bluuebunny/crossref_metadata_2025_split huggingface dataset:
Induction of antioxidant enzyme activity by hyperoxia (60 % O2) in the developing chick embryo
Authors: van Golde Jolanda C. , Borm Paul J. , Wolfs Marion C. , Rhijnsburger Els H. , Blanco Carlos E. 
Published: September 2004

At premature birth, man and animals are exposed to relatively high oxygen levels, compared with intra‐uterine conditions, at a time when their antioxidant enzyme (AOE) system is still immature. Using the chick embryo as a study model, we investigated changes in the AOE system in response to hyperoxia applied at different time points during the incubation period. Relations between hyperoxia and AOE activity were studied in selected organs (brain, heart, liver, intestine and lungs) of developing chick embryos (during the second half of the incubation period).
Incubated White Leghorn eggs were divided into four groups: control (n= 100) and three test groups exposed for 48 h to 60 % O2 on day 10 (test group 1, n= 80), day 14 (test group 2, n= 60) and day 18 (test group 3, n= 30). Superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx) enzyme activities were measured in homogenates of the brain, heart, liver, intestine and lungs.
Exposure to hyperoxia at different time points during incubation resulted in a 2‐ to 10‐fold increase in SOD activity in all organs except the brain. Catalase and GPx enzyme activities were only induced in test group 1, 48 h after initiation of hyperoxia.
In the developing chick embryo, hyperoxia can produce a temporary induction of AOE activity, which is dependent on the AOE, organ, incubation time and time point of exposure.
Ensemble firing of muscle afferents recorded during normal locomotion in cats
Authors: Prochazka Arthur , Gorassini Monica 
Published: September 2004

The main purpose of this study was to collate population data on the firing characteristics of muscle afferents recorded chronically during normal stepping in cats.
Ensemble firing profiles of forty‐seven muscle spindle and tendon organ afferents were compiled from stored data. The relationships between the firing profiles and the displacement and force signals were analysed with the help of mathematical models of the response characteristics of spindle primary and secondary afferents and tendon organs.
Whereas the firing of hamstring spindle afferents could be predicted with reasonable accuracy from the length and velocity signals alone, the firing profiles of triceps surae spindle afferents deviated from the predicted profiles, particularly during electromyogram (EMG) activity. This indicated that the components of fusimotor action linked to extrafusal muscle activity were significant in triceps surae, possibly because this muscle is more strongly recruited in the cat step cycle.
From the limited data available, it was not possible to identify the ‘best’ or most general mathematical function to predict spindle secondary firing. In the two triceps surae spindle secondary units studied, firing was well predicted by using the simplest possible model, rate proportional to displacement, whereas in the hamstring spindle secondary data, a more complex linear transfer function was needed. The results of modelling the spindle secondary data were consistent with a modest amount of phasic, static fusimotor action linked to EMG activity.
The averaged ensemble of tendon organ afferent activity from the triceps surae gave predictions of whole‐muscle force that agreed well with separate triceps force measurements in normal cat locomotion. This supports the idea that ensembles of tendon organ afferents signal whole‐muscle force.
Our overall conclusion is that to a first approximation, large muscle afferents in the cat hindlimb signal muscle velocity, muscle length and muscle force, at least in movements of the speed and amplitude seen in locomotion.
The effect of repeated acute hypoxaemia on fetal cardiovascular development in the sheep
Authors: Steyn Clare , Hanson Mark A. 
Published: September 2004

Hypoxaemia during intrauterine life may be important in the development of cardiovascular diseases in later life. Thus it was the aim of this study to investigate the effect of repeated acute hypoxia on the cardiovascular development and growth of the fetus.
Fourteen fetal sheep (105–109 days gestational age) were instrumented with amniotic and vascular catheters, an electrocardiogram (ECG) electrode and a flow probe around the femoral artery. Seven animals were given repeated acute isocapnic hypoxaemia (Pa,O2 reduced to ca. 13 mmHg) for 1 h every day for 14 days and they were compared to seven animals which remained normoxic throughout with respect to fetal mean arterial blood pressure (MAP), fetal heart rate (FHR), and fetal baro‐ and chemoreflexes.
No differences were found between the two groups of fetuses in FHR, MAP, baro‐ or chemoreflexes, femoral blood flow, femoral vascular resistance or fetal growth.
Repeated acute hypoxaemia of a moderate degree over a period of 2 weeks in late gestation does not affect cardiovascular development or growth in the fetal sheep.
Changes in single motor unit behaviour contribute to the increase in contraction speed after dynamic training in humans
Authors: Van Cutsem Michaël , Duchateau Jacques , Hainaut Karl 
Published: September 2004

The adaptations of the ankle dorsiflexor muscles and the behaviour of single motor units in the tibialis anterior in response to 12 weeks of dynamic training were studied in five human subjects. In each training session ten series of ten fast dorsiflexions were performed 5 days a week, against a load of 30–40 % of the maximal muscle strength.
Training led to an enhancement of maximal voluntary muscle contraction (MVC) and the speed of voluntary ballistic contraction. This last enhancement was mainly related to neural adaptations since the time course of the muscle twitch induced by electrical stimulation remained unaffected.
The motor unit torque, recorded by the spike‐triggered averaging method, increased without any change in its time to peak. The orderly motor unit recruitment (size principle) was preserved during slow ramp contraction after training but the units were activated earlier and had a greater maximal firing frequency during voluntary ballistic contractions. In addition, the high frequency firing rate observed at the onset of the contractions was maintained during the subsequent spikes after training.
Dynamic training induced brief (2–5 ms) motor unit interspike intervals, or ‘doublets’. These doublets appeared to be different from the closely spaced (±10 ms) discharges usually observed at the onset of the ballistic contractions. Motor units with different recruitment thresholds showed doublet discharges and the percentage of the sample of units firing doublets was increased by training from 5.2 to 32.7 %. The presence of these discharges was observed not only at the onset of the series of spikes but also later in the electromyographic (EMG) burst.
It is likely that earlier motor unit activation, extra doublets and enhanced maximal firing rate contribute to the increase in the speed of voluntary muscle contraction after dynamic training.
The role of endothelin‐A receptors in cardiovascular responses to acute hypoxaemia in the late gestation sheep fetus
Authors: Green L. R. , McGarrigle H. H. G. , Bennet L. , Hanson M. A. 
Published: September 2004

In unanaesthetized chronically instumented fetal sheep (118‐121 days gestation) we investigated the effect of acute isocapnic hypoxaemia (arterial Po2, 12.5 ± 0.6 mmHg) on heart rate (FHR), mean systemic arterial blood pressure (MABP), carotid and femoral blood flows (CBF and FBF, respectively), and carotid and femoral vascular resistances (CVR and FVR, respectively) with the infusion of either the endothelin‐A (ETA) receptor antagonist FR139317, or saline vehicle.
During normoxaemia FHR (P < 0.05) and CBF (P < 0.01) were greater, and CVR (P < 0.01) was lower with FR139317 than with vehicle infusion. CVR remained lower with FR139317 than with vehicle infusion during hypoxaemia (P < 0.01) and recovery (P < 0.05). During hypoxaemia the rapid initial bradycardia, the increase in MABP and FVR and the decrease in FBF were similar with vehicle and FR139317 infusion. In both groups plasma endothelin‐1 concentration ([ET‐1]) was unaltered by hypoxaemia. The increase in CBF during hypoxaemia with vehicle (P < 0.01) was absent with FR139317 infusion.
Thus in the late gestation ovine fetus endogenous ET‐1 modulates basal FHR, CBF and CVR via ETA receptors. Modulation of CBF and CVR persists during hypoxaemia but ETA receptors do not appear to contribute to the decrease in femoral blood flow measured during acute hypoxaemia.
Bladder motility and efferent nerve activity during isotonic and isovolumic recording in the cat
Authors: Sasaki Mitsuyoshi 
Published: September 2004

Bladder motility and pelvic nerve efferent activity were recorded in anaesthetized cats under isotonic or isovolumic conditions. In isotonic conditions the bladder was connected to a reservoir and fluid entering or leaving the bladder was monitored for 8 min using different heads of pressure (isotonic recording). Under isovolumic conditions fixed volumes were injected into the bladder and pressure changes recorded (micturition contractions).
In isotonic conditions, at low pressures the bladder filled to a roughly constant level, and then developed small amplitude oscillatory contractions. At higher pressures, after the initial filling, the bladder contracted, expelling part of its volume. Depending on the pressure this contraction was either sustained or led to a gradual expansion of the bladder. In both cases transient periods of expansion were superimposed. In contrast after an initial slow build up, the efferent nerve activity increased reaching a sustained level of activity during which transient decreases in rate were seen.
The firing frequency of the efferent nerve activity during the sustained phase increased as the intravesical pressure was raised until a plateau was reached at high pressures. The plateau pressure (Pplateau) in a bladder was positively correlated with the peak pressure reached by the bladder during micturition contractions under isovolumic conditions, suggesting that micturition contractions were produced by the maximum output of the reflex pathway.
Section of the hypogastric nerves had relatively little effect, but additional section of the pelvic nerves abolished the contractile phase of the bladder response to filling, and resulted in continuous filling of the bladder.
The transient bladder expansions (duration, 3‐33 s) seen when the innervation was intact were closely related to the transient decreases in efferent nerve activity, suggesting involvement of a central inhibitory mechanism. The threshold pressure for triggering transient expansions was similar to the pressure shown to activate myelinated afferent fibres.
Under isovolumic conditions the frequency of micturition contractions increased with increasing vesical volume, and the relaxed interval between contractions shortened. This response could also be evoked by stimulation of the central cut end of the pelvic nerves, suggesting that the central inhibitory mechanism could also be active during isovolumic conditions.
Oestrogen deficiency impairs intestinal calcium absorption in the rat
Authors: O'Loughlin Peter D. , Morris Howard A. 
Published: September 2004

The effects of ovariectomy on the relationships between calcium consumption and calcium balance and its components were assessed in adult (10‐14 months) sham‐operated and ovariectomized (Ovx) rats fed a semi‐synthetic diet with the calcium content varying between 0·02 and 0·4 %.
Adaptation to dietary calcium restriction was monitored for 47 days from commencement of a 0·02 % Ca diet.
Response to 1,25‐dihydroxyvitamin D (20 ng kg−1 day−1) administration in sham and Ovx rats and oestradiol (E2) (20 μg kg−1 day−1) replacement in Ovx rats was assessed in rats fed a 0·05 % Ca diet.
Ovx rats had lower intercepts for the relationships between calcium consumption and both calcium balance (P < 0·005) and intestinal calcium absorption (P < 0·005) compared with sham rats, but 1,25‐dihydroxyvitamin D was not reduced in Ovx rats.
The magnitude of adaptation to dietary calcium restriction was unaffected by ovariectomy.
Intestinal calcium absorption was stimulated by an equivalent amount in sham and Ovx rats following 1,25‐dihydroxyvitamin D administration, although this did not reach statistical significance for sham (sham, t= 1·91, n.s.; Ovx, t= 3·18, P < 0·05).
Oestradiol replacement in Ovx rats induced a marked increase in intestinal calcium absorption (t= 8·25, P < 0·005), without stimulating circulating 1,25‐dihydroxyvitamin D levels and led to a marked increase in calcium balance (t= 6·89, P < 0·005).
These data indicate that the impairment of intestinal calcium absorption following ovariectomy is not the result of reduced circulating 1,25‐dihydroxyvitamin D or reduced intestinal responsiveness to 1,25‐dihydroxyvitamin D. Moreover E2 stimulates intestinal calcium absorption probably by a direct effect on the intestine.
Modulation of reconstituted ATP‐sensitive K+ channels by GTP‐binding proteins in a mammalian cell line
Authors: Sánchez Jorge A. , Gonoi Tohru , Inagaki Nobuya , Katada Toshiaki , Seino Susumu 
Published: September 2004

The action of GTP‐binding proteins on ATP‐sensitive potassium (KATP) channels was investigated. KATP channels were expressed in a mammalian cell line (COS‐1 cells) by cotransfecting vectors carrying the sulphonylurea receptor (SUR1) and BIR (Kir6.2), a member of the inward rectifier K+ channel family. G proteins were also tested on KATP channels composed of an isoform of SUR1, SUR2A, in combination with Kir6.2.
The α and βγ subunits of the GTP binding protein Gi were tested separately in inside‐out patches under continuous recording. Gα‐i1 increases the activity of SUR1‐Kir6.2 and SUR2A‐Kir6.2 channels by 200 and by 30 %, respectively.
Gα‐i2 does not increase the activity of SUR1‐Kir6.2 channels, but increases the activity of SUR2A‐Kir6.2 channels by 30 %.
Control experiments showed that GTPγS, a specific activator of G proteins, and heat‐ inactivated Gα‐i1 do not increase the single channel activity.
No effects of the other subunits (βγ) from either Gi1 or Gi2 on the single channel activity were observed.
The protein kinase C inhibitors H7 and an inhibitory peptide (FARKGALRQKNV) had no effect on the modulatory action of Gα‐i1 on SUR1‐Kir6.2 channels.
We conclude that both types of reconstituted KATP channels are modulated by G proteins.
Opposite modulation of NMDA receptors by lysophospholipids and arachidonic acid: common features with mechanosensitivity
Authors: Casado Mariano , Ascher Philippe 
Published: September 2004

Two classes of amphiphilic compounds, lysophospholipids and arachidonic acid, have been suggested to produce opposite deformations of the lipid bilayer. We have found that their effects on N‐methyl‐D‐aspartate (NMDA) responses are opposite, and resemble those of mechanical deformations of the plasma membrane.
Lysophospholipids inhibited NMDA responses both in nucleated patches taken from cultured neurons and in cells expressing recombinant NMDA receptors. This inhibition was reversible, voltage independent and stronger at non‐saturating doses of agonist. It was not linked to the charge of the polar head, and was not mimicked by lysophosphatidic acid or phosphatidylcholine. In outside‐out patches, lysophospholipids reduced the open probability of NMDA‐activated channels without changing their single‐channel conductance.
The inhibition produced by lysophospholipids occluded that produced by a mechanical compression induced by changes in osmotic or hydrostatic pressure.
The potentiation of NMDA responses by arachidonic acid was observed both in native and recombinant receptors, including those in which the putative ‘fatty acid binding domain’ had been deleted. This suggests that, like lysophospholipids, arachidonic acid alters the NMDA receptor by insertion into the lipid bilayer.
Recombinant receptors in which the cytoplasmic tails had been modified or deleted were still sensitive to mechanical deformation. A linkage to the cytoskeleton is therefore not required for NMDA receptor mechanosensitivity.
The fact that the NMDA responses are depressed similarly by compression and lysophospholipids, and potentiated similarly by stretch and arachidonic acid supports the notion that the modulation of NMDA receptor activity by asymmetrical amphiphilic compounds involves pressure changes transmitted through the lipid bilayer. Compounds with a large hydrophilic head mimic the effects of a compression, and compounds with a small hydrophilic head mimic the effects of stretch.
An ether ‐à‐go‐go K+ current, Ih‐eag, contributes to the hyperpolarization of human fusion‐competent myoblasts
Authors: Bijlenga Philippe , Occhiodoro Teresa , Liu Jian‐Hui , Bader Charles R. , Bernheim Laurent , Fischer‐Lougheed Jacqueline 
Published: September 2004

Two early signs of human myoblast commitment to fusion are membrane potential hyperpolarization and concomitant expression of a non‐inactivating delayed rectifier K+ current, IK(NI). This current closely resembles the outward K+ current elicited by rat ether‐à‐go‐go (r‐eag) channels in its range of potential for activation and unitary conductance.
It is shown that activation kinetics of IK(NI), like those of r‐eag, depend on holding potential and on [Mg2+]o, and that IK(NI), like r‐eag, is reversibly inhibited by a rise in [Ca2+].
Forced expression of an isolated human ether‐à‐go‐go K+ channel (h‐eag) cDNA in undifferentiated myoblasts generates single‐channel and whole‐cell currents with remarkable similarity to IK(NI).
h‐eag current (Ih‐eag) is reversibly inhibited by a rise in [Ca2+]i, and the activation kinetics depend on holding potential and [Mg2+]o.
Forced expression of h‐eag hyperpolarizes undifferentiated myoblasts from −9 to −50 mV, the threshold for the activation of both Ih‐eag and IK(NI). Similarly, the higher the density of IK(NI), the more hyperpolarized the resting potential of fusion‐competent myoblasts.
It is concluded that h‐eag constitutes the channel underlying IK(NI) and that it contributes to the hyperpolarization of fusion‐competent myoblasts. To our knowledge, this is the first demonstration of a physiological role for a mammalian eag K+ channel.
Renal haemodynamic responses to exogenous and endogenous adenosine in conscious dogs
Authors: Berthold Heike , Just Armin , Kirchheim Hartmut R. , Osswald Hartmut , Ehmke Heimo 
Published: September 2004

Adenosine has been suggested to be the mediator of a metabolic feedback mechanism which transfers acute changes in the tubular load into opposite changes in renal blood flow (RBF). The goal of the present experiments was to assess the importance of endogenously formed adenosine as a ‘homeostatic metabolite’ during short‐term changes in metabolic demand.
In nine chronically instrumented conscious foxhounds, both the direct effects of adenosine injections (10, 30 and 100 nmol) into the renal artery and the temporal changes of RBF after short renal artery occlusions (15, 30 and 60 s duration), the most widely used experimental model to study the metabolic feedback mechanism in vivo, were studied.
Intrarenal bolus injections of adenosine (10, 30 and 100 nmol) induced dose‐dependent decreases of RBF (RBF: −34 ± 5, −59 ± 4 and −74 ± 4 %, respectively). This vasoconstrictor effect of adenosine was significantly larger (RBF: −51 ± 4, −68 ± 4 and −83 ± 3 %, respectively) when the dogs received a low salt diet.
The post‐occlusive responses were characterized by a transient hyperaemia with no detectable drop of RBF below the preocclusion level. The post‐occlusive responses were affected neither by changes in local angiotensin II levels, nor by intrarenal infusions of hypertonic NaCl or blockade of A1 adenosine receptors.
When intrarenal adenosine levels were elevated by infusion of the adenosine uptake inhibitor dipyridamole, a transient, although weak, post‐occlusive vasoconstriction was detected.
In summary, the present data demonstrate that adenosine acts as a potent renal vasoconstrictor in the conscious dog. The endogenous production of adenosine during short‐lasting occlusions of the renal artery, however, appears to be too small to induce a post‐occlusive vasoconstrictor response of RBF. These results suggest that a metabolic feedback with adenosine as ‘homeostatic metabolite’ is of minor importance in the short‐term regulation of RBF in the conscious, unstressed animal.
Separable effects of human Kvβ1.2 N‐ and C‐termini on inactivation and expression of human Kv1.4
Authors: Accili E. A. , Kuryshev Y. A. , Wible B. A. , Brown A. M. 
Published: September 2004

The Kvβ subunits of voltage‐gated K+ channels alter the functional expression and gating of non‐ or slowly inactivating Kvα1 subunits via two separate domains. To determine how Kvβ subunits modulate a rapidly inactivating Kvα1 subunit, we did two‐microelectrode voltage clamp experiments on human Kv1.4 voltage‐gated K+ channels expressed heterologously in Xenopus oocytes. In addition we tested a slowly inactivating mutant of Kv1.4 lacking amino acids 2–146 of the N‐terminal α‐ball domain (Kv1.4ΔN2‐146). Kv1.4 or Kv1.4ΔN2‐146 were co‐expressed with either rat Kvβ2 or human Kvβ1.2. To separate domain effects, we also used a mutant of Kvβ1.2 lacking the unique 79 amino acid N‐terminal β‐ball domain (Kvβ1‐C).
For the mutant Kv1.4ΔN2‐146 we found that Kvβ1‐C or Kvβ2 increased current amplitude without altering activation or inactivation. By contrast Kvβ1.2 produced rapid inactivation and slowed deactivation due to block produced by the β‐ball. The β‐ball also increased the rate of C‐type inactivation in 5 mm, but not 50 mm, external K+ consistent with an effect of blockade on K+ efflux.
For Kv1.4, Kvβ1‐C produced a voltage‐independent increase in the rate of inactivation and shifted the inactivation curve to more hyperpolarized potentials, but had no effect on deactivation. Kvβ1‐C, Kvβ2 and Kvβ1.2 slowed recovery from inactivation similarly, thereby excluding involvement of the β‐ball. Kvβ1.2 produced an additional more rapid, voltage‐dependent component of inactivation, significantly reduced peak outward current and shifted steady‐state inactivation towards hyperpolarized potentials.
Yeast two‐hybrid studies showed that α‐β interaction was restricted to the N‐terminus of Kv1.4 and the C‐terminus of Kvβ1.2 or Kvβ2. Direct interaction with the α‐ball did not occur. Our interpretation is that Kvβ1‐C and Kvβ2 enhanced N‐type inactivation produced by the Kv1.4 α‐ball allosterically.
We propose that Kvβ1.2 has three effects on Kv1.4, the first two of which it shares with Kvβ2. First, Kvβ1‐C and Kvβ2 have a current‐enhancing effect. Second, Kvβ1‐C and Kvβ2 increase block by the α‐ball allosterically. Third, the β‐ball of Kβ1.2 directly blocks both Kv1.4 and Kv1.4ΔN2‐146. When both α‐ and β‐balls are present, competition for their respective binding sites slows the block produced by either ball.