Stromal Vascular Fraction Cell Therapy for a Stroke Patient-Cure without Side Effects.

A 48-year-old male, who suffered from a stroke resulting in cerebellum damage and occlusion of the left vertebral artery, underwent stromal vascular fraction therapy. The clinical status of the patient was monitored by a modified Stroke Specific Quality of Life Scale before therapy and at 3, 9, 12, 18, 24, and 32 months after therapy. Three months after therapy, the patient felt a reduction in pain, vertigo, and fatigue.

WITHDRAWN: Autologous adipose tissue-derived stromal vascular fraction cells application in patients with osteoarthritis.

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Components of a Fanconi-like pathway control Pso2-independent DNA interstrand crosslink repair in yeast.

Fanconi anemia (FA) is a devastating genetic disease, associated with genomic instability and defects in DNA interstrand cross-link (ICL) repair. The FA repair pathway is not thought to be conserved in budding yeast, and although the yeast Mph1 helicase is a putative homolog of human FANCM, yeast cells disrupted for MPH1 are not sensitive to ICLs. Here, we reveal a key role for Mph1 in ICL repair when the Pso2 exonuclease is inactivated.

Identification of small molecule regulators of the nuclear receptor HNF4alpha based on naphthofuran scaffolds.

Nuclear receptors are ligand-activated transcription factors involved in all major physiological functions of complex organisms. In this respect, they are often described as drugable targets for a number of pathological states including hypercholesterolemia and atherosclerosis. HNF4alpha (NR2A1) is a recently 'deorphanized' nuclear receptor which is bound in vivo by linoleic acid, although this natural ligand does not seem to promote transcriptional activation.

Non-homologous end-joining factors of Saccharomyces cerevisiae.

DNA double-strand breaks (DSB) are considered to be a severe form of DNA damage, because if left unrepaired, they can cause a cell death and, if misrepaired, they can lead to genomic instability and, ultimately, the development of cancer in multicellular organisms. The budding yeast Saccharomyces cerevisiae repairs DSB primarily by homologous recombination (HR), despite the presence of the KU70, KU80, DNA ligase IV and XRCC4 homologues, essential factors of the mammalian non-homologous end-joining (NHEJ) machinery. S.