Accumulation of Extracellular Matrix in Chronic Lesions of Canine Distemper Demyelinating Encephalitis

2009 ◽  
Vol 141 (4) ◽  
pp. 308
Author(s):  
F. Seehusen ◽  
S. Al-Azreg ◽  
V. Haist ◽  
W. Baumgärtner
PLoS ONE ◽  
2016 ◽  
Vol 11 (7) ◽  
pp. e0159752 ◽  
Author(s):  
Frauke Seehusen ◽  
Seham A. Al-Azreg ◽  
Barbara B. Raddatz ◽  
Verena Haist ◽  
Christina Puff ◽  
...  

2017 ◽  
Vol 156 (1) ◽  
pp. 58
Author(s):  
F. Seehusen ◽  
S. Al-Azreg ◽  
V. Haist ◽  
B. Raddatz ◽  
I. Spitzbarth ◽  
...  

2003 ◽  
Vol 33 (6) ◽  
pp. 1149-1151 ◽  
Author(s):  
Selwyn Arlington Headley ◽  
Taís Berelli Saito

Simultaneous infection of canine distemper virus and canine parvovirus associated with distemper myocardial degeneration and necrosis is described in a pup. The dog demonstrated myoclonus, nystagmus, enamel hypoplasia, abdominal pustules, and bilateral corneal ulceration clinically. Demyelinating encephalitis, myocardial degeneration and necrosis with mineralization, and necrosis, hemorrhage and fusion of intestinal villi were observed. The lesions observed in this dog are characteristic of a dual infection of canine distemper virus and canine parvovirus.


1999 ◽  
Vol 29 (4) ◽  
pp. 741-743 ◽  
Author(s):  
Selwyn Arlington Headley ◽  
Dominguita Lühers Graça ◽  
Mateus Matiuzzi da Costa ◽  
Agueda Castagna de Vargas

Canine distemper virus infection and secondary Bordetella bronchiseptica pneumonia are described in mongrel dogs. Canine distemper was characterised by nonsuppurative demyelinating encephalitis with typical inclusion bodies in astrocytes. B. bronchiseptica was isolated from areas of purulent bronchopneumonia.


Author(s):  
L. Terracio ◽  
A. Dewey ◽  
K. Rubin ◽  
T.K. Borg

The recognition and interaction of cells with the extracellular matrix (ECM) effects the normal physiology as well as the pathology of all multicellular organisms. These interactions have been shown to influence the growth, development, and maintenance of normal tissue function. In previous studies, we have shown that neonatal cardiac myocytes specifically interacts with a variety of ECM components including fibronectin, laminin, and collagens I, III and IV. Culturing neonatal myocytes on laminin and collagen IV induces an increased rate of both cell spreading and sarcomerogenesis.


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