NATURAL LIGHT IN OFFICE BOOSTS HEALTH

Office workers with more light exposure at the office had longer sleep duration, better sleep quality, more physical activity and better quality of life compared to office workers with less light exposure in the workplace, reports a new study from Northwestern Medicine and the University of Illinois at Urbana-Champaign.

The study highlights the importance of exposure to natural light to employee health and the priority architectural designs of office environments should place on natural daylight exposure for workers, the study authors said.

Employees with windows in the workplace received 173 percent more white light exposure during work hours and slept an average of 46 minutes more per night than employees who did not have the natural light exposure in the workplace. There also was a trend for workers in offices with windows to have more physical activity than those without windows.

Workers without windows reported poorer scores than their counterparts on quality of life measures related to physical problems and vitality, as well as poorer outcomes on measures of overall sleep quality and sleep disturbances.

The study was reported in the Journal of Clinical Sleep Medicine in June.

"There is increasing evidence that exposure to light, during the day, particularly in the morning, is beneficial to your health via its effects on mood, alertness and metabolism," said senior study author Phyllis Zee, M.D., a Northwestern Medicine neurologist and sleep specialist. "Workers are a group at risk because they are typically indoors often without access to natural or even artificial bright light for the entire day. The study results confirm that light during the natural daylight hours has powerful effects on health."

Zee is the Benjamin and Virginia T. Boshes Professor of Neurology at Northwestern University Feinberg School of Medicine and director of the Sleep Disorders Center at Northwestern Memorial Hospital.

"Architects need to be aware of the importance of natural light not only in terms of their potential energy savings but also in terms of affecting occupants' health," said co-lead author Mohamed Boubekri, an associate professor of architecture at the University of Illinois at Urbana-Champaign.

A simple design solution to augment daylight penetration in office buildings would be to make sure the workstations are within 20 to 25 feet of the peripheral walls containing the windows, noted Boubekri. "Daylight from side windows almost vanishes after 20 to 25 feet from the windows," he said.

The study group included 49 day-shift office workers; 27 in windowless workplaces and 22 in workplaces with windows. Health-related quality of life and sleep quality were measured with a self-reported form and sleep quality was evaluated with the Pittsburgh Sleep Quality Index (PSQI). Light exposure, activity and sleep were measured by actigraphy in a representative subset of 21 participants; 10 in windowless workplaces and 11 in workplaces with windows.

Actigraphy is a single device worn on the wrist that gives measures of light exposure as well as activity and sleep. This is an ambulatory physiological data logger that records motion and light illuminance. The motion was used to determine activity levels during waking time and to calculate sleep time. The light luminance was used for measures of light exposure during the workday period.

"Light is the most important synchronizing agent for the brain and body," said Ivy Cheung, co-lead author and Ph.D. candidate in neuroscience in Zee's lab at Northwestern. "Proper synchronization of your internal biological rhythms with the earth's daily rotation has been shown to be essential for health."

Also, people who get more light during the day may sleep better at night, which can also help improve health, Zee noted.

ULTRAVIOLET LIGHT INDUCED MUTATIONS DRIVES MANY SKIN CANCERS

A genetic mutation caused by ultraviolet light is likely the driving force behind millions of human skin cancers, according to researchers at the Stanford University School of Medicine

The mutation occurs in a gene called KNSTRN, which is involved in helping cells divide their DNA equally during cell division.

Genes that cause cancer when mutated are known as oncogenes. Although KNSTRN hasn't been previously implicated as a cause of human cancers, the research suggests it may be one of the most commonly mutated oncogenes in the world.

"This previously unknown oncogene is activated by sunlight and drives the development of cutaneous squamous cell carcinomas," said Paul Khavari, MD, PhD, the Carl J. Herzog Professor in Dermatology in the School of Medicine and chair of the Department of Dermatology. "Our research shows that skin cancers arise differently from other cancers, and that a single mutation can cause genomic catastrophe."

Cutaneous squamous cell carcinoma is the second most common cancer in humans. More than 1 million new cases are diagnosed globally each year. The researchers found that a particular region of KNSTRN is mutated in about 20 percent of cutaneous squamous cell carcinomas and in about 5 percent of melanomas.

A paper describing the research will be published online Sept. 7 in Nature Genetics. Khavari, who is also a member of the Stanford Cancer Institute and chief of the dermatology service at the Veterans Affairs Palo Alto Health Care System, is the senior author of the paper. Postdoctoral scholar Carolyn Lee, MD, PhD, is the lead author.

Lee and Khavari made the discovery while investigating the genetic causes of cutaneous squamous cell carcinoma. They compared the DNA sequences of genes from the tumor cells with those of normal skin and looked for mutations that occurred only in the tumors. They found 336 candidate genes for further study, including some familiar culprits. The top two most commonly mutated genes were CDKN2A and TP53, which were already known to be associated with squamous cell carcinoma.

The third most commonly mutated gene, KNSTRN, was a surprise. It encodes a protein that helps to form the kinetochore -- a structure that serves as a kind of handle used to pull pairs of newly replicated chromosomes to either end of the cell during cell division. Sequestering the DNA at either end of the cell allows the cell to split along the middle to form two daughter cells, each with the proper complement of chromosomes.

If the chromosomes don't separate correctly, the daughter cells will have abnormal amounts of DNA. These cells with extra or missing chromosomes are known as aneuploid, and they are often severely dysfunctional. They tend to misread cellular cues and to behave erratically. Aneuploidy is a critical early step toward the development of many types of cancer.

The mutation in the KNSTRN gene was caused by the replacement of a single nucleotide, called a cytosine, with another, called a thymine, within a specific, short stretch of DNA. The swap is indicative of a cell's attempt to repair damage from high-energy ultraviolet rays, such as those found in sunlight.

"Mutations at this UV hotspot are not found in any of the other cancers we investigated," said Khavari. "They occur only in skin cancers."

The researchers found the UV-induced KNSTRN mutation in about 20 percent of actinic keratoses -- a premalignant skin condition that often progresses to squamous cell carcinoma -- but never in 122 samples of normal skin, indicating the mutation is likely to be an early event in the development of squamous cell carcinomas.

Furthermore, overexpression of mutant KNSTRN in laboratory-grown human skin cells disrupted their ability to segregate their DNA during cell division and enhanced the growth of cancer cells in a mouse model of squamous cell carcinoma.

Finally, Lee compared five patient-derived squamous cell carcinomas that had the KNSTRN mutation with five samples that did not have the mutation. Although both sets of cells were aneuploid, those with the mutation had the most severely abnormal genomes.

The identification of a new oncogene will allow researchers to better understand how these types of skin cancers develop. It may also give them clues about how to develop new therapies for the disease. In this case, it also neatly connects the dots between sun exposure and skin cancer.

"Essentially, one ultraviolet-mediated mutation in this region promotes aneuploidy and subsequent tumorigenesis," said Khavari. "It is critical to protect the skin from the sun."