bluuebunny/crossref_metadata_2025_split huggingface dataset:
Using fish-processing time to carry out acoustic surveys from commercial vessels
Authors: O'Driscoll Richard L. , Macaulay Gavin J. 
Published: January 2005

Abstract
In some fisheries large factory freezer trawlers have periods of down time as the catch is processed. By utilizing this time, scientific acoustic surveys can be carried out between commercial-fishing operations without compromising fishing success. Examples are presented from three acoustic surveys for hoki (Macruronus novaezelandiae) in New Zealand waters during 2002 and 2003 conducted from a commercial vessel fitted with a scientifically calibrated SIMRAD ES-60 echosounder. These surveys confirmed the presence of a new spawning area for hoki and provided biomass estimates from known fishing grounds. The approach described works well for small-scale acoustic surveys adjacent to areas of high catch rates and is cost-effective because the vessel “pays for itself” by fishing commercially. The major limitation is that the boundaries of the survey area are determined by the time available during processing, which is related to the size of the catch and the time required to search for a suitable location for the next commercial trawl. In the New Zealand hoki surveys, processing time was typically 3–8 h, which was sufficient to carry out about 10–70 km of acoustic transects. Acoustic research was also limited to periods of relatively good conditions by the use of a hull-mounted transducer.
Effects of preceding birth intervals on neonatal, infant and under‐five years mortality and nutritional status in developing countries: evidence from the demographic and health surveys
Authors: Rutstein S.O. 
Published: January 2005

AbstractObjectiveThis paper examines the association between birth intervals and infant and child mortality and nutritional status.MethodsRepeated analysis of retrospective survey data from the Demographic and Health Surveys (DHS) program from 17 developing countries collected between 1990 and 1997 were used to examine these relationships. The key independent variable is the length of the preceding birth interval measured as the number of months between the birth of the child under study (index child) and the immediately preceding birth to the mother, if any. Both bivariate and multivariate designs were employed. Several child and mother‐specific variables were used in the multivariate analyses in order to control for potential bias from confounding factors. Adjusted odds ratios were calculated to estimate relative risk.ResultsFor neonatal mortality and infant mortality, the risk of dying decreases with increasing birth interval lengths up to 36 months, at which point the risk plateaus. For child mortality, the analysis indicates that the longer the birth interval, the lower the risk, even for intervals of 48 months or more. The relationship between chronic malnutrition and birth spacing is statistically significant in 6 of the 14 surveys with anthropometric data and between general malnutrition and birth spacing in 5 surveys. However, there is a clear pattern of increasing chronic and general undernutrition as the birth interval is shorter, as indicated by the averages of the adjusted odds ratios for all 14 countries.ConclusionConsidering both the increased risk of mortality and undernutrition for a birth earlier than 36 months and the great number of births that occur with such short intervals, the author recommends that mothers space births at least 36 months. However, the tendency for increased risk of neonatal mortality for births with intervals of 60 or more months leads the author to conclude that the optimal birth interval is between 36 and 59 months. This information can be used by health care providers to counsel women on the benefits of birth spacing.
The HDL2/HDL3 ratio in menopause
Authors: Ushiroyama T. , Sakuma K. , Ikeda A. , Ueki M. 
Published: January 2005

AbstractObjectivesThe influence of the menopause on the HDL2/HDL3 ratio was assessed in association with hypertriglyceridemia.MethodsFasting blood samples were collected from 607 patients. Commercially available enzymatic methods were used for determination of TG, and total HDL‐C. HDL2 and HDL3 were measured by ultracentrifugation.ResultsThe HDL2/HDL3 ratio had a strong negative correlation with TG (r=−0.272, P<0.0001 and r=‐0.314, P<0.0001) in both pre‐ and postmenopausal women. No significant differences were observed in HDL2, HDL3, and HDL2/HDL3 ratio between pre‐ and postmenopausal women without hypertriglyceridemia. Postmenopausal women had a significantly higher HDL2/HDL3 ratio than premenopausal women with hypertriglyceridemia.ConclusionsThese results indicate that menopausal status not only increases plasma LDL‐cholesterol and triglyceride levels, but also increases the HDL2/HDL3 ratio when associated with elevation of plasma triglyceride levels. These changes may increase the risk for CHD due to enlargement of the lipid pool.
Ultrasound stimulation of tendon cell proliferation and upregulation of proliferating cell nuclear antigen
Authors: Tsai Wen‐Chung , Hsu Chih‐Chin , Tang Fuk‐Tan , Chou Shih‐Wei , Chen Ying‐Jen , Pang Jong‐Hwei S. 
Published: January 2005

AbstractTherapeutic ultrasound has been widely used in sports‐related tendon injuries. However, previous research has not examined the molecular mechanism of this therapeutic effect on tendon cell proliferation. This study was designed to determine the in vitro effect of ultrasound on the proliferation of tendon cells intrinsic to rat Achilles tendon. Furthermore, the existence of a correlation between this effect and the expression of the proliferating cell nuclear antigen (PCNA) was also examined. Using cultured tendon cells, cell viability was evaluated by MTT assay. The expression of PCNA protein in cells was evaluated by immunocytochemistry. The mRNA expression of PCNA was determined by reverse transcniption‐polymerase chain reaction (RT‐PCR). A dose‐dependent increase in the cellularity of tendon cells by either, pulsed or continuous mode ultrasound was demonstrated by MTT assay (p = 0.044 for the pulsed mode; p = 0.004 for the continuous mode). Ten minutes of treatment achieved maximum cellularity compared to 5 min of treatment time (p = 0.010 for pulsed ultrasound; p = 0.004 for continuous ultrasound). Immunocyto‐chemical staining revealed that ultrasound treated tendon cells were stained more strongly for PCNA than were control cells. Upregulation of PCNA at the mRNA level was also confirmed by RT‐PCR. In conclusion, ultrasound stimulates tendon cell proliferation in a process that is probably mediated by the upregulation of PCNA. © 2004 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved.
Postsynaptic 5‐HT1B receptors modulate electroshock‐induced generalised seizures in rats
Authors: Stean Tania O , Atkins Alan R , Heidbreder Christian A , Quinn Leann P , Trail Brenda K , Upton Neil 
Published: January 2005

Although an important regulatory role for serotonin (5‐HT) in seizure activation and propagation is well established, relatively little is known of the function of specific 5‐HT receptor subtypes on seizure modulation.
The aim of the present study was to investigate the role of 5‐HT1A, 1B and 1D receptors in modulating generalised seizures in the rat maximal electroshock seizure threshold (MEST) test.
The mixed 5‐HT receptor agonists SKF 99101 (5–20 mg kg−1 i.p.) and RU 24969 (1–5 mg kg−1 i.p.), 0.5 h pretest, both produced marked dose‐related increases in seizure threshold. These agents share high affinity for 5‐HT1A, 1B and 1D receptors.
Antiseizure effects induced by submaximal doses of these agonists were maintained following p‐chlorophenylalanine (150 mg kg−1 i.p. × 3 days)‐induced 5‐HT depletion.
The anticonvulsant action of both SKF 99101 (15 mg kg−1 i.p.) and RU 24969 (2.5 mg kg−1 i.p.) was dose‐dependently abolished by the selective 5‐HT1B receptor antagonist SB‐224289 (0.1–3 mg kg−1 p.o., 3 h pretest) but was unaffected by the selective 5‐HT1A receptor antagonist WAY 100635 (0.01–0.3 mg kg−1 s.c., 1 h pretest). This indicates that 5‐HT1B receptors are primarily involved in mediating the anticonvulsant properties of these agents.
In addition, the ability of the 5‐HT1B/1D receptor antagonist GR 127935 (0.3–3 mg kg−1 s.c., 60 min pretest) to dose‐dependently inhibit SKF 99101‐induced elevation of seizure threshold also suggests possible downstream involvement of 5‐HT1D receptors in the action of this agonist, although confirmation awaits the identification of a selective 5‐HT1D receptor antagonist.
Overall, these data demonstrate that stimulation of postsynaptic 5‐HT1B receptors inhibits electroshock‐induced seizure spread in rats.

British Journal of Pharmacology (2005) 144, 628–635. doi:10.1038/sj.bjp.0706027
Effects of NS1608, a BKCa channel agonist, on the contractility of guinea‐pig urinary bladder in vitro
Authors: Mora Ticiana Camila , Suarez‐Kurtz Guilherme 
Published: January 2005

The functional effects of NS1608 ((N‐(3‐(trifluoromethyl)phenyl)‐N′‐(2‐hydroxy‐5‐chlorophenyl)urea), an opener of the large conductance, Ca2+‐activated K+ (BKCa) channel, on the contractility of guinea‐pig urinary bladder muscle are described.
NS1608 (0.3–30 μM) had no significant effect on the integrated myogenic activity (tension integral) or the electrically evoked twitches of detrusor muscle strips. Possible mechanisms for the discrepancy between the lack of functional effects of NS1608 per se on detrusor contractility and this drug's agonistic effect on BKCa currents in isolated bladder myocytes are discussed.
4‐Aminopyridine (1 mM), a blocker of voltage‐gated K+ (KV) channels, increased the tension integral 2.7‐fold, on average. NS1608 (30 μM) counteracted this effect.
Apamin (100 nM), a selective blocker of the small conductance, Ca2+‐activated K+ (SKCa) channel, increased the tension integral 1.7‐fold, on average. This effect was reversed by NS1608 (30 μM).
Ryanodine (10 μM), a modulator of the sarcoplasmic reticulum (SR) Ca2+‐release channel, increased the tension integral 1.9‐fold, on average. This effect was reversed by NS1608 (30 μM).
Iberiotoxin (IbTX, 50 nM), a selective blocker of the BKCa channel, caused additional increases in the tension integral of detrusor strips pretreated with apamin or ryanodine and prevented the inhibitory effects of NS1608 (30 μM) in detrusor contractility.
The present study shows that blockade of repolarizing currents carried by, respectively apamin‐ and 4‐aminopyridine‐sensitive K+ channels unmasks an activation of BKCa in guinea‐pig urinary bladder smooth muscle strips.

British Journal of Pharmacology (2005) 144, 636–641. doi:10.1038/sj.bjp.0706034
AT2 receptors mediate tonic renal medullary vasoconstriction in renovascular hypertension
Authors: Duke Lisa M , Widdop Robert E , Kett Michelle M , Evans Roger G 
Published: January 2005

Renal medullary blood flow is relatively insensitive to angiotensin II (Ang II)‐induced vasoconstriction, due partly to AT1‐mediated release of nitric oxide and/or prostaglandins. AT2‐receptor activation appears to blunt AT1‐mediated vasodilatation within the medullary circulation. This could affect long‐term efficacy of antihypertensive pharmacotherapies targeting the renin/angiotensin system, particularly in Ang II‐dependent forms of hypertension.
We tested the effects of AT1‐ and AT2‐receptor blockade on basal cortical and medullary laser Doppler flux (CLDF and MLDF), and on responses to renal arterial infusion of Ang II, in rats with 2 kidney, 1 clip (2K1C) hypertension and sham‐operated controls. Studies were carried out in thiobutabarbital (175 mg kg−1, i.p.) anaesthetised rats, 4 weeks after clipping, or sham surgery (n=6 in each of eight groups).
Candesartan (10 μg kg−1 h−1, intravenous (i.v.)) reduced mean arterial pressure (∼17%) and increased CLDF (∼24%), similarly in both sham and 2K1C rats, but did not significantly affect MLDF. PD123319 (1 mg kg−1 h−1, i.v.) increased basal MLDF (19%) in 2K1C but not sham rats, without significantly affecting other variables.
In sham rats, renal arterial infusion of Ang II (1–100 ng kg−1 min−1) dose dependently decreased CLDF (up to 44%), but did not significantly affect MLDF. These effects were markedly blunted in 2K1C rats. After PD123319, Ang II dose dependently increased MLDF (up to 38%) in sham but not 2K1C rats. Candesartan abolished all effects of Ang II, including those seen after PD123319.
Our data indicate that AT1 receptors mediate medullary vasodilatation, which is opposed by AT2‐receptor activation. In 2K1C hypertension, AT2‐receptor activation tonically constricts the medullary circulation.

British Journal of Pharmacology (2005) 144, 486–492. doi:10.1038/sj.bjp.0706036
Role of central and peripheral adenosine receptors in the cardiovascular responses to intraperitoneal injections of adenosine A1 and A2A subtype receptor agonists
Authors: Schindler Charles W , Karcz‐Kubicha Marzena , Thorndike Eric B , Müller Christa E , Tella Srihari R , Ferré Sergi , Goldberg Steven R 
Published: January 2005

The cardiovascular effects of the adenosine A1 receptor agonist N6‐cyclopentyladenosine (CPA) and the adenosine A2A receptor agonist 2‐p‐(2‐carboxyethyl)phenethylamino‐5′‐N‐ethylcarboxamidoadenosine (CGS 21680) were investigated in rats implanted with telemetry transmitters for the measurement of blood pressure and heart rate.
Intraperitoneal (i.p.) injections of the adenosine A1 receptor agonist CPA led to dose‐dependent decreases in both blood pressure and heart rate. These effects of 0.3 mg kg−1 CPA were antagonized by i.p. injections of the adenosine A1 receptor antagonist 8‐cyclopentyl‐1,3‐dimethyl‐xanthine (CPT), but not by i.p. injections of the adenosine A2A receptor antagonist 3‐(3‐hydroxypropyl)‐8‐(m‐methoxystyryl)‐7‐methyl‐1‐propargylxanthine phosphate disodium salt (MSX‐3). Injections (i.p.) of the peripherally acting nonselective adenosine antagonist 8‐sulfophenyltheophylline (8‐SPT) and the purported nonselective adenosine antagonist caffeine also antagonized the cardiovascular effects of CPA.
The adenosine A2A agonist CGS 21680 given i.p. produced a dose‐dependent decrease in blood pressure and an increase in heart rate. These effects of 0.5 mg kg−1 CGS 21680 were antagonized by i.p. injections of the adenosine A2A receptor antagonist MSX‐3, but not by i.p. injections of the antagonists CPT, 8‐SPT or caffeine.
Central administration (intracerebral ventricular) of CGS 21680 produced an increase in heart rate, but no change in blood pressure. MSX‐3 given i.p. antagonized the effects of the central injection of CGS 21680.
These results suggest that adenosine A1 receptor agonists produce decreases in blood pressure and heart rate that are mediated by A1 receptors in the periphery, with little or no contribution of central adenosine A1 receptors to those effects.
The heart rate increasing effect of adenosine A2A agonists appears to be mediated by adenosine A2A receptors in the central nervous system. The blood pressure decreasing effect of adenosine A2A agonists is most probably mediated in the periphery.

British Journal of Pharmacology (2005) 144, 642–650. doi:10.1038/sj.bjp.0706043
Selective release of ATP from sympathetic nerves of rat vas deferens by the toxin TsTX‐I from Brazilian scorpion Tityus serrulatus
Authors: Conceição Isaltino M , Jurkiewicz Aron , Fonseca Daniela R , Opperman Andrea R , Freitas Thalma A , Lebrun Ivo , Garcez‐do‐Carmo Lúcia 
Published: January 2005

The effects of the main component of the Tityus serrulatus scorpion venom, toxin TsTX‐I, were studied on the contractility and release of neurotransmitters in the rat vas deferens. Since TsTX‐I is known to act on sodium channels, we used veratridine, another sodium channel agent, for comparison.
Toxin TsTX‐I induced concentration‐dependent contractions with an EC50 value of 47.8±0.1 nM and a maximum effect of 84.4±10.4% of that for BaCl2.
Contractions by TsTX‐I were abolished by denervation or tetrodotoxin (0.1 μM), showing that the toxin effects depend on the integrity of sympathetic nerve terminals.
To check for the presence of a noradrenergic component, experiments were conducted after removal of adrenergic stores in nerve terminals by reserpinization (10 mg kg−1, 24 h prior to experiments) or blockade of α1 adrenoceptors by prazosin (30 μM), showing that these procedures did not modify the response to TsTX‐I, and therefore that adrenoceptors were not involved in contractions.
To check for the presence of a purinergic component, experiments were carried out after blockade of P2X receptors by suramin (0.1 mM) or desensitization by α,β‐methylene‐ATP (30 μM). These agents greatly abolished the contractile response to TsTX‐I (about 83% by desensitization and 96% by suramin), showing the involvement of purinergic receptors.
The release of noradrenaline and purinergic agents (ATP, ADP, AMP and adenosine) was detected by HPLC. Together, the total release of purines in the presence of TsTX‐I was about 42 times higher than in the control group. In contrast, TsTX‐I did not modify the overflow of noradrenaline, showing that the release was selective for purines.
The release of purinergic agents was reduced by the N‐type calcium channel blocker ω‐conotoxin GVIA (1 μM) and by the P/Q‐type blocker ω‐conotoxin MVIIC (1 μM), showing that the effects of TsTX‐I are calcium‐dependent.
The results show that TsTX‐I produced a selective release of purines from postganglionic sympathetic nerves in the rat vas deferens.

British Journal of Pharmacology (2005) 144, 519–527. doi:10.1038/sj.bjp.0706062
Vasomotion: cellular background for the oscillator and for the synchronization of smooth muscle cells
Authors: Aalkjær Christian , Nilsson Holger 
Published: January 2005

Vasomotion is the oscillation of vascular tone with frequencies in the range from 1 to 20 min−1 seen in most vascular beds. The oscillation originates in the vessel wall and is seen both in vivo and in vitro.
Recently, our ideas on the cellular mechanisms responsible for vasomotion have improved. Three different types of cellular oscillations have been suggested. One model has suggested that oscillatory release of Ca2+ from intracellular stores is important (the oscillation is based on a cytosolic oscillator). A second proposed mechanism is an oscillation originating in the sarcolemma (a membrane oscillator). A third mechanism is based on an oscillation of glycolysis (metabolic oscillator). For the two latter mechanisms, only limited experimental evidence is available.
To understand vasomotion, it is important to understand how the cells synchronize. For the cytosolic oscillators synchronization may occur via activation of Ca2+‐sensitive ion channels by oscillatory Ca2+ release. The ensuing membrane potential oscillation feeds back on the intracellular Ca2+ stores and causes synchronization of the Ca2+ release. While membrane oscillators in adjacent smooth muscle cells could be synchronized through the same mechanism that sets up the oscillation in the individual cells, a mechanism to synchronize the metabolic‐based oscillators has not been suggested.
The interpretation of the experimental observations is supported by theoretical modelling of smooth muscle cells behaviour, and the new insight into the mechanisms of vasomotion has the potential to provide tools to investigate the physiological role of vasomotion.

British Journal of Pharmacology (2005) 144, 605–616. doi:10.1038/sj.bjp.0706084
Addition of a signal peptide sequence to the α1D‐adrenoceptor gene increases the density of receptors, as determined by [3H]‐prazosin binding in the membranes
Authors: Petrovska Ramona , Kapa Ivo , Klovins Janis , Schiöth Helgi B , Uhlén Staffan 
Published: January 2005

Both in mammalian tissues and in transfected cells, only low levels of α1D‐adrenoceptors are detected in radioligand binding studies. It has been implicated that the comparatively long N‐terminal tail of the α1D‐adrenoceptor is responsible for the inefficient surface expression of the receptor.
In the present study, we created gene constructs for six N‐terminally truncated variants of the human α1D‐adrenoceptor. These constructs were used to transfect Neuro2A cells. We show that the density of α1D‐adrenoceptors, observed by [3H]‐prazosin binding, gradually increased with longer truncations of the N‐terminus. This seems to indicate that the long N‐terminal tail nonspecifically interferes with receptor translocation to the plasma membrane.
The addition of a 16 amino acids long signal peptide to the N‐terminus of the wild‐type α1D‐adrenoceptor increased the density of receptor binding sites 10‐fold in Neuro2A and COS‐7 cells. This indicates that, after the addition of a signal peptide, the long N‐terminal tail of the α1D‐adrenoceptor does not interfere with proper translocation of the receptor to the plasma membrane. This, in turn, indicates that the N‐terminal tail of the wild‐type α1D‐adrenoceptor, merely by its long length, hinders the first transmembrane helix of the receptor from being a signal anchor.
Neither the wild‐type α1D‐adrenoceptor (for which the expression level of [3H]‐prazosin binding sites is low) nor the truncated α1D‐adrenoceptor variant (for which the expression level of [3H]‐prazosin binding sites is high) showed any constitutive activity in stimulating inositol phosphate accumulation. This indicates that the low expression level of [3H]‐prazosin binding sites, after transfection with the wild‐type α1D‐adrenoceptor, is not caused by constitutive activity of the receptor and subsequent receptor downregulation.

British Journal of Pharmacology (2005) 144, 651–659. doi:10.1038/sj.bjp.0706087
Effects of connexin‐mimetic peptides on gap junction functionality and connexin expression in cultured vascular cells
Authors: Martin Patricia E M , Wall Colin , Griffith Tudor M 
Published: January 2005

We have investigated the effects of connexin‐mimetic peptides homologous to the Gap 26 and Gap 27 domains of Cxs 37, 40 and 43 against gap junctional communication and connexin expression in rat aortic endothelial cells (RAECs) and A7r5 myocytes.
Immunostaining and Western blot analysis confirmed the presence of gap junction plaques containing Cx43, but not Cx40, in RAECs, whereas plaques containing Cxs 40 and 43 were evident in A7r5 cells. Expression of Cx37 was limited in RAECs and absent from A7r5 cells.
Under control conditions calcein‐loaded RAECs transferred dye to ∼70% of subjacent A7r5 cells after coculture for 4–5 h. Dye transfer was inhibited by a peptide targeted to Cxs 37 and 43 (37,43Gap 27), but minimally affected by peptides targeted to Cxs 37 and 40 (37,40Gap 26 and 40Gap 27). These findings suggest that the myoendothelial gap junctions that couple RAECs and A7r5 cells are constructed principally from Cx43.
Inhibition of dye transfer from RAECs to A7r5 cells cocultured in the presence of 37,43Gap 27 plus 37,40Gap 26 for 5 h was fully reversible.
In A7r5 cells, endogenous expression of Cx40 and Cx43 was unaffected by incubation with 37,43Gap 27, 37,40Gap 26, either individually or in combination, and the peptide combination did not impair connexin trafficking or the de novo formation of gap plaques in A7r5 cells transfected to express Cx43‐GFP.
Treatment of A7r5 cells with 37,43Gap 27 plus 37,40Gap 26 abolished synchronized oscillations in intracellular [Ca2+] induced by the α1‐adrenoceptor agonist phenylephrine.
The reversibility and lack of effect of the peptides on plaque formation suggests that they may be considered ideal probes for functional studies of connexin‐mediated communication in the vascular wall.

British Journal of Pharmacology (2005) 144, 617–627. doi:10.1038/sj.bjp.0706102