The study has shown that a protein lost in people with Werner’s syndrome, a rare hereditary premature aging disease, is also decreased in smokers suffering from emphysema. The decrease causes damage to those lung cells that typically heal wounds. This is the first time that a connection has been made between the effects of smoking and the accelerated aging protein, pointing to potential therapeutic targets for smoking-related diseases.

The study, which was published in the Feb. 6 issue of the American Journal of Respiratory and Critical Care Medicine, focused on “what happens within the lungs because of the similar aging effects, including atherosclerotic diseases and cancer, seen in people with Werner’s syndrome and people who smoke,” explains Toru Nyunoya, M.D., assistant professor of internal medicine at the University of Iowa Carver College of Medicine and a pulmonologist with University of Iowa Hospitals and Clinics.

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An interesting paper from the owner of senescence.info and collegues: “Numerous microarray studies of aging have been conducted, yet given the noisy nature of gene expression changes with age, elucidating the transcriptional features of aging and how these relate to physiological, biochemical, and pathological changes remains a critical problem. … We performed a meta-analysis of age-related gene expression profiles using 27 datasets from mice, rats, and humans. Our results reveal several common signatures of aging, including 56 genes consistently overexpressed with age, the most significant of which was APOD, and 17 genes underexpressed with age. We characterized the biological processes associated with these signatures and found that age-related gene expression changes most notably involve an overexpression of inflammation and immune response genes and of genes associated with the lysosome. An underexpression of collagen genes and of genes associated with energy metabolism, particularly mitochondrial genes, as well as alterations in the expression of genes related to apoptosis, cell cycle, and cellular senescence biomarkers, were also observed. … We suggest these molecular signatures reflect a combination of degenerative processes but also transcriptional responses to the process of aging.” Supplementary data are available over at senescence.info.

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Stratatech Corp., a privately-held regenerative medicine company, announced that it has genetically modified its StrataGraft® living human skin substitute to actively fight costly bacterial infections that routinely develop at the site of burns and other severe skin injuries, such as skin ulcers. Bacterial infection is a primary cause of skin graft rejection and can significantly increase the hospital costs of burn and other skin injury patients. Stratatech’s skin-substitute innovation, detailed in an article published online this morning by the journal Molecular Therapy, enables the immediate topical delivery of a potent anti-infective that actively inhibits bacterial growth and promotes regrowth of the patient’s own cells.

Stratatech’s genetically-engineered skin substitute was generated using a non-viral vector, or carrier. The company believes it is the first time a virus-free approach has been used to genetically modify a living, cell-based tissue substitute. The data published in Molecular Therapy demonstrate that the modified tissue contained 139-fold more anti-infective proteins called host defense peptides than unmodified tissue in vitro.

Your mother’s wrinkles - or lack there of, may not be the best predictor of how you’ll age. In fact, a new study claims just the opposite. The study, involving identical twins, suggests that despite genetic make-up, certain environmental factors can add years to a person’s perceived age. Results just published on the web-based version of Plastic and Reconstructive Surgery®, the official medical journal of the American Society of Plastic Surgeons (ASPS), reveal that factors like divorce or the use of antidepressants are the real culprits that can wreak havoc on one’s face.

“A person’s heritage may initially dictate how they age - but if you introduce certain factors into your life, you will certainly age faster. Likewise, if you avoid those factors you can slow down the hands of time,” said ASPS Member Surgeon and study author Bahaman Guyuron, MD, professor and chairman, department of plastic surgery, University Hospitals Case Medical Center.

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Researchers have unraveled crucial details of how aging causes broken bones to heal slowly, or not at all, according to study results published in the Journal of Bone and Mineral Research. The research team also successfully conducted preclinical tests on a potential new class of treatments designed to “rescue” healing capability lost to aging.

In the worst cases, an age-related delay in healing keeps the two sides of a fractured bone from ever rejoining (non-union), leaving many confined to wheelchairs, unable to walk or to live independently.

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