XXXX treatment in a @entity19 model of @entity5 reduces serum @entity51946 and raises heart @entity460 .

@entity51945 @entity5 @entity19 @entity1372 @entity730 @entity2265 @entity1391 @entity460 @entity4571 @entity51946
Mutations in the @entity51945 gene result in @entity5 , characterized by persistent @entity2265 and ectopic calcific masses in soft tissues. Since calcific masses often recur after surgical removal, a more permanent solution to the problem is required. @entity4571 is reported to lower serum @entity1391 by decreasing @entity1372 -dependent @entity1391 co-transporters in the gut and kidney. However, its effectiveness in @entity5 remains unknown. In this study, we investigated @entity4571 as a potential therapy for @entity5 , using a @entity19 model of the disease- @entity51945 knockout @entity19 . Initially, five different doses of @entity4571 were given to normal heterozygous @entity19 intraperitoneally or orally. Treatment had no effect on serum @entity1391 levels, but serum levels of a phosphaturic hormone, @entity51946 ( @entity51946 ), decreased in a dose-dependent manner. Subsequently, high-dose @entity4571 (40mM) was tested in @entity51945 knockout @entity19 fed a high @entity1391 diet. The radiographic data pre- and post-treatment showed that @entity4571 did not reverse the @entity730 . However, the treatment retarded @entity730 growth after 4weeks, while in the untreated animals, @entity730 increased in size. The therapy did not affect serum @entity1391 levels, but intact @entity51946 decreased in the treated @entity19 . The treated @entity19 also had increased @entity460 in the heart. In summary, @entity4571 did not alter serum @entity1391 levels, likely due to compensatory decrease in @entity51946 to counteract the @entity1391 lowering effect of @entity4571 . Although increased @entity460 accumulation in the heart is a concern, the therapy appears to slow down the progression of ectopic @entity730 .
