Diabetes startup brews up $11M after ‘serendipitous spill’ led to creation of new CGM tech was reported by Andrea Park for FierceBioTech.com, 12 August 2021. Israeli startup Hagar, with its GWave technology that measures blood sugar levels using noninvasive radio waves rather than an implanted sensor or repeated fingersticks.
According to Hagar lore, the technology came about after Geri Waintraub, the company’s co-founder and chief technology officer, accidentally spilled a cup of tea on a radio frequency device during a separate research project and concluded that the ensuing reaction was caused by the sugar in his tea. Thus, GWave was born.
The first generation of the GWave sensor is a device about a third the size of a standard smartphone, inserted into a ceramic bracelet. It uses Bluetooth to transmit its glucose readings to an accompanying mobile app that tracks readings and alerts users to fluctuations in their blood sugar levels. While radio waves are a form of electromagnetic radiation, GWave produces “significantly less” amounts than a smartphone, according to Hagar.
A proof-of-concept study found the company’s radio frequency technology was able to continuously measure glucose levels with at least 90% accuracy, compared to the estimated 70% rate for traditional continuous glucose monitors. According to the company, that difference stems from the fact that Hagar’s system directly measures glucose in the blood in real time. Other CGMs may use a sensor implanted under the skin to take measurements from the interstitial fluid between cells and may often have to be calibrated throughout the day with routine fingerstick blood tests.
Backed by those promising results, and with Hagar now planning to launch clinical trials to pursue FDA approval of the GWave system, the company has raised $11.7 million in series B funding.
Pancreatic beta-cell boost in mice paves way for future diabetes treatments was reported by the Center for Genomic Regulation for MedicalXpress.com, 12 August 2021.
A research team has uncovered the role of a gene that is critical to boosting the number of insulin-producing cells during the early development of the pancreas. The findings could bolster diabetes research efforts and eventually lead to new replacement therapies for the disease. The findings are published in the journal Genes and Development.
Researchers at the Centre for Genomic Regulation (CRG), the Bellvitge Biomedical Research Institute (IDIBELL) and the University of Barcelona studied the RE1 Silencing Transcription Factor gene, also known as REST, in mouse and zebrafish models, as well as in human pancreatic organoids. Researchers have previously suspected a role for this gene in pancreas development, though studies so far have been inconclusive.
They found that REST is expressed in embryonic pancreatic cells which are yet to differentiate, also known as progenitor cells, as well as in adult cells which form the pancreatic duct. The researchers did not detect REST activity in adult beta-cells that produce insulin.
Inactivating REST was not able to boost beta cell formation after the pancreas has already formed. “Though important for the development of the pancreas, we have shown that REST is not the sole guardian of endocrine differentiation. However, if one day we come up with a future cocktail of drugs to boost insulin-producing cells in the pancreas, I suspect that REST inhibitors would be part of the recipe. We are now testing whether REST inhibitors can be used to artificially boost the formation of beta cells in a dish,” says Jorge Ferrer, senior author of the study and Group Leader of the Regulatory Genomics and Diabetes at the CRG.
Researchers unlock genetic ‘treasure map’ for chronic kidney disease was published by the Perelman School of Medicine at the University of Pennsylvania for MedicalXpress.com, 13 August 2021.
Despite impacting an estimated 850 million people and being responsible for 1 in 60 deaths worldwide, few treatments are available for chronic kidney disease. Understanding the genetic variations associated with the disease represents an important step for drug development. Now, in one of the most comprehensive genome-wide association studies of its kind, researchers in the Perelman School of Medicine at the University of Pennsylvania have identified 182 genes likely responsible for kidney function — many of which can be targeted with existing drugs and 88 genes for hypertension. Additionally, the research team has mapped the key cell types and mechanisms that are linked to disease. The findings were published Thursday in Nature Genetics.
The study provides one of the clearest pictures to date of the genetic underpinnings of chronic kidney disease. And it paves the way for the identification of potential treatments, which are critically needed, according to principal investigator Katalin Susztak, MD, Ph.D., a professor in the division of Renal-Electrolyte and Hypertension at Penn, who led the research with lead author Xin Sheng, Ph.D., a postdoctoral fellow at Penn.
“This is a key roadmap for understanding the mechanisms of chronic kidney disease,” Susztak said. “Fortunately, some of the genes we’ve identified for kidney disease can be targeted with existing drugs.”