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  • Lahti, A-M, 1959, et al. (författare)
  • Effect of alpha-trinositol on secretion induced by Escherichia coli ST-toxin in rat jejunum.
  • 2003
  • Ingår i: Acta physiologica Scandinavica. - 0001-6772. ; 179:4, s. 373-9
  • Tidskriftsartikel (refereegranskat)abstract
    • d-myo-inositol-1,2,6-trisphosphate (alpha-trinositol, PP56), is a synthetic isomer of the intracellular second messenger, d-myo-inositol-1,4,5-trisphospahate. The pharmacological actions of alpha-trinositol include potent anti-inflammatory properties and inhibition of the secretion induced by cholera toxin and obstructive ileus. In the present study, we investigated whether alpha-trinositol was able to influence the secretion induced by heat-stable ST-toxin from Escherichia coli in the rat jejunum.
  • Malm, Christer, et al. (författare)
  • Immune system alteration in response to two consecutive soccer games.
  • 2004
  • Ingår i: Acta Physiologica Scandinavica. - 0001-6772 .- 1365-201X. ; 180:2, s. 143-55
  • Tidskriftsartikel (refereegranskat)abstract
    • AIM: Changes in leucocyte and monocyte subpopulations were investigated in 10 elite male soccer players aged 16-19 years. The purpose was to perform a descriptive study of immunological alterations in elite soccer players in response to two consecutive games separated by 20 h. It was hypothesized that in response to two games the players would show signs of short-term immunosuppression. METHODS: Blood samples were taken before the first soccer game, immediately after the second game and after 6, 24, 48 and 72 h. Cell surface antigens, testosterone and cortisol were investigated. RESULTS: During the first 6 h after the second game there was a significant increase in number of circulating neutrophils, mature (CD20+ CD5+) B cells and CD4/CD8 ratio. A significant decrease was observed in the number of natural killer (NK) cells, monocytes and adhesion on lymphocytes and monocytes. In a delayed phase, 48 h after the second game the expression of both adhesion and signalling molecules increased on lymphocytes and monocytes. Changes in adhesion and signalling molecules at 48 h correlated negatively to the subjects VO2max, suggesting larger immunological response to similar exercise in subjects with lower aerobic exercise capacity. CONCLUSION: In response to competitive soccer exercise some immunological variables are enhanced while others are depressed. Observed changes may serve a purpose in adaptation to exercise by signalling via adhesion.
  • Zhang, Qiuxia, 1960, et al. (författare)
  • Muscle blood flow in response to concentric muscular activity vs passive venous compression
  • 2004
  • Ingår i: Acta Physiol Scand. - 0001-6772 .- 1365-201X. ; 180:1, s. 57-62
  • Tidskriftsartikel (refereegranskat)abstract
    • AIM: To measure muscle blood flow (MBF) using photoplethysmography (PPG) following concentric muscular activity of the leg (active treatment) or passive venous compression (passive treatment) with or without venous obstruction. METHODS: In study A, blood flow in the anterior tibial muscle was measured in 15 healthy subjects with a mean age of 30 years. In study B, blood flow in the gastrocnemius muscle was measured in nine healthy subjects with a mean age of 34 years. Subjects performed concentric muscular activity in one leg. Passive venous compression by a venous foot pump was applied in the contralateral leg. RESULTS: MBF increased significantly following concentric muscular activity, but not following passive venous compression. MBF decreased in both legs when venous obstruction, induced by a thigh tourniquet, was applied. However, MBF was significantly higher following concentric muscular activity than passive venous compression. CONCLUSION: We conclude that concentric muscular activity produces higher MBF values than passive venous compression.
  • Abdul-Rahman, A, et al. (författare)
  • Local cerebral blood flow in the rat during severe hypoglycemia, and in the recovery period following glucose injection
  • 1980
  • Ingår i: Acta Physiologica Scandinavica. - : Wiley-Blackwell. - 0001-6772. ; 109:3, s. 307-314
  • Tidskriftsartikel (refereegranskat)abstract
    • In order to assess the influence of severe hypoglycemia on local cerebral blood flow (1-CBF) artificially ventilated rats, maintained on 70% N2O, were injected with insulin to provide either an EEG pattern of slow-wave polyspikes, or cessation of spontaneous EEG activity for 5, 15 or 30 min ("coma"). In other animals, glucose was injected at the end of a 30 min period of "coma" and 1-CBF was measured after recovery periods of 5, 30, 90, or 180 min. Local CBF was measured autoradiographically with 14C-iodoantipyrine as the diffusible tracer. In the slow-wave polyspike period 1-CBF was increased in most of the structures studied, and reached values that were 1.4 to 3.2 times greater than control. In many structures, cessation of EEG activity was accompanied by a further increase in 1-CBF, with some structures (thalamus, hypothalamus, pontine gray, and cerebellar cortex) showing flow rates of 400--500% of control. The increase in 1-CBF was unrelated to arterial hypertension, hypercapnia, or hypoxia. 5 min after glucose injection the hyperemia persisted in only some of the structures studied; in others, the 1-CBF were close to, or below, control values. During the subsequent recovery period 1-CBF was markedly reduced with some structures (cerebral cortical areas, hippocampus, and caudate-putamen) showing flow rates of only 20--35% of control. In others, notably pontine gray and cerebellar cortex, secondary hypoperfusion was never observed. The hypoperfusion was unrelated to arterial hypertension, hypocapnia, or increase in intracranial pressure. It is concluded that, like hypoxia and ischemia, substrate deficiency due to hypoglycemia is accompanied by vasodilatation in the brain. Furthermore, like long-lasting ischemia, severe hypoglycemia is followed by a delayed hypoperfusion syndrome that, by restricting oxygen supply, may well contribute to the final cell damage incurred.
  • Abletshauser, C, et al. (författare)
  • Biosensing of arteriosclerotic nanoplaque formation and interaction with an HMG-CoA reductase inhibitor
  • 2002
  • Ingår i: Acta Physiologica Scandinavica. - 0001-6772 .- 1365-201X. ; 176, s. 131-146
  • Tidskriftsartikel (refereegranskat)abstract
    • Proteoheparan sulphate can be adsorbed to a methylated silica surface in a monomolecular layer via its transmembrane hydrophobic protein core domain. As a result of electrostatic repulsion, its anionic glycosaminoglycan side chains are stretched out into the blood substitute solution, thereby representing one receptor site for specific lipoprotein binding through basic amino acid-rich residues within their apolipoproteins. The binding process was studied by ellipsometric techniques suggesting that high-density lipoprotein (HDL) has a high binding affinity and a protective effect on interfacial heparan sulphate proteoglycan layers with respect to low-density lipoprotein (LDL) and Ca2+ complexation. Low-density lipoprotein was found to deposit strongly at the proteoheparan sulphate-coated surface, particularly in the presence of Ca2+, apparently through complex formation 'proteoglycan-LDL-calcium'. This ternary complex build-up may be interpreted as arteriosclerotic nanoplaque formation on the molecular level responsible for the arteriosclerotic primary lesion. On the other hand, HDL bound to heparan sulphate proteoglycan protected against LDL deposition and completely suppressed calcification of the proteoglycan-lipoprotein complex. In addition, HDL was able to decelerate the ternary complex deposition. Therefore, HDL attached to its proteoglycan receptor sites is thought to raise a multidomain barrier, selection and control motif for transmembrane and paracellular lipoprotein uptake into the arterial wall. Although much remains unclear regarding the mechanism of lipoprotein depositions at proteoglycan-coated surfaces, it seems clear that the use of such systems offers possibilities for investigating lipoprotein deposition at a 'nanoscopic' level under close to physiological conditions. In particular, Ca2+-promoted LDL deposition and the protective effect of HDL even at high Ca2+ and LDL concentrations agree well with previous clinical observations regarding risk and beneficial factors for early stages of atherosclerosis. Considering this, the system was tested on its reliability in a biosensor application in order to unveil possible acute pleiotropic effects of the lipid lowering drug fluvastatin. The very low-density lipoprotein (VLDL)/intermediate-density lipoprotein (IDL)/LDL plasma fraction from a high risk patient with dyslipoproteinaemia and type 2 diabetes mellitus showed beginning arteriosclerotic nanoplaque formation already at a normal blood Ca2+ concentration, with a strong increase at higher Ca2+ concentrations. Fluvastatin, whether applied to the patient (one single 80 mg slow release matrix tablet) or acutely in the experiment (2.2 μmol L-1), markedly slowed down this process of ternary aggregational nanoplaque complexation at all Ca2+ concentrations used. This action resulted without any significant change in lipid concentrations of the patient. Furthermore, after ternary complex build-up, fluvastatin, similar to HDL, was able to reduce nanoplaque adsorption and size. These immediate effects of fluvastatin have to be taken into consideration while interpreting the clinical outcome of long-term studies.
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