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  • Malmqvist, Ulf, et al. (författare)
  • Contractile properties during development of hypertrophy of the smooth muscle in the rat portal vein
  • 1988
  • Ingår i: Acta Physiologica Scandinavica. - Wiley-Blackwell. - 0001-6772. ; 133:1, s. 49-61
  • Tidskriftsartikel (refereegranskat)abstract
    • Structural and mechanical alterations during hypertrophy of the rat portal vein were investigated. Growth of the vessel was induced by a partial ligature of the vessel causing an increased transmural pressure. Vessel segments from animals kept with ligature for 1, 3, 5 and 7 days, were compared with vessels from sham-operated animals. Maximal active force and vessel cross-sectional area increased with time in the ligated group. On day 7, force and cross-sectional area at the optimal length, were markedly increased in the ligated group (21.1 +/- 1.0 mN, 0.55 +/- 0.04 mm2, n = 9) compared with the control vessels (11.7 +/- 1.0 mN, 0.30 +/- 0.02 mm2, n = 7). Light and electron microscopy of preparations fixed at optimal length showed that the amount of smooth muscle and the cross-sectional area of cell profiles were almost doubled in the ligated group on day 7, consistent with hypertrophy of the smooth muscle. The force per smooth muscle cell area was similar in the two groups (ligated: 132 +/- 15; control: 145 +/- 16 mN mm-2, n = 4-5). The maximal shortening velocity was significantly lower in the hypertrophied group (ligated: 0.28 +/- 0.02; control: 0.41 +/- 0.01 optimal length s-1, n = 6). In chemically skinned preparations, activated by maximal thiophosphorylation of the myosin light chains, force was higher in the ligated group compared to the controls but no difference in maximal shortening velocity was observed. In conclusion, the increased transmural pressure is associated with a rapid increase in the amount of smooth muscle in the portal vein. The mechanical data show that after 7 days the force generating ability of the contractile system has increased in proportion to the smooth muscle cell mass. The unaltered maximal shortening velocity in the skinned hypertrophied preparations suggests that the kinetic properties of the maximally activated contractile system are unaltered. The decreased maximal shortening velocity in the intact hypertrophied preparations may reflect alterations in the excitation-contraction coupling.
  • Malmqvist, Ulf, et al. (författare)
  • Cytoskeletal and contractile proteins in detrusor smooth muscle from bladders with outlet obstruction--a comparative study in rat and man
  • 1991
  • Ingår i: Scandinavian Journal of Urology and Nephrology. - Taylor & Francis. - 0036-5599. ; 25:4, s. 261-267
  • Tidskriftsartikel (refereegranskat)abstract
    • Detrusor biopsies were obtained from patients with urinary outlet obstruction due to prostatic enlargement and from age-matched control patients. The relative amounts of actin and myosin and their isoforms, as well as desmin and filamin were determined and compared with corresponding results from bladders from control rats and rats with 10 days of experimental outlet obstruction of the urinary bladder. In the human control detrusor the actin/myosin ratio was similar to that in the control rat. The isoform distribution of the myosin heavy chains differed between man and rat. In the biopsies from the patients with outlet obstruction and in the obstructed rat bladders the actin/myosin ratio was increased. A change in the myosin heavy chain distribution in the obstructed bladders was observed for both species. The filamin/actin ratio increased significantly in the obstructed rat bladders and tended to increase in the obstructed human bladders. Desmin was the dominating intermediate filament protein. The desmin/actin ratio increased in obstructed bladders in man and in rat.
  • Malmqvist, Ulf, et al. (författare)
  • Mechanics and Ca(2+)-sensitivity of human detrusor muscle bundles studied in vitro
  • 1991
  • Ingår i: Acta Physiologica Scandinavica. - Wiley-Blackwell. - 0001-6772. ; 143:4, s. 373-380
  • Tidskriftsartikel (refereegranskat)abstract
    • Mechanical properties of isolated smooth muscle strips from human urinary bladder were investigated in vitro. Bladder tissue was obtained from tumour-free wall regions of bladders from male patients undergoing cystectomy for bladder carcinoma. In intact muscle strips, activated with high-K+ solution, half-maximal force occurred at about 0.9 mM extracellular [Ca2+]. The length-active force relation was determined and the muscle strips were fixed for light and electron microscopy at optimal length for active force (1o). The maximal active force per unit smooth muscle cross-sectional area was 208 +/- 49 mN/mm2, n = 6. Chemically skinned preparations were obtained by treatment with triton X-100. These preparations had a steep [Ca2+]-force relation in the micromolar range which was influenced by calmodulin. The skinned preparations could be maximally activated by irreversible thiophosphorylation of the regulatory light chains. The force-velocity relation was determined in the maximally activated skinned muscle at 22 degrees C at 0.51o. When the muscle was shortened by 10%, force was reduced by 35% whereas the maximal shortening velocity was little affected.
  • Nilsson, Bengt-Olof, et al. (författare)
  • Effects of polyamine synthesis inhibition on polyamines, growth and mechanical properties in hypertrophic rat urinary bladder
  • 1998
  • Ingår i: Pharmacology and Toxicology. - Wiley-Blackwell. - 1600-0773. ; 82:6, s. 287-294
  • Tidskriftsartikel (refereegranskat)abstract
    • The polyamines putrescine, spermidine and spermine, are ubiquitous intracellular metabolites associated with growth and protein synthesis. In this study effects of polyamine synthesis inhibition on bladder growth, polyamine levels and mechanical properties were investigated in rat urinary bladder subjected to partial outflow obstruction that causes bladder hypertrophy. The S-adenosyl methionine decarboxylase inhibitor CGP-48664 (5 and 20 mg kg-1) was administered alone or in combination with the ornithine decarboxylase inhibitor DFMO (500 mg kg-1), starting one day before creation of partial outflow obstruction and then daily for 7 days. The bladder muscle level of putrescine was increased 38 times and that of spermine reduced by 4 times while spermidine was unchanged after treatment with CGP-48664 (20 mg kg-1). The increase in putrescine was abolished in animals receiving CGP-48664 in combination with DFMO. Treatment with polyamine synthesis inhibitors could not prevent or reduce the hypertrophy of the bladder as judged by bladder wet weight and protein contents. The effects on polyamine quantities were not associated with changes in Ca(2+)-force relationship or in agonist and electrically stimulated force. In summary, treatment of rats with polyamine synthesis inhibitors resulted in changes in polyamine levels in the growing urinary bladder but did not affect growth or mechanical properties.
  • Rodriguez, Juan, 1983- (författare)
  • Targeting apoptosis-inducing factor as a novel therapeutic strategy for preventing perinatal brain injury
  • 2020
  • Doktorsavhandling (övrigt vetenskapligt)abstract
    • Perinatal complications such as asphyxia can cause brain injuries that are often associated with subsequent neurological deficits. The mechanisms of perinatal brain injury are not fully understood, but mitochondria play a prominent role, not only due to their central function in metabolism, but also because many proteins with apoptosisrelated functions are located in the mitochondrion. Among these proteins, CHCHD4 and apoptosis-inducing factor (AIF) have already been shown to make important contributions to neuronal cell death upon hypoxia-ischemia (HI), but a better understanding of the mechanisms behind these processes is required for the development of improved treatments. By inducing HI in 9-day-old mice, leading to moderate brain injury, we studied these mechanisms from multiple perspectives. First, we determined the effect of chchd4 haploinsufficiency, and we showed that neonatal mice with this genotype experienced less brain damage due to reduced translocation of AIF and Cytochrome c from the mitochondrion. Second, we characterized the role of a newly discovered AIF isoform (AIF2), which is only expressed in the brain and the functions of which are unknown. By using Aif2 knockout mice, we showed that under physiological conditions there is an increase in Aif1 expression (the ubiquitously expressed isoform) due to a compensatory effect of loss of Aif2 expression. As a result, these mice showed a higher degree of brain damage after HI and were more vulnerable to oxidative stress. Third, we used another transgenic mouse in which Aif was overexpressed by knocking in a proviral insertion of Aif, leading to an increased expression of Aif1 without affecting the expression of Aif2. This mouse also showed a higher degree of brain damage and higher levels of oxidative stress. Finally, we used a peptide designed to block the apoptotic function of AIF. The results in young mice showed that the neuroprotective effect of the peptide was greater in male mice than in female mice. In summary, this PhD project has opened new perspectives in the comprehension of the mechanisms by which CHCHD4 and AIF are crucial proteins for brain damage after HI, and it has showed that AIF is a promising therapeutic target for improving outcome after perinatal brain injury.
  • Sukhovey, Yurij G., et al. (författare)
  • Functional Conjugation of the Different Regulatory Responses to the Stress Stimuli in Healthy Human Subjects
  • 2016
  • Ingår i: Open Journal of Applied Sciences. - 2165-3917. ; 6, s. 489-500
  • Tidskriftsartikel (refereegranskat)abstract
    • Present article discusses the physiological mechanisms of the state employees adaptation duringactive training in temporary groups. It is suggested that adaptive mechanisms to adverse effectsmay be studied basing on the concept of functional isomorphism of the psychic and immune systems.Adaptive mechanisms were studied through the monitoring of the stress factors’ impact upon thelaw enforcement officers when training outside the places of permanent deployment. The specificpurpose of present study was to evaluate the physiological indicators of the psychic, immune andendocrine systems dynamics at different stages of adaptation of the live organism to a stressfulsituation, hoping to get better insight into possible relations between psychic and immune domains.Through monitoring of the dynamics of the endocrine and immune responses to the psychic stimuli,it was possible to correlate the stages of the stress onset to the phases of specific immune reactions.Strong correlations between the parameters characterizing activation of the psychic and immuneresponses support the hypothesis of the presence of “strong cooperation” between psychic andimmune domains. It supports earlier hypothesis that we are monitoring
  • Zhu, Changlian, 1964-, et al. (författare)
  • X chromosome-linked inhibitor of apoptosis protein reduces oxidative stress after cerebral irradiation or hypoxia-ischemia through up-regulation of mitochondrial antioxidants.
  • 2007
  • Ingår i: The European journal of neuroscience. - 1460-9568. ; 26:12, s. 3402-10
  • Tidskriftsartikel (refereegranskat)abstract
    • We demonstrate that X chromosome-linked inhibitor of apoptosis protein (XIAP) counteracts oxidative stress in two essentially different disease-related models of brain injury, hypoxia-ischemia and irradiation, as judged by lower expression of nitrotyrosine (5-fold) and 4-hydroxy-2-nonenal (10-fold) in XIAP-overexpressing compared with wild-type mice. XIAP overexpression induced up-regulation of at least three antioxidants residing in mitochondria, superoxide dismutase 2, thioredoxin 2 and lysine oxoglutarate reductase. Cytochrome c release from mitochondria was reduced in XIAP-overexpressing mice. Hence, in addition to blocking caspases, XIAP can regulate reactive oxygen species in the brain, at least partly through up-regulation of mitochondrial antioxidants. XIAP-induced prevention of oxidative stress was not secondary to tissue protection because although XIAP overexpression provides tissue protection after hypoxia-ischemia, it does not prevent tissue loss after irradiation. This is a previously unknown role of XIAP and may provide the basis for development of novel protective strategies for both acute and chronic neurodegenerative diseases, where oxidative stress is an integral component of the injury mechanisms involved.
  • Österman, Å, et al. (författare)
  • Effects of 2,3-butanedione monoxime on activation of contraction and crossbridge kinetics in intact and chemically skinned smooth muscle fibres from guinea pig taenia coli
  • 1993
  • Ingår i: Journal of Muscle Research and Cell Motility. - Springer. - 0142-4319. ; 14:2, s. 186-194
  • Tidskriftsartikel (refereegranskat)abstract
    • The effects of 2,3-butanedione monoxime (BDM) were studied in smooth muscle fibres from guinea pig taenia coli. In intact muscle, active force during contractions induced by high-K+ was inhibited by about 10% in 1 mM BDM and by approximately 70% in 10 mM BDM. Intracellular [Ca2+] during contraction, measured with the fura-2 technique, was reduced in the presence of BDM. The reduction in force and [Ca2+] in the presence of 1 and 10 mM BDM could be reproduced by reduction in extracellular Ca2+, suggesting that BDM influences the Ca2+ entry or release. In skinned muscle preparations, BDM decreased the Ca2+ sensitivity of active force. This change could be explained by a decreased level of myosin light chain phosphorylation. In fibres maximally activated by thiophosphorylation, the effect of BDM on force occurred at higher concentrations; 10 mM gave no reduction of force and 60 mM 15% reduction. The maximal shortening velocity (Vmax) and force were unaffected by 30 mM BDM in thiophosphorylated muscle and decreased almost in parallel in Ca(2+)-activated contractions. The present results suggest that BDM inhibits myosin light chain phosphorylation, directly decreases force generation at the crossbridge level and inhibits the Ca2+ translocation in smooth muscle. The effect on force in skinned fibres is observed at higher BDM concentrations than those reported to be required for inhibition of force in striated muscle. The inhibition of force in intact smooth muscle could be explained by an influence on Ca2+ translocation.
  • Fälker, Knut, 1971-, et al. (författare)
  • ADP secretion and subsequent P2Y12 receptor signalling play a crucial role in thrombin-induced ERK2 activation in human platelets
  • 2004
  • Ingår i: Thrombosis and Haemostasis. - Stuttgart, Germany : Schattauer Gmbh. - 0340-6245. ; 92:1, s. 114-23
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Stimulating human platelets with thrombin induces the activation of the extracellular signal-regulated kinase 2 (ERK2). We demonstrate that this effect is highly dependent on ADP secretion and P2Y12 receptor signalling. AR-C69931MX (10 microM), a specific antagonist of the Gi-coupled P2Y12 ADP receptor, inhibits ERK2 activation induced by thrombin. Antagonists of the Gq-coupled P2Y1 ADP receptor, A3P5P (500 microM) and MRS2179 (100 microM), have no effect. ADP and its more potent analogue 2-methylthio-ADP alone (both up to 100 microM) do not induce ERK2 activation. Furthermore, we show that the inhibitory effect of AR-C69931MX on ERK2 activation induced by 0.1 U/ml thrombin as well as on platelet aggregation can be bypassed by epinephrine (1 and 10 microM), whereas epinephrine alone has no effect. Epinephrine acts on platelets mainly via alpha(2A)-adrenergic receptors, which, like P2Y12 receptors, couple to inhibitory G proteins. In addition, 2-methylthio-ADP as well as epinephrine provoke ERK2 activation at a thrombin concentration that alone has no detectable effect (0.05 U/ml). Thromboxane A2 (TXA2), which, like ADP, is released by activated platelets, acts as a positive feedback mediator. Stimulating the Gq-coupled TXA2 -receptor with U46619 (10 microM), which leads to ADP secretion and P2Y12 receptor-dependent platelet aggregation, also induces P2Y12-related ERK2 activation. The inhibition of U46619-induced ERK2 activation and platelet aggregation by AR-C69931MX are also rescued by epinephrine. Pretreatment with aspirin inhibits ERK2 activation induced by 0.1 U/ml thrombin, but has no effect at high concentrations of thrombin. The combination of U46619 and thrombin, at concentrations which alone have no effect, provokes ERK2 activation, suggesting that thrombin and released TXA2 act synergistically. Our data indicate that both primary signalling through Gq, which evokes ADP secretion, as well as subsequent coupling via Gi by the P2Y12 receptor are required for ERK2 activation.</p>
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