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  • 1.
    Birznieks, Ingvars
    et al.
    UNSW Sydney, Australia; Neurosci Res Australia, Australia; Western Sydney Univ, Australia.
    Mcintyre, Sarah
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten. Neurosci Res Australia, Australia; Western Sydney Univ, Australia.
    Nilsson, Hanna Maria
    Linköpings universitet. Sweden; Neurosci Res Australia, Australia.
    Nagi, Saad
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten. Western Sydney Univ, Australia.
    Macefield, Vaughan G.
    Neurosci Res Australia, Australia; Western Sydney Univ, Australia; Baker Heart and Diabet Inst, Australia.
    Mahns, David A.
    Western Sydney Univ, Australia.
    Vickery, Richard M.
    UNSW Sydney, Australia; Neurosci Res Australia, Australia.
    Tactile sensory channels over-ruled by frequency decoding system that utilizes spike pattern regardless of receptor type2019Inngår i: eLIFE, E-ISSN 2050-084X, Vol. 8, artikkel-id e46510Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The established view is that vibrotactile stimuli evoke two qualitatively distinctive cutaneous sensations, flutter (frequencies amp;lt; 60 Hz) and vibratory hum (frequencies amp;gt; 60 Hz), subserved by two distinct receptor types (Meissners and Pacinian corpuscle, respectively), which may engage different neural processing pathways or channels and fulfil quite different biological roles. In psychological and physiological literature, those two systems have been labelled as Pacinian and non-Pacinian channels. However, we present evidence that low-frequency spike trains in Pacinian afferents can readily induce a vibratory percept with the same low frequency attributes as sinusoidal stimuli of the same frequency, thus demonstrating a universal frequency decoding system. We achieved this using brief low-amplitude pulsatile mechanical stimuli to selectively activate Pacinian afferents. This indicates that spiking pattern, regardless of receptor type, determines vibrotactile frequency perception. This mechanism may underlie the constancy of vibrotactile frequency perception across different skin regions innervated by distinct afferent types.

  • 2.
    Larsson, Johan
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelning för neurobiologi. Linköpings universitet, Medicinska fakulteten.
    Larsson, H. Peter
    Univ Miami, FL USA.
    Liin, Sara
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelning för neurobiologi. Linköpings universitet, Medicinska fakulteten.
    KCNE1 tunes the sensitivity a: K(v)7.1 to polyunsaturated fatty acids by moving turret residues close to the binding site2018Inngår i: eLIFE, E-ISSN 2050-084X, Vol. 7, artikkel-id e37257Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The voltage-gated potassium channel K(v)7.1 and the auxiliary subunit KCNE1 together form the cardiac I-Ks channel, which is a proposed target for future anti-arrhythmic drugs. We previously showed that polyunsaturated fatty acids (PUFAs) activate K(v)7.1 via an electrostatic mechanism. The activating effect was abolished when K(v)7.1 was co-expressed with KCNE1, as KCNE1 renders PUFAs ineffective by promoting PUFA protonation. PUFA protonation reduces the potential of PUFAs as anti-arrhythmic compounds. It is unknown how KCNE1 promotes PUFA protonation. Here, we found that neutralization of negatively charged residues in the S5-P-helix loop of K(v)7.1 restored PUFA effects on K(v)7.1 co-expressed with KCNE1 in Xenopus oocytes. We propose that KCNE1 moves the S5-P-helix loop of K(v)7.1 towards the PUFA-binding site, which indirectly causes PUFA protonation, thereby reducing the effect of PUFAs on K(v)7.1. This mechanistic understanding of how KCNE1 alters K(v)7.1 pharmacology is essential for development of drugs targeting the I-Ks channel.

  • 3.
    Liin, Sara
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Medicinska fakulteten. University of Miami, FL, USA.
    Larsson, Johan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Medicinska fakulteten.
    Berro-Soria, Rene
    University of Miami, FL, USA.
    Hjorth Bentzen, Bo
    The Danish Arrhythmia Research Centre, University of Copenhagen, Copenhagen, Denmark; Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark.
    Larson, H. Peter
    University of Miami, FL, USA.
    Fatty acid analogue N-arachidonoyl taurine restores function of I-Ks channels with diverse long QT mutations2016Inngår i: eLIFE, E-ISSN 2050-084X, Vol. 5, artikkel-id e20272Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    About 300 loss-of-function mutations in the I-Ks channel have been identified in patients with Long QT syndrome and cardiac arrhythmia. How specific mutations cause arrhythmia is largely unknown and there are no approved I-Ks channel activators for treatment of these arrhythmias. We find that several Long QT syndrome-associated IKs channel mutations shift channel voltage dependence and accelerate channel closing. Voltage-clamp fluorometry experiments and kinetic modeling suggest that similar mutation-induced alterations in IKs channel currents may be caused by different molecular mechanisms. Finally, we find that the fatty acid analogue N-arachidonoyl taurine restores channel gating of many different mutant channels, even though the mutations are in different domains of the IKs channel and affect the channel by different molecular mechanisms. N-arachidonoyl taurine is therefore an interesting prototype compound that may inspire development of future IKs channel activators to treat Long QT syndrome caused by diverse IKs channel mutations.

  • 4.
    Rodriguez Curt, Jesús
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. Linköpings universitet, Medicinska fakulteten. Univ Cambridge, England.
    Yaghmaeian Salmani, Behzad
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för hematopoes och utvecklingsbiologi. Linköpings universitet, Medicinska fakulteten. Karolinska Inst, Sweden.
    Thor, Stefan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för hematopoes och utvecklingsbiologi. Linköpings universitet, Medicinska fakulteten. Univ Queensland, Australia.
    Anterior CNS expansion driven by brain transcription factors2019Inngår i: eLIFE, E-ISSN 2050-084X, Vol. 8, artikkel-id e45274Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    During CNS development, there is prominent expansion of the anterior region, the brain. In Drosophila, anterior CNS expansion emerges from three rostral features: (1) increased progenitor cell generation, (2) extended progenitor cell proliferation, (3) more proliferative daughters. We find that tailless (mouse Nr2E1/Tlx), otp/Rx/hbn (Otp/Arx/Rax) and Doc1/2/3 (Tbx2/3/6) are important for brain progenitor generation. These genes, and earmuff (FezF1/2), are also important for subsequent progenitor and/or daughter cell proliferation in the brain. Brain TF comisexpression can drive brain-profile proliferation in the nerve cord, and can reprogram developing wing discs into brain neural progenitors. Brain TF expression is promoted by the PRC2 complex, acting to keep the brain free of anti-proliferative and repressive action of Hox homeotic genes. Hence, anterior expansion of the Drosophila CNS is mediated by brain TF driven super-generation of progenitors, as well as hyper-proliferation of progenitor and daughter cells, promoted by PRC2-mediated repression of Hox activity.

  • 5.
    Salazar, Valerie S.
    et al.
    Harvard Sch Dent Med, MA 02115 USA; Univ Zurich, Switzerland.
    Capelo, Luciane P.
    Harvard Sch Dent Med, MA 02115 USA; Univ Fed Sao Paulo, Brazil.
    Cantù, Claudio
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. Linköpings universitet, Medicinska fakulteten. Univ Zurich, Switzerland.
    Zimmerli, Dario
    Univ Zurich, Switzerland.
    Gosalia, Nehal
    Regeneron Pharmaceut, NY USA.
    Pregizer, Steven
    Harvard Sch Dent Med, MA 02115 USA.
    Cox, Karen
    Harvard Sch Dent Med, MA 02115 USA.
    Ohte, Satoshi
    Harvard Sch Dent Med, MA 02115 USA; Kitasato Univ, Japan.
    Feigenson, Marina
    Harvard Sch Dent Med, MA 02115 USA.
    Gamer, Laura
    Harvard Sch Dent Med, MA 02115 USA.
    Nyman, Jeffry S.
    Vanderbilt Univ, TN USA.
    Carey, David J.
    Geisinger Hlth Syst, PA USA.
    Economides, Aris
    Regeneron Pharmaceut, NY USA.
    Basler, Konrad
    Harvard School of Dental Medicine, Boston, United States.
    Rosen, Vicki
    Harvard Sch Dent Med, MA 02115 USA.
    Reactivation of a developmental Bmp2 signaling center is required for therapeutic control of the murine periosteal niche2019Inngår i: eLIFE, E-ISSN 2050-084X, Vol. 8, artikkel-id e42386Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Two decades after signals controlling bone length were discovered, the endogenous ligands determining bone width remain unknown. We show that postnatal establishment of normal bone width in mice, as mediated by bone-forming activity of the periosteum, requires BMP signaling at the innermost layer of the periosteal niche. This developmental signaling center becomes quiescent during adult life. Its reactivation however, is necessary for periosteal growth, enhanced bone strength, and accelerated fracture repair in response to bone-anabolic therapies used in clinical orthopedic settings. Although many BMPs are expressed in bone, periosteal BMP signaling and bone formation require only Bmp2 in the Prx1-Cre lineage. Mechanistically, BMP2 functions downstream of Lrp5/6 pathway to activate a conserved regulatory element upstream of Sp7 via recruitment of Smad1 and Grhl3. Consistent with our findings, human variants of BMP2 and GRHL3 are associated with increased risk of fractures.

  • 6.
    Shahul Hameed, L.
    et al.
    Karolinska Institute, Sweden.
    Berg, Daniel A.
    Karolinska Institute, Sweden.
    Belnoue, Laure
    Karolinska Institute, Sweden.
    Jensen, Lasse
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för kardiovaskulär medicin. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Diagnostikcentrum, Klinisk farmakologi. Karolinska Institute, Sweden.
    Cao, Yihai
    Linköpings universitet, Institutionen för medicin och hälsa. Linköpings universitet, Medicinska fakulteten. Karolinska Institute, Sweden; University of Leicester, England.
    Simon, Andras
    Karolinska Institute, Sweden.
    Environmental changes in oxygen tension reveal ROS-dependent neurogenesis and regeneration in the adult newt brain2015Inngår i: eLIFE, E-ISSN 2050-084X, ELIFE SCIENCES PUBLICATIONS LTD, SHERATON HOUSE, CASTLE PARK, CAMBRIDGE, CB3 0AX, ENGLAND, ISSN 2050-084X, Vol. 4, nr e08422Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Organisms need to adapt to the ecological constraints in their habitat. How specific processes reflect such adaptations are difficult to model experimentally. We tested whether environmental shifts in oxygen tension lead to events in the adult newt brain that share features with processes occurring during neuronal regeneration under normoxia. By experimental simulation of varying oxygen concentrations, we show that hypoxia followed by re-oxygenation lead to neuronal death and hallmarks of an injury response, including activation of neural stem cells ultimately leading to neurogenesis. Neural stem cells accumulate reactive oxygen species (ROS) during re-oxygenation and inhibition of ROS biosynthesis counteracts their proliferation as well as neurogenesis. Importantly, regeneration of dopamine neurons under normoxia also depends on ROS-production. These data demonstrate a role for ROS-production in neurogenesis in newts and suggest that this role may have been recruited to the capacity to replace lost neurons in the brain of an adult vertebrate.

  • 7.
    Stratmann, Johannes
    et al.
    Linköpings universitet, Medicinska fakulteten. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin.
    Gabilondo, Hugo
    Linköpings universitet, Medicinska fakulteten. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. University of Autonoma Madrid, Spain.
    Benito-Sipos, Jonathan
    University of Autonoma Madrid, Spain.
    Thor, Stefan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. Linköpings universitet, Medicinska fakulteten.
    Neuronal cell fate diversification controlled by sub-temporal action of Kruppel2016Inngår i: eLIFE, E-ISSN 2050-084X, Vol. 5, artikkel-id e19311e19311Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    During Drosophila embryonic nervous system development, neuroblasts express a programmed cascade of five temporal transcription factors that govern the identity of cells generated at different time-points. However, these five temporal genes fall short of accounting for the many distinct cell types generated in large lineages. Here, we find that the late temporal gene castor sub-divides its large window in neuroblast 5-6 by simultaneously activating two cell fate determination cascades and a sub-temporal regulatory program. The sub-temporal program acts both upon itself and upon the determination cascades to diversify the castor window. Surprisingly, the early temporal gene Kruppel acts as one of the sub-temporal genes within the late castor window. Intriguingly, while the temporal gene castor activates the two determination cascades and the sub-temporal program, spatial cues controlling cell fate in the latter part of the 5-6 lineage exclusively act upon the determination cascades.

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