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Propranolol and atenolol, current therapies for problematic infantile hemangioma (IH), are composed of R(+) and S(-) enantiomers: the R(+) enantiomer is largely devoid of beta blocker activity. We investigated the effect of R(+) enantiomers of propranolol and atenolol on the formation of IH-like blood vessels from hemangioma stem cells (HemSCs) in a murine xenograft model. Both R(+) enantiomers inhibited HemSC vessel formation in vivo. In vitro, similar to R(+) propranolol, both atenolol and its R(+) enantiomer inhibited HemSC to endothelial cell differentiation. As our previous work implicated the transcription factor sex-determining region Y (SRY) box transcription factor 18 (SOX18) in propranolol-mediated inhibition of HemSC to endothelial differentiation, we tested in parallel a known SOX18 small-molecule inhibitor (Sm4) and show that this compound inhibited HemSC vessel formation in vivo with efficacy similar to that seen with the R(+) enantiomers. We next examined how R(+) propranolol alters SOX18 transcriptional activity. Using a suite of biochemical, biophysical, and quantitative molecular imaging assays, we show that R(+) propranolol directly interfered with SOX18 target gene transactivation, disrupted SOX18-chromatin binding dynamics, and reduced SOX18 dimer formation. We propose that the R(+) enantiomers of widely used beta blockers could be repurposed to increase the efficiency of current IH treatment and lower adverse associated side effects., Introduction Infantile hemangioma (IH) is a common benign vascular tumor of infancy that occurs in 4%-5% of mature neonates, with a predominance in females and infants of European descent (1). [...]

This article focuses on the development of an efficient method for directly converting somatic cells into induced neural stem cells (iNSCs) without passing through a pluripotent state. It is reported that the researchers used an engineered version of the Sox17 transcription factor, called eSox17FNV, to reprogram embryonic and aged mouse fibroblasts into iNSCs. It is further reported that this approach bypasses pluripotency reprogramming and produces iNSCs more rapidly and efficiently.

The article looks at the Caribbean history of the Sooty Tern in New Mexico through mitochondrial and weather-based information. The bird was discovered dead in the Laguna Grande area closer to Carlsbad, California, where it was admitted to the Museum of Southwestern Biology to be studied through a DNA analysis. Results of the study showed that the sequence of the mitochondrial region of the bird is connected to a dataset of the Sooty Terns, proving that the dead tern has similarities to the Sooty Terns living in the Caribbean islands of Puerto Rico and Ascension Island.

The article presents research which confirmed the first record of the Long-billed Murrelet for New Mexico. The researchers performed DNA sequencing from the mitochondrial gene cytochrome-b but revealed an unrecognized variant of the bird species. The specimen that they found from a brine pool associated with a potash mine in Eddy County, New Mexico on July 12, 2009, offers the first documentation of the species which was anticipated by ornithologists since it established pattern of vagrancy across North America.

Infantile hemangioma (IH) is the most common tumor in children and a paradigm for pathological vasculogenesis, angiogenesis and regression. Propranolol is the mainstay of treatment for IH. It inhibits hemangioma vessel formation via a β-adrenergic receptor independent off-target effect of its R(+) enantiomer on the endothelial specific transcription factor sex-determining region Y (SRY) box transcription factor 18 (SOX18). Transcriptomic profiling of patient-derived hemangioma stem cells uncovered the mevalonate pathway (MVP) as a target of R(+) propranolol. Loss of SOX18 function confirmed R(+) propranolol mode of action on the MVP. Functional validation in preclinical IH models revealed that statins - targeting the MVP - are potent inhibitors of hemangioma vessel formation. We propose a novel SOX18-MVP-axis as a central regulator of IH pathogenesis and suggest statin repurposing to treat IH. Our findings reveal novel pleiotropic effects of beta-blockers and statins acting on the SOX18-MVP axis to disable an endothelial specific program in IH, which may impact other scenarios involving pathological vasculogenesis and angiogenesis.