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Sökning: (AMNE:(MEDICIN OCH HÄLSOVETENSKAP Medicinska och farmaceutiska grundvetenskaper Andra medicinska och farmaceutiska grundvetenskaper)) srt2:(2000-2009) > (2005)

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1.
  • Kaczmarczyk, Aneta, et al. (författare)
  • Plasma bikunin : half-life and tissue uptake.
  • 2005
  • Ingår i: Molecular and Cellular Biochemistry. - : Springer Science and Business Media LLC. - 0300-8177 .- 1573-4919. ; 271:1-2, s. 61-67
  • Tidskriftsartikel (refereegranskat)abstract
    • Bikunin is a chondroitin sulfate-containing plasma protein synthesized in the liver. In vitro, it has been shown to inhibit proteases and to have additional activities, but its biological function is still unclear. Here we have studied the dynamics of plasma bikunin in rats and mice. A half-life of 7 +/- 2 min was obtained from the time course of the decrease of the plasma level of bikunin following hepatectomy. Clearance experiments with intravenously injected radiolabeled bikunin with or without the chondroitin sulfate chain showed that the polysaccharide had little influence on the elimination rate of the protein. The uptake of bikunin by different tissues was studied using bikunin labeled with the residualizing agent 125I-tyramine cellobiose; 60 min after intravenous injection, 49% of the radioactivity was recovered in the kidneys and 6-11% in the liver, bones, skin, intestine and skeletal muscle. The uptake in the liver was analyzed by intravenous injection of radiolabeled bikunin followed by collagenase perfusion and dispersion of the liver cells. These experiments indicated that bikunin is first trapped extracellularly within the liver before being internalized by the cells.
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2.
  • Medina-Gomez, Gema, et al. (författare)
  • The link between nutritional status and insulin sensitivity is dependent on the adipocyte-specific peroxisome proliferator-activated receptor-gamma2 isoform
  • 2005
  • Ingår i: Diabetes. - : American Diabetes Association. - 0012-1797 .- 1939-327X. ; 54:6, s. 1706-1716
  • Tidskriftsartikel (refereegranskat)abstract
    • The nuclear receptor peroxisome proliferator-activated receptor-gamma (PPARgamma) is critically required for adipogenesis. PPARgamma exists as two isoforms, gamma1 and gamma2. PPARgamma2 is the more potent adipogenic isoform in vitro and is normally restricted to adipose tissues, where it is regulated more by nutritional state than PPARgamma1. To elucidate the relevance of the PPARgamma2 in vivo, we generated a mouse model in which the PPARgamma2 isoform was specifically disrupted. Despite similar weight, body composition, food intake, energy expenditure, and adipose tissue morphology, male mice lacking the gamma2 isoform were more insulin resistant than wild-type animals when fed a regular diet. These results indicate that insulin resistance associated with ablation of PPARgamma2 is not the result of lipodystrophy and suggests a specific role for PPARgamma2 in maintaining insulin sensitivity independently of its effects on adipogenesis. Furthermore, PPARgamma2 knockout mice fed a high-fat diet did not become more insulin resistant than those on a normal diet, despite a marked increase in their mean adipocyte cell size. These findings suggest that PPARgamma2 is required for the maintenance of normal insulin sensitivity in mice but also raises the intriguing notion that PPARgamma2 may be necessary for the adverse effects of a high-fat diet on carbohydrate metabolism.
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3.
  • Liu, Rong, et al. (författare)
  • Preparation of the four stereoisomers of 3-bromo-2-butanol or their acetates via lipase-catalysed resolutions of the racemates derived from dl- or meso-2,3-butanediol
  • 2005
  • Ingår i: Tetrahedron. - : Elsevier BV. - 0957-4166 .- 1362-511X. ; 16:15, s. 2607-2611
  • Tidskriftsartikel (refereegranskat)abstract
    • The four stereoisomeric 3-bromo-2-butanols and/or their acetates were prepared via lipase-catalysed kinetic resolution by hydrolyses of the acetates of the (+/-)-syn- and (+/-)-anti-3-bromo-2-butanols, or via esterifications of the alc hols. The diastereomeric bromoacetates were obtained by syntheses from the dl- and meso-2,3-butanediols, respectively. On a preparative scale, the four stereoisomers, either as the free alcohols or as their acetates, were obtained in > 95% ee, and in 35-40% yield (based on the starting racemates).
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4.
  • Persson, Bertil R.R., et al. (författare)
  • Effects of microwaves from GSM mobile phones on the blood-brain barrier and neurons in rat brain
  • 2005
  • Ingår i: PIERS 2005 - Progress in Electromagnetics Research Symposium, Proceedings. - 1933077077 - 9781933077079 ; , s. 638-641
  • Konferensbidrag (refereegranskat)abstract
    • Our group has since 1988 studied the effects of different intensities and modulations of 915MHz RF in a rat model where the exposure takes place in a TEM-cell during various time periods and post exposure recovery times. The power fed into TEM-cells was 0.125, 1.25, 12.5 or 125mW corresponding to whole body SAR (determined experimentally): 0.2, 2, 20 or 200mW/kg. The rats were awake and not restrained during exposure and after the recovery period the animals were anaesthetized and sacrificed by perfusion-fixation with 4% formaldehyde. Paraffin embedded 5 μm. thick brain slices were stained for albumin by applying albumin antibodies (Dakopatts), by which albumin is revealed as brownish discolorations. Dark neurons were revealed by staining for RNA/DNA with cresyl violet. In series of more than 1800 Fisher rats, we have proven that sub thermal power levels from both pulse-modulated and continuous RF fields - including those from real GSM mobile phones - have the potency to significantly open the BBB for the animals' own albumin (but not fibrinogen) to pass out into the brain and to accumulate in the neurons and glial cells surrounding the capillaries. Albumin extravasations are most prominent at the lower SAR values. This dose-response behaviour suggests some kind of energy or electromagnetic field strength windowing effect. A linear dose-response relationship for dark neurons was found at 50 days after exposure, with most prominent occurrence at SAR 200mW/kg.
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7.
  • Abbasi, Alireza, et al. (författare)
  • Highly hydrated cations : Deficiency, mobility and coordination of water in crystalline nonahydrated scandium(III), yttrium(III) and lanthanoid(III) trifluoromethanesulfonate
  • 2005
  • Ingår i: Chemistry - A European Journal. - : Wiley. - 0947-6539 .- 1521-3765. ; 11:14, s. 4065-4077
  • Tidskriftsartikel (refereegranskat)abstract
    • Trivalent lanthanide-like metal ions coordinate nine water oxygen atoms, which form a tricapped trigonal prism in a large number of crystalline hydrates. Water deficiency, randomly distributed over the capping positions, was found for the smallest metal ions in the isomorphous nonahydrated trifluoromethanesulfonates, [M(H2O)(n)]CF3SO3)(3), in which M=Sc-III, Lu-III, Yb-III, Tm-III or Er-III. The hydration number n increases (n=8.0(1), 8.4(1), 8.7(1), 8.8(1) and 8.96(5), respectively) with increasing ionic size. Deuterium (H-2) solid-state NMR spectroscopy revealed fast positional exchange between the coordinated capping and prism water molecules; this exchange started at temperatures higher than about 280 K for lutetium(m) and below 268 K for scandium(m). Similar positional exchange for the fully nonahydrated yttrium(m) and lanthanum(m) compounds started at higher temperatures, over about 330 and 360 K, respectively. An exchange mechanism is proposed that can exchange equatorial and capping water molecules within the restrictions of the crystal lattice, even for fully hydrated lanthanoid(III) ions. Phase transitions occurred for all the water-deficient compounds at; 185 K. The hydrated scandium(III) trifluoromethanesulfonate transforms reversibly (Delta H degrees= -0.80(1) kJ mol(-1) on cooling) to a trigonal unit cell that is almost nine times larger, with the scandium ion surrounded by seven fully occupied and two partly occupied oxygen atom positions in a distorted capped trigonal prism. The hydrogen bonding to the trifluoromethanesulfonate anions stabilises the trigonal prism of water ligands, even for the crowded hydration sphere of the smallest metal ions in the series. Implications for the Lewis acid catalytic activity of the hydrated scandium(III) and lanthanoid(III) trifluoromethanesulfonates for organic syntheses performed in aqueous media are discussed.
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8.
  • Andersen, Sonja, et al. (författare)
  • Monoclonal B-cell hyperplasia and leukocyte imbalance precede development of B-cell malignancies in uracil-DNA glycosylase deficient mice
  • 2005
  • Ingår i: DNA Repair. - : Elsevier BV. - 1568-7864 .- 1568-7856. ; 4:12, s. 1432-1441
  • Tidskriftsartikel (refereegranskat)abstract
    • Ung-deficient mice have reduced class switch recombination, skewed somatic hypermutation, lymphatic hyperplasia and a 22-fold increased risk of developing B-cell lymphomas. We find that lymphomas are of follicular (FL) and diffuse large B-cell type (DLBCL). All FLs and 75% of the DLBCLs were monoclonal while 25% were biclonal. Monoclonality was also observed in hyperplasia, and could represent an early stage of lymphoma development. Lymphoid hyperplasia occurs very early in otherwise healthy Ung-deficient mice, observed as a significant increase of splenic B-cells. Furthermore, loss of Ung also causes a significant reduction of T-helper cells, and 50% of the young Ung(-/-) mice investigated have no detectable NK/NKT-cell population in their spleen. The immunological imbalance is confirmed in experiments with spleen cells where the production of the cytokines interferon gamma, interleukin 6 and interleukin 2 is clearly different in wild type and in Ung-deficient mice. This suggests that Ung-proteins, directly or indirectly, have important functions in the immune system, not only in the process of antibody maturation, but also for production and functions of immunologically important cell types. The immunological imbalances shown here in the Ung-deficient mice may be central in the development of lymphomas in a background of generalised lymphoid hyperplasia.
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9.
  • Arend, A, et al. (författare)
  • Prostaglandins of the E-series inhibit connective tissue proliferation in the liver wound of the rat
  • 2005
  • Ingår i: Annals of Anatomy. - Jena : Urban & Fischer. - 0940-9602 .- 1618-0402. ; 187:1, s. 57-62
  • Tidskriftsartikel (refereegranskat)abstract
    • The present study was undertaken to relate wound heating of an internal organ to prostaglandins of the E and F series. A small liver wound was induced by a galvanic cauter via the abdominal route under general anesthesia and prostaglandin E-1, E-2 and F-2 alpha were injected twice daily at a dose of 250 mu g/kg. Proliferation of the connective tissue in the liver wound was estimated morphometrically 6 days after liver wound infliction. Levels of prostaglandins E-2 and F-2 alpha were measured in the liver wound as well as in normal liver tissue from adjacent lobes using radioimmunoassay. The results show that exogenous prostaglandins of the E-series suppress connective tissue proliferation. Three minutes after the last prostaglandin E-2 injection, high prostaglandin concentrations were measured both in the tiver wound and in the liver tissue of the adjacent lobe. Prostaglandin F-2 alpha injections had no effect on wound heating. We believe that the rat thermic liver wound model can be used for different studies on wound heating mechanisms and that prostaglandins of the E-series are involved in wound heating in the specific time period studied.
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10.
  • Asin-Cayuela, Jorge, et al. (författare)
  • The human mitochondrial transcription termination factor (mTERF) is fully active in vitro in the non-phosphorylated form.
  • 2005
  • Ingår i: The Journal of biological chemistry. - 0021-9258. ; 280:27, s. 25499-505
  • Tidskriftsartikel (refereegranskat)abstract
    • The human mitochondrial transcription termination factor (mTERF) is a 39-kDa protein that terminates transcription at the 3'-end of the 16 S rRNA gene and thereby controls expression of the ribosomal transcription unit of mitochondrial DNA. The transcription termination activity of human mTERF has been notoriously difficult to study in vitro, and it has been suggested that the activity of the protein is regulated by posttranslational modifications or by protein polymerization. We here characterize the activity of recombinant human mTERF expressed in insect cells. We observed that mTERF efficiently promotes sequence-specific termination in a completely recombinant and highly purified in vitro system for mitochondrial transcription. The termination activity has a distinct polarity, and we observed complete transcription termination when the mTERF-binding site is oriented in a forward position relative the heavy strand promoter but only partial transcription termination when the binding site is in the reverse position. We analyzed the biochemical characteristics of the active mTERF protein and found that it is a stable monomer at physiological salt concentration. Structural analysis, including phosphostaining, two-dimensional electrophoresis, and electrospray mass spectrometry, detected no evidence of phosphorylation. We conclude that the monomeric human mTERF is fully active in its non-phosphorylated form and that the protein does not require additional cellular factors to terminate mitochondrial transcription in vitro.
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