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Scientists have long
experimented with organs - on - chips: tiny representations of human organs, such as lungs,
hearts and intestines, made from
cells embedded on plastic about the size of a computer memory stick.
«Before this study, it was not known if it is possible to produce sufficient numbers of these
cells and successfully use them to remuscularize damaged
hearts in a large animal whose
heart size and physiology is similar to that of the human
heart,» said Dr. Charles Murry, UW professor of pathology and bioengineering, who led the research team that conducted the
experiment.
The results of the
experiment appear in the April 30 advanced online edition of the journal Nature in a paper titled, «Human embryonic - stem
cell derived cardiomyocytes regenerate non-human primate
hearts.»
The team's further
experiments on cultured
heart cells confirmed that GDF - 11 stops the thickening growth seen with age.
The second key
experiment showed the effect of transferring activated T -
cells from
heart - attack mice to healthy mice.
Two key
experiments demonstrated this necessary and sufficient role for the activated T -
cells, which presumably attack
heart muscle tissue in an auto - immune fashion.
The day after his disciplinary dismissal from University of Tokyo for «damaging the university's honor or credibility,» Hisashi Moriguchi maintained in an interview with ScienceInsider that he really did participate in a groundbreaking
experiment to treat a
heart disease patient with cardiac muscle
cells derived from the patient's own induced pluripotent stem (iPS)
cells.
After the pig
experiment worked well, he used his Boston area facility to culture the 30 million cardiac muscle
cells that he says were injected into a
heart disease patient in mid-2011.
The
experiments reveal that the sudden loss of energy supply to the
heart cells and the subsequent rapid «reboot» during treatment causes mitochondria to falter and trigger a whirlwind of aberrant electrical signals.
In their
experiments, the researchers noted that the mitochondria of
heart cells that lost oxygen and nutrient supply for a half - hour recovered smoothly.
But the scientists noticed something odd when they ran control
experiments in which they injected the hydrogel without added
cells: Some of the animals»
hearts still showed improvement compared with untreated animals.
Experiments on mice and on
heart cells obtained from infants born with congenital
heart disease suggest that neuregulin 1, a human growth factor, can put infant
heart cells on a path that mimics normal growth rather than stalling out.
In the case of the Circulation paper, which reported a surprisingly high turnover rate for muscle
cells in the adult
heart, Leri and Anversa say that Kajstura apparently altered, without their knowledge, data from mass spectrometry
experiments performed at Lawrence Livermore National Laboratory (LLNL) in California.
Sean Wu, who studies
heart stem
cells at Stanford University in Palo Alto, California, says the NIH notice prompted Stanford to urge scientists to be sure their
experiments didn't violate the new rules.
In previous
experiments, neural stem
cells have been able to integrate into developing embryos and turn into many different types of
cells, including
heart and liver (ScienceNOW, 1 June) and even blood (21 January 1999).
Then an
experiment in 2005 found that young blood returned the liver and skeletal stem
cells of old mice to a more youthful state, and work in 2012 discovered that young blood can reverse
heart decline in old mice.
Stem
cells in parts of the
heart that have survived a
heart attack can be prodded to regenerate tissue that was killed by the attack, recent
experiments suggest.
In these
experiments, exactly how the stem
cells improved
heart function remains controversial.
In a series of
experiments, Haldar discovered that JQ1 stops the harmful gene expression that enlarges the
heart and damages
heart cells.
His studies, ranging from molecular
experiments to clinical trials, have generated comprehensive evidence for the efficacy of omega - 3 in preventing cardiac sudden death and established the mechanism by which omega - 3 fatty acids can reduce cardiac arrhythmia by interacting with membrane ion channels and stabilizing the electrical activity of
heart cells.
But initial
experiments on human fibroblasts from three sources — fetal
heart cells, embryonic stem
cells and neonatal skin
cells — revealed that the GMT combination alone was not sufficient.