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Träfflista för sökning "WFRF:(Hansen T) srt2:(1990-1994)"

Search: WFRF:(Hansen T) > (1990-1994)

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1.
  • Hultin, M, et al. (author)
  • Metabolism of emulsions containing medium- and long-chain triglycerides or interesterified triglycerides.
  • 1994
  • In: Journal of Lipid Research. - 0022-2275 .- 1539-7262. ; 35:10, s. 1850-60
  • Journal article (peer-reviewed)abstract
    • This study compares the clearing and metabolism of three different lipid emulsions. They had the same phospholipid emulsifier and similar particle sizes. In one (LLL) the core component was long-chain triglycerides (TG), the second (MMM/LLL) contained equal molar amounts of medium- and long-chain TG, the third (MLM) contained synthetic TG with medium-chain (M) fatty acids in the 1,3-positions and a long-chain (L) fatty acid in the 2-position. In model experiments with bovine lipoprotein lipase, the MMM component was hydrolyzed preferentially in the MMM/LLL emulsion so that the initial products were M fatty acids and M monoglycerides. The MLM emulsion, in contrast, gave M fatty acids and formation of L-MG (monoglyceride) throughout hydrolysis. For in vivo studies [3H]oleic acid was incorporated into the emulsion TG as marker for the long-chain component. After bolus injection to rats, the MMM/LLL and MLM emulsions were cleared more rapidly than the LLL emulsion. This was true at all TG loads studied (4-64 mg for a 200 g rat). The labeled oleic acid was oxidized somewhat more rapidly when administered in the MLM emulsion compared to the MMM/LLL emulsion. There were only slight differences in tissue distribution of label. Hence, differences in in vivo metabolism of the long-chain fatty acids were small compared to the marked differences in TG structure and in patterns of product release during in vitro lipolysis.
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2.
  • Amann, F., et al. (author)
  • A search for murarregamma at the level of 10-13
  • 1991
  • In: Proceedings of the 25th International Conference on High Energy Physics. - 9810024347 ; , s. 1070-1071
  • Conference paper (peer-reviewed)abstract
    • The MEGA experiment, which is a search for the decay murarregamma with a branching ratio sensitivity of about 10-13, employs highly modular, fast detectors, state-of-the-art electronics, and a staged trigger with on-line filters. The detectors are contained in a 1.5-T solenoidal field produced by a superconducting magnet. Positrons are confined to the central region and are measured by a set of thin MWPCs. Photons are measured by one of four layers of pair spectrometers in the outer region. Most aspects of the design have been validated in engineering runs; data taking will begin in 1990 with much of the electron arm and one pair spectrometer layer installed.
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3.
  • Lanne, T, et al. (author)
  • Differences in mechanical properties of the common carotid artery and abdominal aorta in healthy males
  • 1994
  • In: Journal of Vascular Surgery. - 1097-6809. ; 20:2, s. 218-225
  • Journal article (peer-reviewed)abstract
    • PURPOSE: Vascular disease is differentiated throughout the vascular regions, with central arteries more prone to dilation and with peripheral arteries more prone to occlusive disease. In this study we investigated the diameter and compliance in the common carotid artery and abdominal aorta in healthy males at varying ages to assess potential differences in the aging process. METHODS: An ultrasound phase-locked echo-tracking system was used to determine differences in diameter and pulsatile diameter changes of the common carotid artery and abdominal aorta in 56 healthy Caucasian males ages 10 to 74 years. Pressure strain elastic modulus (Ep) and stiffness (beta) were calculated from diameter, pulsatile diameter change, and blood pressure obtained by the auscultatory method. Compliance was defined as the inverse of Ep and stiffness. RESULTS: The diameter of both common carotid artery and abdominal aorta increases not only when a person is a child, but also when they are between 25 and 70 years old. The dilation in adults seems to be more accentuated in the abdominal aorta (27%) than in the common carotid artery (17%). Ep and stiffness (beta) are higher in the common carotid artery when a person is 10 years of age (p < 0.01 and 0.05). However, during aging, Ep and stiffness (beta) increase to a higher extent in the aorta than in the common carotid artery, with a significantly higher Ep and stiffness (beta) in the aorta when a person is 45 years and older (45 years: p < 0.05 and p = NS; 60 years: p < 0.001 and p < 0.001; 70 years: p < 0.01 and p < 0.01). CONCLUSIONS: This investigation demonstrates regional differences in diameter change and compliance in the common carotid artery and abdominal aorta and implies that the abdominal aorta is more prone to degenerative changes than the common carotid artery. This may be one etiologic factor for the regional differences in vascular disease.
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4.
  • Lauritzen, M., et al. (author)
  • Cortical spreading depression is associated with arachidonic acid accumulation and preservation of energy charge
  • 1990
  • In: Journal of Cerebral Blood Flow and Metabolism. - : SAGE Publications. - 0271-678X .- 1559-7016. ; 10:1, s. 115-122
  • Journal article (peer-reviewed)abstract
    • The present study aimed to study the relation between the release of arachidonic acid (AA) and the energy state in cerebral cortices of rats during single episodes of cortical spreading depression (CSD). The changes in concentrations of AA, labile phosphate compounds [ATP, ADP, AMP, and phosphocreatine (PCr)], and glycolytic metabolites (lactate, pyruvate, glucose, and glycogen) were studied during and following the large change of the local direct current (DC) potential. Free AA increased markedly during the DC shift, continued to increase during the subsequent 3 min, and returned to control levels at 4-5 min after CSD. PCr decreased by 38% in the first minutes following the DC shift, while ADP increased by 38%. Both returned to normal within a few minutes. ATP, AMP, and energy charge remained constant throughout the experimental period. Glucose decreased by 47% and glycogen by 34% for a few minutes following CSD, while lactate increased by 105% at 2-3 min and by 77% at 4-5 min after CSD. The metabolites returned to control levels at 10 min after CSD. Considering the constant energy charge at all time points during CSD, it is suggested that the AA rise reflects augmented phospholipase activity due to either increased intracellular [Ca2+] or receptor stimulation or both. The possibility that N-methyl-D-aspartate receptors play a role in the release of AA, and that free AA in turn could be part of the mechanism of CSD, is discussed.
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5.
  • Zhang, E., et al. (author)
  • Influence of MK-801 on brain extracellular calcium and potassium activities in severe hypoglycemia
  • 1990
  • In: Journal of Cerebral Blood Flow and Metabolism. - : SAGE Publications. - 0271-678X .- 1559-7016. ; 10:1, s. 136-139
  • Journal article (peer-reviewed)abstract
    • The purpose of the present study was to examine the effect of blockade of N-methyl-D-aspartate (NMDA) receptors on the depolarization associated with severe hypoglycemia, which is commonly preceded by one or a few transient depolarizations reminiscent of cortical spreading depression (CSD). In the cerebral cortices of rats [K+](e) and [Ca2+](e) were measured with ion-selective microelectrodes. NMDA blockade was achieved by injection of MK801 in doses that block CSD. In control rats, the latency from the time point when blood glucose reached minimal levels to onset of ionic shifts was 33.2 ± 3.5 min, and [K+](e) rose from 3.2 ± 0.2 to 55 ± 5 mM. All variables remained unchanged in rats treated with MK801. In another four rats treated with MK801, [Ca2+](e) declined from 1.06 ± 0.22 to 0.12 ± 0.02 mM. Plasma glucose measurements indicated that the cortex depolarized at a plasma glucose concentration between 0.7 and 0.8 mM, i.e., within a narrow range, suggesting a threshold phenomenon. In conclusion, activation of NMDA receptors seems of minor importance for hypoglycemic depolarization. The ionic transients that precede the persistent hypoglycemic depolarization are probably mediated by mechanisms distinct from those of electrically induced CSD.
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