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Träfflista för sökning "WFRF:(Kuhn M) srt2:(2000-2004)"

Search: WFRF:(Kuhn M) > (2000-2004)

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  • Cooper-Kuhn, Christiana M, 1971, et al. (author)
  • Decreased neurogenesis after cholinergic forebrain lesion in the adult rat.
  • 2004
  • In: Journal of neuroscience research. - : Wiley. - 0360-4012 .- 1097-4547. ; 77:2, s. 155-65
  • Journal article (peer-reviewed)abstract
    • Adult neurogenesis has been shown to be regulated by a multitude of extracellular cues, including hormones, growth factors, and neurotransmitters. The cholinergic system of the basal forebrain is one of the key transmitter systems for learning and memory. Because adult neurogenesis has been implicated in cognitive performance, the present work aims at defining the role of cholinergic input for adult neurogenesis by using an immunotoxic lesion approach. The immunotoxin 192IgG-saporin was infused into the lateral ventricle of adult rats to selectively lesion cholinergic neurons of the cholinergic basal forebrain (CBF), which project to the two main regions of adult neurogenesis: the dentate gyrus and the olfactory bulb. Five weeks after lesioning, neurogenesis, defined by the number of cells colocalized for bromodeoxyuridine (BrdU) and the neuronal nuclei marker NeuN, declined significantly in the granule cell layers of the dentate gyrus and olfactory bulb. Furthermore, immunotoxic lesions to the CBF led to increased numbers of apoptotic cells specifically in the subgranular zone, the progenitor region of the dentate gyrus, and within the periglomerular layer of the olfactory bulb. We propose that the cholinergic system plays a survival-promoting role for neuronal progenitors and immature neurons within regions of adult neurogenesis, similar to effects observed previously during brain development. As a working hypothesis, neuronal loss within the CBF system leads not only to cognitive deficits but may also alter on a cellular level the functionality of the dentate gyrus, which in turn may aggravate cognitive deficits.
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  • Jostarndt, K, et al. (author)
  • Enzymatically modified low-density lipoprotein upregulates CD36 in low-differentiated monocytic cells in a peroxisome proliferator-activated receptor-γ-dependent way
  • 2004
  • In: Biochemical Pharmacology. - : Elsevier BV. - 0006-2952 .- 1356-1839. ; 67:5, s. 841-854
  • Journal article (peer-reviewed)abstract
    • Peroxisome proliferator-activated receptor-γ (PPARγ) has been suggested to upregulate CD36. Since free oxidized polyunsaturated fatty acids are PPARγ ligands, we studied the effects of LDL modified by the simultaneous action of sPLA2 and 15-lipoxygenase (15LO) on CD36 expression and PPARγ activation in monocytic cells. Exposure of MM6 cells, which do not express CD36 or other scavenger receptors, to such enzymatically modified LDL (enzLDL) resulted in upregulation of CD36 surface protein and mRNA expression. Similar effects were observed with free 13-hydroperoxyoctadecadienoic acid but not its esterified counterpart. Less pronounced effects were observed with LDL modified by 15LO alone. Upregulation of CD36 was inversely correlated to the state of cell differentiation, as showed by lower response to enzLDL of the scavenger receptor-expressing MM6-sr and THP1 cells. Importantly, LDL modified by sPLA2 and 15LO did not efficiently induce upregulation CD36 in PPARγ-deficient macrophage-differentiated embryonic stem cells confirming a role of PPARγ in CD36 expression in cells stimulated with enzLDL. Our data show that LDL modified with physiologically relevant enzymes stimulates CD36 expression in non-differentiated monocytes and that this process involves PPARγ activation. These effects of enzLDL can be considered pro-atherogenic in the context of early atherosclerosis.
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  • Kasic, A., et al. (author)
  • Phonons and free-carrier properties of binary, ternary, and quaternary group-III nitride layers measured by infrared Spectroscopic Ellipsometry
  • 2003
  • In: Physica Status Solidi. C, Current topics in solid state physics. - : Wiley. - 1610-1634 .- 1610-1642. ; 0:6 SPEC. ISS., s. 1750-1769
  • Conference paper (other academic/artistic)abstract
    • This work reviews recent ellipsometric investigations of the infrared dielectric functions of binary, ternary, and quaternary group-III nitride films. Spectroscopic Ellipsometry in the mid-infrared range is employed for the first time to determine phonon and free-carrier properties of individual group-III nitride heterostructure components, including layers of some ten nanometer thickness. Assuming the effective carrier mass, the free-carrier concentration and mobility parameters can be quantified upon model analysis of the infrared dielectric function. In combination with Hall-effect measurements, the effective carrier masses for wurtzite n- and p-type GaN and n-type InN are obtained. The mode behavior of both the E1(TO) and A1(LO) phonons are determined for ternary compounds. For strain-sensitive phonon modes, the composition and strain dependences of the phonon frequencies are differentiated and quantified. Information on the crystal quality and compositional homogeneity of the films can be extracted from the phonon mode broadening parameters. A comprehensive IR dielectric function database of group-III nitride materials has been established and can be used for the analysis of complex thin-film heterostructures designed for optoelectronic device applications. Information on concentration and mobility of free carriers, thickness, alloy composition, average strain state, and crystal quality of individual sample constituents can be derived. © 2003 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
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  • Rasmusson, M, et al. (author)
  • Photodissociation of bromobenzene in solution
  • 2003
  • In: Chemical Physics Letters. - 0009-2614 .- 1873-4448. ; 367:5-6, s. 759-766
  • Journal article (peer-reviewed)abstract
    • The photodissociation of bromobenzene in solution was investigated with ultrafast transient absorption spectroscopy following excitation at 266 nm. Ab initio calculations of lower singlet and triplet states were performed in order to guide the interpretations. The main feature of the kinetics measured between 300 and 930 nm in acetonitrile is a 9 +/- 1ps decay, which we mainly assign to predissociation. Similar decays were observed in hexane, dichloromethane and tetrachloromethane at 400 and 800 nm. Other features in acetonitrile, such as complicated short-time dynamics between 420 and 620 nm and a long-lived component, might indicate the involvement of lower triplet states.
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  • Schänzer, Anne, et al. (author)
  • Direct stimulation of adult neural stem cells in vitro and neurogenesis in vivo by vascular endothelial growth factor.
  • 2004
  • In: Brain pathology (Zurich, Switzerland). - 1015-6305. ; 14:3, s. 237-48
  • Journal article (peer-reviewed)abstract
    • Hypoxia as well as global and focal ischemia are strong activators of neurogenesis in the adult mammalian central nervous system. Here we show that the hypoxia-inducible vascular endothelial growth factor (VEGF) and its receptor VEGFR-2/Flk-1 are expressed in clonally-derived adult rat neural stem cells in vitro. VEGF stimulated the expansion of neural stem cells whereas blockade of VEGFR-2/Flk-1-kinase activity reduced neural stem cell expansion. VEGF was also infused into the lateral ventricle to study changes in neurogenesis in the ventricle wall, olfactory bulb and hippocampus. Using a low dose (2.4 ng/d) to avoid endothelial proliferation and changes in vascular permeability, VEGF stimulated adult neurogenesis in vivo. After VEGF infusion, we observed reduced apoptosis but unaltered proliferation suggesting a survival promoting effect of VEGF in neural progenitor cells. Strong expression of VEGFR-2/Flk-1 was detected in the ventricle wall adjacent to the choroid plexus, a site of significant VEGF production, which suggests a paracrine function of endogenous VEGF on neural stem cells in vivo. We propose that VEGF acts as a trophic factor for neural stem cells in vitro and for sustained neurogenesis in the adult nervous system.These findings may have implications for the pathogenesis and therapy of neurodegenerative diseases.
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  • Result 1-10 of 24

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