@article{BeckerSchmidtkeStoeberetal.1994,
  author    = {Becker, T. and Schmidtke, A. and St{\"o}ber, Gerald and Franzek, E. and Teichmann, E. and Hofmann, E.},
  title     = {Hyperintense Marklagerl{\"a}sionen bei psychiatrischen Patienten: r{\"a}umliche Verteilung und psychopathologische Symptome},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-78288},
  year      = {1994},
  abstract  = {In einem Kollektiv von 130 MR-tomographisch untersuchten psychiatrischen Patienten (axiale T2-SE-Sequenz) wurden Zahl und r{\"a}umliche Verteilung von hyperintensen Marklagerl{\"a}sionen ("white matter lesions"; WM L) erfaßt und die Ventricle-to-brain-Ratio (VBR) bestimmt. Eine Konfigurationsfrequenzanalyse auf der Grundlage der r{\"a}umlichen WMLVerteilung erlaubte die Abgrenzung von vier Patientengruppen: 1. keine WML (n = 35), 2. WML rechts frontotemporal (n = 23), 3. WML bifrontal (n = 12), 4. WML ubiquit{\"a}r (n = 16). Die w{\"a}hrend 3 Jahren beobachteten psychopathologischen Symptome dieser Patienten wurden retrospektiv nach dem AMDP-Systemdokumentiert. In der Gruppe mit ubiquit{\"a}ren WML {\"u}berwogen organisch-psychopathologische Ttems, die VER war gr{\"o}ßer als in den anderen Gruppen (ANOVA;p < 0,001). Die r{\"a}umliche W M L- Verteilung erkl{\"a}rte 10,24 \% der Gesamtvarianz psychopathologischer M erkmalsverteilung in den Gruppen. Das Patientenalter (MANCOVA; p < 0,021), nicht aber die VER hattesignifikanten Einfluß auf das psychopathologische Symptomprofil. Nach Ausblendung der Patientengruppe mit ubiquit{\"a}ren WMLblieb der Einfluß der WML-Verteilung auf die psychopathologische Symptomatiksignifikantc (p <0,05). Bifrontale WML waren mit Denkst{\"o}rung, rechts frontotemporale WML mit affektiven Symptomen assoziiert. Die Befunde sprechen f{\"u}r einen Einfluß der r{\"a}umlichen Verteilung unspezifischer Marklagerl{\"a}sionen auf die psychopathologische Symptomatik.},
  subject      = {Medizin},
  language  = {de}
}
@phdthesis{Fischer2008,
  author    = {Fischer, Stefan Martin},
  title     = {Regulation and functional consequences of MCP-1 expression in a model of Charcot-Marie-Tooth 1B disease},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-29189},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2008},
  abstract  = {Charcot-Marie-Tooth 1B (CMT1B) is a progressive inherited demyelinating disease of human peripheral nervous system leading to sensory and/or motor function disability and is caused by mutations in the P0 gene. Mice heterozygously deficient for P0 (P0+/-) are an adequate model of this human disorder showing myelin degeneration, formation of onion bulbs, remyelination and a reduced motor conduction velocity of around 30m/s similar to patients. Previously, it had been shown that T-lymphocytes and macrophages play a crucial role during pathogenesis in peripheral nerves of P0+/- mice. Both, T-lymphocytes and macrophages increase in number in the endoneurium and deletion of T-lymphocytes or deletion of a macrophage-directed cytokine ameliorates the disease. In this study the monocyte chemoattractant protein-1 (MCP-1) was identified as an early regulated cytokine before onset of disease is visible at the age of six months. MCP-1 mRNA and protein expression could be detected in femoral quadriceps and sciatic nerves of P0+/- mice already at the age of one month but not in cutaneous saphenous nerves which are never affected by the disease. MCP-1 was shown to be expressed by Schwann cells and to mediate the immigration of immune cells into peripheral nerves. Deletion of MCP-1 in P0+/- mice accomplished by crossbreeding P0 and MCP-1 deficient mice revealed a substantial reduction of immune cells in peripheral nerves of P0+/-/MCP-1+/- and P0+/-/MCP-1-/- mice at the age of six months. In twelve months old mice reduction of immune cells in peripheral nerves is accompanied by amelioration of demyelinating disease in P0+/-/MCP-1+/- and aggravation of demyelinating disease in lumbar ventral roots of P0+/ /MCP-1-/- mice in comparison to P0+/ /MCP 1+/+ mice. Furthermore, activation of the MEK1/2-ERK1/2 signalling cascade could be demonstrated to take place in Schwann cells of affected peripheral nerves of P0+/- mice overlapping temporarily and spatially with MCP-1 expression. An animal experiment using a MEK1/2-inhibitor in vivo, CI-1040, revealed that upon reduction of ERK1/2 phosphorylation MCP-1 mRNA expression is diminished suggesting that the activation of the MEK1/2-ERK1/2 signalling cascade is necessary for MCP-1 expression. Additionally, peripheral nerves of P0+/- mice showing reduced ERK1/2 phosphorylation and MCP-1 mRNA expression also show reduced numbers of macrophages in the endoneurium. This study shows a molecular link between a Schwann cell based mutation and immune cell function. Inhibition of the identified signalling cascade might be a putative target for therapeutic approaches.},
  subject      = {Schwann-Zelle},
  language  = {en}
}