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Kirjailija

Michael Streppel

Kirjat ja teokset yhdessä paikassa: 2 kirjaa, julkaisuja vuosilta 1998-2005, suosituimpien joukossa Axonal Branching and Recovery of Coordinated Muscle Activity after Transsection of the Facial Nerve in Adult Rats. Vertaile teosten hintoja ja tarkista saatavuus suomalaisista kirjakaupoista.

2 kirjaa

Kirjojen julkaisuhaarukka 1998-2005.

Axonal Branching and Recovery of Coordinated Muscle Activity after Transsection of the Facial Nerve in Adult Rats

Axonal Branching and Recovery of Coordinated Muscle Activity after Transsection of the Facial Nerve in Adult Rats

Doychin N. Angelov; Orlando Guntinas-Lichius; Konstantin Wewetzer; Wolfram Neiss; Michael Streppel

Springer-Verlag Berlin and Heidelberg GmbH Co. K
2005
nidottu
Facial nerve surgery inevitably leads to partial pareses, abnormally associated movements and pathologically altered reflexes. The reason for this "post-paralytic syndrome" is the misdirected reinnervation of targets, which consists of two major components. First, due to malfunctioning axonal guidance, a muscle gets reinnervated by a "foreign" axon, that has been misrouted along a "wrong" fascicle. Second, the supernumerary collateral branches emerging from all transected axons simultaneously innervate antagonistic muscles and cause severe impairment of their coordinated activity. Since it is hardly possible to influence the first major component and improve the guidance of several thousands axons, the authors concentrated on the second major component and tried to reduce the collateral axonal branching.
The Cerebral Perivascular Cells

The Cerebral Perivascular Cells

Doychin N. Angelov; Michael Walther; Michael Streppel; Orlando Guntinas-Lichius; Wolfram F. Neiss

Springer-Verlag Berlin and Heidelberg GmbH Co. K
1998
nidottu
References ...77 Subject Index...89 XI 1 Introduction 1.1 Antigen Presentation and Antigen Presenting Cells A key issue in the pathogenesis of any chronic degenerative (auto )immune disease of the central nervous system (CNS) is how pathologically altered autologous neuronal proteins can trigger a reaction of the immune system. The specific and greatly multi- plied immune response is decisive for the outcome of the disease. Current knowledge shows that the immune system gets involved and potentiates a progressive neuronal degeneration in two ways, which are not mutually exclusive. First, provided the immunogenic autologous protein occurs in the interstitial fluid of CNS in amounts which cannot be phagocytized and cleared by the leptomeningeal macrophages, it reaches the cervical lymph nodes passively along the perivascular spaces, the cerebrospinal fluid compartment above the cribriform plate, and the lymphatics of the nasal mucosa (Cserr and Ostrach 1974; Weller et al. 1992; Zhang et al. 1992; Kida et al. 1993). The immunological significance of this "late" pathway typical for advanced neurodegeneration has been confirmed by Harling-Berg et al. (1989), who showed that the cervical lymph nodes are the main site of antibody production against foreign protein injected into the central gray matter of the rat brain.