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You could try manually updating the libraries. Try to open Windows Update, search for Google, and click through until it tells you that there are updates available. If you do not have any updates, click the “check now” button.
If that fails, download and install the latest update for Google Chromium. I know the Google website uses a separate browser, but the underlying libraries are not updated when installing the browser.
If you want to remove Chrome and install Chromium instead, delete the old version of Google Chrome, then download and install Chromium. You will still need to manually update the libraries, but this should work for you.

Duchenne muscular dystrophy (DMD) is a lethal, recessive disorder characterized by progressive muscle degeneration and early death from respiratory or cardiac failure, affecting about 2.5 million people worldwide. Despite decades of research, there has been no effective treatment for this illness. Gene therapy approaches developed in recent years have shown some promise in mouse models of the disease and, to a lesser extent, in the few patients with DMD treated with adeno-associated virus (AAV) vectors, although clinical trials have not begun yet. Despite the aforementioned progress, there are still many challenges facing this field, including a poor understanding of DMD pathology and a paucity of animal models that faithfully recapitulate disease pathophysiology and features. This application brings together a team of physicians and scientists with expertise in the fields of skeletal muscle biology and muscle disease, genetics, cell biology, gene therapy and preclinical drug development, who propose to develop and optimize an AAV vector platform with multiple applications in DMD and other forms of muscular dystrophy. Specifically, they will (Aim 1) engineer a novel AAV vector containing the human utrophin gene under control of a dual muscle-specific promoter, (Aim 2) test its efficacy in a mouse model of DMD, (Aim 3) test a lead compound from their previous phase II screen against DMD patient fibroblasts, (Aim 4) test the putative beneficial effects of transgene expression on muscle regeneration and fibrosis in myofibers following acute and chronic muscle injury in mice, and (Aim 5) conduct nonclinical toxicology studies required to obtain an Investigational New Drug (IND) for eventual testing in humans.*Enter code for MasterCard® or Visa™ at checkout. Discounts will be applied at checkout and cannot be used with other

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