Image by BlatantNews.com via FlickrInhibition of certain hormone receptors in the brain has been shown to affect cholesterol metabolism and may be a way of protecting against cardiovascular diseases.
Sunday, November 21, 2010
Image by Patrick Hoesly via FlickrResearchers for the first time have induced vigorous regeneration of nerve connections that control voluntary movement after spinal cord injury, revealing the possibility for new therapeutic treatments for paralysis and other motor function impairments.
In a study on lab rodents, University of California (UC) Irvine (UCI; USA), UC San Diego (UCSD; USA), and Harvard University (Cambridge, MA, USA) investigators achieved this breakthrough by turning back the developmental clock in a molecular pathway vital for the growth of corticospinal tract nerve connections. They did this by deleting an enzyme called a phosphatase and tensin homolog (PTEN), which controls a molecular pathway called mTOR that is a key regulator of cell growth. PTEN activity is low early during development, allowing cell proliferation. PTEN then turns on when growth is completed, suppressing mTOR and preventing any ability to regenerate.
Trying to find a way to restore early-developmental-stage cell growth in injured tissue, Dr. Zhigang He, a senior neurology researcher at Children’s Hospital Boston (MA, USA) and Harvard Medical School, first demonstrated in a 2008 study that blocking PTEN in mice enabled the regeneration of connections from the eye to the brain after optic nerve damage. He then collaborated with Drs. Oswald Steward of UCI and Binhai Zheng of UCSD to see if the same approach could promote nerve regeneration in injured spinal cord sites.
An experimental cancer drug is proving effective in treating the of some patients whose tumors carry a certain genetic mutation, new studies show.
Because the mutation can be present in other forms of cancer -- including a rare form of sarcoma (cancer of the soft tissue), childhood neuroblastoma (brain tumor), as well as some lymphomas, breast and colon cancers -- researchers say they are hopeful the drug, crizotinib, will prove effective in treating those cancers as well.
In one study, researchers identified 82 patients from among 1,500 patients with , the most common type of lung malignancy, whose tumors had a mutation in the anaplastic lymphoma kinase (ALK) gene.
Crizotinib targets the ALK "driver kinase," or protein, blocking its activity and preventing the tumor from growing.
Image via WikipediaStem cell researchers have found a way to turn a person's skin into blood, a process that could be used to treat cancer and other ailments, according to a Canadian study published Sunday.
The method uses cells from a patch of a person's skin and transforms it into blood that is a genetic match, without using human , said the study in the journal Nature.
By avoiding the controversial and more complicated processes involved with using human embryonic stem cells to create blood, this approach simplifies the process, researchers said.
"What we believe we can do in the future is generate blood in a much more efficient manner," said study author Mick Bhatia of the McMaster's Stem Cell and Cancer Research Institute in the Michael G. DeGroote School of Medicine.
With the ability to create blood for transfusion from a person's own skin, the advance means someday patients needing blood for surgery or to treat anemia could bypass the blood bank and derive the necessary supply from themselves.
The breakthrough could also see future uses such as allowing patients undergoing chemotherapy to endure a longer regime of treatment without the breaks currently needed to rejuvenate the body.
By substituting a healthy gene for a defective one, scientists were able to partially restore the heart's ability to pump in 39 heart failure patients, researchers report
This is the first time gene therapy has been tested and shown to improve outcomes for patients with advanced heart failure,The therapy works by replenishing levels of an enzyme necessary for the heart to pump more efficiently by introducing the gene for SERCA2a, which is depressed in these patients. If these results are confirmed in future trials, this approach could be an alternative to heart transplant for patients without any other options,The gene for SERCA2a raises levels of the enzyme back to where the heart can pump more efficiently. The enzyme regulates calcium cycling, which, in turn, is involved in how well the heart contracts, the researchers said.
"Heart failure is a defect in contractility related to calcium cycling," explained Dr. Robert Eckel, past president of the and professor of medicine at the University of Colorado Denver.
The study authors hope that, if replicated in larger trials, the gene-therapy treatment could actually delay or obviate the need for heart transplants in .
- Gene Therapy: Mending a Failing Heart? (nlm.nih.gov)