Clemens, a scientist in the UAB Center for Metabolic Bone Disease stressedady lost. Disrupted PTEN in bone cells called osteoblasts in mice gastroesophageal reflux disease . The mice with Pten disruption, while normal size had dramatic and progressive increase in bone density throughout life compared with the control group. Longer in the mice without Pten, osteoblasts survived and set a new bone long after they died have died, Clement said. This increased osteoblast production run greater bone density. If we translate these findings to human diseases such as osteoporosis or bone fracture, we to not only prevent to not only prevent bone loss, but actually increase bone density in men as they age. .
Clemens stressed 20th St at a very early stage and it could take years to therapies for human conditions would be possible. ‘The key will be to find a way to selectively turn off Pten only in bone osteoblasts make and leave the other are are not affected,’said Clement. ‘Pten plays an important role in the body by the killing of cell lines proliferating out of control, such as in tumors. ‘.
Twenty participants aged from 18 to 50 with with a body mass index 29 to 39 to the for the study and the type of feed been randomly assigned to participants. Weight loss, the river mediated dilation of, blood pressure and of insulin and blood sugar have been measured the participants every other week for six-week trial.
Gutmann plans Saint the mouse model in an new collaborative network the child Tumor Foundation. His party and four between laboratories test a variety of connections against certain tumor types in subjects with Neurofibromatose influences affected. – ‘We want find out whether these new medicines work the same in all the aspects of the disease, ‘Gutmann say. ‘We are the things we learn to an efficient, strict pipeline on movement of promising new drugs from the the laboratory to clinical trials. ‘.