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Archive - Oct 9, 2018


EXOSOME NEWS: Avalon GloboCare Teams with Weill Cornell Medicine to Co-Develop Standardization of cGMP-Grade Exosome Isolation and Application of Tissue-Specific Exosomes

On October 9, 2018, Avalon GloboCare Corp. (OTCQB: AVCO), a leading global developer of cell-based technologies and therapeutics, headquartered in New Jersey, USA, announced that Weill Cornell Medicine has selected its subsidiary Genexosome Technologies’ proprietary exosome isolation system as a key component in the world’s first standardization processing of cGMP-grade exosomes for clinical studies. This co-development program is led by Yen-Michael Hsu, MD, PhD, Director of cGMP Cellular Therapy Facility and Laboratory for Advanced Cellular Engineering at Weill Cornell. This co-development program will focus on two main objectives: (1) standardization of cGMP-grade exosome isolation from human endothelial cells, essential for vascular health and organ regeneration; and (2) identification and isolation of tissue-specific exosomes for liquid biopsy and clinical use. A material transfer agreement will accompany this announcement to facilitate and authorize the use of GenExosome’s isolation system by Weill Cornell. “Identification and isolation of tissue-specific exosomes is considered by many as the “Holy Grail” in this area. This co-development and standardization initiative with Weill Cornell has further enhanced the global recognition, intellectual property, as well as our leading role in this industry sector,” stated Yu Zhou, MD, PhD, Founder and Co-CEO of GenExosome Technologies, Inc. "This strategic co-development endeavor will synergize Genexosome Technologies’ top-rated isolation platform with Weill Cornell’s world-class cGMP cellular therapy/cell-derived product processing facility to accelerate innovative exosome technology development, as well as standardization in clinical-grade exosome bio-production process,” stated David Jin, MD, PhD, CEO and President of Avalon GloboCare Corp.

Two Genes Responsible for Remarkable Difference in Flower Color of Nearby Snapdragons Identified; Islands of Divergence Established by Gene Flow & Multiple Selective Sweeps; Bee Pollination a Key Factor

Snapdragons are charming tall plants that flower in a range of bright colors. In Spain, where snapdragons grow wild, these flower colors show a remarkable pattern: When driving up a road from Barcelona to the Pyrenees, snapdragons of the species Antirrhinum majus bloom in magenta at the beginning of the road, before a population of yellow flowering snapdragons takes over - separated by just a two kilometer c long stretch in which flower colors mix. Such hybrid zones of snapdragons are quite infrequent; only a few others are known. But why don't the snapdragons mix, with yellow and magenta flowers growing together over a wide area? Dr. Nick Barton at the Institute of Science and Technology Austria (IST Austria), together with Dr. David Field, previously a postdoc in Dr. Barton's group and now Assistant Professor at the University of Vienna, collaborated with molecular geneticists at the John Innes Center in Norwich, UK, to investigate the causes of this pattern. In an article published online on October 8, 2018 in PNAS, the scientists report that they identified the genes responsible for flower color difference from DNA sequence data. The open-access article is titled “Selection and Gene Flow Shape Genomic Islands That Control Floral Guides.” "DNA sequencing is becoming cheaper and cheaper. But analyzing sequence data and interpreting the patterns seen is very hard,” Dr. Barton explains. “In this study, we used sequence data from Antirrhinum plants to locate the individual genes that are responsible for the difference in flower color across the hybrid zone." The researchers compared the genome sequences of 50 snapdragons of each color, and measured how much the sequences diverged between magenta and yellow snapdragon populations.

Phenylketonuria Cured in Mouse Model by Adaptation of CRISPR/Cas9 Gene Editing—60% Gene Correction Rate Achieved Employing Base Editor Cytidine Deaminase

Parents of newborns may be familiar with the metabolic disorder phenylketonuria: in Switzerland, all newborn babies are screened for this genetic disease. If a baby is found to have phenylketonuria, he or she requires a special diet so that the amino acid phenylalanine does not accumulate in the body. Excess phenylalanine delays mental and motor development. If left untreated, the children may suffer massive mental disability. The cause of this metabolic disorder is a mutation in a gene that provides the blueprint for the enzyme phenylalanine hydroxylase (Pah). This enzyme, which is produced by the cells of the liver, metabolizes phenylalanine. The disorder is referred to as "autosomal recessive"--the child develops the disease if he or she inherits one mutated Pah gene from the mother and one from the father. There has been no cure for this disorder to date. A team of researchers led by ETH Zurich professor Gerald Schwank has now taken advantage of a method to correct both mutated genes in the liver cells and thus heal the disease. (Editor’s Note: ETH Zurich is a science, technology, engineering, and mathematics university in the city of Zürich, Switzerland.) Dr. Schwank’s team has succeeded, at least in mice. With the help of a CRISPR/Cas9 system extended by one enzyme, the researchers changed the sequence of the DNA building blocks for the Pah corresponding gene in adult mice. The mouse liver cells were subsequently able to produce functioning Pah enzymes, and the mice were healed. The work was reported online on October 8, 2018 in Nature Medicine. The article is titled “Treatment of a Metabolic Liver Disease by In Vivo Genome Base Editing in Adult Mice.” Following are more details on the work.