Heart damage is also a prominent phenotype in various strains of dko mice, including the utrophin/dystrophin dko, α7-integrin/dystrophin dko, myoD/dystrophin dko and mTR/dystrophin dko mice (Grady et al., 1997; Guo et al., 2006; Megeney et al., 1999; Mourkioti et al., 2013) (supplementary material Table S1).
The idea of growing new heart tissue to repair heart damage is not new.
But both approaches would primarily benefit patients whose heart damage is not very severe, Taylor says.
Emerging evidence indicates that the "bad genes" are more common among Chinese women, in whom permanent iatrogenic heart damage is much more frequent, which changes the risk-benefit calculations for use of this drug.
It was not investigated whether heart damage was the primary cause of death or a secondary complication of antibody administration.
To scrutinize this hypothesis, Balb/c mice, either untreated or pre-treated with lovastatin were exposed to a single dose of doxorubicin and acute heart damage was analyzed 48 h later by measuring the mRNA levels of pro-inflammatory and pro-fibrotic cytokines.
The drug's connection to heart damage was unknown when the experiments were conducted.
So-called "recognized" heart attacks were identified when signs of heart damage were evident, and the patient's medical record indicated that medical attention had been sought and a diagnosis rendered.
The children's heart damage was repaired in December at St. Francis Hospital in Roslyn, thanks to the hospital's pediatric cardiologists, a host family and the Gift of Life Foundation in Great Neck.
Heart damage was quantified by measuring release of cardiac troponin 1 into the serum of mock-infected or infected mice at days 3 and 7 PI using a commercially available ELISA kit (Life Diagnostics, West Chester, PA) according to manufacturer's instruction.
