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1.	Gyllensten, Hanna, 1979, et al. (author) Cost-effectiveness of the behavioral antenatal care intervention programme Mighty Mums 2016 In: European Obesity Summit (EOS) - Joint Congress of EASO and IFSO-EC, Gothenburg, Sweden, June 1-4, 2016. Obesity Facts.. - : S. Karger AG. - 1662-4025 .- 1662-4033. - 9783318058956 Conference paper (peer-reviewed)
2.	Abbott, N. Joan, et al. (author) Astrocyte-endothelial interactions at the blood-brain barrier 2006 In: Nature Reviews Neuroscience. - : Springer Science and Business Media LLC. - 1471-0048 .- 1471-003X. ; 7:1, s. 41-53 Research review (peer-reviewed)
3.	Adermark, Louise, 1974, et al. (author) Ethanol acutely decreases astroglial gap junction permeability in primary cultures from defined brain regions 2004 In: Neurochemistry International. - : Elsevier BV. - 0197-0186. ; 45:7, s. 971-978 Journal article (peer-reviewed)abstract The acute effect of hyperosmotic ethanol on gap junction permeability was examined in astroglial cells in primary culture from five different brain regions. Gap junction permeability was analyzed by measuring dye spreading from cell to cell with the low molecular weight dye Lucifer Yellow. Ethanol concentrations 25-300 mM significantly decreased dye spreading in cultures from the cerebral cortex in a dose-dependent but time-independent manner for up to 60 min. Besides cerebral cortex, exposure to 150 mM ethanol decreased dye spreading in astroglial cultures from the hippocampus and from the brain stem, while cultures from the olfactory bulb and from the hypothalamus were not significantly affected. The ethanol-induced decrease in dye spreading in cultures from the cerebral cortex was not mediated through changes in cell volume, osmolarity, protein kinase C (PKC) phosphorylation, intracellular pH, or intracellular calcium concentration ([Ca 2+ ] i ). The decrease in dye spreading was abolished upon incubation in sodium-reduced buffer, and after blockage of the Na + /K + /2Cl - cotransporter with furosemide. The results presented here indicate that ethanol-mediated decrease in dye spreading is directly or indirectly dependent on sodium. © 2004 Elsevier Ltd. All rights reserved.
4.	Adermark, Louise, 1974, et al. (author) Implications for glycine receptors and astrocytes in ethanol-induced elevation of dopamine levels in the nucleus accumbens. 2011 In: Addiction biology. - : Wiley. - 1369-1600 .- 1355-6215. ; 16:1, s. 43-54 Journal article (peer-reviewed)abstract ABSTRACT Elevated dopamine levels are believed to contribute to the rewarding sensation of ethanol (EtOH), and previous research has shown that strychnine-sensitive glycine receptors in the nucleus accumbens (nAc) are involved in regulating dopamine release and in mediating the reinforcing effects of EtOH. Furthermore, the osmoregulator taurine, which is released from astrocytes treated with EtOH, can act as an endogenous ligand for the glycine receptor, and increase extracellular dopamine levels. The aim of this study was to address if EtOH-induced swelling of astrocytes could contribute to elevated dopamine levels by increasing the extracellular concentration of taurine. Cell swelling was estimated by optical sectioning of fluorescently labeled astrocytes in primary cultures from rat, and showed that EtOH (25-150 mM) increased astrocyte cell volumes in a concentration- and ion-dependent manner. The EtOH-induced cell swelling was inhibited in cultures treated with the Na(+)/K(+)/2Cl(-) cotransporter blocker furosemide (1 mM), Na(+)/K(+)-ATPase inhibitor ouabain (0.1 mM), potassium channel inhibitor BaCl(2) (50 microM) and in cultures containing low extracellular sodium concentration (3 mM). In vivo microdialysis performed in the nAc of awake and freely moving rats showed that local treatment with EtOH enhanced the concentrations of dopamine and taurine in the microdialysate, while glycine and beta-alanine levels were not significantly modulated. EtOH-induced dopamine release was antagonized by local treatment with the glycine receptor antagonist strychnine (20 microM) or furosemide (100 microM or 1 mM). Furosemide also prevented EtOH-induced taurine release in the nAc. In conclusion, our data suggest that extracellular concentrations of dopamine and taurine are interconnected and that swelling of astrocytes contributes to the acute rewarding sensation of EtOH.
5.	Andersson, Anna, et al. (author) Lactate contributes to ammonia-mediated astroglial dysfunction during hyperammonemia. 2009 In: Neurochemical research. - : Springer Science and Business Media LLC. - 1573-6903 .- 0364-3190. ; 34:3, s. 556-65 Journal article (peer-reviewed)abstract Even though ammonia is considered to underlie nervous system symptoms of dysfunction during hyperammonemia, lactate, which increases as a metabolic consequence of high ammonia levels, might also be a contributing factor. The data presented here show that NH4Cl (5 mM) mediates astroglial cell swelling, and that treatment with NH4Cl or lactate (25 mM) causes rearrangements of actin filaments and reduces astroglial glutamate uptake capacity. Co-application with BaCl2, which blocks astroglial uptake of NH4+, prevents NH4Cl-mediated cell swelling and rearrangement of actin filaments, but does not reduce NH4Cl-induced glutamate uptake capacity inhibition. Neither NH4Cl nor lactate affected glutamate uptake or protein expression in microglial cultures, indicating that astroglial cells are more susceptible to the neurotoxic affects of ammonia. Our results suggest that ammonium underlies brain edema, but that lactate can contribute to some of the cellular dysfunctions associated with elevated cerebral levels of ammonia.
6.	Andersson, Anna, et al. (author) Lactate induces tumour necrosis factor-alpha, interleukin-6 and interleukin-1 beta release in microglial- and astroglial-enriched primary cultures 2005 In: Journal of Neurochemistry. - : Wiley. - 0022-3042 .- 1471-4159. ; 93:5, s. 1327-1333 Journal article (peer-reviewed)
7.	Björklund, Ulrika, 1970, et al. (author) Primary cultures from cerebral cortex and hippocampus enriched in glutamatergic and GABAergic neurons. 2010 In: Neurochemical research. - : Springer Science and Business Media LLC. - 1573-6903 .- 0364-3190. ; 35:11, s. 1733-42 Journal article (peer-reviewed)abstract The aim was to define a primary culture system enriched in neurons using a defined culture medium, and characterize the model system as to cellular morphology and neuronal phenotypes. We found that these primary neuron enriched cultures from either newborn rat cerebral cortex or hippocampus contain small GABAergic and large glutamatergic neurons as well as astrocytes and microglia. Astrocytes in these cultures are morphologically differentiated with long, slender processes and interact with soluble factors responsible for induction and expression of the glutamate transporter GLT-1. The cultures achieve the highest expression of the vesicular glutamate transporter 1 (VGLUT1) and GLT-1 after 20 days in vitro. Conditioned media from these neuron enriched cultures also induced GLT-1 expression in primary astrocytic cultures, which were free from neurons. The amount of glutamatergic neurons guides the morphological maturation of astrocytes and GLT-1 expression both in the neuron enriched cultures and in the conditioned media supplemented astrocytic cultures. Interestingly, these cultures were not influenced or activated by the inflammatory stimulus lipopolysaccharide. This suggests that soluble factors from neurons protect microglia and astrocytes to become inflammatory reactive. In conclusion we have developed a well characterized culture model system enriched in neurons, taken from newborn rats and cultured in defined media. The neurons express different neuronal phenotypes. Such a model system is valuable when studying interactions between neurons and glial cells.
8.	Block, Linda, et al. (author) A new concept affecting restoration of inflammation-reactive astrocytes. 2013 In: Neuroscience. - : Elsevier BV. - 1873-7544 .- 0306-4522. ; 250, s. 536-45 Journal article (peer-reviewed)abstract Long-lasting pain may partly be a consequence of ongoing neuroinflammation, in which astrocytes play a significant role. Following noxious stimuli, increased inflammatory receptor activity, influences in Na(+)/K(+)-ATPase activity and actin filament organization occur within the central nervous system. In astrocytes, the Ca(2+) signaling system, Na(+) transporters, cytoskeleton, and release of pro-inflammatory cytokines change during inflammation. The aim of this study was to restore these cell parameters in inflammation-reactive astrocytes. We found that the combination of (1) endomorphin-1, an opioid agonist that stimulates the Gi/o protein of the μ-opioid receptor; (2) naloxone, an opioid antagonist that inhibits the Gs protein of the μ-opioid receptor at ultralow concentrations; and (3) levetiracetam, an anti-epileptic agent that counteracts the release of IL-1β, managed to activate the Gi/o protein and Na(+)/K(+)-ATPase activity, inhibit the Gs protein, and decrease the release of IL-1β. The cell functions of astrocytes in an inflammatory state were virtually restored to their normal non-inflammatory state and it could be of clinical significance and may be useful for the treatment of long-term pain.
9.	Block, Linda, et al. (author) Naloxone in ultralow concentration restores endomorphin-1-evoked Ca(2+) signaling in lipopolysaccharide pretreated astrocytes. 2012 In: Neuroscience. - : Elsevier BV. - 1873-7544 .- 0306-4522. ; 205, s. 1-9 Journal article (peer-reviewed)abstract Long-term pain is a disabling condition that affects thousands of people. Pain may be sustained for a long time even after the physiological trigger has resolved. Possible mechanisms for this phenomenon include low-grade inflammation in the CNS. Astrocytes respond to inflammatory stimuli and may play an important role as modulators of the inflammatory response in the nervous system. This study aimed first to assess how astrocytes in a primary culture behave when exposed to the endogenous μ-opioid receptor agonist endomorphin-1 (EM-1), in a concentration-dependent manner, concerning intracellular Ca(2+) responses. EM-1 stimulated the μ-opioid receptor from 10(-15) M up to 10(-4) M with increasing intensity, usually reflected as one peak at low concentrations and two peaks at higher concentrations. Naloxone, pertussis toxin (PTX), or the μ-opioid receptor antagonists CTOP did not totally block the EM-1-evoked Ca(2+) responses. However, a combination of ultralow concentration naloxone (10(-12) M) and PTX (100 ng/ml) totally blocked the EM-1-evoked Ca(2+) responses. This suggests that ultralow (picomolar) concentrations of naloxone should block the μ-opioid receptor coupled G(s) protein, and that PTX should block the μ-opioid receptor coupled G(i/o) protein. The second aim was to investigate exposure of astrocytes with the inflammatory agent lipopolysaccharide (LPS). After 4 h of LPS incubation, the EM-1-evoked Ca(2+) transients were attenuated, and after 24 h of LPS incubation, the EM-1-evoked Ca(2+) transients were oscillated. To restore the EM-1-evoked Ca(2+) transients, naloxone was assessed as a proposed anti-inflammatory substance. In ultralow picomolar concentration, naloxone demonstrated the ability to restore the Ca(2+) transients.
10.	Block, Linda, et al. (author) Ultralow concentrations of bupivacaine exert anti-inflammatory effects on inflammation-reactive astrocytes. 2013 In: The European journal of neuroscience. - : Wiley. - 1460-9568 .- 0953-816X. ; 38:11, s. 3669-3678 Journal article (peer-reviewed)abstract Bupivacaine is a widely used, local anesthetic agent that blocks voltage-gated Na(+) channels when used for neuro-axial blockades. Much lower concentrations of bupivacaine than in normal clinical use, <10(-8) m, evoked Ca(2+) transients in astrocytes from rat cerebral cortex, that were inositol trisphosphate receptor-dependent. We investigated whether bupivacaine exerts an influence on the Ca(2+) signaling and interleukin-1β (IL-1β) secretion in inflammation-reactive astrocytes when used at ultralow concentrations, <10(-8) m. Furthermore, we wanted to determine if bupivacaine interacts with the opioid-, 5-hydroxytryptamine- (5-HT) and glutamate-receptor systems. With respect to the μ-opioid- and 5-HT-receptor systems, bupivacaine restored the inflammation-reactive astrocytes to their normal non-inflammatory levels. With respect to the glutamate-receptor system, bupivacaine, in combination with an ultralow concentration of the μ-opioid receptor antagonist naloxone and μ-opioid receptor agonists, restored the inflammation-reactive astrocytes to their normal non-inflammatory levels. Ultralow concentrations of bupivacaine attenuated the inflammation-induced upregulation of IL-1β secretion. The results indicate that bupivacaine interacts with the opioid-, 5-HT- and glutamate-receptor systems by affecting Ca(2+) signaling and IL-1β release in inflammation-reactive astrocytes. These results suggest that bupivacaine may be used at ultralow concentrations as an anti-inflammatory drug, either alone or in combination with opioid agonists and ultralow concentrations of an opioid antagonist.
11.	Block, Linda, et al. (author) Ultralow Dose of Naloxone as an Adjuvant to Intrathecal Morphine Infusion Improves Perceived Quality of Sleep but Fails to alter Persistent Pain: A Randomized, Double-blind, Controlled Study. 2015 In: The Clinical journal of pain. - 1536-5409. ; 31:11, s. 968-975 Journal article (peer-reviewed)abstract This randomized, cross-over, double-blind, controlled study of continuous intrathecal morphine administration in patients with severe, long-term pain addresses whether the supplementation of low doses of naloxone in this setting is associated with beneficial clinical effects. All of the study subjects (n=11) provided informed consent and were recruited from a subset of patients who were already undergoing long-term treatment with continuous intrathecal morphine because of difficult-to-treat pain. The patients were (in a randomized order) also given intrathecal naloxone (40 ng/24 h or 400 ng/24 h). As control, the patients' ordinary dose of morphine without any additions was used. The pain (Numeric Rating Scale, NRS) during activity, perceived quality of sleep, level of activity and quality of life as well as the levels of several pro- and anti-inflammatory cytokines in the blood were assessed. The pre-study pain (NRS during activity) in the study group ranged from 3 to 10. 64% of the subjects reported improved quality of sleep during treatment with naloxone at a dose of 40 ng/24 hours compared with 9% with sham treatment (P=0.024). Although not statistically significant, pain was reduced by 2 NRS steps or more during supplemental treatment with naloxone in 36% of subjects when using the 40 ng/24 hours dose and in 18% of the subjects when using a naloxone 400 ng/24 hours dose. The corresponding percentage among patients receiving unaltered treatment was 27%. To conclude, the addition of an ultralow dose of intrathecal naloxone (40 ng/24 h) to intrathecal morphine infusion in patients with severe, persistent pain improves perceived quality of sleep. We were not able to show any statistically significant effects of naloxone on pain relief, level of activity or quality of life.This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivitives 3.0 License, where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially. http://creativecommons.org/licenses/by-nc-nd/3.0.
12.	Blomstrand, Fredrik, 1969, et al. (author) Extent of intercellular calcium wave propagation is related to gap junction permeability and level of connexin-43 expression in astrocytes in primary cultures from four brain regions. 1999 In: Neuroscience. - 0306-4522. ; 92:1, s. 255-65 Journal article (peer-reviewed)abstract Astrocytes are coupled via gap junctions, predominantly formed by connexin-43 proteins, into cellular networks. This coupling is important for the propagation of intercellular calcium waves and for the spatial buffering of K+. Using the scrape-loading/dye transfer technique, we studied gap junction permeability in rat astrocytes cultured from four different brain regions. The cultures were shown to display regional heterogeneity with the following ranking of the gap junction coupling strengths: hippocampus = hypothalamus > cerebral cortex = brain stem. Similar relative patterns were found in connexin-43 messenger RNA and protein levels using solution hybridization/RNase protection assay and western blots, respectively. The percentages of the propagation area of mechanically induced intercellular calcium waves for cortical, brain stem and hypothalamic astrocytes compared with hippocampal astrocytes were approximately 77, 42, and 52, respectively. Thus, the extent of calcium wave propagation was due to more than just gap junctional permeability as highly coupled hypothalamic astrocytes displayed relatively small calcium wave propagation areas. Incubation with 5-hydroxytryptamine decreased and incubation with glutamate increased the calcium wave propagation area in hippocampal (67% and 170% of the control, respectively) and in cortical astrocytes (82% and 163% of the control, respectively). Contrary to hippocampal and cortical astrocytes, the calcium wave propagation in brain stem astrocytes was increased by 5-hydroxytryptamine incubation (158% of control), while in hypothalamic astrocytes, no significant effects were seen. Similar effects from 5-hydroxytryptamine or glutamate treatments were observed on dye transfer, indicating an effect on the junctional coupling strength. These results demonstrate a strong relationship between connexin-43 messenger RNA levels, protein expression, and gap junction permeability among astroglial cells. Furthermore, our results suggest heterogeneity among astroglial cells from different brain regions in intercellular calcium signaling and in its differential modulation by neurotransmitters, probably reflecting functional requirements in various brain regions.
13.	Caesar, Ulla, et al. (author) A sense of being rejected : Patients’ lived experiences of cancelled knee or hip replacement surgery 2021 In: Scandinavian Journal of Caring Sciences. - : John Wiley & Sons. - 0283-9318 .- 1471-6712. Journal article (peer-reviewed)abstract BackgroundGrowing care queues, reduced access to care and cancelled surgery are realities for some patients being treated with total hip or knee replacement surgery in Sweden.Most of the patients on the waiting lists have experienced pain and limited motion for a varying period of time, with a negative effect on their everyday lives. Overbooked surgical schedules are already contributing to the lengthy waiting times, but, with the addition of cancellations, longer waiting times will increase still further and may affect patients’ well‐being.MethodsIn the present study, we aimed to illuminate the experience of having planned surgery cancelled, based on narratives from 10 participants. The interview transcriptions were analysed using a phenomenological hermeneutic approach.ResultsThe comprehensive analyses revealed that the participants described the agony of being deselected and the additional impression of being excluded. Metaphors of being damaged and feeling physical pain were used and the interpretations referred to the cancellations as unpleasant. Additionally, the important relationship and the trust between the health workers and the patient were negatively affected by the cancellation.ConclusionAfter the cancellation, the participants expressed being vulnerable and from their perspective the cancelled surgery affected them deeply; in fact, much more than the healthcare workers appeared to understand. Therefore, information around the cancellation must be given respectfully and with dignity, in a dialogue between the patient and the healthcare workers. Taken together, to enable an opportunity to be involved in the continued care. The cancellations should be seen as an interruption, in which the patients’ chance of living a pain‐free, active life is postponed.
14.	Carlström, Eric, 1957, et al. (author) The unannounced patient in the corridor - trust, friction and person centered care. 2017 In: International Journal of Health Planning and Management. - : Wiley. - 0749-6753 .- 1099-1751. ; 32:1 Journal article (peer-reviewed)abstract In this study, a Swedish cancer clinic was studied where three to four unscheduled patients sought support from the hospital on a daily basis for pain and nutrition problems. The clinic was neither staffed nor had a budget to handle such return visits. In order to offer the patients a better service and decrease the workload of the staff in addition to their everyday activities, a multidisciplinary team was established to address the unscheduled return visits. The team was supposed to involve the patient, build trust, decrease the friction, and contribute to a successful rehabilitation process. Data were collected from the patients and the staff. Patients who encountered the team (intervention) and patients who encountered the regular ad hoc type of organization (control) answered a questionnaire measuring trust and friction. Nurses in the control group spent 35% of their full‐time employment, and the intervention group staffed with nurses spent 30% of their full‐time employment in addressing the needs of these return patients. The patients perceived that trust between them and the staff was high. In summary, it was measured as being 4.48 [standard deviation (SD) = 0.82] in the intervention group and 4.41 (SD = 0.79) in the control group using the 5‐point Likert scale. The data indicate that using a multidisciplinary team is a promising way to handle the problems of unannounced visits from patients. Having a team made it cost effective for the clinic and provided a better service than the traditional ad hoc organization.
15.	Delbro, Dick, 1950, et al. (author) In inflammatory reactive astrocytes co-cultured with brain endothelial cells nicotine-evoked Ca(2+) transients are attenuated due to interleukin-1beta release and rearrangement of actin filaments. 2009 In: Neuroscience. - : Elsevier BV. - 0306-4522. ; 159:2, s. 770-9 Journal article (peer-reviewed)abstract The aim of this study was to investigate whether nicotine acetylcholine receptors (nAChRs) are expressed in a more pronounced way in astrocytes co-cultured with microvascular endothelial cells from adult rat brain, compared with monocultured astrocytes, as a sign of a more developed signal transduction system. Also investigated was whether nicotine plays a role in the control of neuroinflammatory reactivity in astrocytes. Ca(2+) imaging experiments were performed using cells loaded with the Ca(2+) indicator Fura-2/AM. Co-cultured astrocytes responded to lower concentrations of nicotine than did monocultured astrocytes, indicating that they are more sensitive to nicotine. Co-cultured astrocytes also expressed a higher selectivity for alpha7nAChR and alpha4/beta2 subunits and evoked higher Ca(2+) transients compared with monocultured astrocytes. The Ca(2+) transients referred to are activators of Ca(2+)-induced Ca(2+) release from intracellular stores, both IP(3) and ryanodine, triggered by influx through receptor channels. The nicotine-induced Ca(2+) transients were attenuated after incubation with the inflammatory mediator lipopolysaccharide (LPS), but were not attenuated after incubation with the pain-transmitting peptides substance P and calcitonin-gene-related peptide, nor with the infection and inflammation stress mediator, leptin. Furthermore, LPS-induced release of interleukin-1beta (IL-1beta) measured by enzyme-linked immunosorbent assay (ELISA) was more pronounced in co-cultured versus monocultured astrocytes. Incubation with both LPS and IL-1beta further attenuated nicotine-induced Ca(2+) response. We also found that LPS and IL-1beta induced rearrangement of the F-actin filaments, as measured with an Alexa488-conjugated phalloidin probe. The rearrangements consisted of increases in ring formations and a more dispersed appearance of the filaments. These results indicate that there is a connection between a dysfunction of nicotine Ca(2+) signaling in inflammatory reactive astrocytes and upregulation of IL-1beta and the rearrangements of actin filaments in the cells.
16.	Forshammar, Johan, et al. (author) Anti-inflammatory substances can influence some glial cell types but not others. 2013 In: Brain research. - : Elsevier BV. - 1872-6240 .- 0006-8993. ; 1539, s. 34-40 Journal article (peer-reviewed)abstract In rat microglial enriched cultures, expressing Toll-like receptor 4, we studied cytokine release after exposure with 1ng/ml LPS for 0.5-24h. Dexamethasone and corticosterone exposure served as controls. We focused on whether naloxone, ouabain, and bupivacaine, all agents with reported anti-inflammatory effects on astrocytes, could affect the release of TNF-α and IL-1β in microglia. Our results show that neither ultralow (10(-12)M) nor high (10(-6)M) concentrations of these agents had demonstrable effects on cytokine release in microglia. The results indicate that anti-inflammatory substances exert specific influences on different glial cell types. Astrocytes seem to be functional targets for anti-inflammatory substances while microglia respond directly to inflammatory stimuli and are thus more sensitive to anti-inflammatory substances like corticoids. The physiological relevance might be that astrocyte dysfunction influences neuronal signalling both due to direct disturbance of astrocyte functions and in the communication within the astrocyte networks. When the signalling between astrocytes is working, then microglia produce less pro-inflammatory cytokines.
17.	Forshammar, Johan, et al. (author) Naloxone and Ouabain in Ultralow Concentrations Restore Na+/K+-ATPase and Cytoskeleton in Lipopolysaccharide-treated Astrocytes. 2011 In: The Journal of biological chemistry. - 1083-351X. ; 286:36, s. 31586-97 Journal article (peer-reviewed)abstract Astrocytes respond to inflammatory stimuli and may be important modulators of the inflammatory response in the nervous system. This study aimed first to assess how astrocytes in primary culture behave in response to inflammatory stimuli concerning intracellular Ca(2+) responses, expression of Toll-like receptor 4 (TLR4), Na(+)/K(+)-ATPase, actin filament organization, and expression of cytokines. In a cell culture model with lipopolysaccharide (LPS), astrocyte response was assessed first in the acute phase and then after incubation with LPS for 1-48 h. The concentration curve for LPS-stimulated Ca(2+) responses was bell-shaped, and the astrocytes expressed TLR4, which detects LPS and evokes intracellular Ca(2+) transients. After a long incubation with LPS, TLR4 was up-regulated, LPS-evoked Ca(2+) transients were expressed as oscillations, Na(+)/K(+)-ATPase was down-regulated, and the actin filaments were disorganized. Interleukin-1β (IL-1β) release was increased after 24 h in LPS. A second aim was to try to restore the LPS-induced changes in astrocytes with substances that may have dose-dependent anti-inflammatory properties. Naloxone and ouabain were tested separately in ultralow or high concentrations. Both substances evoked intracellular Ca(2+) transients for all of the concentrations from 10(-15) up to 10(-4) m. Neither substance blocked the TLR4-evoked Ca(2+) responses. Naloxone and ouabain prevented the LPS-induced down-regulation of Na(+)/K(+)-ATPase and restored the actin filaments. Ouabain, in addition, reduced the IL-1β release from reactive astrocytes. Notably, ultralow concentrations (10(-12) m) of naloxone and ouabain showed these qualities. Ouabain seems to be more potent in these effects of the two tested substances.
18.	Gerard, Frank, 1974, et al. (author) Inflammatory activation enhances NMDA-triggered Ca2+ signalling and IL-1 beta secretion in primary cultures of rat astrocytes 2012 In: Brain Research. - : Elsevier BV. - 0006-8993. ; 1473, s. 1-8 Journal article (peer-reviewed)abstract The aim of the present study was to measure the effects of NMDA receptor antagonists on rat astroglial-enriched primary cultures after incubation with lipopolysaccharide (LPS), with a view to explaining the role of NMDA receptors in the inflammatory activation of astrocytes. First, the presence of NMDA receptor subunits was confirmed at the protein level by immunocytochemical methods. The presence of functional NMDA receptors containing GluN2B subunits was then established by ratiometric fluorescent Ca2+ imaging which revealed transient NMDA-triggered Ca2+ responses. These responses could be blocked by the competitive antagonist 2-amino-5-phosphonopentoate (APV) and the non-competitive GluN2B subunit-selective antagonist ifenprodil. The NMDA-evoked Ca2+ transients were dependent on Ca2+ release from intracellular stores via interaction with InsP3-sensitive receptors as they were blocked by thapsigargin or xestospongin C. Following 24 h incubation with LPS, astroglial inflammatory activation increased IL-1 beta secretion and NMDA-triggered Ca2+ transients. The addition of APv or ifenprodil inhibited these enhanced responses, suggesting that LPS exposure stimulates IL-1 beta release from astrocytes through a mechanism that requires NMDA receptor stimulation. (c) 2012 Elsevier B.V. All rights reserved. BOTT NJ, 1992, JOURNAL OF CELL SCIENCE, V103, P23
19.	Giunta, Riccardo E, et al. (author) ESPRAS Survey on Breast Reconstruction in Europe. : ESPRAS Umfrage zur Brustrekonstruktion in Europa. 2021 In: Handchirurgie, Mikrochirurgie, plastische Chirurgie : Organ der Deutschsprachigen Arbeitsgemeinschaft fur Handchirurgie : Organ der Deutschsprachigen Arbeitsgemeinschaft fur Mikrochirurgie der Peripheren Nerven und Gefasse : Organ der V.... - : Georg Thieme Verlag KG. - 1439-3980. ; 53:4, s. 340-348 Journal article (peer-reviewed)abstract The European Leadership Forum (ELF) of the European Society of Plastic, Reconstructive and Aesthetic Surgery (ESPRAS) previously identified the need for harmonisation of breast reconstruction standards in Europe, in order to strengthen the role of plastic surgeons. This study aims to survey the status, current trends and potential regional differences in the practice of breast reconstruction in Europe, with emphasis on equity and access.A largescale web-based questionnaire was sent to consultant plastic and reconstructive surgeons, who are experienced in breast reconstruction and with understanding of the national situation in their country. Suitable participants were identified via the Executive Committee (ExCo) of ESPRAS and national delegates of ESPRAS. The results were evaluated and related to evidence-based literature.A total of 33 participants from 29 European countries participated in this study. Overall, the incidence of breast reconstruction was reported to be relatively low across Europe, comparable to other large geographic regions, such as North America. Equity of provision and access to breast reconstruction was distributed evenly within Europe, with geographic regions potentially affecting the type of reconstruction offered. Standard practices with regard to radiotherapy differed between countries and a clear demand for European guidelines on breast reconstruction was reported.This study identified distinct lack of consistency in international practice patterns across European countries and a strong demand for consistent European guidance. Large-scale and multi-centre European clinical trials are required to further elucidate the presented areas of interest and to define European standard operating procedures.
20.	Gustafsson Asting, Annika, et al. (author) Genetic Copy Number Variations in Colon Mucosa Indicating Risk for Colorectal Cancer. 2014 In: Journal of Cancer Therapy. - : Scientific Research Publishing, Inc.. - 2151-1934 .- 2151-1942. ; 5:14 Journal article (peer-reviewed)abstract Background: Sporadic colorectal tumors probably carry genetic alterations that may be related to familiar clusters according to risk loci visualized by SNP arrays on normal tissues. The aim of the present study was therefore to search for DNA regions (copy number variations, CNVs) as biomarkers associated to genetic susceptibility for early risk predictions of colorectal cancer. Such sequence alterations could provide additional information on phenotypic grouping of patients. Material and Methods: High resolution 105K oligonucleotide microarrays were used in search for CNV loci in DNA from tumor-free colon mucosa at primary operations for colon cancer in 60 unselected patients in comparison to DNA in buffy coat cells from 44 confirmed tumor-free and healthy blood donors. Array-detected CNVs were confirmed by Multiplex ligation-dependent probe amplification (MLPA). Results: A total number of 205 potential CNVs were present in DNA from colon mucosa. 184 (90%) of the 205 potential CNVs had been identified earlier in mucosa DNA from healthy individuals as reported to the Database of Genomic Variants. Remaining 21 (10%) CNVs were potentially novel sites. Two CNVs (3q23 and 10q21.1) were significantly related to colon cancer, but not confirmed in buffy coat DNA from the cancer patients. Conclusion: Our study reveals two CNVs that indicate increased risk for colon cancer; these DNA alterations may have been acquired by colon stem cells with subsequent appearance among epithelial mucosa cells. Impact: Certain mucosa CNV alterations may indicate individual susceptibility for malignant transformation in relationship to intestinal toxins and bacterial growth.
21.	Gyllensten, Hanna, 1979, et al. (author) Economic evaluation of a person-centred care intervention in head and neck oncology: results from a randomized controlled trial. 2019 In: Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer. - : Springer Science and Business Media LLC. - 1433-7339. ; 27:5, s. 1825-1834 Journal article (peer-reviewed)abstract Head and neck cancer and its treatment deteriorate quality of life, but symptoms improve with person-centred care. We examined the cost-effectiveness of a person-centred care intervention versus standard medical care.In this randomized clinical trial of a person-centred intervention, patients were planned for outpatient oncology treatment in a Swedish university hospital between 2012 and 2014 and were followed during 1year. Annual healthcare costs were identified from medical records and administrative register data. Productivity costs were calculated from reported sick leave. Health-related quality of life was collected using the EuroQol Group's five-dimension health state questionnaire.Characteristics were similar between 53 patients in the intervention group and 39 control patients. The average total cost was Euro (EUR) 55,544 (95% confidence interval: EUR 48,474-62,614) in the intervention group and EUR 57,443 (EUR 48,607-66,279) among controls, with similar health-related quality of life.This person-centred intervention did not result in increased costs and dominated the standard medical care.ClinicalTrials.gov (registration number: NCT02982746).
22.	Hansson, Elisabeth, 1955 (author) Actin Filament Reorganization in Astrocyte Networks is a Key Functional Step in Neuroinflammation Resulting in Persistent Pain: Novel Findings on Network Restoration 2015 In: Neurochemical Research. - : Springer Science and Business Media LLC. - 0364-3190 .- 1573-6903. ; 40:2, s. 372-379 Journal article (peer-reviewed)abstract In recent years, the importance of glial cell activation in the generation and maintenance of long-term pain has been investigated. One novel mechanism underlying long-lasting pain is injury-induced inflammation in the periphery, followed by microglial activation in the dorsal horn of the spinal cord, which results in local neuroinflammation. An increase in neuronal excitability may follow, with intense signaling along the pain tracts to the thalamus and the parietal cortex along with other cortical regions for the identification and recognition of the injury. If the local neuroinflammation develops into a pathological state, then the astrocytes become activated. Previous studies in which lipopolysaccharide (LPS) was used to induce inflammation have shown that in a dysfunctional astrocyte network, the actin cytoskeleton is reorganized from the normally occurring F-actin stress fibers into the more diffusible, disorganized, ring-form globular G-actin. In addition, Ca2+ signaling systems are altered, Na+- and glutamate transporters are downregulated, and pro-inflammatory cytokines, particularly IL-1 beta, are released in dysfunctional astrocyte networks. In a series of experiments, we have demonstrated that these LPS-induced changes in astrocyte function can be restored by stimulation of G(i/o) and inhibition of G(s) with a combination of a mu-receptor agonist and ultralow concentrations of a mu-receptor antagonist and by inhibition of cytokine release, particularly IL-1 beta, by the antiepileptic drug levetiracetam. These findings could be of clinical significance and indicate a novel treatment for long-term pain.
23.	Hansson, Elisabeth, 1955, et al. (author) Altered neuronal-glial signaling in glutamatergic transmission as a unifying mechanism in chronic pain and mental fatigue 2004 In: NEUROCHEMICAL RESEARCH. - 0364-3190. ; 29:5, s. 989-996 Journal article (peer-reviewed)
24.	Hansson, Elisabeth, 1955, et al. (author) Anti-inflammatory effects induced by pharmaceutical substances on inflammatory active brain astrocytes-promising treatment of neuroinflammation 2018 In: Journal of Neuroinflammation. - : Springer Science and Business Media LLC. - 1742-2094. ; 15:1 Journal article (peer-reviewed)abstract BACKGROUND: Pharmaceutical treatment with probable anti-inflammatory substances that attack cells in various ways including receptors, ion channels, or transporter systems may slow down the progression of inflammatory conditions. Astrocytes and microglia are the most prominent target cells for inflammation in the central nervous system. Their responses upon inflammatory stimuli work through the NO/cyclic GMP/protein kinase G systems that can downregulate the ATP-induced Ca2+ signaling, as well as G protein activities which alter Na+ transporters including Na+/K+-ATPase pump activity, Toll-like receptor 4 (TLR4), glutamate-induced Ca2+ signaling, and release of pro-inflammatory cytokines. The rationale for this project was to investigate a combination of pharmaceutical substances influencing the NO and the Gi/Gs activations of inflammatory reactive cells in order to make the cells return into a more physiological state. The ATP-evoked Ca2+ signaling is important maybe due to increased ATP release and subsequent activation of purinergic receptors. A balance between intercellular Ca2+ signaling through gap junctions and extracellular signaling mediated by extracellular ATP may be important for physiological function. METHODS: Astrocytes in primary cultures were incubated with lipopolysaccharide in a physiological glucose concentration for 24h to induce inflammatory reactivity. The probable anti-inflammatory substances sildenafil and 1α,25-Dihydroxyvitamin D3 together with endomorphin-1, naloxone, and levetiracetam, were used in the presence of high glucose concentration in the medium to restore the cells. Glutamate-, 5-HT-, and ATP-evoked intracellular Ca2+ release, Na+/K+-ATPase expression, expression of inflammatory receptors, and release of tumor necrosis factor alpha were measured. RESULTS: Sildenafil in ultralow concentration together with 1α,25-Dihydroxyvitamin D3 showed most prominent effects on the ATP-evoked intracellular Ca2+ release. The μ-opioid agonist endomorphin-1, the μ-opioid antagonist naloxone in ultralow concentration, and the antiepileptic agent levetiracetam downregulated the glutamate-evoked intracellular Ca2+ release and TLR4. The combination of the pharmaceutical substances in high glucose concentration downregulated the glutamate- and ATP-evoked Ca2+ signaling and the TLR4 expression and upregulated the Na+/K+-ATPase pump. CONCLUSION: Pharmaceutical treatment with the combination of substances that have potential anti-inflammatory effects, which attack different biochemical mechanisms in the cells may exert decisive effects to downregulate neuroinflammation in the nervous system.
25.	Hansson, Elisabeth, 1955, et al. (author) Anti-inflammatory effects induced by ultralow concentrations of bupivacaine in combination with ultralow concentrations of sildenafil (Viagra) and vitamin D3 on inflammatory reactive brain astrocytes 2019 In: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 14:10 Journal article (peer-reviewed)abstract Network coupled cells, such as astrocytes, regulate their cellular homeostasis via Ca2+ signals spread between the cells through gap junctions. Intracellular Ca2+ release is controlled by different signaling pathways that can be stimulated by ATP, glutamate and serotonin (5-HT). Based on our findings, all these pathways are influenced by inflammatory agents and must be restored to fully recover the Ca2+ signaling network. An ultralow concentration of the local anesthetic agent bupivacaine reduced 5-HT-evoked intracellular Ca2+ release, and an ultralow concentration of the phosphodiesterase-5 inhibitor sildenafil in combination with vitamin D3 reduced ATP-evoked intracellular Ca2+ release. Combinations of these three substances downregulated 5-HT-, glutamate- and ATP-evoked intracellular Ca2+ release to a more normal Ca2+ signaling state. Furthermore, inflammatory Toll-like receptor 4 expression decreased with a combination of these three substances. Substance P receptor neurokinin (NK)-1 expression was reduced by ultralow concentrations of bupivacaine. Here, bupivacaine and sildenafil (at extremely low concentrations) combined with vitamin D3 have potential anti-inflammatory properties. According to the present study, drug combinations at the right concentrations, especially extremely low concentrations of bupivacaine and sildenafil, affect different cellular biochemical mechanisms and represent a potential solution for downregulating inflammatory parameters, thereby restoring cells or networks to normal physiological homeostasis. © 2019 Hansson, Skiöldebrand. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
26.	Hansson, Elisabeth, 1955, et al. (author) Bupivacaine in combination with sildenafil (Viagra) and vitamin D3 have anti-inflammatory effects in osteoarthritic chondrocytes 2021 In: Current Research in Pharmacology and Drug Discovery. - : Elsevier BV. - 2590-2571. ; 2 Journal article (peer-reviewed)abstract Aims: To treat osteoarthritic chondrocytes and thereby reduce the inflammation with a drug combination that primarily affects 5-HT- and ATP-evoked Ca2+ signaling. In osteoarthritic chondrocytes, Ca2+ signaling is elevated, resulting in increased production of ATP and inflammatory mediators. The expression of TLR4 and Na+/K+-ATPase was used to evaluate the inflammatory status of the cells. Main methods: Equine chondrocytes were collected from joints with mild structural osteoarthritic changes and cultured in monolayers. The cells were treated with a combination of bupivacaine (1 pM) and sildenafil (1 μM) in combination with vitamin D3 (100 nM). A high-throughput screening system, the Flexstation 3 microplate reader, was used to measure intra- and extracellular Ca2+ signaling after exposure to 5-HT, glutamate, or ATP. Expression of inflammatory receptors was assessed by Western blotting. Key findings: Drug treatment substantially reduced 5-HT- and ATP-evoked intracellular Ca2+ release and TLR4 expression compared to those in untreated chondrocytes. The combination of sildenafil, vitamin D3 together with metformin, as the ability to take up glucose is limited, increased Na+/K+-ATPase expression. Significance: The combination of these three therapeutic substances at concentrations much lower than usually used, reduced expression of the inflammatory receptor TLR4 and increased the cell membrane enzyme Na+/K+-ATPase, which regulates cell volume and reduces increased intracellular Ca2+ concentrations. These remarkable results indicate that this drug combination has disease-modifying osteoarthritis drug (DMOAD) properties and may be a new clinical therapy for osteoarthritis (OA). © 2021 The Authors
27.	Hansson, Elisabeth, 1955 (author) Could chronic pain and spread of pain sensation be induced and maintained by glial activation? 2006 In: Acta physiologica (Oxford, England). - : Wiley. - 1748-1708 .- 1748-1716. ; 187:1-2, s. 321-7 Journal article (peer-reviewed)abstract An injury often starts with acute physiological pain, which becomes inflammatory or neuropathic, and may sometimes become chronic. It has been proposed recently that activated glial cells, astrocytes and microglia within the central nervous system could maintain the pain sensation even after the original injury or inflammation has healed, and convert it into chronic by altering neuronal excitability. Glial cell activation has also been proposed to be involved in the phenomenon of spread of pain sensation ipsilaterally or to the contralateral side (i.e. mirror image pain). Substance P and calcitonin gene-related peptide, released due to an inflammatory process, interact with the endothelial cells of the blood-spinal cord and blood-brain barriers. The barriers open partially and substances may influence adjacent glial cells. Such substances are also released from neurones carrying the 'pain message' all the way from the injury to the cerebral cortex. Pro-inflammatory cytokines may be released from the microglial cells, and astroglial Ca2+-transients or oscillations may spread within the astroglial networks. One theory is that Ca2+-oscillations could facilitate the formation of new synapses. These new synapses could establish neuronal contacts for maintaining and spreading the pain sensation. If this theory holds true, it is possible that Ca2+ waves, production of cytokines and growth factors could be modified by selective anti-inflammatory drugs to achieve a balance in the activities of the different intercellular and intracellular processes. This paper reviews current knowledge about glial mechanisms underlying the phenomena of chronic pain and spread of the pain sensation.
28.	Hansson, Elisabeth, 1955, et al. (author) Coupled cell networks are target cells of inflammation, which can spread between different body organs and develop into systemic chronic inflammation 2015 In: Journal of Inflammation-London. - : Springer Science and Business Media LLC. - 1476-9255. ; 12 Research review (peer-reviewed)abstract Several organs in the body comprise cells coupled into networks. These cells have in common that they are excitable but do not express action potentials. Furthermore, they are equipped with Ca2+ signaling systems, which can be intercellular and/or extracellular. The transport of small molecules between the cells occurs through gap junctions comprising connexin 43. Examples of cells coupled into networks include astrocytes, keratinocytes, chondrocytes, synovial fibroblasts, osteoblasts, connective tissue cells, cardiac and corneal fibroblasts, myofibroblasts, hepatocytes, and different types of glandular cells. These cells are targets for inflammation, which can be initiated after injury or in disease. If the inflammation reaches the CNS, it develops into neuroinflammation and can be of importance in the development of systemic chronic inflammation, which can manifest as pain and result in changes in the expression and structure of cellular components. Biochemical parameters of importance for cellular functions are described in this review.
29.	Hansson, Elisabeth, 1955, et al. (author) Glial-neuronal signaling and astroglial swelling in physiology and pathology. 2004 In: Advances in experimental medicine and biology. - 0065-2598. ; 559, s. 313-23 Journal article (peer-reviewed)
30.	Hansson, Elisabeth K, 1954, et al. (author) Can a person-centred-care intervention improve health-related quality of life in patients with head and neck cancer? A randomized, controlled study 2017 In: Bmc Nursing. - : Springer Science and Business Media LLC. - 1472-6955. ; 16:9, s. 1-12 Journal article (peer-reviewed)abstract Background: The incidence of head and neck cancer is increasing slightly. Head and neck cancer but also it's necessary and often successful treatment may affect general domains of health-related quality of life and provoke a variety of adverse symptoms and side effects, both during and after treatment. The objective of this study was to compare a person-centred care intervention in terms of health-related quality of life, disease-specific symptoms or problems, with traditional care as a control group for patients with head and neck cancer. Methods: In this randomized controlled trial, person-centred-care intervention and traditional care (control) groups comprised 54 and 42 patients, respectively. Outcome measures used were: the EORTC QLQ-C30 and the EORTC QLQ-C35. Both groups answered the questionnaires at baseline and after 4, 10, 18 and 52 weeks from start of treatment. The questionnaires' scores were compared between groups by using independent samples test and non-parametric test for continuous variables. For categorical data, Fisher's exact test was used. Longitudinal data were analysed using generalized linear models for normally distributed repeated measures data. Results: At baseline, the intervention and control groups were comparable in terms of medical and sociodemographic variables, clinical characteristics, health-related quality of life and disease-specific symptoms or problems. At all the follow-up points, even during the worst period for the patients, the person-centred-care group consistently reported better scores than the control group. The differences were numerically but not always statistically significant. When testing longitudinal data, statistically significant results were found for head and neck cancer-specific problems, swallowing (p = 0.014), social eating (p = 0.048) and feeling ill (p = 0.021). Conclusions: The results from this study suggest that adopting the person-centred-care concept practiced here could be a way to improve function and wellbeing in patients with head and neck cancer.
31.	Hansson, Elisabeth, 1955 (author) Long-term pain, neuroinflammation and glial activation 2010 In: Scandinavian Journal of Pain. - : Walter de Gruyter GmbH. - 1877-8860 .- 1877-8879. ; 1:2, s. 67-72 Journal article (peer-reviewed)abstract Nociceptive and neuropathic pain signals are known to result from noxious stimuli, which are converted into electrical impulses within tissue nociceptors. There is a complex equilibrium of pain-signalling and pain-relieving pathways connectingPNSand CNS. Drugs against long-term pain are today directed against increased neuronal excitability, mostly with less success. An injury often starts with acute physiological pain, which becomes inflammatory, nociceptive, or neuropathic, and may be transferred into long-term pain. Recently a low-grade inflammation was identified in the spinal cord and along the pain pathways to thalamus and the parietal cortex. This neuroinflammation is due to activation of glial cells, especially microglia, with production of cytokines and other inflammatory mediators within the CNS. Additionally, substances released to the blood from the injured region influence the blood–brain barrier, and give rise to an increased permeability of the tight junctions of the capillary endothelial cells, leading to passage of blood cells into the CNS. These cells are transformed into reactivemicroglia. If the inflammation turns into a pathological state the astrocytes will be activated. They are coupled into networks and respond to substances released by the capillary endothelial cells, to cytokines released from microglia, and to neurotransmitters and peptides released from neurons. As the astrocytes occupy a strategic position between the vasculature and synapses, they monitor the neuronal activity and transmitter release. Increased release of glutamate and ATP leads to disturbances in Ca2+ signalling, increased production of cytokines and free radicals, attenuation of the astrocyte glutamate transport capacity, and conformational changes in the astrocytic cytoskeleton, the actin filaments, which can lead to formation and rebuilding of new synapses. New neuronal contacts are established for maintaining and spreading pain sensation with the astrocytic networks as bridges. Thereby the glial cells can maintain the pain sensation even after the original injury has healed, and convert the pain into long-term by altering neuronal excitability. It can even be experienced from other parts of the body. As astrocytes are intimate co-players with neurons in the CNS, more knowledge on astrocyte responses to inflammatory activators may give new insight in our understanding of mechanisms of low-grade inflammation underlying long-term pain states and pain spreading. Novel treatment strategies would be to restore glial cell function and thereby attenuate the neuroinflammation.
32.	Hansson, Elisabeth, 1955, et al. (author) Low-grade inflammation causes gap junction-coupled cell dysfunction throughout the body, which can lead to the spread of systemic inflammation 2019 In: Scandinavian Journal of Pain. - : Walter de Gruyter GmbH. - 1877-8860 .- 1877-8879. ; 19:4, s. 639-649 Journal article (peer-reviewed)abstract Gap junction-coupled cells form networks in different organs in the body. These networks can be affected by inflammatory stimuli and become dysregulated. Cell signaling is also changed through connexin-linked gap junctions. This alteration affects the surrounding cells and extracellular matrix in organs. These changes can cause the spread of inflammatory substances, thus affecting other network-linked cells in other organs in the body, which can give rise to systemic inflammation, which in turn can lead to pain that can turn into chronic. This is a review based on literature search and our own research data of inflammatory stimuli that can affect different organs and particularly gap-junction-coupled cells throughout the body. A remaining question is which cell type or tissue is first affected by inflammatory stimuli. Can endotoxin exposure through the air, water and body start the process and are mast cells the first target cells that have the capacity to alter the physiological status of gap junction-coupled cells, thereby causing breakdown of different barrier systems? Is it possible to address the right cellular and biochemical parameters and restore inflammatory systems to a normal physiological level by therapeutic strategies? © 2019 Elisabeth Hansson et al., Scandinavian Association for the Study of Pain. Published by Walter de Gruyter GmbH, Berlin/Boston. All rights reserved.
33.	Hansson, Elisabeth, 1955, et al. (author) PACAP attenuates 5-HT, histamine, and ATP-evoked Ca2+ transients in astrocytes. 2009 In: Neuroreport. - 1473-558X. ; 20:10, s. 957-62 Journal article (peer-reviewed)abstract Pituitary adenylate cyclase-activating polypeptide (PACAP) has neuroprotective properties and plays an important role in neuroinflammation. PACAP38 interacts with its receptors, PAC1, and VPAC, on astrocytes at 10(-8) M to induce biphasic Ca2+ transients, which were reduced to a single transient by the PAC1-blocking PACAP antagonist PACAP6-38. At 10(-12) M even the single transient, corresponding to PAC1 was blocked. PACAP-induced Ca2+ transients were more pronounced in astrocytes cocultured with brain endothelial cells than in monocultured astrocytes, indicating that astrocytes that receive signals from microvessels develop more sensitive signal transduction systems for Ca. In this sensitive system, PACAP38 attenuated 5-HT, histamine, and ATP-evoked Ca2+ transients, showing the anti-inflammatory properties of PACAP.
34.	Hansson, Elisabeth, 1955, et al. (author) Roles of astrocytes and microglia in pain memory 2007 In: Immune and glial regulation of pain. Eds J.A. DeLeo, L.S. Sorkin & L.R. Watkins. - Seattle, USA : IASP Press. - 9780931092671 ; , s. 21-42 Book chapter (other academic/artistic)
35.	Hansson, Elisabeth, 1955, et al. (author) Therapeutic innovation: Inflammatory-reactive astrocytes as targets of inflammation 2016 In: IBRO Reports. - : Elsevier BV. - 2451-8301. ; 1, s. 1-9 Journal article (peer-reviewed)abstract This study aimed to test pharmaceutical compounds targeting astrocytes showing inflammatory dysregulation. The primary rat brain cultures were treated with different batches of serum with or without microglia added to make the cells inflammatory-reactive. Lipopolysaccharide (LPS) and tryptase were used as inflammatory inducers. Expression levels of Toll-like receptor 4 (TLR4), Na+/K+-ATPase, and matrix metalloprotease-13 (MMP-13), as well as actin filament organization, pro-inflammatory cytokines, and intracellular Ca2+ release, were evaluated. LPS combined with tryptase upregulated TLR4 expression, whereas Na+/K+-ATPase expression was downregulated, ATP-evoked Ca2+ transients were increased, actin filaments were reorganized and ring structures instead of stress fibers were observed. Other aims of the study were to prevent astrocytes from becoming inflammatory-reactive and to restore inflammatory dysregulated cellular changes. A combination of the μ-opioid antagonist (−)-naloxone in ultra-low concentrations, the non-addictive μ-opioid agonist (−)-linalool, and the anti-epileptic agent levetiracetam was examined. The results indicated that this drug cocktail prevented the LPS- and tryptase-induced inflammatory dysregulation. The drug cocktail could also restore the LPS- and tryptase-treated cells back to a normal physiological level in terms of the analyzed parameters. © 2016 The Author(s)
36.	Hansson, Elisabeth, 1955, et al. (author) μ-Opioid agonists inhibit the enhanced intracellular Ca2+ responses in inflammatory activated astrocytes co-cultured with brain endothelial cells 2008 In: Neuroscience. - : Elsevier BV. - 0306-4522. ; 155:4, s. 1237-1249 Journal article (peer-reviewed)abstract In order to imitate the in vivo situation with constituents from the blood–brain barrier, astrocytes from newborn rat cerebral cortex were co-cultured with adult rat brain microvascular endothelial cells. These astrocytes exhibited a morphologically differentiated appearance with long processes. 5-HT, synthetic μ-, δ- or κ-opioid agonists, and the endogenous opioids endomorphin-1, β-endorphin, and dynorphin induced higher Ca2+ amplitudes and/or more Ca2+ transients in these cells than in astrocytes in monoculture, as a sign of more developed signal transduction systems. Furthermore, stimulation of the co-cultured astrocytes with 5-HT generated a pronounced increase in intracellular Ca2+ release in the presence of the inflammatory or pain mediating activators substance P, calcitonin gene-related peptide (CGRP), lipopolysaccharide (LPS), or leptin. These Ca2+ responses were restored by opioids so that the δ- and κ-opioid receptor agonists reduced the number of Ca2+ transients elicited after incubation in substance P+CGRP or leptin, while the μ- and δ-opioid receptor agonists attenuated the Ca2+ amplitudes elicited in the presence of LPS or leptin. In LPS treated co-cultured astrocytes the μ-opioid receptor antagonist naloxone attenuated not only the endomorphin-1, but also the 5-HT evoked Ca2+ transients. These results suggest that opioids, especially μ-opioid agonists, play a role in the control of neuroinflammatory activity in astrocytes and that naloxone, in addition to its interaction with μ-opioid receptors, also may act through some binding site on astrocytes, other than the classical opioid receptor.
37.	Hultman, Karin, 1980, et al. (author) Potentiating effect of endothelial cells on astrocytic plasminogen activator inhibitor type-1 gene expression in an in vitro model of the blood-brain barrier. 2010 In: Neuroscience. - : Elsevier BV. - 1873-7544 .- 0306-4522. ; 166:2, s. 408-15 Journal article (peer-reviewed)abstract There is accumulating evidence of the importance of cellular communication between the cells that compose the blood-brain barrier (BBB). Astrocytes are known to affect the expression of tissue-type plasminogen activator (t-PA) and its inhibitor plasminogen activator inhibitor type-1 (PAI-1) in endothelial cells. We investigated the influence of endothelial cells on astrocytic gene expression of PAI-1, protease nexin-1 (PN-1) and t-PA using an in vitro model of the BBB. Primary rat astrocyte-enriched cultures were cocultured with primary adult rat brain microvascular endothelial cells on opposite sides of a transwell membrane. After coculturing for 9-11 days, the cultures were treated with lipopolysaccharide (LPS) for 8 h or 24 h. The levels of PAI-1, PN-1 and t-PA mRNA in untreated and treated monocultures and cocultures were analyzed by Real-Time RT-PCR. Cocultivation of astrocytes and endothelial cells increased astrocytic PAI-1 mRNA expression, and this response was further amplified by LPS treatment. The levels of PN-1 and t-PA mRNA expression in astrocytes were unaffected by cocultivation and/or LPS treatment. Analysis of endothelial PAI-1 and t-PA gene expression revealed increased PAI-1 mRNA levels in cocultured cells, whereas t-PA mRNA levels remained unchanged. These results demonstrate that the cocultivation of astrocytes and endothelial cells induces a pronounced increase in astrocytic PAI-1 gene expression, and that this effect is amplified by LPS treatment. These findings imply an important role for intercellular crosstalk in modulating PAI-1 gene expression within the BBB, under both physiologic and pathophysiologic conditions.
38.	Isaac, Giorgis, et al. (author) Sulfatide with short fatty acid dominates in astrocytes and neurons 2006 In: FEBS Journal. - : Wiley. - 1742-464X .- 1742-4658. ; 273:8, s. 1782-1790 Journal article (peer-reviewed)abstract Glycosphingolipids are located in cell membranes and the brain is especially enriched. We speculated that the subcellular location of glycosphingolipids depends on their fatty acid chain length because their sugar residues are constant, whereas fatty acid chain length can vary within the same molecule. To test this hypothesis we analysed the glycosphingolipid sulfatide, which is highly abundant in myelin and has mostly long fatty acids. We used a negative ion electrospray tandem mass spectrometry precursor ion scan to analyse the molecular species of sulfatide in cultured astrocytes and a mouse model of the human disease metachromatic leukodystrophy. In these arylsulfatase A (ASA)-deficient mice sulfatide accumulates intracellularly in neurons and astrocytes. Immunocytochemistry was also performed on cultured astrocytes and analysed using confocal laser scanning microscopy. Analyses of the molecular species showed that cultured astrocytes contained sulfatide with a predominance of stearic acid (C18), which was located in large intracellular vesicles throughout the cell body and along the processes. The same was seen in ASA-deficient mice, which accumulated a higher proportion (15 mol% compared with 8 mol% in control mice) of sulfatide with stearic acid. We conclude that the major fatty acid composition of sulfatide differs between white and grey matter, with neurons and astrocytes containing mostly short-chain fatty acids with an emphasis on stearic acid. Based on our results, we speculate that the fatty acid chain length of sulfatide might determine its intracellular (short chain) or extracellular (long chain) location and thereby its functions.
39.	Jacobsson, Jenny, et al. (author) Corticosterone inhibits expression of the microglial glutamate transporter GLT-1 in vitro 2006 In: Neuroscience. - : Elsevier BV. - 0306-4522. ; 139:2, s. 475-483 Journal article (peer-reviewed)
40.	Kendall, Anna, et al. (author) Nerve growth factor in the equine joint 2021 In: Veterinary Journal. - : Elsevier BV. - 1090-0233 .- 1532-2971. ; 267 Journal article (peer-reviewed)abstract Nerve growth factor (NGF) is a neurotrophin with many functions. In humans, it is involved in inflammation, nerve growth, apoptosis and pain signalling. Increased concentrations of NGF in synovial fluid has been shown in humans and dogs with osteoarthritis. Despite osteoarthritis being a common problem in horses, no studies have previously been published on NGF in the equine joint. The aim of this study was to quantify NGF in equine synovial fluid from healthy joints, acutely inflamed septic joints and joints with structural changes associated with osteoarthritis. A secondary aim was to identify the localisation of NGF and its two receptors, TrkA and p75(NTR) in healthy and osteoarthritic articular cartilage. NGF concentrations in synovial fluid from osteoarthritic joints (n = 27), septic joints (n = 9) and healthy joints (n = 16) were determined by ELISA. In addition, articular cartilage from osteoarthritic and healthy joints was examined for NGF, TrkA and P75(NTR) using immunohistochemistry staining. NGF was present in equine synovial fluid and articular cartilage. Compared to synovial fluid from healthy joints, NGF concentration was higher in synovial fluid from joints with structural osteoarthritic changes (P = 0.032) or acute septic inflammation (P = 0.006). In articular cartilage with severe osteoarthritic changes, there was more abundant positive immunohistochemistry staining for NGF and its receptors than in normal articular cartilage. Further studies should focus on identifying precursor forms of NGF, and on receptor expression and downstream signalling of TrkA and P75(NTR) in health and disease. (C) 2020 The Author(s). Published by Elsevier Ltd.
41.	Koinberg, Ingalill, 1955, et al. (author) Impact of a person-centered intervention for patients with head and neck cancer: A qualitative exploration 2018 In: BMC Nursing. - : Springer Science and Business Media LLC. - 1472-6955. ; 17:1 Journal article (peer-reviewed)abstract Background: People affected by head and neck cancer (HNC) experience a variety of multifaceted health-related problems during the treatment process, based on both the disease and side effects, several years after the treatment is complete. This study investigated a person-centred intervention using transition theory as a framework. Aim: Thus, the aim of the present study was to explore patients' experience of the transition and person centred care from diagnosis to the end of the treatment period. Methods: Interviews were conducted with 12 persons included in the person-centred intervention group. The patients were recruited from a randomised controlled study. We used a directed deductive content analysis as an analysis method. Results: There was a distinct transition between being a healthy person to being diagnosed with a serious disease. The majority of the participants felt that the diagnosis had put their lives in the balance; they felt both healthy and sick at the same time, and all participants described that their symptoms and side effects were the worst possible and totally unexpected. Of great importance was the health-care plan, comprising self-management goals which were formed in partnership between the patient and the nurse. The participants experienced that their interaction and engagement with lay persons and healthcare professionals supported a gradual acceptance of the situation and a sense of relief with a kind of awareness of the disease. Conclusion: The intervention played a significant role in promoting a healthy transition. Person-centredness and transition theory can help healthcare professionals to be more confident and resourceful in supporting people affected by HNC. © 2018 The Author(s).
42.	Leonova, Julia, et al. (author) Endothelin-1 decreases glutamate uptake in primary cultured rat astrocytes. 2001 In: American journal of physiology. Cell physiology. - 0363-6143. ; 281:5 Journal article (peer-reviewed)abstract Endothelin-1 (ET-1) is a potent vasoconstrictor peptide that is also known to induce a wide spectrum of biological responses in nonvascular tissue. In this study, we found that ET-1 (100 nM) inhibited the glutamate uptake in cultured astrocytes expressing the glutamate/aspartate transporter (GLAST); astrocytes did not express the glutamate transporter-1 (GLT-1). The V(max) and the K(m) of the glutamate uptake were reduced by 57% and 47%, respectively. Application of the ET(A) and ET(B) receptor antagonists BQ-123 and BQ-788 partly inhibited the ET-1-evoked decrease in the glutamate uptake, whereas the nonspecific ET receptor antagonist bosentan completely inhibited this decrease. Incubation of the cultures with pertussis toxin abolished the effect of ET-1 on the uptake. The ET-1-induced decrease in the glutamate uptake was independent of extracellular free Ca(2+) concentration, whereas the intracellular Ca(2+) antagonists thapsigargin and 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester abolished the effect of ET-1 on the glutamate uptake. Incubation with the protein kinase C (PKC) antagonist staurosporine, but not with the fatty acid-binding protein bovine serum albumin, prevented the ET-1-induced decrease in the glutamate uptake. These results suggest that ET-1 impairs the high-affinity glutamate uptake in cultured astrocytes through a G protein-coupled mechanism, involving PKC and changes in intracellular Ca(2+).
43.	Lundborg, Christopher, 1965, et al. (author) Glial cell line-derived neurotrophic factor is increased in cerebrospinal fluid but decreased in blood during long-term pain. 2010 In: Journal of Neuroimmunology. - : Elsevier BV. - 1872-8421 .- 0165-5728. ; 220:1-2, s. 108-113 Journal article (peer-reviewed)abstract Glial cell line-derived neurotrophic factor (GDNF) is involved in inflammation and pain, roles which remain to be delineated clinically. We aimed to evaluate the role of central nervous and peripheral GDNF in long-term pain patients and in controls by analysing intrathecal and blood concentrations of GDNF. Simultaneous measurements of pro-inflammatory cytokines IL-1beta, TNF-alpha and IL-6, anti-inflammatory cytokine IL-10 and chemokine IL-8 served to define inflammatory responses. Generally, blood levels of GDNF were higher than corresponding intrathecal levels. Pain was associated with levels of GDNF that were increased intrathecally, but decreased in blood. IL-8 was uniformly higher in pain patients.
44.	Lundborg, Christopher, 1965, et al. (author) Ifenprodil restores GDNF-evoked Ca(2+) signalling and Na(+) /K(+) -ATPase expression in inflammation-pretreated astrocytes. 2011 In: Journal of neurochemistry. - : Wiley. - 1471-4159 .- 0022-3042. ; 119:4, s. 686-696 Journal article (peer-reviewed)abstract ABSTRACT: Glial cell line-derived neurotrophic factor (GDNF) plays an important role in neuroinflammatory and neuropathic pain conditions. Astrocytes produce and secrete GDNF, which interacts with its receptors to induce Ca(2+) transients. This study aimed first to assess intracellular Ca(2+) responses of astrocytes in primary culture when exposed to the neuroprotective and anti-inflammatory peptide GDNF. Furthermore, incubation with the inflammatory inducers lipopolysaccharide (LPS), NMDA, or interleukin 1-β (IL-1β) attenuated the GDNF-induced Ca(2+) transients. The next aim was to try to restore the suppressed GDNF responses induced by inflammatory changes in the astrocytes with an anti-inflammatory substance. Ifenprodil, an NMDA receptor antagonist at the NR2B subunit, was tested. It was shown to restore the GDNF-evoked Ca(2+) transients and increased the Na(+) /K(+) -ATPase expression. Ifenprodil seems to be a potent anti-inflammatory substance for astrocytes which have been pre-activated by inflammatory stimuli.
45.	Nunes, A. K. D., et al. (author) Sildenafil (Viagra (R)) prevents and restores LPS-induced inflammation in astrocytes 2016 In: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 630, s. 59-65 Journal article (peer-reviewed)abstract Astrocytes are effectively involved in the pathophysiological processes in the central nervous system (CNS) and may contribute to or protect against development of inflammatory and degenerative diseases. Sildenafil is a potent and selective phosphodiesterase-5 (PDE-5) inhibitor, which induces cyclic GMP accumulation. However, the mechanisms of actions on glial cells are not clear. The aim of the present work is to evaluate the role of sildenafil in lipopolysaccharide (LPS)-stimulated astrocytes. The cytoskeleton integrity and Ca2+ waves were assessed as indicators of inflammatory state. Two main groups were done: (A) one prevention and (B) one restoration. Each of these groups: A1: control; A2: LPS for 24h; A3: sildenafil 1 or 10 mu M for 4h and then sildenafil 1 or 10 mu M + LPS for 24 h. B1: control; B2: LPS for 24 h; B3: LPS for 24 h and then LPS + sildenafil 1 or 10 mu M for 24 h. Cytoskeleton integrity was analyzed through GFAP immunolabeling and actin labeling with an Alexa 488-conjugated phalloidin probe. Calcium responses were assessed through a Ca2+-sensitive fluorophore Fura-2/AM. The results show that both preventive and restorative treatments with sildenafil (in both concentrations) reduced the Ca2+ responses in intensity and induced a more organized actin fiber pattern, compared to LPS treated cells. This work demonstrated for the first time that astrocytes are a key part of the sildenafil protective effects in the CNS.
46.	Persson, Mikael, 1979, et al. (author) Lipopolysaccharide increases microglial GLT-1 expression and glutamate uptake capacity in vitro by a mechanism dependent on TNF-alpha 2005 In: Glia. - : Wiley. - 0894-1491 .- 1098-1136. ; 51:2, s. 111-120 Journal article (peer-reviewed)
47.	Persson, Mikael, 1979, et al. (author) Microglial GLT-1 is upregulated in response to herpes simplex virus infection to provide an antiviral defence via glutathione. 2007 In: Glia. - : Wiley. - 0894-1491 .- 1098-1136. ; 55:14, s. 1449-58 Journal article (peer-reviewed)abstract Herpes simplex virus (HSV) can enter the central nervous system and cause encephalitis (HSV-1) or meningitis (HSV-2). Microglia, the immunocompetent cells of the central nervous system, are potentially able to detect viral infections. Microglia have been shown to express the glutamate transporter GLT-1 during pathological events, leading to increased microglial glutamate uptake and glutathione synthesis. This study aims to address the role of GLT-1 and glutathione, a major antioxidant with antiviral properties, during HSV infections. Using neuron-enriched mixed primary cultures from rat, it was found that microglia have higher resistance to HSV infections than neurons or astrocytes after 24 h incubation with HSV. Purified microglia in culture were used to further address this. It was found that microglia were able to detect HSV and responded by releasing tumor necrosis factor-alpha (TNF-alpha) and upregulating GLT-1 after 24 h incubation with 1 PFU/cell HSV-1 or HSV-2. Furthermore, the microglial glutathione levels were not significantly diminished after 24 h. Inhibition of the microglial glutathione synthesis with 200 microM buthionine sulfoximide (BSO) led to significantly more infected cells after 24 h incubation with 1 PFU/cell HSV-1 or HSV-2. These data indicate that the higher resistance in microglia against HSV infections may be due to the expression of GLT-1, which can maintain the glutathione levels and provide a mechanism for microglial self-defense against HSV.
48.	Persson, Mikael, 1979, et al. (author) Microglial glutamate uptake is coupled to glutathione synthesis and glutamate release. 2006 In: The European journal of neuroscience. - : Wiley. - 0953-816X .- 1460-9568. ; 24:4, s. 1063-70 Journal article (peer-reviewed)abstract The physiological function of microglial glutamate uptake has been debated as it is about 10% of that measured for astrocytes. This study addresses how glutamate, taken up from the extracellular space, is utilized by microglia. It was found that purified rat microglia incubated for 60 min with (3)H-glutamate had an increased intracellular accumulation of (3)H-glutamate after 12 h incubation with tumour necrosis factor alpha (TNF-alpha) but not after incubation with lipopolysaccharide (LPS). Furthermore, LPS- but not TNF-alpha-treated cells showed an increased efflux of (3)H-labelled compounds, presumably glutamate through the X(C) (-) system and treatment with LPS or TNF-alpha increased the microglial glutathione concentrations and led to an increased incorporation of (3)H-glutamate into glutathione. Depending on the stimuli, 3-6% of the total labelled contents were found in the form of glutathione and 25-35% in the form of glutamate. These results show that microglial glutamate uptake is directly coupled to glutathione synthesis and release of glutamate and/or glutamate metabolites. Additionally, the increased glutathione contents after LPS or TNF-alpha treatment were able to reduce microglial cell death after H(2)O(2) challenge, showing a potential (self)-protective function for microglial glutamate transporter expression and glutathione synthesis.
49.	Persson, Mikael, 1979, et al. (author) The complement-derived anaphylatoxin C5a increases microglial GLT-1 expression and glutamate uptake in a TNF-alpha-independent manner. 2009 In: The European journal of neuroscience. - : Wiley. - 1460-9568 .- 0953-816X. ; 29:2, s. 267-74 Journal article (peer-reviewed)abstract Microglia can express Na+-dependent high-affinity glutamate transporters during pathological conditions in the CNS. The transporter expression seems to be activation dependent, and we therefore sought to identify factors that could induce it, in addition to the well-known effect of lipopolysaccharide (LPS) that is mediated by tumour necrosis factor-alpha (TNF-alpha). The complement-derived anaphylatoxins C3a and C5a are of potential interest as the complement system is activated in nearly all insults to the nervous system, and both C3a and C5a have been shown to protect against excitotoxicity. We have found that C5a, but not C3a, increased the expression of the microglial glutamate transporter GLT-1 in a dose-dependent manner without eliciting or modulating the release of TNF-alpha. However, the increase was not as prominent as the one induced by LPS, indicating that the microglia are in different activity states. The increase in microglial GLT-1 expression led to an increased functional uptake of glutamate without affecting the release. This suggests that C5a-stimulated microglia can be self- and neuroprotective by removing extracellular glutamate.
50.	Raposo, C., et al. (author) Neuropharmacological effects of Phoneutria nigriventer venom on astrocytes 2016 In: Neurochemistry International. - : Elsevier BV. - 0197-0186. ; 96, s. 13-23 Journal article (peer-reviewed)abstract Bites from genus Phoneutria (Ctenidae, Araneomorpha) are the second most frequent source of spider accidents in Southeast Brazil. Severe envenoming from Phoneutria nigriventer produces vision disturbance, tremor and convulsion, suggesting that the CNS is involved; however, the mechanisms by which P. nigriventer venom (PNV) affects the CNS remain poorly understood. The present study aimed to investigate whether PNV directly impairs astrocytes. Cultured astrocytes were exposed to PNV, and intracellular Ca2+ release and signaling were measured (Fura-2/AM), Na+/K+-ATPase and Toll-like receptor 4 (TLR4) involvement were investigated, actin filaments were stained (Alexa (TM) 488-conjugated phalloidin probe), the G-actin/F-actin ratio was determined, and the expression level of connexin 43 (Cx43) was assessed. Incubation in Ca2+-free buffer did not change the Ca2+ responses. However, pre-incubation in thapsigargin/caffeine completely abolished these responses, suggesting that PNV-evoked Ca2+ transients were from intracellular Ca2+ stores. Pretreatment with a Na+/K+-ATPase antagonist (ouabain) or a TLR4 antagonist (LPS-RS) decreased or increased the Ca2+-evoked transients, respectively. Astrocytes showed altered actin filament structure after PNV exposure. PNV treatment increased the expression levels of Na+/K+-ATPase and Cx43 but decreased those of TLR4. The present results suggest that PNV directly affects astrocytes. Na+/K+-ATPase may thus represent a more specific drug target for controlling the neurotoxicity of PNV. (C) 2016 Elsevier Ltd. All rights reserved.

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