uu.seUppsala University Publications
Change search
Refine search result
3456 251 - 255 of 255
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Rows per page
  • 5
  • 10
  • 20
  • 50
  • 100
  • 250
Sort
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
  • Standard (Relevance)
  • Author A-Ö
  • Author Ö-A
  • Title A-Ö
  • Title Ö-A
  • Publication type A-Ö
  • Publication type Ö-A
  • Issued (Oldest first)
  • Issued (Newest first)
  • Created (Oldest first)
  • Created (Newest first)
  • Last updated (Oldest first)
  • Last updated (Newest first)
  • Disputation date (earliest first)
  • Disputation date (latest first)
Select
The maximal number of hits you can export is 250. When you want to export more records please use the Create feeds function.
  • 251. Zheng, Wen
    et al.
    Kuhlicke, Johannes
    Jäckel, Kristian
    Eltzschig, Holger K
    Singh, Anurag
    Sjöblom, Markus
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Physiology.
    Riederer, Brigitte
    Weinhold, Cornelia
    Seidler, Ursula
    Colgan, Sean P
    Karhausen, Jörn
    Hypoxia inducible factor-1 (HIF-1)-mediated repression of cystic fibrosis transmembrane conductance regulator (CFTR) in the intestinal epithelium.2009In: The FASEB journal : official publication of the Federation of American Societies for Experimental Biology, ISSN 1530-6860, Vol. 23, no 1, p. 204-213Article in journal (Refereed)
    Abstract [en]

    Diarrhea is widespread in intestinal diseases involving ischemia and/or hypoxia. Since hypoxia alters stimulated Cl(-) and water flux, we investigated the influence of such a physiologically and pathophysiologically important signal on expression of the cystic fibrosis transmembrane conductance regulator (CFTR). Located on the apical membrane, this cAMP-activated Cl(-) channel determines salt and fluid transport across mucosal surfaces. Our studies revealed depression of CFTR mRNA, protein, and function in hypoxic epithelia. Chromatin immunoprecipitation identified a previously unappreciated binding site for the hypoxia inducible factor-1 (HIF-1), and promoter studies established its relevance by loss of repression following point mutation. Consequently, HIF-1 overexpressing cells exhibited significantly reduced transport capacity in colorimetric Cl(-) efflux studies, altered short circuit measurements, and changes in transepithelial fluid movement. Whole-body hypoxia in wild-type mice resulted in significantly reduced small intestinal fluid and HCO(3)(-) secretory responses to forskolin. Experiments performed in Cftr(-/-) and Nkcc1(-/-) mice underlined the role of altered CFTR expression for these functional changes, and work in conditional Hif1a mutant mice verified HIF-1-dependent CFTR regulation in vivo. In summary, our study clarifies CFTR regulation and introduces the concept of a HIF-1-orchestrated response designed to regulate ion and fluid movement across hypoxic intestinal epithelia.

  • 252.
    Zidar, Josefina
    et al.
    Linkoping Univ, Dept Phys Chem & Biol, IFM Biol, SE-58183 Linkoping, Sweden.
    Campderrich, Irene
    Swedish Univ Agr Sci, Dept Anim Environm & Hlth, SE-75007 Uppsala, Sweden;Neiker Tecnalia, Dept Anim Prod, Vitoria 01080, Spain.
    Jansson, Emelie
    Linkoping Univ, Dept Phys Chem & Biol, IFM Biol, SE-58183 Linkoping, Sweden.
    Wichman, Anette
    Swedish Univ Agr Sci, Dept Anim Environm & Hlth, SE-75007 Uppsala, Sweden.
    Winberg, Svante
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Physiology.
    Keeling, Linda
    Swedish Univ Agr Sci, Dept Anim Environm & Hlth, SE-75007 Uppsala, Sweden.
    Løvlie, Hanne
    Linkoping Univ, Dept Phys Chem & Biol, IFM Biol, SE-58183 Linkoping, Sweden.
    Environmental complexity buffers against stress-induced negative judgement bias in female chickens2018In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 8, article id 5404Article in journal (Refereed)
    Abstract [en]

    Cognitive processes are often biased by emotions. In humans, affective disorders are accompanied by pessimistic judgement, while optimistic judgement is linked to emotional stability. Similar to humans, animals tend to interpret ambiguous stimuli negatively after experiencing stressful events, although the long-lasting impact on judgement bias has rarely been investigated. We measure judgement bias in female chicks (Gallus gallus domesticus) after exposure to cold stress, and before and after exposure to additional unpredictable stressors. Additionally, we explore if brain monoamines can explain differences in judgement bias. Chicks exposed to cold stress did not differ in judgement bias compared to controls, but showed sensitivity to additional stressors by having higher motivation for social reinstatement. Environmental complexity reduced stress-induced negative judgement bias, by maintaining an optimistic bias in individuals housed in complex conditions even after stress exposure. Moreover, judgement bias was related to dopamine turnover rate in mesencephalon, with higher activity in individuals that had a more optimistic response. These results demonstrate that environmental complexity can buffer against negative effects of additive stress and that dopamine relates to judgement bias in chicks. These results reveal that both internal and external factors can mediate emotionally biased judgement in animals, thus showing similarities to findings in humans.

    Download full text (pdf)
    fulltext
  • 253. Zygmunt, Peter M.
    et al.
    Ermund, Anna
    Movahed, Pouya
    Andersson, David A.
    Simonsen, Charlotte
    Jonsson, Bo A. G.
    Blomgren, Anders
    Birnir, Bryndis
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Physiology.
    Bevan, Stuart
    Eschalier, Alain
    Mallet, Christophe
    Gomis, Ana
    Hogestatt, Edward D.
    Monoacylglycerols Activate TRPV1-A Link between Phospholipase C and TRPV12013In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 8, no 12, p. e81618-Article in journal (Refereed)
    Abstract [en]

    Phospholipase C-mediated hydrolysis of phosphatidylinositol 4,5-bisphosphate generates diacylglycerol, inositol 1,4,5-trisphosphate and protons, all of which can regulate TRPV1 activity via different mechanisms. Here we explored the possibility that the diacylglycerol metabolites 2-arachidonoylglycerol and 1-arachidonoylglycerol, and not metabolites of these monoacylglycerols, activate TRPV1 and contribute to this signaling cascade. 2-Arachidonoylglycerol and 1-arachidonoylglycerol activated native TRPV1 on vascular sensory nerve fibers and heterologously expressed TRPV1 in whole cells and inside-out membrane patches. The monoacylglycerol lipase inhibitors methylarachidonoyl-fluorophosphonate and JZL184 prevented the metabolism of deuterium-labeled 2-arachidonoylglycerol and deuterium-labeled 1-arachidonoylglycerol in arterial homogenates, and enhanced TRPV1-mediated vasodilator responses to both monoacylglycerols. In mesenteric arteries from TRPV1 knock-out mice, vasodilator responses to 2-arachidonoylglycerol were minor. Bradykinin and adenosine triphosphate, ligands of phospholipase C-coupled membrane receptors, increased the content of 2-arachidonoylglycerol in dorsal root ganglia. In HEK293 cells expressing the phospholipase C-coupled histamine H-1 receptor, exposure to histamine stimulated the formation of 2-AG, and this effect was augmented in the presence of JZL184. These effects were prevented by the diacylglycerol lipase inhibitor tetrahydrolipstatin. Histamine induced large whole cell currents in HEK293 cells co-expressing TRPV1 and the histamine H-1 receptor, and the TRPV1 antagonist capsazepine abolished these currents. JZL184 increased the histamine-induced currents and tetrahydrolipstatin prevented this effect. The calcineurin inhibitor ciclosporin and the endogenous "entourage'' compound palmitoylethanolamide potentiated the vasodilator response to 2-arachidonoylglycerol, disclosing TRPV1 activation of this monoacylglycerol at nanomolar concentrations. Furthermore, intracerebroventricular injection of JZL184 produced TRPV1-dependent antinociception in the mouse formalin test. Our results show that intact 2-arachidonoylglycerol and 1-arachidonoylglycerol are endogenous TRPV1 activators, contributing to phospholipase C-dependent TRPV1 channel activation and TRPV1-mediated antinociceptive signaling in the brain.

    Download full text (pdf)
    fulltext
  • 254.
    Åkerman, Karl E. O.
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Physiology.
    Shariatmadari, Ramin
    Courtney, Michael J.
    Kukkonen, Jyrki P.
    Voltage gated calcium channels potentiate muscarinic receptor-mediated calcium responses in SH-SY5Y human neuroblastoma cells1997In: Life Sciences, ISSN 0024-3205, E-ISSN 1879-0631, Vol. 60, no 13-14, p. 1189-Article in journal (Other academic)
    Abstract [en]

    Muscarinic receptor-mediated Ca2+ elevations were investigated using the fura-2 method and image analysis. Typical responses consisted of an initial fast and transient phase followed by a sustained phase. Removal of external Ca2+ did not affect the magnitude of the initial phase of the signal whereas the sustained phase was abolished. Hence they may mainly consist of a release from intracellular stores and an influx, respectively. Depolarization of the cells with 30 mM KCl in the presence of external Ca2+ caused a small elevation of [Ca2+]i. In these conditions a considerable potentiation of the fast phase of muscarinic Ca2+ response was seen. The potentiation was dependent on the extracellular Ca2+ as it was abolished in the presence of antagonists of voltage-gated Ca2+ channels or by removal of external Ca2+ prior to KCl. Removal of external Ca2+ after the KCl-induced increase in [Ca2+]i partially inhibited the potentiation. If Ca2+ was readded together with the muscarinic stimulation a maximum potentiation was seen. The results suggest that the muscarinic response is potentiated by a Ca2+-mediated priming of both a fast and transient receptor associated Ca2+ influx pathway and release from the intracellular stores.

  • 255.
    Åkerman, Karl
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Physiology.
    Shariatmadari, Ramin
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Physiology.
    Krjukova, Jelena
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Physiology.
    Larsson, Kim
    Courtney, Michael
    Kukkonen, Jyrki
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Physiology.
    Ca2+-Dependent Potentiation of Muscarinic Receptor-Mediated Ca2+ Elevation2004In: Cell Calcium, ISSN 0143-4160, E-ISSN 1532-1991, Vol. 36, no 5, p. 397-408Article in journal (Refereed)
    Abstract [en]

    Muscarinic receptor-mediated increases in Ca(2+) in SH-SY5Y neuroblastoma cells consist of an initial fast and transient phase followed by a sustained phase. Activation of voltage-gated Ca(2+) channels prior to muscarinic stimulation resulted in a several-fold potentiation of the fast phase. Unlike the muscarinic response under control conditions, this potentiated elevation of intracellular Ca(2+) was to a large extent dependent on extracellular Ca(2+). In potentiated cells, muscarinic stimulation also activated a rapid Mn(2+) entry. By using known organic and inorganic blockers of cation channels, this influx pathway was easily separated from the known Ca(2+) influx pathways, the store-operated pathway and the voltage-gated Ca(2+) channels. In addition to the Ca(2+) influx, both IP(3) production and Ca(2+) release were also enhanced during the potentiated response. The results suggest that a small increase in intracellular Ca(2+) amplifies the muscarinic Ca(2+) response at several stages, most notably by unravelling an apparently novel receptor-activated influx pathway.

3456 251 - 255 of 255
CiteExportLink to result list
Permanent link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf