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  • 301.
    Witt, Suzanne Tyson
    et al.
    Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV. Linköpings universitet, Medicinska fakulteten.
    Bednarska, Olga
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för Kirurgi, Ortopedi och Onkologi. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Magtarmmedicinska kliniken.
    Keita, Åsa
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för Kirurgi, Ortopedi och Onkologi. Linköpings universitet, Medicinska fakulteten.
    Icenhour, Adriane
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten. Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV.
    Jones, Michael P.
    Department of Psychology, Macquarie University, NSW, Australia.
    Elsenbruch, Sigrid
    Institute of Medical Psychology & Behavioral Immunobiology, Essen University Hospital, Essen, Germany.
    Söderholm, Johan D
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för Kirurgi, Ortopedi och Onkologi. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Centrum för kirurgi, ortopedi och cancervård, Kirurgiska kliniken US.
    Engström, Maria
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för radiologiska vetenskaper. Linköpings universitet, Medicinska fakulteten. Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV.
    Mayer, Emeran A.
    Department of Medicine, UCLA, Los Angeles, CA, United States of America.
    Walter, Susanna
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Magtarmmedicinska kliniken. Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV.
    Interactions between gut permeability and brain structure and function in health and irritable bowel syndrome2019Ingår i: NeuroImage: Clinical, ISSN 0353-8842, E-ISSN 2213-1582, Vol. 21, artikel-id 101602Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Changes in brain-gut interactions have been implicated in the pathophysiology of chronic visceral pain in irritable bowel syndrome (IBS). Different mechanisms of sensitization of visceral afferent pathways may contribute to the chronic visceral pain reports and associated brain changes that characterize IBS. They include increased gut permeability and gut associated immune system activation, and an imbalance in descending pain inhibitory and facilitatory mechanisms. In order to study the involvement of these mechanisms, correlations between gut epithelial permeability and live bacterial passage, and structural and functional brain connectivity were measured in women with moderate-to-severe IBS and healthy women. The relationships between gut permeability and functional and anatomical connectivity were significantly altered in IBS compared with the healthy women. IBS participants with lower epithelial permeability reported increased IBS symptoms, which was associated with increased functional and structural connectivity in endogenous pain facilitation regions. The findings suggest that relationships between gut permeability and the brain are significantly altered in IBS and suggest the existence of IBS subtypes based on these interactions.

  • 302.
    Yaghmaeian Salmani, Behzad
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. Linköpings universitet, Medicinska fakulteten.
    Genetic Mechanisms Regulating the Spatiotemporal Modulation of Proliferation Rate and Mode in Neural Progenitors and Daughter Cells during Embryonic CNS Development2018Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
    Abstract [en]

    The central nervous system (CNS) is a hallmark feature of animals with a bilateral symmetry: bilateria and can be sub-divided into the brain and nerve cord. One of the prominent properties of the CNS across bilateria is the discernible expansion of its anterior part (brain) compared with the posterior one (nerve cord). This evolutionarily conserved feature could be attributed to four major developmental agencies: First, the existence of more anterior progenitors. Second, anterior progenitors are more proliferative. Third, anterior daughter cells, generated by the progenitors, are more proliferative. Forth, fewer cells are removed by programmed cell death (PCD) anteriorly. My thesis has addressed these issues, and uncovered both biological principles and genetic regulatory networks that promote these A-P differences. I have used the Drosophila and mouse embryonic CNSs as model systems. Regarding the 1st issue, while the brain indeed contains more progenitors, my studies demonstrate that this only partly explains the anterior expansion. Indeed, with regard to the 2nd issue, my studies, on both the Drosophila and mouse CNS, demonstrate that anterior progenitors divide more extensively. Concerning the 3rd issue, in Drosophila we identified a gradient of daughter proliferation along the AP axis of the developing CNS with brain daughter cells being more proliferative. Specifically, in the brain, progenitors divide to generate a series of daughter cells that divide once (Type I), to generate two neurons or glia. In contrast, in the nerve cord, progenitors switch during later stages, from first generating dividing daughters to subsequently generating daughters that directly differentiate (Type 0). Hence, nerve cord progenitors undergo a programmed Type I->0 proliferation switch. In the Drosophila posterior CNS, this switch occurs earlier and is more prevalent, contributing to the generation of smaller lineages in the posterior regions. Similar to Drosophila, in the mouse brain we also found that progenitor and daughter cell proliferation was elevated and extended into later developmental stages, when compared to the spinal cord. DNA-labeling experiments revealed faster cycling cells in the brain when compared to the nerve cord, in both Drosophila and mouse. In both Drosophila and mouse, we found that the suppression of progenitor and daughter proliferation in the nerve cord is controlled by the Hox homeotic gene family. Hence, the absence of Hox gene expression in the brain provides a logical explanation for the extended progenitor proliferation and lack of Type I->0 switch. The repression of Hox genes in the brain is mediated by the histonemodifying Polycomb Group complex (PcG), which thereby is responsible for the anterior expansion. With respect to the 4th issue, we found no effect of PCD on anterior expansion in Drosophila, while this cannot be asserted for the mouse embryonic neurodevelopment as there are no genetic tools to abolish PCD effectively in mammals. Taken together, the studies presented in this thesis identified global and evolutionarily-conserved genetic programs that promote anterior CNS expansion, and pave the way for understanding the evolution of size along the anterior-posterior CNS axis.

    Delarbeten
    1. Global Programmed Switch in Neural Daughter Cell Proliferation Mode Triggered by a Temporal Gene Cascade
    Öppna denna publikation i ny flik eller fönster >>Global Programmed Switch in Neural Daughter Cell Proliferation Mode Triggered by a Temporal Gene Cascade
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    2014 (Engelska)Ingår i: Developmental Cell, ISSN 1534-5807, E-ISSN 1878-1551, Vol. 30, nr 2, s. 192-208Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    During central nervous system (CNS) development, progenitors typically divide asymmetrically, renewing themselves while budding off daughter cells with more limited proliferative potential. Variation in daughter cell proliferation has a profound impact on CNS development and evolution, but the underlying mechanisms remain poorly understood. We find that Drosophila embryonic neural progenitors (neuroblasts) undergo a programmed daughter proliferation mode switch, from generating daughters that divide once (type I) to generating neurons directly (type 0). This typelgreater than0 switch is triggered by activation of Dacapo (mammalian p21(CIP1)/p27(KIP1)/p57(Kip2)) expression in neuroblasts. In the thoracic region, Dacapo expression is activated by the temporal cascade (castor) and the Hox gene Antennapedia. In addition, castor, Antennapedia, and the late temporal gene grainyhead act combinatorially to control the precise timing of neuroblast cell-cycle exit by repressing Cyclin E and E2f. This reveals a logical principle underlying progenitor and daughter cell proliferation control in the Drosophila CNS.

    Ort, förlag, år, upplaga, sidor
    Elsevier (Cell Press), 2014
    Nationell ämneskategori
    Medicinska och farmaceutiska grundvetenskaper
    Identifikatorer
    urn:nbn:se:liu:diva-109588 (URN)10.1016/j.devcel.2014.06.021 (DOI)000339641500012 ()25073156 (PubMedID)
    Tillgänglig från: 2014-08-21 Skapad: 2014-08-21 Senast uppdaterad: 2019-03-13
    2. Anterior-Posterior Gradient in Neural Stem and Daughter Cell Proliferation Governed by Spatial and Temporal Hox Control
    Öppna denna publikation i ny flik eller fönster >>Anterior-Posterior Gradient in Neural Stem and Daughter Cell Proliferation Governed by Spatial and Temporal Hox Control
    2017 (Engelska)Ingår i: Current Biology, ISSN 0960-9822, E-ISSN 1879-0445, Vol. 27, nr 8, s. 1161-1172Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    A readily evident feature of animal central nervous systems (CNSs), apparent in all vertebrates and many invertebrates alike, is its "wedge-like appearance, with more cells generated in anterior than posterior regions. This wedge could conceivably be established by an antero-posterior (A-P) gradient in the number of neural progenitor cells, their proliferation behaviors, and/or programmed cell death (PCD). However, the contribution of each of these mechanisms, and the underlying genetic programs, are not well understood. Building upon recent progress in the Drosophila melanogaster (Drosophila) ventral nerve cord (VNC), we address these issues in a comprehensive manner. We find that, although PCD plays a role in controlling cell numbers along the A-P axis, the main driver of the wedge is a gradient of daughter proliferation, with divisions directly generating neurons (type 0) being more prevalent posteriorly and dividing daughters (type I) more prevalent anteriorly. In addition, neural progenitor (NB) cell-cycle exit occurs earlier posteriorly. The gradient of type I amp;gt; 0 daughter proliferation switch and NB exit combine to generate radically different average lineage sizes along the A-P axis, differing by more than 3-fold in cell number. We find that the Hox homeotic genes, expressed in overlapping A-P gradients and with a late temporal onset in NBs, trigger the type I amp;gt; 0 daughter proliferation switch and NB exit. Given the highly evolutionarily conserved expression of overlapping Hox homeotic genes in the CNS, our results point to a common mechanism for generating the CNS wedge.

    Ort, förlag, år, upplaga, sidor
    CELL PRESS, 2017
    Nationell ämneskategori
    Utvecklingsbiologi
    Identifikatorer
    urn:nbn:se:liu:diva-137604 (URN)10.1016/j.cub.2017.03.023 (DOI)000399986500023 ()28392108 (PubMedID)
    Anmärkning

    Funding Agencies|Swedish Research Council [621-2013-5258]; Knut and Alice Wallenberg Foundation [KAW2011.0165, KAW2012.0101]; Swedish Cancer Foundation [150663]

    Tillgänglig från: 2017-05-22 Skapad: 2017-05-22 Senast uppdaterad: 2018-05-09
    3. Evolutionarily conserved anterior expansion of the central nervous system promoted by a common PcG-Hox program
    Öppna denna publikation i ny flik eller fönster >>Evolutionarily conserved anterior expansion of the central nervous system promoted by a common PcG-Hox program
    Visa övriga...
    2018 (Engelska)Ingår i: Development, ISSN 0950-1991, E-ISSN 1477-9129, Vol. 145, nr 7, artikel-id dev160747Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    A conserved feature of the central nervous system (CNS) is the prominent expansion of anterior regions (brain) compared with posterior (nerve cord). The cellular and regulatory processes driving anterior CNS expansion are not well understood in any bilaterian species. Here, we address this expansion in Drosophila and mouse. We find that, compared with the nerve cord, the brain displays extended progenitor proliferation, more elaborate daughter cell proliferation and more rapid cell cycle speed in both Drosophila and mouse. These features contribute to anterior CNS expansion in both species. With respect to genetic control, enhanced brain proliferation is severely reduced by ectopic Hox gene expression, by either Hox misexpression or by loss of Polycomb group (PcG) function. Strikingly, in PcG mutants, early CNS proliferation appears to be unaffected, whereas subsequent brain proliferation is severely reduced. Hence, a conserved PcG-Hox program promotes the anterior expansion of the CNS. The profound differences in proliferation and in the underlying genetic mechanisms between brain and nerve cord lend support to the emerging concept of separate evolutionary origins of these two CNS regions.

    Ort, förlag, år, upplaga, sidor
    Cambridge, United Kingdom: The Company of Biologists Ltd., 2018
    Nyckelord
    Asymmetric division, Cell cycle, Combinatorial control, Evolution of the CNS, Lineage size, Nervous system development
    Nationell ämneskategori
    Utvecklingsbiologi
    Identifikatorer
    urn:nbn:se:liu:diva-147741 (URN)10.1242/dev.160747 (DOI)000438944000010 ()29530878 (PubMedID)2-s2.0-85045513794 (Scopus ID)
    Tillgänglig från: 2018-05-09 Skapad: 2018-05-09 Senast uppdaterad: 2018-12-10Bibliografiskt granskad
  • 303.
    Zajdel, Joanna
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Centrum för social och affektiv neurovetenskap. Linköpings universitet, Medicinska fakulteten.
    Interactions between the brain and the immune system in pain and inflammation2019Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
    Abstract [en]

    Reciprocal interactions between the nervous and immune systems have gained a lot of attention in the last two decades, especially after demonstrating that cytokine immunotherapies can induce depression and after describing the inflammatory reflex. A lot of effort has been dedicated to understanding how the signals from the immune system reach the brain and vice versa, and on their role in health and disease. However, it is not well-known which of the brain circuits, receptors and signalling molecules give rise to behavioural and affective changes induced by inflammation, such as reduced food intake and induction of negative mood. Moreover, although it is well established that early life stress leads to an increased risk of developing inflammatory diseases in adulthood, the acute effects of stress on the inflammatory response in childhood are not well described. Using mouse models of systemic and local inflammation, I studied (1) how inflammatory pain elicits negative affect, (2) if CGRPα is necessary for parabrachial-amygdaloid pathway-mediated behaviours associated with pain and inflammation, and finally, (3) what are the effects of stress on the inflammatory process during early life. The results indicate that (1) the negative affect of inflammatory pain is triggered by inhibition of serotonergic neurons of the dorsal raphe nucleus, as a result of prostaglandin E2 binding to EP3 receptors; (2) CGRPα is dispensable for most pain- and inflammation-related protective behaviours; (3) acute stress potentiates the pro-inflammatory cytokine expression after an inflammatory challenge in mouse pups. The phenomena studied here can contribute to understanding how immune system activation induces changes in mood and behaviour common for inflammation and depression.

    Delarbeten
    1. Prostaglandin-mediated inhibition of serotonin signaling controls the affective component of inflammatory pain
    Öppna denna publikation i ny flik eller fönster >>Prostaglandin-mediated inhibition of serotonin signaling controls the affective component of inflammatory pain
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    2017 (Engelska)Ingår i: Journal of Clinical Investigation, ISSN 0021-9738, E-ISSN 1558-8238, Vol. 127, nr 4, s. 1370-1374Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    Pain is fundamentally unpleasant and induces a negative affective state. The affective component of pain is mediated by circuits that are distinct from those mediating the sensory-discriminative component. Here, we have investigated the role of prostaglandins in the affective dimension of pain using a rodent pain assay based on conditioned place aversion to formalin injection, an inflammatory noxious stimulus. We found that place aversion induced by inflammatory pain depends on prostaglandin E-2 that is synthesized by cyclooxygenase 2 in neural cells. Further, mice lacking the prostaglandin E-2 receptor EP3 selectively on serotonergic cells or selectively in the area of the dorsal raphe nucleus failed to form an aversion to formalininduced pain, as did mice lacking the serotonin transporter. Chemogenetic manipulations revealed that EP3 receptor activation elicited conditioned place aversion to pain via inhibition of serotonergic neurons. In contrast to their role in inflammatory pain aversion, EP3 receptors on serotonergic cells were dispensable for acute nociceptive behaviors and for aversion induced by thermal pain or a kappa opioid receptor agonist. Collectively, our findings show that prostaglandin-mediated modulation of serotonergic transmission controls the affective component of inflammatory pain.

    Ort, förlag, år, upplaga, sidor
    AMER SOC CLINICAL INVESTIGATION INC, 2017
    Nationell ämneskategori
    Neurovetenskaper
    Identifikatorer
    urn:nbn:se:liu:diva-136568 (URN)10.1172/JCI90678 (DOI)000398183300026 ()28287401 (PubMedID)
    Anmärkning

    Funding Agencies|European Research Council; Swedish Medical Research Council; Knut and Alice Wallenberg Foundation; Swedish Brain Foundation; County Council of Ostergotland; National Institute of Neurological Disorders and Stroke (NINDS)

    Tillgänglig från: 2017-04-24 Skapad: 2017-04-24 Senast uppdaterad: 2019-04-08
    2. Acute maternal separation potentiates the gene expression and corticosterone response induced by inflammation
    Öppna denna publikation i ny flik eller fönster >>Acute maternal separation potentiates the gene expression and corticosterone response induced by inflammation
    Visa övriga...
    2019 (Engelska)Ingår i: Brain, behavior, and immunity, ISSN 0889-1591, E-ISSN 1090-2139, Vol. 77, s. 141-149Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    Maternal care is crucial for infants and profoundly affects their responses to different kinds of stressors. Here, we examined how maternal separation affects inflammatory gene expression and the corticosterone response to an acute immune challenge induced by lipopolysaccharide (LPS; 40 µg/kg ip) in mouse pups, 8–9 days old. Maternal separation initially attenuated LPS-induced hypothalamic pro-inflammatory gene expression, but later, at 3 h after immune challenge, robustly augmented such gene expression and increased serum corticosterone levels. Providing the pups with a warm and soft object prevented the separation-induced augmented hypothalamic-pituitary-adrenal (HPA)-axis response. It also prevented the potentiated induction of some, but not all, inflammatory genes to a similar extent as did the dam. Our results show that maternal separation potentiates the inflammatory response and the resulting HPA-axis activation, which may have detrimental effects if separation is prolonged or repeated.

    Ort, förlag, år, upplaga, sidor
    Elsevier, 2019
    Nyckelord
    Lipopolysaccharide, Hypothalamus, Cytokines, Inflammation, Maternal separation, Corticosterone
    Nationell ämneskategori
    Farmakologi och toxikologi Utvecklingsbiologi Medicinsk bioteknologi Immunologi
    Identifikatorer
    urn:nbn:se:liu:diva-154886 (URN)10.1016/j.bbi.2018.12.016 (DOI)30590109 (PubMedID)2-s2.0-85059128986 (Scopus ID)
    Tillgänglig från: 2019-03-04 Skapad: 2019-03-04 Senast uppdaterad: 2019-04-08Bibliografiskt granskad
  • 304.
    Zeitooni, Mehrnaz
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Teknisk audiologi. Linköpings universitet, Hälsouniversitetet.
    Stenfelt, Stefan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Teknisk audiologi. Linköpings universitet, Hälsouniversitetet.
    Mäki-Torkko, Elina
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Teknisk audiologi. Linköpings universitet, Hälsouniversitetet.
    Binaural hearing with bone conduction stimulation in normal hearing subjects2013Konferensbidrag (Refereegranskat)
  • 305. Zha, Dingjun
    et al.
    Chen, Fangyi
    Ramamoorthy, Sripriya
    Fridberger, Anders
    Karolinska Institutet / Karolinska University Hospital, Stockholm, Sweden.
    Choudhury, Niloy
    Jacques, Steven L
    Wang, Ruikang K
    Nuttall, Alfred L
    In vivo outer hair cell length changes expose the active process in the cochlea2012Ingår i: PloS one, ISSN 1932-6203, Vol. 7, nr 4, s. e32757-Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Mammalian hearing is refined by amplification of the sound-evoked vibration of the cochlear partition. This amplification is at least partly due to forces produced by protein motors residing in the cylindrical body of the outer hair cell. To transmit power to the cochlear partition, it is required that the outer hair cells dynamically change their length, in addition to generating force. These length changes, which have not previously been measured in vivo, must be correctly timed with the acoustic stimulus to produce amplification.

    METHODOLOGY/PRINCIPAL FINDINGS: Using in vivo optical coherence tomography, we demonstrate that outer hair cells in living guinea pigs have length changes with unexpected timing and magnitudes that depend on the stimulus level in the sensitive cochlea.

    CONCLUSIONS/SIGNIFICANCE: The level-dependent length change is a necessary condition for directly validating that power is expended by the active process presumed to underlie normal hearing.

  • 306.
    Zhang, Fei
    et al.
    Oregon Health and Science University, Portland, USA.
    Dai, Min
    Oregon Health and Science University, Portland, USA.
    Neng, Lingling
    Oregon Health and Science University, Portland, USA.
    Zhang, Jin Hui
    Oregon Health and Science University, Portland, USA.
    Zhi, Zhongwei
    University of Washington, Seattle, USA.
    Fridberger, Anders
    Karolinska Institutet, Stockholm, Sweden.
    Shi, Xiaorui
    Oregon Health and Science University, Portland, USA.
    Perivascular macrophage-like melanocyte responsiveness to acoustic trauma--a salient feature of strial barrier associated hearing loss2013Ingår i: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 27, nr 9, s. 3730-3740Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Tissue perivascular resident macrophages (PVM/Ms), a hybrid cell type with characteristics of both macrophages and melanocytes, are critical for establishing and maintaining the endocochlear potential (EP) required for hearing. The PVM/Ms modulate expression of tight- and adherens-junction proteins in the endothelial barrier of the stria vascularis (intrastrial fluid-blood barrier) through secretion of a signaling molecule, pigment epithelium growth factor (PEDF). Here, we identify a significant link between abnormalities in PVM/Ms and endothelial barrier breakdown from acoustic trauma to the mouse ear. We find that acoustic trauma causes activation of PVM/Ms and physical detachment from capillary walls. Concurrent with the detachment, we find loosened tight junctions between endothelial cells and decreased production of tight- and adherens-junction protein, resulting in leakage of serum proteins from the damaged barrier. A key factor in the intrastrial fluid-blood barrier hyperpermeability exhibited in the mice is down-regulation of PVM/M modulated PEDF production. We demonstrate that delivery of PEDF to the damaged ear ameliorates hearing loss by restoring intrastrial fluid-blood barrier integrity. PEDF up-regulates expression of tight junction-associated proteins (ZO-1 and VE-cadherin) and PVM/M stabilizing neural cell adhesion molecule (NCAM-120). These studies point to the critical role PVM/Ms play in regulating intrastrial fluid-blood barrier integrity in healthy and noise-damaged ears.

  • 307. Zhang, Wenjing
    et al.
    Dai, Min
    Fridberger, Anders
    Karolinska Institutet, Stockholm, Sweden.
    Hassan, Ahmed
    Degagne, Jacqueline
    Neng, Lingling
    Zhang, Fei
    He, Wenxuan
    Ren, Tianying
    Trune, Dennis
    Auer, Manfred
    Shi, Xiaorui
    Perivascular-resident macrophage-like melanocytes in the inner ear are essential for the integrity of the intrastrial fluid-blood barrier2012Ingår i: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 109, nr 26, s. 10388-10393Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The microenvironment of the cochlea is maintained by the barrier between the systemic circulation and the fluids inside the stria vascularis. However, the mechanisms that control the permeability of the intrastrial fluid-blood barrier remain largely unknown. The barrier comprises endothelial cells connected to each other by tight junctions and an underlying basement membrane. In a recent study, we found that the intrastrial fluid-blood barrier also includes a large number of perivascular cells with both macrophage and melanocyte characteristics. The perivascular-resident macrophage-like melanocytes (PVM/Ms) are in close contact with vessels through cytoplasmic processes. Here we demonstrate that PVM/Ms have an important role in maintaining the integrity of the intrastrial fluid-blood barrier and hearing function. Using a cell culture-based in vitro model and a genetically induced PVM/M-depleted animal model, we show that absence of PVM/Ms increases the permeability of the intrastrial fluid-blood barrier to both low- and high-molecular-weight tracers. The increased permeability is caused by decreased expression of pigment epithelial-derived factor, which regulates expression of several tight junction-associated proteins instrumental to barrier integrity. When tested for endocochlear potential and auditory brainstem response, PVM/M-depleted animals show substantial drop in endocochlear potential with accompanying hearing loss. Our results demonstrate a critical role for PVM/Ms in regulating the permeability of the intrastrial fluid-blood barrier for establishing a normal endocochlear potential hearing threshold.

  • 308. Zheng, Jiefu
    et al.
    Ramamoorthy, Sripriya
    Ren, Tianying
    He, Wenxuan
    Zha, Dingjun
    Chen, Fangyi
    Magnusson, Anna
    Nuttall, Alfred L
    Fridberger, Anders
    Karolinska Institutet, Stockholm, Sweden.
    Persistence of past stimulations: storing sounds within the inner ear2011Ingår i: Biophysical Journal, ISSN 0006-3495, E-ISSN 1542-0086, Vol. 100, nr 7, s. 1627-1634Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Tones cause vibrations within the hearing organ. Conventionally, these vibrations are thought to reflect the input and therefore end with the stimulus. However, previous recordings of otoacoustic emissions and cochlear microphonic potentials suggest that the organ of Corti does continue to move after the end of a tone. These after-vibrations are characterized here through recordings of basilar membrane motion and hair cell extracellular receptor potentials in living anesthetized guinea pigs. We show that after-vibrations depend on the level and frequency of the stimulus, as well as on the sensitivity of the ear. Even a minor loss of hearing sensitivity caused a sharp reduction in after-vibration amplitude and duration. Mathematical models suggest that after-vibrations are driven by energy added into organ of Corti motion after the end of an acoustic stimulus. The possible importance of after-vibrations for psychophysical phenomena such as forward masking and gap detection are discussed.

  • 309.
    Zheng, Lin
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Geriatrik.
    Cedazo-Minguez, Angel
    KI-AlzheimerDisease Research Center, NVS, Novum, Karolinska Institutet, Stockholm, Sweden.
    Hallbeck, Martin
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Experimentell patologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Diagnostikcentrum, Klinisk patologi och klinisk genetik.
    Jerhammar, Fredrik
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Experimentell patologi. Linköpings universitet, Hälsouniversitetet.
    Marcusson, Jan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Geriatrik. Linköpings universitet, Hälsouniversitetet.
    Terman, Alexei
    Department of Clinical Pathology and Cytology, Karolinska University Hospital, Stockholm, Sweden.
    Intracellular distribution of amyloid beta peptide and its relationship to the lysosomal system.2012Ingår i: Translational Neurodegeneration, ISSN 2047-9158, Vol. 1, nr 1, s. 19-Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background

    Amyloid beta peptide (Aβ) is the main component of extraneuronal senile plaques typical of Alzheimer’s disease (AD) brains. Although Aβ is produced by normal neurons, it is shown to accumulate in large amounts within neuronal lysosomes in AD. We have recently shown that under normal conditions the majority of Aβ is localized extralysosomally, while oxidative stress significantly increases intralysosomal Aβ content through activation of macroautophagy. It is also suggested that impaired Aβ secretion and resulting intraneuronal increase of Aβ can contribute to AD pathology. However, it is not clear how Aβ is distributed inside normal neurons, and how this distribution is effected when Aβ secretion is inhibited.

    Methods

    Using retinoic acid differentiated neuroblastoma cells and neonatal rat cortical neurons, we studied intracellular distribution of Aβ by double immunofluorescence microscopy for Aβ40 or Aβ42 and different organelle markers. In addition, we analysed the effect of tetanus toxin-induced exocytosis inhibition on the intracellular distribution of Aβ.

    Results

    Under normal conditions, Aβ was found in the small cytoplasmic granules in both neurites and perikarya. Only minor portion of Aβ was colocalized with trans-Golgi network, Golgi-derived vesicles, early and late endosomes, lysosomes, and synaptic vesicles, while the majority of Aβ granules were not colocalized with any of these structures. Furthermore, treatment of cells with tetanus toxin significantly increased the amount of intracellular Aβ in both perikarya and neurites. Finally, we found that tetanus toxin increased the levels of intralysosomal Aβ although the majority of Aβ still remained extralysosomally.

    Conclusion

    Our results indicate that most Aβ is not localized to Golgi-related structures, endosomes, lysosomes secretory vesicles or other organelles, while the suppression of Aβ secretion increases intracellular intra- and extralysosomal Aβ.

  • 310.
    Österholm, Johannes H
    Linköpings universitet, Institutionen för samhälls- och välfärdsstudier, NISAL - Nationella institutet för forskning om äldre och åldrande. Linköpings universitet, Filosofiska fakulteten.
    Assessment meetings between care managers and persons living with dementia: Citizenship as practice2016Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
    Abstract [sv]

    Den här avhandlingen berör möten mellan personer med demenssjukdom och biståndshandläggare. Demenssjukdomar medför ofta komplexa omsorgsbehov, vilka kan mötas med hjälp av olika stödinsatser. Personens omsorgsbehov bedöms i ett biståndshandläggningssamtal där personen och dennes anhöriga träffar en biståndshandläggare för att förhandla dennes behov och eventuella insatser. Konversation är centralt i dessa möten. Demenssjukdomar medför kognitiva nedsättningar och nedsatt förmåga att kommunicera och interagera med andra. Det kan därför vara svårt för personer med demenssjukdom att deltaga i diskussioner om behov och insatser. 15 ljudinspelade samtal har studerats för att förstå hur personer med demens använder sina kvarvarande kommunikativa, kognitiva och språkliga resurser för att åberopa, förhandla och använda sina rättigheter som medborgare i den institutionella kontext där deras omsorgsbehov bedöms. I samtalet medverkar personen med demens, handläggaren samt ofta någon familjemedlem. Analysen fokuserar på organiseringen av samtal som en gemensam aktivitet; hur sociala aktörer skapas i samtal; hur det institutionella samtalets särdrag påverkar konversationen. Sammanfattningsvis visar denna avhandling på att hur medborgarskap praktiseras är situationsbaserat och varierar beroende på vilka som deltar i mötet. Biståndshandläggare kan underlätta för personer med demenssjukdom att övervinna kommunikativa problem genom att använda olika samtalsstrategier och göra det möjlig för dem att delta eller att åtminstone inkluderas i förhandlingen angående olika stödinsatser. Personer med demenssjukdom positioneras ofta som mindre kompetenta än andra personer som deltar i behovsbedömningssamtal, vilket kan medföra konsekvenser på personens delaktighet i planerandet av framtida insatser. Berättelser i dessa samtal positionerar ofta personen med demenssjukdom som beroende av andra, vilket kan underminera deras identitet och uppfattning av sig själva.

    Delarbeten
    1. Citizenship as practice: Handling communication problems in encounters between persons with dementia and social workers
    Öppna denna publikation i ny flik eller fönster >>Citizenship as practice: Handling communication problems in encounters between persons with dementia and social workers
    2016 (Engelska)Ingår i: Dementia, ISSN 1471-3012, E-ISSN 1741-2684, Vol. 15, nr 6, s. 1457-1473Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    The overall aim of the study was to investigate if and how persons with dementia were able to take part in negotiations for formal support, as cases of citizenship as practice. The transcripts used for analysis were from 11 assessment meetings conducted in Sweden, in which the formal applicant was a person with dementia. The findings suggest that the actual participation of persons with dementia in assessment meetings varies. Communication problems were found in the meetings to different degrees and were dealt with differently and with various consequences. For those persons with dementia contributing at the same levels as the other participants, there was an attempt at mutual understanding. For those making fewer contributions, the other interlocutors took over the initiative and thus affected the practice of citizenship by persons with dementia in a negative way. The practice of citizenship is situation based and varies depending on all participants. When the person with dementia is able to participate in the conversation, social workers can facilitate for them to overcome communication problems by giving them more time and signaling acceptance. If the person with dementia has great problems in participating, the other participants can find different strategies to at least involve her or him in the conversation

    Ort, förlag, år, upplaga, sidor
    Sage Publications, 2016
    Nationell ämneskategori
    Gerontologi, medicinsk/hälsovetenskaplig inriktning
    Identifikatorer
    urn:nbn:se:liu:diva-119105 (URN)10.1177/1471301214563959 (DOI)000387007700009 ()25525075 (PubMedID)
    Anmärkning

    Funding agencies: Solstickan Foundation; Swedish Riksbankens Jubileumsfond [M10-0187:1]

    Tillgänglig från: 2015-06-09 Skapad: 2015-06-09 Senast uppdaterad: 2018-05-16
    2. Handling the dilemma of self-determination and dementia: A study of case managers’ discursive strategies in assessment meetings.
    Öppna denna publikation i ny flik eller fönster >>Handling the dilemma of self-determination and dementia: A study of case managers’ discursive strategies in assessment meetings.
    2015 (Engelska)Ingår i: Journal of Gerontological Social Work, ISSN 0163-4372, Vol. 58, nr 6, s. 613-636Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    In assessment meetings concerning care services for people with dementia, Swedish case managers face a dilemma. On the one hand, according to the law, the right to self-determination of every adult citizen must be respected, but on the other hand cognitive disabilities make it difficult to fulfill obligations of being a full-fledged citizen. In this article, we examine 15 assessment meetings to identify discursive strategies used by case managers to handle this dilemma. We also examine how these affect the participation of persons with dementia, and indicate implications of our study for social work practice and research.

    Ort, förlag, år, upplaga, sidor
    Routledge, 2015
    Nationell ämneskategori
    Socialt arbete
    Identifikatorer
    urn:nbn:se:liu:diva-122384 (URN)10.1080/01634372.2015.1067851 (DOI)000213302600005 ()26207822 (PubMedID)
    Tillgänglig från: 2015-10-30 Skapad: 2015-10-30 Senast uppdaterad: 2018-03-09
    3. Orally positioning persons with dementia in assessment meetings
    Öppna denna publikation i ny flik eller fönster >>Orally positioning persons with dementia in assessment meetings
    2015 (Engelska)Ingår i: Ageing & Society, ISSN 0144-686X, E-ISSN 1469-1779, Vol. 35, nr 2, s. 367-388Artikel i tidskrift (Refereegranskat) Published
    Abstract [en]

    In this paper the authors study if and how persons with dementia are orally positioned by others, and how they position themselves while participating in assessment meetings held in order to discuss access to supportive services. We analysed five assessment meetings where two older persons (one diagnosed with dementia and one without a dementia diagnosis) participated to investigate whether the person with dementia is positioned differently than the other old person. Interactional phenomena used to position the person with dementia were identified by interactional analysis.

    The paperidentifies six phenomena that positioned the person with dementia as an individual with less interactional competence than the other participants: ignoring the person with dementia; voicing the feelings, capacity or opinion of the person with dementia; posing questions implying lack of competence; others' use of diagnosis; self-(re)positioning; and elderspeak. Persons with dementia are often orally positioned as less competent, indicating that they suffer further from discrimination than other older persons. We suggest that this has an impact on the participation of people with dementia in negotiations regarding their future care. The results indicate that social workers should be made aware that negative positioning exists and how it may affect the ability of people with dementia to contribute to discussions about their everyday life. Social workers should be encouraged to find strategies to reduce negative positioning in interaction.

    Ort, förlag, år, upplaga, sidor
    Cambridge: Cambridge University Press, 2015
    Nyckelord
    Äldreriktat tal positionerna biståndshandläggarsamtal demens
    Nationell ämneskategori
    Hälsovetenskaper
    Identifikatorer
    urn:nbn:se:liu:diva-103361 (URN)10.1017/S0144686X13000755 (DOI)000357881000007 ()
    Tillgänglig från: 2014-01-17 Skapad: 2014-01-17 Senast uppdaterad: 2018-05-16
  • 311.
    Österholm, Johannes H
    et al.
    Linköpings universitet, Institutionen för samhälls- och välfärdsstudier, Avdelningen för arbetsterapi. Linköpings universitet, Medicinska fakulteten.
    Taghizadeh Larsson, Annika
    Linköpings universitet, Institutionen för samhälls- och välfärdsstudier, Avdelningen Åldrande och social förändring. Linköpings universitet, Filosofiska fakulteten.
    Audio recorded data as a method to understand encounters between people living with dementia and social workers2018Ingår i: Social research methods in dementia studies: inclusion and innovation / [ed] John Keady, Lars-Christer Hydén, Ann Johnson, Caroline Swarbrick, Abingdon, Oxon: Routledge, 2018, s. 38-55Kapitel i bok, del av antologi (Övrigt vetenskapligt)
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