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Beatrix Fauler

Researcher at Max Planck Society

Publications -  23
Citations -  8748

Beatrix Fauler is an academic researcher from Max Planck Society. The author has contributed to research in topics: Induced pluripotent stem cell & Biology. The author has an hindex of 9, co-authored 20 publications receiving 7172 citations.

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Neutrophil extracellular traps kill bacteria

TL;DR: It is described that, upon activation, neutrophils release granule proteins and chromatin that together form extracellular fibers that bind Gram-positive and -negative bacteria, which degrade virulence factors and kill bacteria.
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The senescence-related mitochondrial/oxidative stress pathway is repressed in human induced pluripotent stem cells.

TL;DR: It is demonstrated that somatic mitochondria within human iPSCs revert to an immature ESC‐like state with respect to organelle morphology and distribution, expression of nuclear factors involved in mitochondrial biogenesis, content of mitochondrial DNA, intracellular ATP level, oxidative damage, and lactate generation, and suggest that cellular reprogramming can modulate the mitochondrial/oxidative stress pathway, thus inducing a rejuvenated state capable of escaping cellular senescence.
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Mitochondrial-associated cell death mechanisms are reset to an embryonic-like state in aged donor-derived iPS cells harboring chromosomal aberrations

TL;DR: It will be essential to develop reprogramming protocols capable of safeguarding the integrity of the genome of aged somatic cells, before employing iPSC-based therapies for age-associated disorders, according to concerns over the oncogenic potential of reprogrammed cells.
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FGF Inhibition Directs BMP4-Mediated Differentiation of Human Embryonic Stem Cells to Syncytiotrophoblast

TL;DR: It is shown that FGF inhibition alone, or in combination with either ACTIVIN/NODAL inhibition or BMP activation, supports hESC differentiation to hCG-secreting syncytiotrophoblast, and that the inhibition of the FGF pathway acts as a key in directing BMP4-mediated hESCs differentiation to syn Cytiotrophicoblast.