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Sökning: L773:0002 9513 OR L773:2163 5773

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1.
  • Aronson, D., et al. (författare)
  • Extracellular-regulated protein kinase cascades are activated in response to injury in human skeletal muscle
  • 1998
  • Ingår i: American Journal of Physiology. - : HighWire Press. - 0002-9513 .- 2163-5773. ; 275:2, s. C555-C561
  • Tidskriftsartikel (refereegranskat)abstract
    • The mitogen-activated protein (MAP) kinase signaling pathways are believed to act as critical signal transducers between stress stimuli and transcriptional responses in mammalian cells. However, it is not known whether these signaling cascades also participate in the response to injury in human tissues. To determine whether injury to the vastus lateralis muscle activates MAP kinase signaling in human subjects, two needle biopsies or open muscle biopsies were taken from the same incision site 30-60 min apart. The muscle biopsy procedures resulted in striking increases in dual phosphorylation of the extracellular-regulated kinases (ERK1 and ERK2) and in activity of the downstream substrate, the p90 ribosomal S6 kinase. Raf-1 kinase and MAP kinase kinase, upstream activators of ERK, were also markedly stimulated in all subjects. In addition, c-Jun NH2-terminal kinase and p38 kinase, components of two parallel MAP kinase pathways, were activated following muscle injury. The stimulation of the three MAP kinase cascades was present only in the immediate vicinity of the injury, a finding consistent with a local rather than systemic activation of these signaling cascades in response to injury. These data demonstrate that muscle injury induces the stimulation of the three MAP kinase cascades in human skeletal muscle, suggesting a physiological relevance of these protein kinases in the immediate response to tissue injury and possibly in the initiation of wound healing.
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2.
  • Ask, Per, et al. (författare)
  • Effect of time interval between swallows on esophageal peristalsis.
  • 1980
  • Ingår i: American Journal of Physiology. - 0002-9513 .- 2163-5773. ; 238:6, s. G485-90
  • Tidskriftsartikel (refereegranskat)abstract
    • Esophageal peristaltic pressure amplitude, peristaltic incidence, speed of peristalsis, and wave duration were investigated as a function of swallow interval. In the distal half of the esophagus, the amplitude decreased at swallow intervals of 8 s and shorter. At intervals of 8 and 4 s, dropouts of contractions that were obtained were most frequent in the distal esophagus and for the 4-s interval. At continuous swallows no contractions were obtained below the upper esophageal sphincter until the end of the swallow sequence, after which a peristaltic wave of high amplitude propagated along the esophagus. The peristaltic speed increased toward a level 5 cm above the lower esophageal sphincter. The peristaltic wave duration was approximately the same in different parts of the esophagus and at different swallow intervals. The findings indicate an impairment of esophageal transport function by short swallow intervals.
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3.
  • Ask, Per, et al. (författare)
  • Frequency content of esophageal peristaltic pressure.
  • 1979
  • Ingår i: American Journal of Physiology. - 0002-9513 .- 2163-5773. ; 236:3, s. E296-300
  • Tidskriftsartikel (refereegranskat)abstract
    • Fourier analysis of esophageal peristaltic pressure waves was performed by computer fast Fourier transform. The highest power spectral density was obtained in the frequency range below 1 Hz. The Fourier analysis showed spectral components up to about 12 Hz in the upper esophageal sphincter (UES). The significance of different frequency components was investigated by low-pass filtering at different cut-off frequencies. A reduction in the amplitude of UES contractions was obtained at a cut-off frequency of 4 Hz, whereas the cut-off frequency of 8 Hz did not show any distortion. For perfused manometry systems, only a low-compliance perfusion pump will have sufficient bandwidth for accurate recording of esophageal peristaltic pressures.
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4.
  • Ask, Per, et al. (författare)
  • Peripheral nerve as an osmometer : role of the perineurium in frog sciatic nerve.
  • 1983
  • Ingår i: American Journal of Physiology. - 0002-9513 .- 2163-5773. ; 244:1, s. C75-81
  • Tidskriftsartikel (refereegranskat)abstract
    • Measurements of volume and hydrostatic pressure in the frog sciatic nerve in vitro demonstrate that the nerve acts as an osmometer, in large part because the perineurium is a semipermeable membrane for water flow. Endoneurial hydrostatic pressure in nerves in isotonic Ringer exceeds bath pressure by about 7 mmHg. In Ringer made hypertonic by addition of sucrose, nerve volume and endoneurial pressure fall linearly in relation to 1/osmolality. The slope of the plot of pressure against volume provides a value for nerve compliance equal to 0.006 mm2/mmHg. Calculations based on the model of the nerve as an osmometer indicate that the nerve has an osmotically "inactive" volume equal to 0.19 mm3/mm, which is about 75% of the total volume of a nerve segment of unit length in normal Ringer. Perineurial hydraulic conductivity (Lp) equals 7.5 x 10(-13) cm3.s-1.dyn-1, a value characteristic of nonleaky epithelia. The perineurium is an elastic tissue with a constant modulus of elasticity equal to 3 x 10(6) dyn/cm2 when not markedly stretched and may limit nerve swelling under pathological conditions of nerve edema.
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5.
  • Balagopal, P., et al. (författare)
  • Skeletal muscle heavy-chain synthesis rate in healthy humans
  • 1997
  • Ingår i: American Journal of Physiology. - : HighWire Press. - 0002-9513 .- 2163-5773. ; 272:1, s. 45-50
  • Tidskriftsartikel (refereegranskat)abstract
    • Mixed muscle protein synthetic rate has been measured in humans. These measurements represent the average of synthetic rates of all muscle proteins with variable rates. We determined to what extent the synthesis rate of mixed muscle protein in humans reflects that of myosin heavy chain (MHC), the main contractile protein responsible for the conversion of ATP to mechanical energy as muscle contraction. Fractional synthetic rates of MHC and mixed muscle protein were measured from the increment of [C-13]leucine in these proteins in vastus lateralis biopsy samples taken at 5 and 10 h during a primed continuous infusion of L-[1-C-13]leucine in 10 young healthy subjects. Calculations were done by use of plasma [C-13]ketoisocaproate (KIC) and muscle tissue fluid [C-13]leucine as surrogate measures of leucyl-tRNA. Fractional synthetic rate of MHC with plasma KIC (0.0299 +/- 0.0043%/h) and tissue fluid leucine (0.0443 +/- 0.0056%/h) were only 72 +/- 3% of that of mixed muscle protein (0.0408 +/- 0.0032 and 0.0603 +/- 0.0059%/h, respectively, with KIC and tissue fluid leucine). Contribution of MHC (7 +/- 1 mg . kg(-1) . h(-1)) to synthetic rates of whole body mixed muscle protein (36 +/- 5 mg . kg(-1) . h(-1)) and whole body protein (127 +/- 4 mg . kg(-1) . h(-1)) is only 18 +/- 1 and 5 +/- 1%, respectively. This relatively low contribution of MHC to whole body and mixed muscle protein synthesis warrants direct measurement of synthesis rate of MHC in conditions involving abnormalities of muscle contractile function.
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6.
  • Barg, Sebastian, et al. (författare)
  • Different interactions of cardiac and skeletal muscle ryanodine receptors with FK-506 binding protein isoforms
  • 1997
  • Ingår i: American Journal of Physiology: Cell Physiology. - 1522-1563. ; 272:5 Pt 1, s. C1726-C1733
  • Tidskriftsartikel (refereegranskat)abstract
    • In the present study, we compare functional consequences of dissociation and reconstitution of binding proteins FKBP12 and FKBP12.6 with ryanodine receptors from cardiac (RyR2) and skeletal muscle (RyR1). The skeletal muscle RyR1 channel became activated on removal of endogenously bound FKBP12, consistent with previous reports. Both FKBP12 and FKBP12.6 rebind to FKBP-depleted RyR1 and restore its quiescent channel behavior by altering ligand sensitivity, as studied by single-channel recordings in planar lipid bilayers, and macroscopic behavior of the channels (ryanodine binding and net energized Ca2- uptake). By contrast, removal of FKBP12.6 from the cardiac RyR2 did not modulate the function of the channel using the same types of assays as for RyR1. FKBP12 or FKBP12.6 had no effect on channel activity of FKBP12.6-depleted cardiac RyR2, although FKBP12.6 rebinds. Our studies reveal important differences between the two ryanodine receptor isoforms with respect to their functional interaction with FKBP12 and FKBP12.6.
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7.
  • El-Khoury, Antoine E, et al. (författare)
  • Moderate exercise at energy balance does not affect 24-h leucine oxidation or nitrogen retention in healthy men
  • 1997
  • Ingår i: American Journal of Physiology. - 0002-9513 .- 2163-5773. ; 273:2, s. E394-E407
  • Tidskriftsartikel (refereegranskat)abstract
    • Short-term metabolic experiments have revealed that physical exercise increases the oxidation of leucine, which has been interpreted to indicate an increased requirement for dietary protein in physically active subjects. Because it may be inaccurate to extrapolate measurements of amino acid oxidation made over a few hours to the entire day, we have carried out a continuous 24-h intravenous [1-13C]leucine/[15N]urea tracer study in eight healthy adult men. Their diet supplied 1 g protein.kg-1.day-1, and exercise (mean maximal O2 consumption 46%) was for 90 min during the 12-h fast and 12-h fed periods of the day. Subjects were adapted to the diet and exercise regimen for 6 days. Then, on day 7, they were dressed in the University of Uppsala energy metabolic unit's direct calorimeter suit, were connected to an open-hood indirect calorimeter, and received the tracers. Exercise increased leucine oxidation by approximately 50 and 30% over preexercise rates for fast and fed periods, respectively. This increase amounted to approximately 4-7% of daily leucine oxidation. Subjects remained in body leucine equilibrium (balance -4.6 +/- 10.5 mg.kg-1.day-1; -3.6 +/- 8.3% of intake; P = not significant from zero balance). Therefore, moderate exercise did not cause a significant deterioration in leucine homeostasis at a protein intake of 1 g.kg-1.day-1. These findings underscore the importance of carrying out precise, continuous, 24-h measurements of whole body leucine kinetics; this model should be of value in studies concerning the quantitative interactions among physical exercise, energy/protein metabolism, and diet in humans.
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8.
  • Holm, Lena, et al. (författare)
  • Histamine is not involved in pentagastrin-induced gastric mucosal vasodilation in the rat.
  • 1994
  • Ingår i: American Journal of Physiology. - 0002-9513 .- 2163-5773. ; 266:1 Pt 1, s. G55-61
  • Tidskriftsartikel (refereegranskat)abstract
    • The effects of histamine and its role in the gastric mucosal vascular response to pentagastrin were studied in anesthetized rats. Blood flow was measured with laser-Doppler flowmetry (LDF) and with red blood cell velocity measurements in the superficial mucosal microcirculation. Acid secretion was determined by titration of the saline covering 0.8 cm2 of the fundic mucosa. Pentagastrin (40 micrograms.kg-1 x h-1 i.v. induced a blood flow increase (+40%), which was not significantly altered by ranitidine (H2-receptor antagonist, 2 mg/kg iv bolus), whereas the stimulated acid output was abolished. In experiments in which the H1-receptor antagonist pyrilamine (2.5 mg/kg i.v. bolus) was administered before pentagastrin stimulation, pentagastrin still increased blood flow by approximately 60%. Intravenous histamine (4 mg.kg-1 x h-1) induced a blood flow reduction in parallel with the reduction in blood pressure (vascular resistance unchanged). Even during intra-arterial (thoracic aorta) infusion of histamine (1 or 4 mg.kg-1 x h-1), gastric vascular resistance was unchanged. In animals pretreated with pyrilamine, histamine (4 mg.kg-1 x h-1 i.v.) left the gastric blood flow and blood pressure unchanged. These results indicate that the pentagastrin-induced increase in the rat gastric blood flow is not dependent on histamine.
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9.
  • Holm, Lena, et al. (författare)
  • Influence of tactile stimulation of the rat gastric mucosa on blood flow and acid output.
  • 1993
  • Ingår i: American Journal of Physiology. - 0002-9513 .- 2163-5773. ; 265:2 Pt 1, s. G303-9
  • Tidskriftsartikel (refereegranskat)abstract
    • The influence of tactile stimulation of the gastric mucosa (mimics the mechanical influence of the food bolus) on the gastric mucosal blood flow and acid output was studied in rats anesthetized with Inactin. Blood flow was measured with laser-Doppler flowmetry (LDF) with the probe positioned above the gastric mucosa, and acid secretion was measured at regular intervals by titration of the saline covering 0.8 cm2 of the mucosa. After gentle tactile stimulation (wiping with cotton tips) of the mucosa for 20 s, blood flow increased to approximately 250% of the control value and then returned to the control level 15 min later, whereas acid output was transiently reduced immediately after tactile stimulation. Pretreatment with lidocaine, methysergide, or hexamethonium did not change the results of tactile stimulation on the blood flow. After indomethacin (3 mg/kg i.v.) LDF was significantly reduced by 33% and the hyperemic response to tactile stimulation was almost abolished. This suggests that endogenously released prostaglandins, not evoked through activation of intramural reflexes that can be blocked by lidocaine, methysergide or hexamethonium, are responsible for the hyperemia seen after tactile stimulation of the gastric mucosa.
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10.
  • Holm, Lena, et al. (författare)
  • Role of prostaglandins in regulation of gastric mucosal blood flow and acid secretion.
  • 1992
  • Ingår i: American Journal of Physiology. - 0002-9513 .- 2163-5773. ; 263:4 Pt 1, s. G446-51
  • Tidskriftsartikel (refereegranskat)abstract
    • The role of prostaglandins in the rat gastric mucosal vascular response to acid stimulation was studied. Blood flow was measured with laser-Doppler flowmetry (LDF) and with red blood cell velocity measurements in the superficial mucosa; acid secretion was determined by titration. Baseline acid output was calculated to be 0.026 +/- 0.011 mueq/min. Pentagastrin (20 and 40 micrograms.kg-1.h-1 iv) significantly increased acid output to 0.387 +/- 0.104 and 0.546 +/- 0.220 mueq/min and LDF to 119 +/- 10 and 132 +/- 13% of control, respectively. LDF was significantly reduced by 15% after indomethacin (3 mg/kg iv) and was not changed by pentagastrin, whereas acid secretion increased to similar levels as without indomethacin pretreatment. The H2-agonist impromidine (100 and 500 micrograms.kg-1.h-1 iv) induced a dose-dependent increase in acid secretion (0.178 +/- 0.068 and 0.330 +/- 0.072 mueq/min, respectively) while blood flow was unchanged. Despite a substantial blood flow reduction (-38%) by indomethacin, impromidine did not alter blood flow, and acid secretion was dose dependently increased to similar values as without indomethacin pretreatment. These results provide further evidence that there is not necessarily any correlation between blood flow and acid secretion and that the pentagastrin-induced blood flow increase depends on prostaglandin release.
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