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Sökning: AMNE:(MEDICIN OCH HÄLSOVETENSKAP Medicinska grundvetenskaper Läkemedelskemi) > Simonsson Per

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1.
  • Ding, W Q, et al. (författare)
  • Effects of ethanol on muscarinic receptor-stimulated c-fos expression in human neuroblastoma cells
  • 1997
  • Ingår i: Brain Research. Molecular Brain Research. - 0169-328X. ; 46:1-2, s. 77-84
  • Tidskriftsartikel (refereegranskat)abstract
    • The effect of ethanol exposure on muscarinic receptor-stimulated expression of c-fos was investigated in SH-SY5Y cells. Four days of ethanol exposure enhanced carbachol-stimulated c-fos mRNA expression, analyzed with Northern blot, and Fos/AP-1 binding activity, measured with gel mobility super shift assay. Pre-incubation with muscarinic antagonists or the protein kinase C inhibitor GF109203X demonstrated that, in both control and ethanol-treated cells, carbachol-induced c-fos expression was mediated via muscarinic M1 receptors and to a large extent through protein kinase C. However, phorbol ester-induced c-fos expression was unaffected in ethanol-treated cells. Acute exposure to ethanol caused a suppression of both carbachol- and phorbol ester-stimulated c-fos expression. These results demonstrate that muscarinic receptor-stimulated gene expression is sensitive to both acute and long-term ethanol exposure.
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2.
  • Strandberg, Karin, et al. (författare)
  • Fyra nya instrument för analys av blodgaser testade: Behändiga kassetter skall ge bättre användarvänlighet
  • 2000
  • Ingår i: Läkartidningen. - : Swedish Medical Association. - 0023-7205 .- 1652-7518. ; 97:7, s. 698-701
  • Tidskriftsartikel (refereegranskat)abstract
    • An entirely new type of blood gas analyser has made its way into the marketplace, to be used, for example, in emergency rooms, intensive care units, ambulances, and bedside with quarantined patients in infectious diseases units. The instruments reviewed here employ new miniaturised analysis circuitry, integrated into the cassette on which the blood sample is applied. These instruments are designed for use by care-givers without specific laboratory training. Four point-of-care blood gas analysers are tested: OPTI 1 (AVL), I-STAT (HP), IRMA (Infiniti) och ABL 70 (Radiometer).
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3.
  • Björk, Jonas, et al. (författare)
  • Prediction of relative glomerular filtration rate in adults: New improved equations based on Swedish Caucasians and standardized plasma-creatinine assays.
  • 2007
  • Ingår i: Scandinavian Journal of Clinical & Laboratory Investigation. - : Informa UK Limited. - 1502-7686 .- 0036-5513. ; 67:7, s. 678-695
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: To evaluate newly developed equations predicting relative glomerular filtration rate(GFR) in adult Swedish Caucasians and to compare with the Modification of Diet in Renal Disease(MDRD) and Mayo Clinic equations using enzymatic and zero-calibrated plasma creatinine assays. MATERIAL AND METHODS: GFR was measured with iohexol clearance adjusted to 1.73 m(2). One population sample (n=436/Lund) was used to derive an equation based on plasma-creatinine/age/gender, and a second with the addition of lean body mass (LBM). Both equations were validated in a separate sample (n=414/Malmö). The coefficients of the equations were eventually fine-tuned using all 850 patients and yielding Lund-Malmö equations without (LM) and with LBM-term (LM(LBM)).Their performance was compared with the MDRD(CC) (conventional creatinine calibration), MDRD(IDMS) (isotope dilution mass spectroscopy traceable calibration) and Mayo Clinic equations. RESULTS: The Lund equations performed similarly in both samples. In the combined set, the Mayo Clinic/MDRD(CC) resulted in +19.0/+10.2 % median bias, while bias for the other equations was < 10 %. LM(LBM) had the highest accuracy (86 % of estimates within 30 % of measured GFR), significantly (p < 0.001) better than for MDRD(IDMS) (80 %). In men with BMI < 20 kg/m(2), MDRD(IDMS)/LM had +46 %/+19 % median bias. MDRD(IDMS) also overestimated GFR by 22 %/14 % in men/women above 80 years of age. The LM(LBM) equation had < 10 % bias irrespective of BMI, age or GFR except for a 15 % negative bias at GFR > 90 mL/min/1.73 m(2). CONCLUSION: The newly developed Lund-Malmö equations for GFR estimation performed better than the MDRD(IDMS) and Mayo Clinic equations in a Swedish Caucasian sample. Inclusion of an LBM term improved performance markedly in certain subgroups.
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5.
  • Alling, Christer, et al. (författare)
  • Adaptation of signal transduction in brain
  • 1994
  • Ingår i: EXS. - 1023-294X. ; 71, s. 19-28
  • Tidskriftsartikel (refereegranskat)abstract
    • Cell culture models were used to study the effects of long-term ethanol exposure on neuronal cells. Effects on phospholipase C and phospholipase D mediated signal transduction were investigated by assaying receptor-binding, G protein function, activities of lipases, formation of second messengers and c-fos mRNA. The signal transduction cascades displayed abnormal activities from 2 to 7 days of exposure which differed from the acute effects. Phosphatidylethanol formed by phospholipase D is an abnormal lipid that may harmfully affect nerve cell function.
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6.
  • Alling, Christer, et al. (författare)
  • Continuous and intermittent exposure to ethanol: effect on NG 108-15 cell membrane phospholipids
  • 1991
  • Ingår i: Alcohol and alcoholism. Supplement. - 1358-6173. ; 1, s. 227-231
  • Tidskriftsartikel (refereegranskat)abstract
    • The effect of continuous and intermittent ethanol exposure on the phospholipid composition of Neuroblastoma x Glioma (NG 108-15) cell membranes was investigated. The cells were treated with ethanol for three weeks. Continuous ethanol exposure (150 mM) produced an increase (27%) in the amount of phosphatidylcholine, whereas intermittent ethanol treatment (150 mM) induced a 22% reduction of this lipid. Decreases of phosphatidylethanolamine plasmalogen (8.5%), phosphatidylinositol (16%) and phosphatidylserine (24%) were also seen after intermittent exposure. After binge administration, the concentration of total phospholipids was reduced by 17%, whereas continuous exposure produced a 19% increase. Both intermittent and continuous exposure induced a reduction in the total protein content. No changes in phosphatidic acid, sphingomyelin, phosphatidylcholine plasmalogen or phosphatidylethanolamine (diacyl form) were detected with either treatment. The importance of this study is that ethanol, irrespective of amount, can elicit different effects depending on the pattern of administration.
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7.
  • Alling, Christer, et al. (författare)
  • Evaluation of ethanol effects on PLC signal transduction pathways using cell lines of neuronal origin
  • 1993
  • Ingår i: Alcohol and alcoholism. Supplement. - 1358-6173. ; 2, s. 295-299
  • Tidskriftsartikel (refereegranskat)abstract
    • Human neuroblastoma cells SH-SY5Y and neuroblastoma-glioma cells NG 108-15 have been used as models for the elucidation of the effects of ethanol on receptor-mediated phospholipase C activity, c-fos mRNA expression and protein kinase C activity. Cells were exposed to ethanol (0-200 mM) for varying periods up to seven days. Agonist stimulated events were obtained in NG 108-15 cells with bradykinin and in SH-SY5Y cells with carbachol. Chronic ethanol exposure reduced the agonist-stimulated formation of inositol 1,4,5-trisphosphate in NG 108-15 cells and in SH-SY5Y cells. 100 mM ethanol for seven days increased the membrane bound and cytosolic forms of protein kinase C activity in SH-SY5Y cells. Carbachol (1 mM) induced a maximal c-fos mRNA response after 40 minutes in SH-SY5Y cells, an effect that could be mimicked through protein kinase C stimulation by phorbol esters.
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8.
  • Larsson, Christer, et al. (författare)
  • Ethanol inhibits the peak of muscarinic receptor-stimulated formation of inositol 1,4,5-trisphosphate in neuroblastoma SH-SY5Y cells
  • 1995
  • Ingår i: Biochemical Pharmacology. - : Elsevier BV. - 0006-2952. ; 50:5, s. 647-654
  • Tidskriftsartikel (refereegranskat)abstract
    • The effect of ethanol on muscarinic receptor-stimulated formation of inositol 1,4,5-trisphosphate was studied in human neuroblastoma SH-SY5Y cells. Stimulation with carbachol induced a biphasic increase of inositol 1,4,5-triphosphate with an initial peak after 10 sec declining to a plateau phase of elevation above basal levels, which was sustained for at least 5 min in the presence of agonist. The peak, but not the plateau phase, was concentration-dependently decreased by exposure to ethanol. Maximal inhibition was obtained within 30 sec of exposure to ethanol. Ethanol caused an increase in the EC50 value of carbachol for the initial rate of inositol 1,4,5-trisphosphate formation, measured after 10 sec of stimulation, from 98 microM in the absence to 196 microM in the presence of 100 mM ethanol. The potencies of pirenzepine and hexahydro-sila-difenidol hydrochloride for inhibiting [3H]quinuclidinyl benzilate binding and inositol 1,4,5-trisphosphate formation suggest that both phases are mediated via the muscarinic M1 receptor. Phorbol 12-myristate 13-acetate inhibited both phases of inositol 1,4,5-trisphosphate formation, whereas okadaic acid and modulators of cAMP-dependent protein kinase were without any effect. There was no inhibitory effect of ethanol when protein kinase C was inhibited by H7 and calphostin C, indicating that the ethanol effect is dependent on protein kinase C activity.
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9.
  • Larsson, Christer, et al. (författare)
  • Long-term exposure to ethanol increases the number and function of muscarinic M1 receptors in human neuroblastoma cells
  • 1996
  • Ingår i: Journal of Pharmacology and Experimental Therapeutics. - 1521-0103. ; 278:1, s. 313-319
  • Tidskriftsartikel (refereegranskat)abstract
    • The effect of long-term ethanol exposure on muscarinic receptors was investigated in human neuroblastoma SH-SY5Y cells. Exposure to 100 mM ethanol for 4 days enhanced both peak and steady-state levels of carbachol-stimulated inositol 1,4,5-bisphosphate increase. An ethanol concentration of 50 mM was sufficient for an enhancement of this event. The carbachol-stimulated decrease in [3H]inositol-labeled [3H]phosphatidylnositol 4,5-bisphosphate and increase [3H]inositol trisphosphate and [3H]inositol bisphosphate were also potentiated in ethanol-treated cells, which demonstrated that the receptor-stimulated activation of phospholipase C is augmented. Experiments with pirenzepine showed that carbachol-stimulated inositol 1,4,5-trisphosphate increase is mediated via M1 receptors both in ethanol-treated and control cells. Ethanol exposure for 2 or 4 days also caused an increase in [3H]N-methylscopolamine and [3H]quinuclidinyl benzilate binding sites and elevation of [3H]pirenzepine binding, which indicated that the number of muscarinic M1 receptors is increased in ethanol-treated SH-SY5Y cells. These results demonstrate that long-term exposure to ethanol potentiates muscarinic M1 receptor-stimulated activation of phospholipase C in SH-SY5Y cells. This is likely to be explained by an increased number of muscarinic M1 receptors.
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