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Archive - Oct 24, 2019

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New Alpha-Gel; An Environment-Friendly and Easily Producible Surfactant Used to Prepare Effective Water-Retaining Mixture That Can Be Used in Skincare

A layer of lipids covers our skin, and with its help our skin retains moisture and remains healthy. In the lipid layer, a compound called ceramide forms a "lamellar gel" with cholesterol, fatty acids, and water. Lamellar gels are mixtures that are thick, do not flow easily, and can hold large amounts of water. Natural ceramide is therefore an important factor for water retention in our skin. A type of lamellar gel, called the "α-gel," can be formulated by mixing compounds called surfactants with a fatty alcohol and water. As you may have guessed by this explanation, α-gels are widely used in skincare products such as skin creams. In a new study published in Colloids and Surfaces A (https://www.sciencedirect.com/journal/colloids-and-surfaces), scientists from Tokyo University of Science and Miyoshi Oil and Fat Co. Ltd., Japan, led by Dr Kenichi Sakai, synthesized an α-gel using an oleic acid-based surfactant, which can potentially be used in skincare products. This is a surfactant they had previously developed and is structurally similar to natural ceramide (both are amphiphiles with two tails). "I was interested in whether α-gels could be prepared using gemini surfactants (two-tailed and two-headed surfactants), and in what their structural and physical properties would be," Dr Sakai says. Once the α-gel was ready, Dr Sakai and his team used a technique called small- and wide-angle X-ray scattering (SWAXS), another technique called nuclear magnetic resonance (NMR) spectroscopy, and an optical microscope to confirm its characteristics. For this, they prepared several mixtures containing different molar ratios of the oleic acid-based surfactant, water, and 1-tetradecanol (a fatty alcohol). The findings were, indeed, satisfactory.

Breakthrough in Genetic Skin Disease; Epigenetic Modifers DNMT3A and BCOR Are Recurrently Mutated in CYLD Cutaneous Syndrome (CCS)

A breakthrough has been made in understanding a rare genetic skin disease that causes progressively enlarging skin tumors over the scalp, face, and body. For the first time, scientists at Newcastle University, UK, have identified changes in the DNA of the tumor cells in those with CYLD (CYLD lysine 63 deubiquitinase) (image) cutaneous syndrome (CCS) that may help them grow. A study published online on October 17, 2019 in Nature Communications suggest that the tumor cells gain a “survival advantage” when the changes occur - an important step in understanding ways to develop treatments. The open-access article is titled “Epigenetic Modifiers DNMT3A and BCOR Are Recurrently Mutated in CYLD Cutaneous Syndrome.” CCS is a hereditary condition that affects areas of the body where there are hair follicles and leads to skin tumors called "cylindromas" forming and continually growing. The alterations discovered by the experts were in two genes (DNMT3A and BCOR) that are found in the skin tumors. One of the changes highlights a mechanism that the skin tumor cells use to survive and it is hoped that these could be targeted with a new class of drug to inhibit their growth. The change to the second gene is novel for skin tumors and warrants further investigation to establish the significance it has on the growth of the tumors. Dr. Neil Rajan, Senior Lecturer and Honorary Consultant Dermatologist at Newcastle University's Faculty of Medical Sciences, led the research, which was done in collaboration with Dr Serena Nik-Zainal's team at the University of Cambridge.Dr. Rajan said: "This research is an important step in the ongoing work to develop treatments for patients with CCS, which is a central goal of my research group.

Scientists Reveal Novel Oncogenic Driver Gene (DEPDC5) on Chromosome 22q in Human Gastrointestinal Stromal Tumors (GISTs); Intriguing Connection with Focal Epilepsy; DEPCD5 Agonists May Serve As Anti-Cancer Drugs

Sarcomas - cancers that arise from transformed mesenchymal cells (a type of connective tissue) - are quite deadly. Gastrointestinal stromal tumors (GISTs) are the most common human sarcoma and are initiated by activating mutations in the KIT receptor tyrosine kinase. Micro-GISTs are a smaller variation of clinical GISTs and are found in one-third of the general population without clinical symptoms. Although the micro-GISTs and clinical GISTs share the same KIT mutations, micro-GISTs have limited growth potential and do not exceed a centimeter. This size limitation suggests that additional genetic alterations contribute to the progression of clinical GISTs. Chromosome 22q deletions are frequent chromosomal abnormalities in human GISTs, occurring in ~50% of GISTs, and are thought to contribute to the pathogenesis of this disease. However, the crucial gene in 22q was unknown for decades. In a study published online on October 21, 2019 in PNAS, a team led by Professor Yuexiang Wang of the Shanghai Institute of Nutrition and Health (SINH) of the Chinese Academy of Sciences, together with Professor Jonathan Fletcher from Brigham and Women's Hospital and Harvard Medical School, described a novel druggable driver gene in GISTs. The PNAS article is titled “Mutational Inactivation of mTORC1 Repressor Gene DEPDC5 in Human Gastrointestinal Stromal Tumors.” The researchers performed whole exome sequencing and reported recurrent genomic inactivated DEPDC5 gene mutations in GISTs. DEPDC5 was shown to be a chromosome 22q-targeting tumor suppressor, silenced by mutations in GIST specifically. The scientists further provided evidence that inactivation of DEPDC5 promotes GIST cell proliferation by activating the mTORC1 signaling pathway and subsequently inhibiting cell cycle arrest.