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Archive - Oct 14, 2015

Clarifying the Mechanism That Accelerates Aging in Smokers: Smoking Habits Found to Change Blood Serum Concentration of Aging-Related Molecules; α-Klotho, FGF-21, & IL-6 Upregulated in Male Smokers

The average life span of smokers is more than 10 years shorter than that of non-smokers, and it is said that smoking is a factor that accelerates aging. However, the details of the mechanism that accelerates aging due to smoking was not yet clear. Now, a research group led by Dr. Kaori Nakanishi, Assistant Professor, and Dr. Keiko Takihara, Professor, at the Health Care Center, Osaka University, have found that smoking habits affected levels of the aging-related molecule α-klotho (αKl) in blood serum. In addition, this group also elucidated that smoking causes a rise in the blood serum concentration of fibroblast growth factor-21 (FGF-21), a factor related to metabolism that has gained considerable attention in recent years. It is believed that these research results could serve as a key to clarifying the mechanism that accelerates aging in smokers, and provide new knowledge about aging-related diseases caused by smoking and about prevention of smoking-related accelerated aging. The new research results were published online on September 24, 2015 in an open-access article in Nature’s journal Scientific Reports. The article is titled “Klotho-Related Molecules Upregulated by Smoking Habit in Apparently Healthy Men: A Cross-Sectional Study.” The Osaka University group focused on the relationship between smoking and aging, examining the involvement of α-klotho in the advancement of aging due to smoking. It was found that the levels of FGF-21, α-klotho, and interleukin-6 (IL-6), a cytokine related to inflammation, were all significantly higher in smokers than in never-smokers. In addition, the blood serum concentration of α-klotho rose in stressful conditions such as lack of sleep and being under emotional stress outside of smoking.

Scientists Convert Skin Cells into Placenta-Generating Cells in Mice

Regenerative medicine is a new and expanding area that aims to replace lost or damaged cells, tissues, or organs in the human body through cellular transplantation. Embryonic stem cells (ESCs) are pluripotent cells that are capable of long-term growth, self-renewal, and can give rise to every cell, tissue, and organ in the fetus's body. Thus, ESCs hold great promise for cell therapy as a source of diverse differentiated cell-types. Two major bottlenecks to realizing such potential are allogenic immune rejection of ESC-derived cells by recipients and ethical issues. Two Japanese scientists, Nobel laureate Shinya Yamanaka (Gladstone Institutes, San Francicso, and Dr. Kazutoshi Takahashi (now also at Gladstone Institutes, San Francisco), showed, in 2006, that introduction of four genes in skin cells can reprogram fibroblasts into functional embryonic stem-like cells (also termed “induced pluripotent stem cells” (“iPSCs”). The notion that as few as four genes are sufficient to completely change the cell, opened a new avenue which scientists have traveled down in atttempts to convert different adult cells into other somatic cell types. Several subsets of cell types such as blood cells, nerve cells, heart cells, and liver cells have been converted from different adult cells by employing this direct conversion approach. This discovery enabled an attractive approach that resolves both the ethical issue and the immune rejection problem of ESCs and the need for donor cells. Now, researchers from the Hebrew University of Jerusalem, led by Dr.

Gene Therapy with RPGR Gene Preserves Vision in Canine RPGR X-Linked Retinitis Pigmentosa, Even at Later Stages of Blinding Disease After Significant Loss of Photoreceptor Cells

Gene therapy preserved vision in a study involving dogs with naturally occurring, late-stage retinitis pigmentosa, according to research funded by the National Eye Institute (NEI), part of the National Institutes of Health. The findings contribute to the groundwork needed to move gene therapy forward into clinical trials for people with this blinding eye disorder, for which there is currently no cure. Scientists from the University of Pennsylvania and the University of Florida, Gainesville, also determined, for the first time, that gene therapy may be of potential benefit even after there has been significant loss of cells in the eye. Up to this point, animal studies had shown benefits from gene therapy only when it was used in the earliest stages of the disease. "The study shows that a corrective gene can stop the loss of photoreceptors in the retina, and provides good proof of concept for gene therapy at the intermediate stage of the disease, thus widening the therapeutic window," said Neeraj Agarwal, Ph.D., a program director at the NEI. Retinitis pigmentosa is one of the most common inherited diseases that causes degeneration of the retina, the light-sensitive tissue lining the back of the eye. Roughly 1 in 4,000 people are affected and about 10 to 20 percent have a particularly severe form called X-linked retinitis pigmentosa, which predominately affects males, causing night blindness by age 10 and progressive loss of the visual field by age 45. Approximately 70 percent of people with the X-linked form carry mutations that cause loss of function of the retinitis pigmentosa GTPase regulator (RPGR) gene, which encodes a protein important for maintaining the health of photoreceptors. These are cells in the retina that absorb and convert light into electrical signals, which are then sent to the brain.