bluuebunny/crossref_metadata_2025_split huggingface dataset:
Enhanced pulmonary and active skeletal muscle gas exchange during intense exercise after sprint training in men
Authors: McKenna Michael J. , Heigenhauser George J. F. , McKelvie Robert S. , Obminski George , MacDougall J. Duncan , Jones Norman L. 
Published: September 2004

This study investigated the effects of 7 weeks of sprint training on gas exchange across the lungs and active skeletal muscle during and following maximal cycling exercise in eight healthy males.
Pulmonary oxygen uptake (V̇O2) and carbon dioxide output (V̇CO2) were measured before and after training during incremental exercise (n= 8) and during and in recovery from a maximal 30 s sprint exercise bout by breath‐by‐breath analysis (n= 6). To determine gas exchange by the exercising leg muscles, brachial arterial and femoral venous blood O2 and CO2 contents and lactate concentration were measured at rest, during the final 10 s of exercise and during 10 min of recovery.
Training increased (P < 0.05) the maximal incremental exercise values of ventilation (V̇E, by 15.7 ± 7.1%), V̇CO2 (by 9.3 ± 2.1%) and V̇O2 (by 15.0 ± 4.2%). Sprint exercise peak power (3.9 ± 1.0% increase) and cumulative 30 s work (11.7 ± 2.8% increase) were increased and fatigue index was reduced (by −9.2 ± 1.5%) after training (P < 0.05). The highest V̇E, V̇CO2 and V̇O2 values attained during sprint exercise were not significantly changed after training, but a significant (P < 0.05) training effect indicated increased V̇E(by 19.2 ± 7.9%), V̇CO2(by 9.3 ± 2.1%) and V̇O2(by 12.7 ± 6.5%), primarily reflecting elevated post‐exercise values after training.
Arterial O2 and CO2 contents were lower after training, by respective mean differences of 3.4 and 21.9 ml l−1 (P < 0.05), whereas the arteriovenous O2 and CO2 content differences and the respiratory exchange ratio across the leg were unchanged by training.
Arterial whole blood lactate concentration and the net lactate release by exercising muscle were unchanged by training.
The greater peak pulmonary V̇O2 and V̇CO2 with sprint exercise, the increased maximal incremental values, unchanged arterial blood lactate concentration and greater sprint performance all point strongly towards enhanced gas exchange across the lungs and in active muscles after sprint training. Enhanced aerobic metabolism after sprint training may contribute to reduced fatigability during maximal exercise, whilst greater pulmonary CO2 output may improve acid‐base control after training.
Modulation of stimulus—secretion coupling in single rat gonadotrophs
Authors: Thomas Paul , Waring Dennis W. 
Published: September 2004

Exocytosis and intracellular [Ca2+] were determined simultaneously in single anterior pituitary gonadotrophs from ovariectomized female rats. Dispersed cells were cultured for 2–4 days with or without 0.2 nm oestradiol‐17 β (E2) before use. Cells were stimulated with either gonadotrophin releasing hormone (GnRH) or by membrane depolarization. Exocytosis was determined from the change in membrane capacitance (Cm) using the perforated‐patch whole‐cell recording technique. Intracellular [Ca2+] was measured using fura‐2 fluorescence.
The exocytotic response to 1 nm GnRH was characterized by a wide spectrum of responses, ranging from exocytotic bursts to relatively slow, graded increases that were dependent on the evoked intracellular Ca2+ pattern. A kinetic model is presented that incorporates the observed steep dependence of exocytosis on measured intracellular [Ca2+]; simulated exocytosis reasonably approximated observed exocytotic responses, both kinetically and quantitatively. The model also suggests that the modulatory effects of E2 are brought about either by a change in the Ca2+ sensitivity of exocytosis or by a preferential clustering of docked‐secretory granules close to sites of Ca2+ release. The results suggest that in gonadotrophs an oscillatory Ca2+ signal is sensed by the exocytotic apparatus in a modified form of digital encoding.
Exocytosis in E2‐treated cells was 3‐fold greater than in non‐treated cells for GnRH‐evoked secretion, and 38% greater for depolarization; however, there was no effect of E2 on the intracellular Ca2+ response to either stimulus. The results show that maximum expression of the effect of E2 on exocytosis requires activation of GnRH‐dependent pathways.
Extracellular glucose turnover in the striatum of unanaesthetized rats measured by quantitative microdialysis
Authors: Fray Anne E. , Boutelle Martyn , Fillenz Marianne 
Published: September 2004

Steady‐state and time‐resolved quantitative microdialysis was used to measure dialysate concentration, extracellular concentration and the in vivo recovery of glucose in rat striatum.
The extracellular concentration of glucose, determined by the zero net flux method of Lönnroth, was 350 ± 20 μm and the in vivo recovery was 39 ± 2%.
Veratridine caused a steep decrease in dialysate glucose after an initial delay of 7.5 min. When steady‐state glucose levels had been reached in the presence of veratridine the extracellular concentration was reduced to zero, but there was no significant change in in vivo recovery.
Measurement of the dynamic changes during the administration of veratridine showed an immediate decrease in extracellular glucose concentration and a steep rise in in vivo recovery, which accounted for the delay in the decrease in dialysate glucose. When extracellular concentration reached zero, in vivo recovery returned to control levels.
On the nature of anomalous rectification in thalamocortical neurones of the cat ventrobasal thalamus in vitro
Authors: Williams Stephen R. , Turner Jonathan P. , Hughes Stuart W. , Crunelli Vincenzo 
Published: September 2004

Intracellular sharp electrode current clamp and discontinuous single electrode voltage clamp recordings were made from thalamocortical neurones (n= 57) of the cat ventrobasal thalamus in order to investigate the mechanisms underlying anomalous rectification.
Under current clamp conditions, voltage‐current (V–I) relationships in a potential range of −55 to −110 mV demonstrated anomalous rectification with two components: fast rectification, which controlled the peak of negative voltage deviations, and time‐dependent rectification. Time‐dependent rectification was apparent as a depolarizing sag generated during the course of negative voltage deviations, was first formed at potentials in the range −60 to −70 mV, and was sensitive to 3 mm Cs+ (n= 6). Similarly, under voltage clamp conditions, instantaneous and steady‐state I–V relationships demonstrated anomalous rectification. A slowly activating inward current with an activation threshold in the range of −65 to −70 mV formed time‐dependent rectification. This current was sensitive to Cs+ (3 mm) (n= 3) and had properties similar to the slow inward mixed cationic current (Ih).
4‐(N‐Ethyl‐N‐phenylamino)‐l,2‐dimethyl‐6‐(methylamino)‐pyrimidinium chloride (ZD7288) (100–300 μm) irreversibly blocked time‐dependent rectification mediated by Ih (n= 23 of 25 neurones), and led to a hyperpolarization of the resting membrane potential (6.8 ± 0.5 mV). In the presence of ZD 7288, V–I and I–V relationships exhibited fast anomalous rectification, first activated from potential more negative than −80 mV.
Ba2+ (100 μm) (n= 8), in the continuous presence of ZD 7288, reversibly linearized peak V–I and instantaneous I–V relationships over a potential range of −70 to −120 mV, and led to a membrane depolarization (13.3 ± 4.2 mV) or tonic inward current (192 ± 36 pA).
The co‐application of ZD 7288 and Ba2+ revealed a depolarizing sag in negative voltage deviations under current clamp conditions, or a large inward current with kinetics two to three times slower than those of Ih under voltage clamp conditions. This novel form of time‐dependent rectification was first apparent at potentials more negative than about −85 mV, was sensitive to 5 mm Cs+ (n= 4), and is termed Ih,slow. Ih,slow tail currents reversed between −65.3 and −56.6 mV (with potassium acetate electrodes, n= 3) or −57.6 and −50.3 mV (with KCl electrodes, n= 3).
Computer simulations confirmed that the pattern of anomalous rectification in thalamocortical neurones of the cat ventrobasal thalamus is mediated by the concerted action of Ih and a Ba2+ ‐sensitive current with properties similar to an inwardly rectifying K+ current (IKIR).
Phasic activity in the human erector spinae during repetitive hand movements
Authors: Zedka Milan , Prochazka Arthur 
Published: September 2004

Phasic activity in the human back muscle erector spinae (ES) was studied during repetitive hand movements. The hand movements were elicited voluntarily by the subject or induced passively by the experimenter through a servomotor or through cyclical electrical stimulation of muscles acting about the wrist. The aim of the study was to determine whether the rhythmical activation of ES was of supraspinal, intersegmental or segmental origin.
When voluntary rhythmical hand movements were performed as fast as possible, cyclical ES EMG bursts occurred at the same frequency. This frequency was significantly higher than that reached when the task was to contract the back muscles as rapidly as possible. This suggests that the ES activity during the fast hand movements was not generated by direct commands descending to the ES muscles from the motor area of the cerebral cortex responsible for voluntary back muscle activation.
During imposed rhythmical hand movements, ES EMG bursts remained entrained to the hand movements, even when movement frequencies far exceeded those attainable voluntarily either for the hand or the back. This showed that ES EMG responses could be evoked by the hand movements even when these were not generated by descending neural commands. Two alternative mechanisms of ES activation were considered: (a) propriospinal transmission of afferent input entering the spinal cord from the upper extremity; (b) afferent input from ES and other trunk muscles, responding to local oscillations transmitted mechanically from the hand to the lower back.
Activation of ES via proprioceptive signals from the forearm was unlikely since (a) simultaneous electrical stimulation of wrist extensor and wrist flexor muscles did not result in repetitive ES EMG bursting; (b) cyclical vibration of the wrist extensors did not evoke ES EMG bursting; (c) when the forearm was constrained and the hand was moved passively, the lower trunk accelerations and cyclical ES EMG both occurred at a harmonic of the hand movement frequency.
We conclude that the repetitive ES EMG bursting during hand movements was probably due to a local segmental reflex rather than to descending commands. Remote mechanical oscillations of the trunk caused by hand movements evidently elicited proprioceptive reflexes in ES that presumably contributed to trunk stabilization.
Reinterpretation of endothelial cell gaps induced by vasoactive mediators in guinea‐fig, mouse and rat: many are transcellular pores
Authors: Feng Dian , Nagy Janice A. , Hipp John , Pyne Kathryn , Dvorak Harold F. , Dvorak Ann M. 
Published: September 2004

In response to vascular permeabilizing agents, particulates circulating in the blood extravasate from venules through endothelial cell openings. These openings have been thought to be intercellular gaps though recently this view has been challenged.
To define the precise location of endothelial cell gaps, serial section electron microscopy and three‐dimensional reconstructions were performed in skin and cremaster muscle of guinea‐Pigs, mice and rats injected locally with agents that enhance microvascular permeability: vascular permeability factor, histamine or serotonin. Ferritin and colloidal carbon were injected intravenously as soluble and particulate macromolecular tracers, respectively.
Both tracers extravasated from venules in response to all three permeability enhancing agents. The soluble plasma protein ferritin extravasated primarily by way of vesiculo‐vacuolar organelles (VVOs), interconnected clusters of vesicles and vacuoles that traverse venular endothelium. In contrast, exogenous particulates (colloidal carbon) and endogenous particulates (erythrocytes, platelets) extravasated from plasma through transendothelial openings.
Serial electron microscopic sections and three‐dimensional reconstructions demonstrated that eighty‐nine of ninety‐two openings were transendothelial pores, not intercellular gaps. Pore frequency increased 3‐ to 33‐fold when carbon was used as tracer.
The results demonstrate that soluble and particulate tracers extravasate from venules by apparently different transcellular pathways in response to vasoactive mediators. However, some pores may derive from rearrangements of VVOs.
Pathway‐specific effects of calcitonin gene‐related peptide on irideal arterioles of the rat
Authors: Hill C. E. , Gould D. J. 
Published: September 2004

Arteriolar diameter and membrane voltage have been measured to investigate the actions of calcitonin gene‐related peptide (CGRP) in rat irideal arterioles.
Activation of sensory nerves inhibited sympathetic vasoconstriction, reduced the accompanying 40–50 mV depolarization by 90% and caused a 4 mV hyperpolarization.
The inhibition of vasoconstriction was prevented by either preincubation in l‐NAME (10 μm), to inhibit nitric oxide production, by preincubation in the cell‐permeant adenylate cyclase inhibitor dideoxyadenosine (1 mm) or by preincubation in the ATP‐sensitive potassium channel blocker glibenclamide (10 μM). The subsequent addition of a nitric oxide donor to the glibenclamide solution inhibited nerve‐mediated vasoconstriction, suggesting that the potassium channel involvement preceded the production of nitric oxide. The small hyperpolarization was not affected by l‐NAME.
Nerve‐mediated vasodilatation persisted in the presence of l‐NAME (10 μm) but was abolished with the CGRP1 receptor antagonist CGRP8–37.
In arterioles preconstricted with the α2‐adrenoceptor agonist UK‐14304 (100 nm), exogenous CGRP caused a hyperpolarization and a dose‐dependent vasodilatation, neither of which was affected by l‐NAME (10 μm).
In arterioles preconstricted with 30 mm KCl, CGRP (10 nm) caused vasodilatation but not hyperpolarization, suggesting that the hyperpolarization was not causal to the vasodilatation.
Forskolin (30 nm), in the presence of l‐NAME to prevent effects due to nitric oxide, caused vasodilatation.
These results suggest that CGRP inhibits sympathetic nerve‐mediated vasoconstriction through sequential increases in cyclic AMP and nitric oxide, while vasodilatation results from increases in cyclic AMP alone. The production of nitric oxide, but not its mechanism of action, appears to be dependent on the activation of ATP‐sensitive potassium channels. The possible sites of action of these two pathways are discussed.
Sympathetic and parasympathetic interaction in vascular and secretory control of the nasal mucosa in anaesthetized dogs
Authors: Revington Maureen , Lacroix J. Silvain , Potter Erica K. 
Published: September 2004

In dogs anaesthetized with pentobarbitone, electrical stimulation of the parasympathetic nerve fibres to the nasal mucosa evoked frequency dependent increases in both nasal arterial blood flow and nasal secretion. Blood flow was measured using a transonic flow probe placed around the artery.
Sympathetic nerve stimulation for 3 min at 10 Hz evoked significant and prolonged (> 30 min) attenuation of the vasodilator and secretory responses to subsequent parasympathetic stimulation.
Intravenous and intranasal administration of the neuropeptide Y (NPY) analogue N‐acetyl [Leu28,Leu31] NPY 24–36, a selective NPY Y2 receptor agonist (20 nmol kg−1), significantly attenuated both vasodilator and secretory effects of subsequent parasympathetic nerve stimulation. When given intravenously, the inhibitory effect of this Y2 receptor agonist on vascular and secretory effects of parasympathetic nerve stimulation was rapid in onset (5 min) and lasted for more than 60 min. The modulatory effect of the Y2 receptor agonist was also seen with intranasal administration, but was slower in onset (15 min), and lasted less than 45 min. The effects of the intranasal pretreatment with the Y2 receptor agonist were significantly prolonged in the presence of the endopeptidase inhibitor phosphoramidon (10 nm).
Atropine pretreatment did not significantly reduce the change in vascular conductance evoked by parasympathetic nerve stimulation. Subsequent pretreatment with the NPY Y2 receptor agonist N‐acetyl [Leu28,Leu31] NPY 24–36 reduced the stimulation induced increase in conductance by 30%. Nasal secretion was reduced by 70% following pretreatment with atropine and a further 30% by pretreatment with the NPY Y2 receptor agonist. Dose dependent vasodilator and secretory effects of local intra‐arterial infusion of acetylcholine and vasoactive intestinal peptide were not modified by the NPY Y2 agonist.
Total protein and albumin concentration were measured in nasal lavage fluid collected after nerve stimulation. Atropine pretreatment increased the percentage of the total protein that was albumin in nasal lavage fluid. Neither sympathetic nerve stimulation nor Y2 receptor agonist pretreatment further modified the albumin exudation (a marker of vascular permeability) in nasal fluid lavage collected after parasympathetic nerve stimulation.
We propose that sympathetic nerve stimulation releases NPY, which acts on Y2 receptors, probably located on parasympathetic nerve endings, to attenuate both vasodilatation and nasal secretion evoked by subsequent parasympathetic nerve stimulation. This effect is also observed after pretreatment with the Y2‐selective NPY analogue N‐acetyl [Leu28,Leu31] NPY 24–36.
Serving seniors better: service guidelines for general practitioners
Authors: Pettigrew Simone , Mizerski Katherine , Donovan Robert 
Published: September 2004

Objective:  Generate a list of service guidelines that will enable general practitioners (GPs) to appreciate and accommodate the needs of older patients. Method:  Focus groups and a national telephone survey were conducted with Australian seniors to generate 10 service guidelines for GPs. Results:  The issues covered by the 10 guidelines are considered highly important by Australian seniors, with some apparent differences in ratings between age categories. Conclusion:  Seniors have distinct preferences for the ways they wish to interact with their GPs. In particular, they seek prompt referrals and up‐to‐date medical knowledge.
Healthy ageing: how is it defined and measured?
Authors: Peel Nancye , Bartlett Helen , McClure Roderick 
Published: September 2004

A review of existing studies which defined and measured healthy ageing as an outcome was undertaken to clarify the term for the purposes of informing policy development and further research into positive health outcomes in older age. Studies which measured the prevalence of healthy (or successful) ageing in population‐based settings were identified from a search of health and gerontology databases. Eighteen studies met the selection criteria. The arbitrary nature of the definition, populations sampled, domains selected and measures within the domains resulted in considerable variation between the studies in the proportion of the study population classified as ‘healthy ageing’, which ranged from 3% to 80%. The present review shows the need to establish a standard for defining and quantifying the concept of healthy ageing. Despite the differences, there was consensus in the studies that the multidimensional, positive health outcome should measure the capacity to function well and adapt to environmental challenges in domains assessing physical, mental and social well‐being.
It is part of your life until you die: older refugees in Australia
Authors: Hugman Richard , Bartolomei Linda , Pittaway Eileen 
Published: September 2004

Objective:  To explore perceptions of the issues facing older refugees, from the perspective of older refugees themselves and from workers in their communities who assist them. Method:  A qualitative approach, consisting of five focus groups with older refugees, and 10 interviews and one focus group with community workers. Results:  The impact of being a refugee can be seen in the effects of trauma and of forced migration on the experience of growing old. Conclusion:  Older refugees have a sense of ‘ageing in the wrong place’, to which policy and practice need to respond.
Using the Nursing Home Behaviour Problem Scale in an Australian residential care setting
Authors: Crotty Maria , Halbert Julie , Giles Lynne C , Birks Robert , Lange Kylie , Whitehead Craig H 
Published: September 2004

Objective:  To report on the validity of the Nursing Home Behaviour Problem Scale (NHBPS) in an Australian residential care setting. Method:  Cluster randomised controlled trial. As part of this, questionnaires were administered to residential care staff concerning participating residents. The study was carried out in 20 residential care facilities (10 hostels, 10 nursing homes) in metropolitan Adelaide, South Australia. Staff closely associated with the resident's care completed 694 questionnaires. Internal consistency of the scale was examined along with exploratory and confirmatory factor analysis to determine the validity of the NHBPS in the Australian setting. Results:  Analyses indicated that four of the 29 questions should be excluded from the Australian version of the NHBPS. Factor analysis demonstrated five factors accounting for 25 of the questions, grouped around behaviours of uncooperative, inappropriate, attention seeking, unsafe, and agitation. Conclusions:  There is a need for patient‐specific outcome measures, particularly measuring difficult behaviours, for use in residential care settings. Despite the similarities in the prevalence of disturbed behaviours, we were unable to reproduce the six factors reported in the original validation of the instrument, possibly due to differences between the USA and Australia. The results indicate the number of questions should be reduced to 25 in the Australian version of the NHBPS.