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  • 101.
    Saito, Yasuyuki
    et al.
    Gunma University, Gunma University Graduate School of Medicine.
    Iwamura, Hiroko
    Gunma University.
    Kaneko, Tetsuya
    Gunma University.
    Ohnishi, Hiroshi
    Gunma University.
    Murata, Yoji
    Gunma University.
    Okazawa, Hideki
    Gunma University.
    Kanazawa, Yoshitake
    Gunma University.
    Sato-Hashimoto, Miho
    Gunma University.
    Kobayashi, Hisae
    Gunma University.
    Oldenborg, Per-Arne
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Naito, Makoto
    Niigata University Graduate School of Medical and Dental Sciences.
    Kaneko, Yoriaki
    Gunma University Graduate School of Medicine.
    Nojima, Yoshihisa
    Gunma University Graduate School of Medicine.
    Matozaki, Takashi
    Gunma University, Kobe University Graduate School of Medicine.
    Regulation by SIRPα of dendritic cell homeostasis in lymphoid tissues2010Ingår i: Blood, ISSN 0006-4971, E-ISSN 1528-0020, Vol. 116, nr 18, s. 3517-3525Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The molecular basis for regulation of dendritic cell (DC) development and homeostasis remains unclear. Signal regulatory protein α (SIRPα), an immunoglobulin superfamily protein that is predominantly expressed in DCs, mediates cell-cell signaling by interacting with CD47, another immunoglobulin superfamily protein. We now show that the number of CD11c(high) DCs (conventional DCs, or cDCs), in particular, that of CD8-CD4+ (CD4+) cDCs, is selectively reduced in secondary lymphoid tissues of mice expressing a mutant form of SIRPα that lacks the cytoplasmic region. We also found that SIRPα is required intrinsically within cDCs or DC precursors for the homeostasis of splenic CD4+ cDCs. Differentiation of bone marrow cells from SIRPα mutant mice into DCs induced by either macrophage-granulocyte colony-stimulating factor or Flt3 ligand in vitro was not impaired. Although the accumulation of the immediate precursors of cDCs in the spleen was also not impaired, the half-life of newly generated splenic CD4+ cDCs was markedly reduced in SIRPα mutant mice. Both hematopoietic and nonhematopoietic CD47 was found to be required for the homeostasis of CD4+ cDCs and CD8-CD4- (double negative) cDCs in the spleen. SIRPα as well as its ligand, CD47, are thus important for the homeostasis of CD4+ cDCs or double negative cDCs in lymphoid tissues.

  • 102.
    Sato-Hashimoto, Miho
    et al.
    Gunma University.
    Saito, Yasuyuki
    Gunma University.
    Ohnishi, Hiroshi
    Gunma University.
    Iwamura, Hiroko
    Gunma University.
    Kanazawa, Yoshitake
    Gunma University.
    Kaneko, Tetsuya
    Gunma University.
    Kusakari, Shinya
    Gunma University.
    Kotani, Takenori
    Gunma University.
    Mori, Munemasa
    Gunma University.
    Murata, Yoji
    Kobe University Graduate School of Medicine.
    Okazawa, Hideki
    Kobe University Graduate School of Medicine.
    Ware, Carl F
    Sanford-Burnham Medical Research Institute, La Jolla.
    Oldenborg, Per-Arne
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Nojima, Yoshihisa
    Matozaki, Takashi
    Kobe University Graduate School of Medicine.
    Signal regulatory protein α regulates the homeostasis of T lymphocytes in the spleen.2011Ingår i: Journal of Immunology, ISSN 0022-1767, E-ISSN 1550-6606, Vol. 187, nr 1, s. 291-297Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The molecular basis for formation of lymphoid follicle and its homeostasis in the secondary lymphoid organs remains unclear. Signal regulatory protein α (SIRPα), an Ig superfamily protein that is predominantly expressed in dendritic cells or macrophages, mediates cell-cell signaling by interacting with CD47, another Ig superfamily protein. In this study, we show that the size of the T cell zone as well as the number of CD4(+) T cells were markedly reduced in the spleen of mice bearing a mutant (MT) SIRPα that lacks the cytoplasmic region compared with those of wild-type mice. In addition, the expression of CCL19 and CCL21, as well as of IL-7, which are thought to be important for development or homeostasis of the T cell zone, was markedly decreased in the spleen of SIRPα MT mice. By the use of bone marrow chimera, we found that hematopoietic SIRPα is important for development of the T cell zone as well as the expression of CCL19 and CCL21 in the spleen. The expression of lymphotoxin and its receptor, lymphotoxin β receptor, as well as the in vivo response to lymphotoxin β receptor stimulation were also decreased in the spleen of SIRPα MT mice. CD47-deficient mice also manifested phenotypes similar to SIRPα MT mice. These data suggest that SIRPα as well as its ligand CD47 are thus essential for steady-state homeostasis of T cells in the spleen.

  • 103.
    Sehlin, Janove
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Studies on the mechanism of amino acidinduced insulin release1971Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
  • 104.
    Stenberg, Åsa
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Studies of SIRPα-mediated regulation of neutrophil functions2014Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
    Abstract [en]

    Neutrophil granulocytes constitute the front line of defense in the innate immune response to invading microorganisms, but can also contribute to development of inflammatory disease and tissue destruction following e.g. myocardial infarction or stroke. During inflammatory activation, neutrophils leave the blood, interact with extracellular matrix proteins, and migrate into tissues in response to chemotactic factors to phagocytose and kill infectious agents by using toxic granule contents and reactive oxygen metabolites. The functional neutrophil response relies on exocytosis of cytoplasmic granules, each containing membrane proteins, which are thereby mobilized to the plasma membrane. Specific programmed cell death (apoptotic) pathways regulate neutrophil homeostasis, where an inflammatory milieu can prolong the life span of neutrophils to several days, whereas non-activated neutrophils are committed to constitutive/spontaneous apoptosis within hours.

    Signal regulatory protein alpha (SIRPα) is a surface glycoprotein with two intracellular immunoreceptor-tyrosine-based inhibitory motifs (ITIMs), which is highly expressed in neutrophils and other myeloid cells. In other cell types, SIRPα has been shown to regulate cellular functions such as cell migration and phagocytosis. The aim of the present thesis was to investigate neutrophil SIRPα expression in response to inflammatory activation or apoptosis, and how this receptor can regulate neutrophil adhesion and cell migration.

    Neutrophils contain several subcellular granule compartments, including primary (azurophilic), secondary (specific), tertiary (gelatinase) granules, and a fourth compartment called secretory vesicles. In resting neutrophils, SIRPα was found to be present in the plasma membrane and in all types of granules except for the azurophilic granules. Stimulation with the bacterial peptide fMLF in vitro, or inflammatory activation in vivo, was found to rapidly mobilize SIRPα to the neutrophil cell surface. In mice expressing a mutated form of SIRPα, where the cytoplasmic signaling domain was deleted, we found an enhanced accumulation of neutrophils in the peritoneal cavity in a peritonitis model. These findings therefore suggest that an increased amount of SIRPα on the surface of activated neutrophils could serve to negatively fine-tune neutrophil accumulation in inflammation.

    Neutrophil priming means that the cell becomes partially activated, in a way that facilitates subsequent full activation. One part of the priming process is a moderate exocytosis of granules, mostly the secretory vesicles, which increases the density of certain receptors on the cell surface. It also involves the activation of adhesion receptors called integrins. We found that TNFα-induced priming involved an increased accumulation of SIRPα on the cell surface. When comparing wild-type and SIRPα-mutant neutrophils, we found a strongly reduced TNFα-stimulated and β2 integrin-dependent adhesion of mutant neutrophils to type I collagen or fibrinogen. This adhesion defect resulted in a reduced adhesion-dependent activation of the respiratory burst and an increased chemotactic response of SIRPα-mutant neutrophils in vitro.

    During neutrophil apoptosis, several receptors are known to be shed from the cell surface (e.g. CD16 and CD43). We found that also SIRPα is shed from the surface during spontaneous as well as Fas-induced apoptosis. The shedding mechanism was found to involve matrix metalloproteinase (MMP) activity, mostly that of MMP-3 and MMP-8.

    In conclusion, neutrophil cell surface SIRPα expression is regulated during neutrophil activation and seems to play an important role in stimulating β2-integrin-dependent adhesion. This way, SIRPα can negatively fine-tune neutrophil migration and accumulation in inflammation. During apoptosis, SIRPα is shed from the cell surface, which may be one mechanism contributing to the well-known down-regulation in the adhesiveness of apoptotic neutrophils.

  • 105.
    Stenberg, Åsa
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Karlsson, Anna
    Department of Rheumatology and Inflammation Research, Sahlgrenska Academy, University of Gothenburg, Gothenburg.
    Feuk-Lagerstedt, Elisabeth
    Department of Rheumatology and Inflammation Research, Sahlgrenska Academy, University of Gothenburg, Gothenburg.
    Christenson, Karin
    Department of Rheumatology and Inflammation Research, Sahlgrenska Academy, University of Gothenburg, Gothenburg.
    Bylund, Johan
    Department of Rheumatology and Inflammation Research, Sahlgrenska Academy, University of Gothenburg, Gothenburg.
    Oldenborg, Anna
    Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, Mo. , USA.
    Vesterlund, Liselotte
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi. Department of Biosciences and Nutrition at Novum, Karolinska Institute, Stockholm , Sweden.
    Matozaki, Takashi
    Division of Molecular and Cellular Signaling, Department of Biochemistry and Molecular Biology, Kobe University Graduate School of Medicine, Kobe , Japan.
    Sehlin, Janove
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Oldenborg, Per-Arne
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Signal regulatory protein alpha is present in several neutrophil granule populations and is rapidly mobilized to the cell surface to negatively fine-tune neutrophil accumulation in inflammation2014Ingår i: Journal of Innate Immunity, ISSN 1662-811X, E-ISSN 1662-8128, Vol. 6, nr 4, s. 553-560Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Signal regulatory protein alpha (SIRPα) is a cell surface glycoprotein with inhibitory functions, which may regulate neutrophil transmigration. SIRPα is mobilized to the neutrophil surface from specific granules, gelatinase granules, and secretory vesicles following inflammatory activation in vitro and in vivo. The lack of SIRPα signaling and the ability to upregulate SIRPα to the cell surface promote neutrophil accumulation during inflammation in vivo.

  • 106.
    Stenberg, Åsa
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Sehlin, Janove
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Matozaki, Takashi
    Oldenborg, Per-Arne
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Signal regulatory protein alpha (SIRPα) negatively regulates neutrophil migration by stimulating β2 integrin-mediated adhesionManuskript (preprint) (Övrigt vetenskapligt)
  • 107.
    Stenberg, Åsa
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Sehlin, Janove
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Oldenborg, Per-Arne
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Neutrophil apoptosis is associated with loss of signal regulatory protein alpha (SIRP alpha) from the cell surface2013Ingår i: Journal of Leukocyte Biology, ISSN 0741-5400, E-ISSN 1938-3673, Vol. 93, nr 3, s. 403-412Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Cells of the innate immune system, including monocytes, macrophages, and neutrophils, play a major role in the development of inflammatory diseases. During inflammation, large numbers of neutrophils are recruited from the blood and subsequently undergo apoptosis, which involves changes in the cell surface expression of a number of receptors. Neutrophils express the Ig superfamily member, SIRP alpha, which is a receptor involved in regulating cell adhesion and migration. As apoptotic neutrophils down-regulate their capacity for adhesion and migration, we here investigated whether neutrophil expression of SIRP alpha was affected during apoptosis. We found that apoptotic neutrophils lost SIRP alpha from their cell surface with kinetics similar to the loss of CD16. The majority of neutrophils with reduced SIRP alpha also expressed PS on their surface, and the loss of the receptor was reduced proportional to the reduction of apoptosis by caspase inhibitors during Fas-induced apoptosis but less so during spontaneous apoptosis. Neutrophil loss of SIRP alpha or CD16 was inhibited by the protease inhibitor TAPI-2, as well as specific inhibitors of MMP3 or -8, suggesting that proteolytic mechanisms were involved. Finally, SIRP alpha was also found on smaller membrane vesicles released from the cells during apoptosis. Our data suggest that neutrophils reduce their SIRP alpha expression during apoptosis, which may be part of the functional down-regulation seen in apoptotic neutrophils. J. Leukoc. Biol. 93: 403-412; 2013.

  • 108.
    Strömberg, Ingrid
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Bickford, Paula
    University of South Florida.
    Gerhardt, Greg A
    University of Kentucky Health Sciences Center.
    Grafted dopamine neurons: Morphology, neurochemistry, and electrophysiology2010Ingår i: Progress in Neurobiology, ISSN 0301-0082, E-ISSN 1873-5118, Vol. 90, nr 2, s. 190-197Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Grafting of dopamine-rich tissue to counteract the symptoms in Parkinson's disease became a promising tool for future treatment. This article discusses how to improve the functional outcome with respect to graft outgrowth and functions of dopamine release and electrophysiological responses to graft implantation in the host brain striatal target. It has been documented that a subpopulation of the dopamine neurons innervates the host brain in a target-specific manner, while some of the grafted dopamine neurons never project to the host striatum. Neurochemical studies have demonstrated that the graft-induced outgrowth synthesize, store, metabolize and release dopamine and possibly other neurotransmitters such as 5-HT. Furthermore, the released dopamine affects the dopamine-depleted brain in areas that are larger than the graft-derived nerve fibers reach. While stem cells will most likely be the future source of cells to be used in grafting, it is important to find the guiding cues for how to reinnervate the dopamine-depleted striatum in a proper way with respect to the dopamine subpopulations of A9 and A10 to efficiently treat the motor abnormalities seen in Parkinson's disease.

  • 109.
    Strömberg, Ingrid
    et al.
    Umeå universitet, Medicinsk fakultet, Integrativ medicinsk biologi, Histologi med cellbiologi.
    Gemma, Carmelina
    Vila, Jennifer
    Bickford, Paula C
    Blueberry- and spirulina-enriched diets enhance striatal dopamine recovery and induce a rapid, transient microglia activation after injury of the rat nigrostriatal dopamine system.2005Ingår i: Experimental Neurology, ISSN 0014-4886, Vol. 196, nr 2, s. 298-307Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Neuroinflammation plays a critical role in loss of dopamine neurons during brain injury and in neurodegenerative diseases. Diets enriched in foods with antioxidant and anti-inflammatory actions may modulate this neuroinflammation. The model of 6-hydroxydopamine (6-OHDA) injected into the dorsal striatum of normal rats, causes a progressive loss of dopamine neurons in the ventral mesencephalon. In this study, we have investigated the inflammatory response following 6-OHDA injected into the striatum of adult rats treated with diet enriched in blueberry or spirulina. One week after the dopamine lesion, a similar size of dopamine degeneration was found in the striatum and in the globus pallidus in all lesioned animals. At 1 week, a significant increase in OX-6- (MHC class II) positive microglia was found in animals fed with blueberry- and spirulina-enriched diets in both the striatum and the globus pallidus. These OX-6-positive cells were located within the area of tyrosine hydroxylase (TH) -negativity. At 1 month after the lesion, the number of OX-6-positive cells was reduced in diet-treated animals while a significant increase beyond that observed at 1 week was now present in lesioned control animals. Dopamine recovery as revealed by TH-immunohistochemistry was significantly enhanced at 4 weeks postlesion in the striatum while in the globus pallidus the density of TH-positive nerve fibers was not different from control-fed lesioned animals. In conclusion, enhanced striatal dopamine recovery appeared in animals treated with diet enriched in antioxidants and anti-inflammatory phytochemicals and coincided with an early, transient increase in OX-6-positive microglia.

  • 110.
    Strömberg, Ingrid
    et al.
    Umeå universitet, Medicinsk fakultet, Integrativ medicinsk biologi, Histologi med cellbiologi.
    Hansson, Anita C
    Rimondini, Roberto
    Sommer, Wolfgang
    c-fos antisense oligonucleotides increase firing rate of striatal neurons in the anaesthetized rat.2004Ingår i: Brain Research, ISSN 0006-8993, Vol. 1000, nr 1-2, s. 192-4Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Extracellular electrophysiological recordings were used to study the firing rate of striatal neurons before and up to 4 h after intrastriatal c-fos antisense oligonucleotide injections in urethane-anesthetized rats. A four-fold increase from baseline neuronal activity was observed between 1 and 3 h upon antisense treatment, but not after control oligonucleotide injections. We conclude that, under urethane anesthesia, which here does not affect c-fos expression in the striatum by itself, neuronal activity appears to be tonically suppressed by basal striatal c-fos expression.

  • 111.
    Strömberg, Ingrid
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Rehnmark, Anna
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Orädd, Greger
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Virel, Ana
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Neuroinflammation Using MRI: Phagocytes From Blood to Brain With the Help of Bilberries2013Ingår i: Cell Transplantation, ISSN 0963-6897, E-ISSN 1555-3892, Vol. 22, nr 5, s. 917-917Artikel i tidskrift (Övrigt vetenskapligt)
  • 112.
    Thrybom, T
    et al.
    Huddinge University Hospital.
    Rooth, P
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Lindström, P
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Effect of serotonin reuptake inhibitor on syndrome development in obese hyperglycemic mice (Umeå ob/ob).2001Ingår i: Metabolism: Clinical and Experimental, ISSN 0026-0495, E-ISSN 1532-8600, Vol. 50, nr 2, s. 144-50Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    These experiments tested the effect of 10 to 30 mg, citalopram/kg body weight on food intake, weight increase, and blood glucose levels in young obese hyperglycemic mice (Umeå ob/ob). A leptin defect in ob/ob mice results in hyperphagia, hyperglycemia, and increased body weight compared with normal mice. Citalopram had no effect on weight increase in ob/ob mice aged 3 to 10 weeks, when the weight increase is most rapid. Citalopram reduced the weight increase at the age 10 to 19 weeks. Food intake reaches a maximum at age 7 to 10 weeks and then decreases. The reduction was more rapid in citalopram-treated mice. The weight of feces paralleled the food intake. Citalopram treatment had no effect on serum insulin levels in 15-week-old mice. Blood sugar values in fed mice reached a peak at age 7 weeks (21.7 +/- 1.7 mmol/L in controls and 22.3 +/- 1 mmol/L in citalopram-treated mice). After that, blood sugar values decreased. The decrease was more pronounced in citalopram-treated mice (P < .01 compared with controls). Blood glucose levels were lower at ages 12 to 15 weeks in female ob/ob control mice (13.6 +/- 2.5 mmol/L v 19.0 +/- 0.6 mmol/L in male control mice; P < .05). The effect of citalopram was the same in male and female mice. There was a close correlation between accumulated food intake and blood glucose values in individual animals. At age 3 to 10 weeks, ob/ob mice have a high beta-cell proliferation rate, and they have large islets of Langerhans. This was not affected by citalopram treatment. Our findings show that the serotonergic system plays a role as a regulator of food intake over shorter periods, and this is also true in the absence of leptin.

  • 113.
    Täljedal, Inge-Bert
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Esse est percpi and percept identity in C. J. Boström's philosophy2013Ingår i: Idealistic Studies, ISSN 0046-8541, E-ISSN 2153-8239, Vol. 43, nr 1-2, s. 63-70Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Berkeley's 'esse is percipi' has been criticized for implying epistemological solipsism, the main argument being that different minds cannot harbor numerically one and the same idea. Similarly, C. J. Boström, the dominating Swedish philosopher in the 19th century, was early scorned because his principle of esse est percipi allegedly contradicts the simultaneous claim that two spirits (God and a human, or two humans) can perceive the same thing under qualitatively different appearances. Whereas the criticism against Berkeley is here regarded as valid, it is argued that Boström successfully defended himself by employing a dual concept of meaning, resembling Frege's Sinn and Bedeutung some thirty years later, and by postulating an ontology that permits human minds to share in the divine ideas that constitute reality.

  • 114.
    Täljedal, Inge-Bert
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB). Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Linnaeus' Questions to the Sami Herdsman: The ID-versus-Science Issue in a Nut-ShellManuskript (preprint) (Övrigt vetenskapligt)
    Abstract [en]

    According to a United States court ruling, Intelligent Design (ID) theory is religious in nature, not scientific, and must not be taught in schools. In opposition, Fuller argues for a closer rapport between science and religion. Here it is emphasized that any allegedly scientific conclusion from design in Nature to the existence of God is a hypothesis subject to the same quality norms as empirical hypotheses in general. By quotations from his Iter Lapponicum, Linnæus is summoned in support of a strictly immanent conception of science, against Fuller’s suggestion that Linnæus’ personal piety could be reason for considering ID scientific.

  • 115.
    Täljedal, Inge-Bert
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Quantitative studies on phosphatases in isolated pancreatic islets of mammals1967Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
  • 116.
    Täljedal, Inge-Bert
    Umeå universitet, Medicinsk fakultet, Integrativ medicinsk biologi, Histologi med cellbiologi.
    Strong holism, weak holism, and health.2004Ingår i: Med Health Care Philos, ISSN 1386-7423, Vol. 7, nr 2, s. 143-8; discussion 149Artikel i tidskrift (Övrigt vetenskapligt)
    Abstract [en]

    The health theories of Nordenfelt and Boorse are compared. Critical attention is focused on Nordenfelt's description of his theory as one of holistic welfare, contrasting with Boorse's analytical and statistical approach. Neither theory is found to give an entirely satisfactory account of 'health' in scientific medicine or common usage. Because Nordenfelt attenuates the ontological significance of organs and organ parts and simplifies the role of statistics, his theory is regarded as weakly holistic. Boorse underrates the importance of non-statistical evaluation. A mediating position, termed 'strong holism' is suggested as a way of integrating normative and statistical elements in a more adequate health concept.

  • 117.
    Täljedal, Inge-Bert
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    The idea of being is not uniquely innate2016Ingår i: Principia: an International Journal of Epistemology, ISSN 1414-4247, E-ISSN 1808-1711, Vol. 20, nr 3, s. 343-359Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    According to the Italian philosopher Antonio Rosmini (1797-1855), being is an innate idea that is requisite for contemplating anything. He emphatically claims that it is the one and only innate idea. Rosmini makes a sharp distinction between sensations and perceptions. Perceptions are thought to arise when the undetermined idea of being (tantamount to possibility) is combined with sensations, universals when being is combined with perceptions. It is argued here that Rosmini’s explanation of the origin of universals does not work. If the idea of being is regarded as innate, then several others should be similarly regarded, notably the idea of qualitative identity which is an idea necessary for deriving universals.  Although Rosmini holds that certain properties are necessarily present in real objects and therefore implicit in the idea of being, the property of being qualitatively identical with something else is not among those properties. Theological motives may have encouraged  Rosmini to emphasize being as a peculiarly fundamental idea. However, if the idea of being is more fundamental than other universals, it may be regarded so in virtue of its generality,  not because it has a uniquely innate character.

  • 118.
    Täljedal, Inge-Bert
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    The vulnerability of university culture and individual integrity2013Ingår i: Trust and confidence in scientific research / [ed] Göran Hermeren, Kerstin Sahlin, Nils-Eric Sahlin & Kungl. Vitterhets historie och antikvitets akademien, Stockholm: Kungl. Vitterhetsakademien (The Royal Swedish Academy of Letters, History and Antiquities) , 2013, s. 52-58Kapitel i bok, del av antologi (Övrig (populärvetenskap, debatt, mm))
  • 119.
    Virel, Ana
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Saa, Laura
    Pavlov, Valeri
    CIC biomaGUNE, Parque Tecnológico de San Sebastián, San Sebastián, Spain.
    Quantification of prothrombin in human plasma amplified by autocatalytic reaction2012Ingår i: Analytical Chemistry, ISSN 0003-2700, E-ISSN 1520-6882, Vol. 84, nr 5, s. 2380-2387Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    By site directed mutagenesis, we have produced recombinant mutants of human and mouse prethrombin-2 which are able to convert themselves autocatalytically into α-thrombin. We also have created a new method to amplify the signal of bioanalytical assays based on the autocatalytic activation of these mutated proenzymes. The activation of the mutants by active α-thrombin triggers an autocatalytic reaction which leads to more active thrombin resulting in the amplification of the readout signal. Addition of mutated mouse prethrombin-2 into the conventional assay for prothrombin level in human plasma, employing ecarin and the fluorogenic substrate, resulted in improvement of the detection limit by 2 orders of magnitude.

  • 120. Wang, Hui
    et al.
    VerHalen, Jon
    Madariaga, Maria Lucia
    Xiang, Shuanglin
    Wang, Shumei
    Lan, Ping
    Oldenborg, Per-Arne
    Umeå universitet, Medicinsk fakultet, Integrativ medicinsk biologi, Histologi med cellbiologi.
    Sykes, Megan
    Yang, Yong-Guang
    Attenuation of phagocytosis of xenogeneic cells by manipulating CD47.2007Ingår i: Blood, ISSN 0006-4971, Vol. 109, nr 2, s. 836-42Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Signal regulatory protein alpha (SIRPalpha) is a critical immune inhibitory receptor on macrophages, and its interaction with CD47, a ligand for SIRPalpha, prevents autologous phagocytosis. We hypothesized that interspecies incompatibility of CD47 may contribute to the rejection of xenogeneic cells by macrophages. Here, we show that pig CD47 does not interact with mouse SIPRalpha. Similar to CD47-/- mouse cells, porcine red blood cells (RBCs) failed to induce SIRPalpha tyrosine phosphorylation in mouse macrophages. Blocking SIRPalpha with antimouse SIRPalpha mAb (P84) significantly enhanced the phagocytosis of CD47+/+ mouse cells, but did not affect the engulfment of porcine or CD47-/- mouse cells by mouse macrophages. CD47-deficient mice, whose macrophages do not phagocytose CD47-/- mouse cells, showed markedly delayed clearance of porcine RBCs compared with wild-type mouse recipients. Furthermore, mouse CD47 expression on porcine cells markedly reduced their phagocytosis by mouse macrophages both in vitro and in vivo. These results indicate that interspecies incompatibility of CD47 contributes significantly to phagocytosis of xenogeneic cells by macrophages and suggest that genetic manipulation of donor CD47 to improve its interaction with the recipient SIRPalpha may provide a novel approach to prevent phagocyte-mediated xenograft rejection.

  • 121.
    Wang, Hui
    et al.
    Massachusetts General Hospital, Harvard Medical School, Boston.
    Wu, Xiaojian
    Massachusetts General Hospital, Harvard Medical School, Boston, Sun Yat-sen University, Guangzhou.
    Wang, Yuantao
    Massachusetts General Hospital, Harvard Medical School, Boston, First Hospital of Jilin University, Changchun .
    Oldenborg, Per-Arne
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Yang, Yong-Guang
    CD47 is required for suppression of allograft rejection by donor-specific transfusion2010Ingår i: Journal of Immunology, ISSN 0022-1767, E-ISSN 1550-6606, Vol. 184, nr 7, s. 3401-3407Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    CD47 is a ligand of the inhibitory receptor, signal regulatory protein (SIRP)alpha, and its interaction with SIRPalpha on macrophages prevents phagocytosis of autologous hematopoietic cells. CD47-SIRPalpha signaling also regulates dendritic cell (DC) endocytosis, activation, and maturation. In this study, we show that CD47 expression on donor cells plays an important role in suppression of allograft rejection by donor-specific transfusion (DST). DST was performed by i.v. injection of splenocytes from C57BL/6 donors into MHC class I-disparate bm1 mice 7 d prior to donor skin grafting. Administration of wild-type (WT) C57BL/6 donor splenocytes markedly prolonged donor skin survival in bm1 mouse recipients. In contrast, bm1 mice receiving DST from CD47 knockout (KO) donors showed no inhibition or even acceleration of donor skin graft rejection compared with non-DST control (naive) bm1 mice. T cells from bm1 mice receiving CD47 KO, but not WT, DST exhibited strong anti-donor responses. The ability of DST to suppress alloresponses was positively correlated with the density of CD47 molecules on donor cells, as CD47(+/-) DST was able to prolonged donor skin survival, but to a significantly less extent than WT DST. Furthermore, DCs from CD47 KO, but not WT, DST recipients showed rapid activation and contributed to donor skin rejection. These results show for the first time that CD47 on donor cells is required to repress recipient DC activation and suppress allograft rejection after DST, and suggest CD47 as a potential target for facilitating the induction of transplant tolerance.

  • 122.
    Westlund, Jessica
    et al.
    University of Gothenburg.
    Livingston, Megan
    University of Gothenburg.
    Fahlen-Yrlid, Linda
    University of Gothenburg.
    Oldenborg, Per-Arne
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Yrlid, Ulf
    University of Gothenburg.
    CD47-deficient mice have decreased production of intestinal IgA following oral immunization but a maintained capacity to induce oral tolerance2012Ingår i: Immunology, ISSN 0019-2805, E-ISSN 1365-2567, Vol. 135, nr 3, s. 236-244Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Signal regulatory protein a (SIRPa/CD172a), expressed by myeloid cells including CD11b+ dendritic cells, interacts with ubiquitously expressed CD47 to mediate cellcell signalling and therefore, may be pivotal in the development of tolerance or immunity. We show that in mice deficient in CD47 (CD47-/-) the cellularity in gut-associated lymphoid tissues is reduced by 50%. In addition, the frequency of CD11b+ CD172a+ dendritic cells is significantly reduced in the gut and mesenteric lymph nodes, but not in Peyers patches. Activation of ovalbumin (OVA)-specific CD4+ T cells in the mesenteric lymph nodes after feeding OVA is reduced in CD47-/- mice compared with wild-type however, induction of oral tolerance is maintained. The addition of cholera toxin generated normal serum anti-OVA IgG and IgA titres but resulted in reduced intestinal anti-OVA IgA in CD47-/- mice. Replacing the haematopoietic compartment in CD47-/- mice with wild-type cells restored neither the cellularity in gut-associated lymphoid tissues nor the capacity to produce intestinal anti-OVA IgA following immunization. This study demonstrates that CD47 signalling is dispensable for oral tolerance induction, whereas the expression of CD47 by non-haematopoietic cells is required for intestinal IgA B-cell responses. This suggests that differential CD4 T cell functions control tolerance and enterotoxin-induced IgA immunity in the gut.

  • 123.
    Widmark, Anders
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för strålningsvetenskaper, Onkologi.
    Helle, S. I.
    James, N.
    Larsson, Anders
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Staudacher, K.
    Haugen, I.
    Garcia-Vargas, J.
    Nilsson, S.
    Hematologic Safety Profile of Radium-223 Dichloride (Ra-223) From the Phase 3 ALSYMPCA Trial in Castration-Resistant Prostate Cancer (CRPC) Patients With Bone Metastases2013Ingår i: European Journal of Nuclear Medicine and Molecular Imaging, ISSN 1619-7070, E-ISSN 1619-7089, Vol. 40, nr Supplement 2, s. S189-S190Artikel i tidskrift (Övrigt vetenskapligt)
  • 124. Yanagita, Tadahiko
    et al.
    Murata, Yoji
    Tanaka, Daisuke
    Motegi, Sei-ichiro
    Arai, Eri
    Daniwijaya, Edwin Widyanto
    Hazama, Daisuke
    Washio, Ken
    Saito, Yasuyuki
    Kotani, Takenori
    Ohnishi, Hiroshi
    Oldenborg, Per-Arne
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Garcia, Noel Verjan
    Miyasaka, Masayuki
    Ishikawa, Osamu
    Kanai, Yae
    Komori, Takahide
    Matozaki, Takashi
    Anti-SIRP alpha antibodies as a potential new tool for cancer immunotherapy2017Ingår i: JCI Insight, ISSN 2379-3708, Vol. 2, nr 1, artikel-id e89140Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Tumor cells are thought to evade immune surveillance through interaction with immune cells. Much recent attention has focused on the modification of immune responses as a basis for new cancer treatments. SIRP alpha is an Ig superfamily protein that inhibits phagocytosis in macrophages upon interaction with its ligand CD47 expressed on the surface of target cells. Here, we show that SIRP alpha is highly expressed in human renal cell carcinoma and melanoma. Furthermore, an anti-SIRP alpha Ab that blocks the interaction with CD47 markedly suppressed tumor formation by renal cell carcinoma or melanoma cells in immunocompetent syngeneic mice. This inhibitory effect of the Ab appeared to be mediated by dual mechanisms: direct induction of Ab-dependent cellular phagocytosis of tumor cells by macrophages and blockade of CD47-SIRP alpha signaling that negatively regulates such phagocytosis. The antitumor effect of the Ab was greatly attenuated by selective depletion not only of macrophages but also of NK cells or CD8(+) T cells. In addition, the anti-SIRP alpha Ab also enhances the inhibitory effects of Abs against CD20 and programmed cell death 1 (PD-1) on tumor formation in mice injected with SIRP alpha-nonexpressing tumor cells. Anti-SIRP alpha Abs thus warrant further study as a potential new therapy for a broad range of cancers.

  • 125.
    Ylärinne, Janne
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Production of neocartilage tissues using primary chondrocytes2016Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
    Abstract [en]

    Hyaline cartilage is a highly specialized tissue, which plays an important role in the articulating joints of an individual. It provides the joints with a nearly frictionless, impact resisting surface to protect the ends of the articulating bones. Articular cartilage has a poor self-repair capacity and, therefore, it rarely heals back to normal after an injury. Overweight, injuries, overloading and genetic factors may initiate a degenerative disease of the joint called osteoarthritis.

    Osteoarthiritis is a major global public health issue. Currently, the most used treatment for large articular cartilage defects is joint replacement surgery. However, possibilities to replace this highly invasive operation with strategies based on tissue engineering are currently investigated. The idea of the tissue engineering is to optimize the use of the cells, biomaterials and culture conditions to regenerate a new functional tissue for the defect site.

    The goal of this thesis was to manufacture cartilage tissue in cell culture conditions in vitro. Bovine primary chondrocytes isolated from the femoral condyles were used in all the experiments for neocartilage production. The samples were collected for histology, gene expression level quantifications, and analyses of proteoglycan (PG) content and quality. The histological sections were stained for type II collagen and PGs, the quantitative RT-PCR was used to observe the relative expressions of aggrecan, Sox9, procollagen α2(I) and procollagen α1(II) genes. The PGs were quantified using a spectrophotometric method, and agarose gel electrophoresis was used to separate the PGs according to their size.

    In the two first studies, we optimized the culture conditions of in vitro scaffold-free culture technique to produce the native-type hyaline cartilage of a good quality. We found out that high glucose concentration and hypertonic medium at 20% oxygen tension promoted the best hyaline-like neocartilage tissue production. Glucosamine sulfate supplementation, low oxygen tension, 5 mM glucose concentration and a transient TGF-β3 supplementation were not beneficial for the neocartilage formation in the scaffold-free cell culture system.

    In the third study, we used these newly defined, optimized culture conditions to produce the neocartilage tissues in the HyStem™ and the HydroMatrix™ scaffold materials and we compared these tissues to the ones grown as scaffold-free control cultures. We noticed that there was no difference between the controls and the scaffolds, and occasionally the scaffold-free controls had produced better quality cartilage than the ones with the scaffolds. Overall, the neocartilage tissues were of good hyaline-like quality in the third study. Their extracellular matrix contents were close to the native cartilage, although the neotissues lacked the zonal organization typical to the normal articular cartilage. The tissues had the right components, but their ultrastructure differed from the native cartilage.

    In conclusion, we were able to optimize our in vitro neocartilage culture method further, and discovered a good combination of the culture conditions to produce hyaline-like cartilage of good quality. Surprisingly, the scaffold materials were not beneficial for the cartilage formation.

     

  • 126. Zashikhin, A L
    et al.
    Sehlin, Janove
    Umeå universitet, Medicinsk fakultet, Integrativ medicinsk biologi, Histologi med cellbiologi.
    Bolduev, V A
    Agafonov, Iu V
    Organization of the muscular component of the lymphangion wall in different parts of the lymphatic bed2005Ingår i: Morfologiia, ISSN 1026-3543, Vol. 127, nr 1, s. 29-32Artikel i tidskrift (Övrigt vetenskapligt)
    Abstract [en]

    Complex comparative analysis of the organization of smooth muscle (SM) forming the wall of lymphatic vessels in bovine small intestinal mesenterium was performed using the methods of morphometry, quantitative histochemistry (including the analysis of nuclear DNA content, and cytoplasmic protein content) and electron microscopy. SM cells (SMC) isolated by dissociation were studied and were found to possess various levels of differentiation, associated with specific morphometric and metabolic characteristics. The structure of SMC population was shown to vary in both different parts of lymphatic bed and within the wall of an individual lymphangion. The results obtained indicate the cellular heteromorphism of lymphatic bed SM. The peculiarities of SM organization in lymphatic vessels are functionally dependent and are determined not only by the level of SM representation in their wall but also by the proportions of different SMC types.

  • 127.
    Zashikhin, Andrei L
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Sehlin, Janove
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Barmina, Anastasia O
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    [Reactive changes in the smooth muscle tissue of the rat small intestine during experimental intestinal obstruction].2010Ingår i: Morfologiia (Saint Petersburg, Russia), ISSN 1026-3543, Vol. 137, nr 2, s. 48-53Artikel i tidskrift (Refereegranskat)
    Abstract [ru]

    Using light, electron microscopy and immunohistochemical methods, the reactive transformation of smooth muscle tissue (SMT) was studied in the intestinal wall during the development of acute partial high intestinal obstruction. The material of small intestine was taken from 10 male rats in both the zone of ligature application, and proximal and distal zones, 3 cm distant from the ligation zone. The results of the study demonstrate that in partial intestinal obstruction, the nature of structural and functional SMT transformation was variable depending upon differences in functional and destructive loads. During these changes, the remodeling of smooth myocyte population was shown to be one of the mechanisms of SMT adaptation to the changing conditions of functioning. Immunohistochemical analysis found no changes in the pattern of expression of marker and phenotypic proteins in the intestinal zones studied during the dynamics of an experiment.

  • 128.
    Zashikhin, Andrei
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Sehlin, Janove
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Visceral'naja gladkaja myšečnaja tkan'2001Bok (Refereegranskat)
  • 129.
    Zashikhin, Andrey L
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Sehlin, Janove
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Barmina, Anastasia
    Umeå universitet, Medicinska fakulteten, Institutionen för integrativ medicinsk biologi (IMB), Histologi med cellbiologi.
    Mechanisms of the contractile activity control in smooth muscle cells2010Ingår i: Morfologiia, ISSN 1026-3543, Vol. 138, nr 6, s. 56-59Artikel i tidskrift (Refereegranskat)
123 101 - 129 av 129
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