However, the pattern of gene expression of these channels in the heart is a matter of some dispute.2. Here, we used reverse transcription and real‐time quantitative polymerase chain reaction to investigate the pattern of gene expression of nine members of the tandem‐pore K+ channel genes in adult and embryonic rat heart. The genes (TWIK‐1, TWIK‐2, TASK‐1, TASK‐2, TASK‐3, TREK‐1, TREK‐2, TRAAK and KCNK6) were quantified, relative to glyceraldehyde‐3‐phosphate dehydrogenase (GADPH), in all four chambers of adult rat hearts and in the ventricles of embryonic rat hearts.3. All these genes were detected in at least one chamber of the heart, with a predominance of TWIK‐2, TASK‐1 and TREK‐1 expression. The expression of TWIK‐2 was higher in the right atrium than in other cardiac chambers, TASK‐1 was expressed more in atria than in ventricles and TREK‐1 was highly expressed in the right ventricle.4. The expression levels of the three predominant genes in embryonic rat ventricle are much lower than their expression in adult rat ventricles.5. The physiological implications of the differential gene expression of the tandem‐pore K+ channels is discussed.
DIFFERENTIAL EFFECTS OF PYRETHROIDS ON VOLUME‐SENSITIVE ANION AND ORGANIC OSMOLYTE PATHWAYS
Authors: Culliford Steve J , Borg John J , O'Brien Martin J , Kozlowski Roland Z 
Published: February 2004

SUMMARY1. There are no effective ways of screening for potential modulators of volume‐regulated anion channels in their native cell type. Generally, cell lines are used for this purpose. Using HeLa and C6 glioma cells, we identified the pyrethroids as a novel class of compounds that inhibit taurine efflux through volume‐regulated anion transport pathways in these cells. Subsequently, we examined their effects on volume‐regulated anion channels in guinea‐pig ventricular myocytes to determine whether results obtained using cell lines could be extrapolated to other tissues.2. Tetramethrin inhibited taurine efflux in both HeLa and C6 glioma cells with Ki values of approximately 26 and 16 µmol/L, respectively. Bioallethrin and fenpropathrin inhibited volume‐sensitive taurine efflux from C6 glioma cells, but not from HeLa cells. The Ki values for bioallethrin and fenpropathrin were 70 and 59 µmol/L, respectively.3. Volume‐sensitive I– efflux was observed in HeLa cells but not in C6 glioma cells, suggesting that the taurine efflux pathway in C6 glioma cells may be different to that of the I– efflux pathway. Cyfluthrin, tetramethrin, fenpropathrin, tefluthrin and bioallethrin all significantly inhibited volume‐sensitive I– efflux from HeLa cells at 100 µmol/L.4. Patch‐clamp experiments have shown inhibition of ICl,vol in guinea‐pig ventricular myocytes by fenpropathrin, but not tetramethrin or cypermethrin, at 100 µmol/L. This revealed that further differences exist between ICl,vol in guinea‐pig ventricular myocytes and the anion transport pathways in C6 glioma and HeLa cells.5. In conclusion, we have shown that pyrethroids differentially inhibit volume‐regulated anion and taurine efflux in a number of cell types. Because these compounds have different effects in different cells, it is likely that: (i) more than one pathway is involved in the volume‐sensitive transport of anions and organic osmolytes; and (ii) the molecular identities of the channels underlying anion transport are different. Finally, for the reasons given above, care should be taken when extrapolating data from one cell type to another. However, in the absence of an existing high‐throughput screen, taurine efflux still represents a viable route for the identification of potential modulators of volume‐regulated ion channels.
NEW INSIGHT INTO THE SIGNALLING PATHWAYS OF HEAT STRESS‐INDUCED MYOCARDIAL PRECONDITIONING: PROTEIN KINASE Cε TRANSLOCATION AND HEAT SHOCK PROTEIN 27 PHOSPHORYLATION
Authors: Arnaud Claire , Joyeux‐Faure Marie , Bottari Serge , Godin‐Ribuot Diane , Ribuot Christophe 
Published: February 2004

SUMMARY1. Heat stress (HS) is known to induce delayed preconditioning against myocardial infarction 24 h later, but the exact signalling pathway of this response remains to be elucidated. In previous studies, we have shown evidence for the implication of protein kinase C (PKC) and p38 mitogen‐activated protein kinase (MAPK) in the HS‐induced reduction in infarct size. Furthermore, in their phosphorylated state, small heat shock proteins (Hsp27) seem to confer cytoskeletal protection. In the present study, we sought to determine the effect of HS on the subcellular distribution of PKC isoforms and on Hsp27 phosphorylation.2. Rats were subjected to either HS (42°C for 15 min; HS group) or sham anaesthesia (sham group) before their hearts were excised. Myocardial tissue extracts obtained 20 min or 24 h after HS were processed for western blot analysis.3. In the HS group, PKCε translocated from the cytosolic to the particulate fraction (4426 ± 128 vs 6258 ± 316 arbitrary units; P = 0.002). Chelerythrine (5 mg/kg, i.p.), a PKC inhibitor, abolished this translocation. Western blot analysis of Hsp27 24 h after HS showed a marked increase in protein expression and phosphorylation in the particulate fraction.4. In the present study, we have shown that HS induces the translocation of PKCε from the cytosolic to the particulate fraction. Along with our previous observation that PKC is a trigger of HS‐induced myocardial preconditioning, the results of the present study suggest an important role of the ε isoform of PKC in this cardioprotective mechanism. Furthermore, we have also demonstrated that the cytoprotective protein Hsp27 is phosphorylated following HS. Therefore, we can conclude that PKC and MAPK/Hsp27 are involved in the signalling pathway of HS‐induced cardioprotection.
NITRIC OXIDE RELEASE IN THE NUCLEUS TRACTUS SOLITARIUS DURING AND AFTER BILATERAL COMMON CAROTID ARTERY OCCLUSION
Authors: Wu Wun‐Chin , Chai Chok‐Yung 
Published: February 2004

SUMMARY1. The purpose of the present study was to investigate the effect of bilateral common carotid artery occlusion (BCCAO) on cardiovascular responses and nitric oxide (NO) formation in the nucleus tractus solitarius (NTS).2. Twenty‐three adult cats were anaesthetized intraperitoneally with urethane (400 mg/kg) and α‐chloralose (40 mg/kg). The femoral artery was cannulated to allow monitoring of systemic arterial pressure (SAP) and heart rate (HR). The femoral vein was cannulated for intravenous drug administration.3. Extracellular NO levels in the NTS were measured by in vivo voltammetry using an NO microsensor combined with a microcomputer‐controlled apparatus.4. Microinjection of l‐arginine (30 nmol) into the NTS produced hypotension and NO release. This effect of l‐arginine was not changed by 2 min of BCCAO.5. Bilateral common carotid artery occlusion produced increases in SAP and NO levels. These effects were more apparent in vagotomized than in intact animals.6. The onset latency of BCCAO‐induced changes in SAP levels (8.4 ± 2.5 s) was longer than that for changes in NO (4.7 ± 1.7 s).7. Bilateral common carotid artery occlusion induced hypertension and NO release in the NTS of intact and vagotomized animals. These cardiovascular and NO responses to BCCAO were significantly attenuated by NG‐nitro‐l‐arginine methyl ester (10 mg/kg, i.v.) and MK‐801 (2.5 mg/kg, i.v.). These data suggest that NO synthase and activation of N‐methyl‐d‐aspartate receptors are involved in the cardiovascular and NO responses to BCCAO.
EFFECT OF PROPOFOL ON VASOCONSTRICTION AND CALCIUM MOBILIZATION INDUCED BY ANGIOTENSIN II DIFFERS IN AORTAS FROM NORMOTENSIVE AND HYPERTENSIVE RATS
Authors: Samain Emmanuel , Pili‐Floury Sébastien , Bouillier Hélène , Clichet Adeline , Safar Michel , Dagher Georges , Marty Jean , Renaud Jean‐François 
Published: February 2004

SUMMARY1. Angiotensin (Ang) II is a potent vasopressor agent, involved in the short‐term control of arterial blood pressure during anaesthesia. The aim of the present study was to test the hypothesis that propofol, a widely used intravenous anaesthetic agent, could alter the arterial response to AngII and to evaluate its effect in genetic hypertension.2. We studied the effect of increasing concentrations of propofol (5.6 × 10−7 to 5.6 × 10−4 mol/L) on aortic ring maximal isometric tension elicited by AngII and on AngII‐induced Ca2+ mobilization in aortic smooth muscle cells from Wistar‐Kyoto (WKY) rats and spontaneously hypertensive rats (SHR).3. Maximal tension developed by aortic rings from WKY rats was greater than that developed by rings from SHR. In both WKY rats and SHR, propofol at concentrations from 5.6 × 10−6 mol/L decreased maximal tension induced by AngII in a concentration‐dependent manner. The magnitude of inhibition was higher in SHR than in WKY rats, whereas pD2 values were not different. In addition, Ca2+ mobilization induced by AngII was inhibited by propofol in a concentration‐dependent manner, with the same magnitude and pD2 values.4. These results suggest that the arterial response to AngII may be altered during propofol anaesthesia, particularly in hypertension.
MODIFICATION OF TRANSMITTER RELEASE FROM PERIARTERIAL NERVE TERMINALS BY DIPYRIDAMOLE IN CANINE ISOLATED SPLENIC ARTERY
Authors: Naito Makoto , Yang Xiao‐Ping , Chiba Shigetoshi 
Published: February 2004

SUMMARY1. The aim of the present study was to determine the modulatory effects of dipyridamole on purinergic and adrenergic transmission in the canine isolated, perfused splenic artery.2. Periarterial nerve electrical stimulation readily induced a double‐peaked vasoconstriction consisting of an initial transient, predominantly P2X receptor‐mediated constriction followed by a prolonged, mainly α1‐adrenoceptor‐mediated response.3. Exposure of tissues to dipyridamole (0.1–1 µmol/L) dose‐dependently inhibited both the first and second peaks of the vasoconstrictor response at a low frequency of stimulation (1 Hz), whereas at an intermediate frequency of stimulation (4 Hz), the first peak of the response was depressed without any significant effect being observed on the second peak of constriction.4. At a higher dose (1 µmol/L) dipyridamole potentiated vasoconstrictor responses to noradrenaline (0.03–1 nmol). At any doses used, dipyridamole had no effect on the vasoconstrictor responses to ATP (0.03–1 µmol).5. Tyramine (0.01–0.3 µmol) induced vasoconstriction in a dose‐dependent manner. The dose–response curves for tyramine were shifted to the right following treatment with dipyridamole (0.1–1 µmol/L).6. The present results indicate that dipyridamole may inhibit purinergic and adrenergic transmission presynaptically, whereas postsynaptically dipyridamole may potentiate the adrenergic vascular constriction by inhibition of transmitter uptake.
REDUCED HIGH SERUM HEPATOCYTE GROWTH FACTOR LEVELS AFTER SUCCESSFUL CARDIOVERSION IN PATIENTS WITH ATRIAL FIBRILLATION
Authors: Katoh Harumi , Shimada Toshio , Inoue Shin‐ichi , Takahashi Nobuyuki , Shimizu Hiromi , Ohta Yoko , Nakamura Ko , Murakami Yo , Ishibashi Yutaka , Matsumori Akira 
Published: February 2004

SUMMARY1. Serum hepatocyte growth factor (HGF) is considered to be a potent marker of vascular endothelial injury. The present study was designed to examine serum HGF levels in atrial fibrillation and after successful direct current (DC) cardioversion.2. We measured serum HGF levels before and 7 days and 1 month after DC cardioversion in 39 patients with atrial fibrillation in whom sinus rhythm was maintained for at least 7 days after DC cardioversion and in 30 age‐ and sex‐matched normal control subjects with sinus rhythm. We also measured acetylcholine‐induced changes in forearm blood flow (FBF) using venous occlusive plethysmography in 10 patients.3. Serum HGF levels were significantly higher in the atrial fibrillation patients (both lone atrial fibrillation and with underlying heart disease) than in the controls (0.16 ± 0.07 vs 0.10 ± 0.04 ng/mL; P < 0.001). Seven days after successful DC cardioversion, the patients' serum HGF levels had decreased significantly (0.16 ± 0.07 vs 0.12 ± 0.06 ng/mL; P < 0.05) and in the 24 patients maintaining sinus rhythm 1 month after DC cardioversion, serum HGF levels decreased to control values (0.10 ± 0.08 ng/mL at 1 month). Serum HGF levels of the 15 patients who had relapsed into atrial fibrillation 1 month after DC cardioversion tended to decrease 7 days after DC cardioversion, but increased again 1 month after DC cardioversion. Percentage changes in FBF between baseline and the highest dose of acetylcholine before and after DC cardioversion were 180 ± 98 and 323 ± 196%, respectively (P = 0.0051). The rate of increase in FBF at the highest dose of acetylcholine between before and after DC cardioversion correlated negatively with the rate of decrease in serum HGF levels between before and after DC cardioversion (r = −0.837; P = 0.0025).4. This study is the first to demonstrate that serum HGF levels increase in atrial fibrillation and decrease after successful DC cardioversion. This may reflect the fact that atrial fibrillation induces vascular endothelial injury.
DOPAMINERGIC RECEPTORS IN RAT DURA MATER: PHARMACOLOGICAL CHARACTERISTICS
Authors: Cavallotti C , Frati A , Cavallotti D , Tranquilli Leali FM 
Published: February 2004

SUMMARY1. The location and distribution of dopaminergic receptors in rat dura mater was studied by examining several dural zones (vascular, perivascular, intervascular) in different cranial and spinal regions.2. The pharmacological characteristics and anatomical distribution of dopamine D1‐ and D2‐like receptors sites were investigated using combined pharmacological techniques and immunofluorescent microscopy.3. Samples of rat dura mater were obtained from 10 adult Wistar rats. On frozen slices, dopaminergic D1 and D2 receptors were stained immunohistochemically using monoclonal antibodies.4. Inhibition studies were performed using fluorescent and non‐fluorescent agonists or antagonists to define the pharmacological specificity of the immunostaining.5. The greater sensitivity to displacement by amisulpride, bromocryptine, domperidone, haloperidol, raclopride and l‐sulpiride than to displacement by N‐propyl‐nor‐apomorphine, quinpirole and clozapine suggests that the immunofluorescent sites observed in these experiments are likely to belong to the dopamine D2 receptor subtype.6. Our observations provide evidence of the presence of D1 and D2 receptors in the wall of meningeal vessels. The dopaminergic receptors are located in the adventitia, media and intima of dural arteries. Furthermore, the density of receptors is higher in close proximity to arteries and decreases passing from the vascular to the perivascular and intervascular zones.7. In the rat dura mater, dopamine regulates the meningeal blood vessels and, through this action, dopamine and its receptors can play an important role in the pathogenesis of cephalalgia.
ROLE OF LYSOPHOSPHATIDYLCHOLINE IN EOSINOPHIL INFILTRATION AND RESISTANCE IN AIRWAYS
Authors: Nishiyama Osamu , Kume Hiroaki , Kondo Masashi , Ito Yasushi ,   Masafumi Ito and Kenichi Yamaki
Published: February 2004

SUMMARY1. Lysophosphatidylcholine (Lyso‐PC), which is synthesized by phospholipase A2, is generally considered to induce adhesion molecules. However, little is known about the involvement of Lyso‐PC in the pathogenesis of bronchial asthma. The present study was designed to examine whether pre‐exposure to Lyso‐PC causes eosinophil recruitment and an increase in resistance in airways.2. Eosinophils in bronchoalveolar lavage fluid (BALF) and the airway walls were enumerated after inhalation of 0.5 mg/mL Lyso‐PC to guinea‐pigs for 10 min. Respiratory resistance (Rrs) was recorded continuously over 6 h after inhalation of an equi‐dose of Lyso‐PC for an equivalent period.3. The proportion of eosinophils was increased from 10.7 ± 3.3 to 27.5 ± 3.1% (P < 0.0001) in BALF 6 h after inhalation of Lyso‐PC, whereas the proportion of neutrophils and lymphocytes was not increased. Histological examination also showed uniform distribution of eosinophils in the airway wall of bronchi and bronchioles 6 h after inhalation of Lyso‐PC. The number of eosinophils (/10 h.p.f.) in the bronchi and bronchioles was increased from 43.5 ± 16.8 to 154.8 ± 21.7 (P < 0.0001) and from 34.8 ± 0.7 to 106.0 ± 26.6 (P < 0.01), respectively. This eosinophil infiltration was similarly observed 24 h later.4. Next, we examined the effects of eosinophil infiltration induced by Lyso‐PC on Rrs. Inhalation of Lyso‐PC caused a slow increase in Rrs and the percentage increase in Rrs was 19.8 ± 1.9% (P < 0.0001) 6 h later. Eosinophil infiltration and an increase in Rrs did not occur after inhalation of physiological saline. These phenomena induced by Lyso‐PC were diminished by pretreatment with dexamethasone (6 µg/kg per day for 3 days).5. Lysophosphatidylcholine causes eosinophil infiltration and a subsequent increase in resistance in airways. Our results indicate that Lyso‐PC may be involved in the pathophysiology of bronchial asthma.
MICRONIZATION ENHANCES THE PROTECTIVE EFFECT OF PURIFIED FLAVONOID FRACTION AGAINST POSTISCHAEMIC MICROVASCULAR INJURY IN THE HAMSTER CHEEK POUCH
Authors: Cyrino Fátima ZGA , Bottino Daniel A , Lerond Laurence , Bouskela Eliete 
Published: February 2004

SUMMARY1. The present study was designed to evaluate the effect of micronization on the protective effect of the purified flavonoid fraction (MPFF) on increases in macromolecular permeability induced by ischaemia–reperfusion in the hamster cheek pouch microcirculation.2. Male hamsters (Mesocricetus auratus) were treated orally, twice a day, with vehicle (lactose), MPFF and non‐micronized purified flavonoid fraction (PFF) at 5, 20, 80 and 320 mg/kg per day for 10 consecutive days. On the 11th day, cheek pouches of anaesthetized animals were prepared for intravital microscopy.3. Local ischaemia was obtained by clamping the neck of the everted pouch and the increase in microvascular permeability was quantified as leakage (leaks) of intravenously injected fluorescein isothiocyanate‐labelled dextran (FITC–dextran 150; MW = 150 000).4. Reperfusion, after 30 min ischaemia, resulted in an immediate but reversible increase in post‐capillary leakage. The MPFF induced a significant dose‐related reduction in the increased permeability, with 83.4% inhibition compared with control at 320 mg/kg per day (19.2 ± 1.9 vs 115.7 ± 4.1 leaks/cm2; P < 0.0001). Non‐micronized PFF was significantly less effective: only 47.9% inhibition compared with control was observed at 320 mg/kg per day (60.3 ± 1.0 vs 115.7 ± 4.1 leaks/cm2; P < 0.0001) and there was no dose–effect relationship.5. In conclusion, micronization significantly enhances the protective effects of the purified flavonoid fraction on reperfusion injury in the hamster cheek pouch. This improvement is likely to be related to the better absorption of the micronized formulation, which could explain the superior clinical efficacy shown in previous studies.
PROTEINS OF THE BCL‐2 FAMILY IN APOPTOSIS SIGNALLING: FROM MECHANISTIC INSIGHTS TO THERAPEUTIC OPPORTUNITIES
Authors: Chan Shing‐Leng , Yu Victor C 
Published: February 2004

SUMMARY1. Proteins of the Bcl‐2 family are central regulators of apoptosis and are thought to act primarily on the mitochondria.2. Members of the Bcl‐2 family possess either anti‐apoptotic or pro‐apoptotic function. They are characterized by the presence of conserved sequence motifs, known as Bcl‐2 homology (BH) domains. Anti‐apoptotic members share all four BH domains, designated as BH1‐4; the multidomain pro‐apoptotic members contain BH1‐3 domains, whereas another subgroup of pro‐apoptotic members only have a BH3 domain.3. The BH3‐only proteins act as sensors for distinct apoptosis pathways, whereas multidomain pro‐apoptotic Bax and Bak are executioners of death orders relayed by the BH3‐only proteins.4. Anti‐apoptotic Bcl‐2 family members appear to function, at least in part, by interacting with and antagonizing pro‐apoptotic family members. The BH1‐3 domains of BclXL form an elongated hydrophobic groove, which is the docking site for the BH3 domains of pro‐apoptotic binding partners.5. The deregulation of the various Bcl‐2 proteins has been implicated in many pathological conditions.6. Knowledge derived from the understanding of the function and regulation of the Bcl‐2 family of proteins has allowed us to contemplate new therapeutic strategies for diseases where apoptosis signalling mechanisms can potentially be manipulated.7. The anti‐apoptotic Bcl‐2 members have been targeted successfully using an antisense approach, BH3‐peptides and small molecular weight chemicals that are inhibitors of their anti‐apoptotic function.
Different voices: Reviewing and revising the politics of working with consumers in mental health
Authors: McAllister Margaret , Walsh Kenneth 
Published: February 2004

ABSTRACT:
Working with consumers is now a common expectation in contemporary mental health services. Yet health professionals may not entirely understand the difference between patient and consumer roles. Alternatively, they may feel they do not have the skills or resources to deal with people in roles other than patient or carer. Nor may they be able to separate out their personal experiences with particular consumers from the ideals and goals for effective consumer partnerships. This paper reviews a concept known as the politics of difference as well as the rise of the consumer movement in order to explore areas of difference between consumers and providers, to reexamine how power and marginalization practices occur. It reminds professionals that generalizing from one failed experience relating with a consumer is just as invalid as idealizing the current policy of consumer inclusion. Inviting, allowing, amplifying and improving the effectiveness of the consumer voice in mental health services today requires active commitment, educative processes and novel strategies to move beyond superficial relationships so that consumers and professionals work together to make enduring change.