P.1.c.018 Increased serotonin 2c receptor editing in a mouse model of obesity

2010 ◽  
Vol 20 ◽  
pp. S245
Author(s):  
H. Schellekens ◽  
T.G. Dinan ◽  
J.F. Cryan
2020 ◽  
Author(s):  
Jade Hebras ◽  
Virginie Marty ◽  
Jean Personnaz ◽  
Pascale Mercier ◽  
Nicolai Krogh ◽  
...  

2002 ◽  
Vol 22 (24) ◽  
pp. 10529-10532 ◽  
Author(s):  
Ilona Gurevich ◽  
Michael T. Englander ◽  
Mella Adlersberg ◽  
Nathan B. Siegal ◽  
Claudia Schmauss

PLoS ONE ◽  
2012 ◽  
Vol 7 (3) ◽  
pp. e32266 ◽  
Author(s):  
Harriët Schellekens ◽  
Gerard Clarke ◽  
Ian B. Jeffery ◽  
Timothy G. Dinan ◽  
John F. Cryan
Keyword(s):  

Neuroreport ◽  
2010 ◽  
Vol 21 (17) ◽  
pp. 1080-1084 ◽  
Author(s):  
Rebecca Lyddon ◽  
Edwin Cuppen ◽  
Vahram Haroutunian ◽  
Larry J. Siever ◽  
Stella Dracheva

Immunity ◽  
1997 ◽  
Vol 7 (6) ◽  
pp. 765-775 ◽  
Author(s):  
Roberta Pelanda ◽  
Stephan Schwers ◽  
Eiichiro Sonoda ◽  
Raul M Torres ◽  
David Nemazee ◽  
...  

Author(s):  
H. D. Geissinge ◽  
L.D. Rhodes

A recently discovered mouse model (‘mdx’) for muscular dystrophy in man may be of considerable interest, since the disease in ‘mdx’ mice is inherited by the same mode of inheritance (X-linked) as the human Duchenne (DMD) muscular dystrophy. Unlike DMD, which results in a situation in which the continual muscle destruction cannot keep up with abortive regenerative attempts of the musculature, and the sufferers of the disease die early, the disease in ‘mdx’ mice appears to be transient, and the mice do not die as a result of it. In fact, it has been reported that the severely damaged Tibialis anterior (TA) muscles of ‘mdx’ mice seem to display exceptionally good regenerative powers at 4-6 weeks, so much so, that these muscles are able to regenerate spontaneously up to their previous levels of physiological activity.


1998 ◽  
Vol 13 (11-s4) ◽  
pp. S178-S184 ◽  
Author(s):  
PETER KONTUREK ◽  
TOMASZ BRZOZOWSKI ◽  
STANISLAW KONTUREK ◽  
ELZBIETA KARCZEWSKA ◽  
ROBERT PAJDO ◽  
...  

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