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#

A:

You need to install a non-free 32-bit library, libboost_iostreams32.
Pycharm itself is built with the exact same library.
Therefore, you might be able to fix your issue by installing it.
If not, you’ll need to find a 32-bit version of PyCharm, which is not freely available.
(But then, I don’t know what your license is…)
(Disclaimer: my company has been developing PyCharm for Windows since 2014, but I don’t work for them any more.)

To date, there are no proven treatments for Duchenne muscular dystrophy (DMD). However, new stem cell therapy has the potential to reverse the devastating effects of DMD and have a broad translational impact. First, a chronic and inactivated form of dystrophin can be delivered to muscle, and may restore the sarcolemmal membrane integrity and partially restore muscle physiology. Second, a replacement dystrophin may reverse the loss of muscle architecture and prevent or slow-down the progress of histologic and functional muscle degeneration. Third, dystrophin replacement may preserve muscle function and delay the onset of DMD-related complications. Last, dystrophin replacement may lessen the likelihood that DMD boys will develop secondary conditions that complicate the disease, such as cardiomyopathy. We have developed a dystrophin replacement strategy consisting of adeno-associated virus (AAV) expressing the full-length human dystrophin gene delivered to muscle by a lentiviral vector. Our preliminary data indicate that this approach mediates a restoration of the dystrophin network, stabilizes membrane integrity, and has a beneficial effect on muscle force. These data led to the hypothesis that chronic, localized muscle delivery of the dystrophin gene to dystrophin-deficient muscle by AAV results in enhanced functional outcomes in the mdx mouse model of DMD. We will determine whether this dystrophin replacement therapy: 1) reverses the loss of structural features and muscle strength in mdx mice, 2) preserves muscle histology and architecture of mdx mice, 3) preserves muscle force, 4) is stable in muscle over prolonged time, and 5) is maintained in situ by the host muscle cells. We will also assess the effectiveness of dystrophin restoration therapy in a more severe model of DMD. If these studies demonstrate the

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