Most of the people obsess about their daily work and they forget that they need a sound sleep. So many things will take place in your body while you are sleeping, such as the healing process. During sleep, a person’s immune system would work better because when we are awake our body needs to do several other processes, which require our energy.

The process of sleeping has several stages, each stage of this process is very important.

• During the first stage of sleeping cycle, it is quit light and very easy to wake up. The eye movements are slow and the duration of this stage is just few minutes. This can be considered as light sleep stage.
• After sometime the person will enter into second stage. This second stage lasts for a long duration as compared to the first stage. The heart beat would get slow down and brain starts diffusing faster waves. These processes do not occur in sequence. This stage is the true sleep stage.
• Next the stage 3 and stage 4 of sleep starts, which can be considered as deep sleep stage. In this brain releases smaller and faster waves known as delta waves are released. During this stage rhythmic breathing and limited muscular movement is observed.
• After ending of the 4th stage REM sleep stage will start. REM is the stage that contains very unique characteristics. Eye movement, heartbeat, and breathing will become faster. Brain waves become very active and the process of dreaming would begin. Once the dream starts; your muscles may get paralyzed. Suddenly if you wake up during REM stage you would probably remain in that paralyzed stage for a little while. Because at that movement your brain would try to respond for something, which is actually not there; so the rapid transition from dream to reality may creates the problem.

REM Sleep Disorder

REM sleep disorder may also occur at this stage. In some cases the person will have really intense dreams or nightmares and can move the legs and arms as if they were awake.

This may become a serious problem for your sleeping partner. Normally this disorder is caused due to the deterioration of the neurons. Smoking, stress, and alcohol may increase the chances of suffering from the nightmares and paralysis while you are sleeping in a dark and quite room can decrease the chances of experiencing those.

During entire sleep cycle, time spent on REM sleep is highest if the person is a small child or baby. REM sleep has been shown to have ways to learning and memory consolidation. Persons who are suffering from REM sleep disorder may also experience difficulties while learning new things.

The exact causes of REM sleep disorder are unknown, this disorder can occur in accordance with several degenerative neurological situations like multisystem atrophy, shy-dragger syndrome, Parkinson’s disease, and diffuse lewy body dementia. In 45% of people the cause is associated with sedative-hypnotic withdrawal or alcohol and in 55% of people the cause is unknown.

Earlier, getting over jet lag was done in alternative ways itself, but nowadays there are even some medications that can help you. These medications will help you in reducing the sleep debts caused due to jet lag.

Melatonin is a controversial method for getting over jet lag. You can find melatonin in health stores. It is naturally found in our blood, and it plays a vital role in maintaining the body’s internal sleep-wake cycle. The recommended amount of melatonin to be taken is 0.3 to 0.5 mg on the first day of traveling. As a reason of controversy, it is best to consult a physician before going for this.

Light therapy can also help you overcoming the jet lag symptoms. Usually, a person takes one day for one time zone to adjust the sleep-wake cycle. By using light therapy, you can reduce the number of days taken for adjusting.

Simple Thing You Need To Follow For Getting Over Jet Lag

There are certain things you need to do before, during and after travel for getting over jetlag. From about 3 to 4 days before your travel date, adjust your daily sleeping time in accordance to the destination time zone. Exercising, in particularly jogging and swimming is great way of adjusting your sleeping time.

When you are on board, try to drink plenty of water to avoid dehydration, which is the worse effect of jet lag. Avoid alcohol on board. While sleeping on board plan it such a way that, your sleep is in accordance of the destination time zone. Wear eye mask while sleeping.

And after traveling expose your body to daylight, this helps a lot in adjust our body’s internal sleep-wake clock. Take caffeinated drinks to avoid day time sleepiness. But, avoid these drinks hours before going to bed. If you are serious need of sleep during daytime, then try to take a nap, but not more than an hour.

Some people wrongly go for alcohol as a method for getting over jet lag. In fact, alcohol instead of helping out with jet lag, it disrupts the sleep and increases the severity of the problem.

Researchers from Sweden have uncovered an association between shift work and increased risk of multiple sclerosis (MS). Those who engage in off-hour employment before the age of 20 may be at risk for MS due to a disruption in their circadian rhythm and sleep pattern. Findings of this novel study appear today in Annals of Neurology, a journal published by Wiley-Blackwell on behalf of the American Neurological Association and Child Neurology Society.

Previous research has determined that shift work—working during the night or rotating working hours—increases the risk of cardiovascular disease, thyroid disorders, and cancer. Circadian disruption and sleep restriction are associated with working night shifts; these factors are believed to disturb melatonin secretion and increase inflammatory responses, promoting disease states. MS is a central nervous system autoimmune inflammatory disorder that has an important environmental component, thus investigating lifestyle risk factors, such as sleep loss related to shift work, is an important objective and the focus of the current study.

Dr. Anna Karin Hedström and colleagues from the Karolinska Institutet in Stockholm analyzed data from two population-based studies—one with 1343 incident cases of MS and 2900 controls and another with 5129 prevalent MS cases and 4509 controls. The team compared the occurrence of MS among study subjects exposed to shift work at various ages against those who had never been exposed. All study subjects resided in Sweden and were between the ages of 16 and 70. Shift work was defined as permanent or alternating working hours between 9 p.m. and 7 a.m.

“Our analysis revealed a significant association between working shift at a young age and occurrence of MS,” explains Dr. Hedström. “Given the association was observed in two independent studies strongly supports a true relationship between shift work and disease risk.” Results showed that those in the incident MS cohort who had worked off-hour shifts for three years or longer before age 20 had a 2 fold-risk of developing MS compared with those who never worked shifts. Similarly, subjects in the prevalent cohort who engaged in shift work as teens had slightly more than a 2-fold risk of MS than subjects who never worked shifts.

The authors suggest that disruption of circadian rhythm and sleep loss may play a role in the development of MS; however the exact mechanisms behind this increased risk remain unclear and further study is needed.

Source: Dawn Peters, Wiley-Blackwell, via EurekAlert

Now researchers, including a University of Washington biologist, have found hints that differing molecular processes in an area of the brain known as the suprachiasmatic nucleus might play a significant role in those jet lag differences.

Human circadian clocks operate on a period about 20 minutes longer than one day and so must be synchronized to the light-dark cycle of the solar day, delaying or advancing their time in response to light.

Someone whose clock runs faster than a solar day must delay it on a daily basis, and someone whose clock runs slower than a solar day must advance it. These daily adjustments happen naturally, and without our noticing, but the process is disrupted by sudden large shifts in the light-dark cycle because of a radically new geographic location.

Researchers previously learned that delaying the circadian clock happens through different pathways in the suprachiasmatic nucleus than advancing the clock does. The new research shows that, at a molecular level, the mechanisms responsible for resetting the expression of the “clock genes” are drastically different.

“We have known for decades that, in humans and other organisms, advances are always much harder to achieve than delays. For example, compare jet lag going to Europe with that coming back,” said Horacio de la Iglesia, a UW associate professor of biology.

“One of the reasons may be that these two forms of resetting the clock involve different molecular mechanisms at the clock level,” he said.

de la Iglesia and William Schwartz of the University of Massachusetts Medical School are corresponding authors of a paper detailing the research, published online recently (Oct. 3) in the Proceedings of the National Academy of Sciences. Co-authors are Mahboubeh Tavakoli-Nezhad, Christopher Lambert and David Weaver, also of the University of Massachusetts Medical School.

The researchers exposed hamsters to two light-dark cycles, one of 23.33 hours and the other at 24.67 hours, to test the mechanisms that advance and delay the circadian clock. A one-hour light pulse in the shorter cycle acted as dawn, but in the longer cycle it acted as dusk. The scientists confirmed that the pulse of light at dawn advanced the animals’ circadian clocks, while the light at dusk delayed the clocks.

The results suggest that different molecular mechanisms in the suprachiasmatic nucleus are at work when the circadian clocks are advanced than when the clocks are delayed, de la Iglesia said.

That could provide clues for understanding how circadian clocks work in nocturnal animals in natural conditions, and it could help in understanding potential remedies for jet lag.

Source: Vince Stricherz, University of Washington, via EurekAlert

“Cardiovascular disease is still the number one cause of death in developed countries, and we know major adverse cardiovascular events do not occur at random, but are more frequent in the morning,” said lead author Frank Scheer, PhD, Assistant Professor of Medicine at the Division of Sleep Medicine at BWH. “Understanding the underlying factors for this morning peak in adverse events has the potential to address this pattern and decrease the risk.”

In this study, the researchers demonstrated that the body clock regulates platelet function and causes a peak in platelet activation corresponding to the morning peak in adverse cardiovascular events such as myocardial infarction and stroke. A high level of platelet activation can lead to adverse cardiovascular events by influencing blood clotting. According to Scheer, this finding mimics the pattern of morning peaks in cardiovascular risk and tells us that platelet function is likely one of the factors that contributes to this morning peak in adverse cardiovascular events.

“Further study is required to test whether this circadian pattern in platelet activation, as demonstrated here in healthy subjects, is shifted in time or has different rhythm amplitude in people with cardiovascular disease,” Scheer said.

The study used a forced desynchrony protocol during which required healthy young subjects to live on a 20-hour day for 12 cycles in a dim-light, time-free, and controlled environment. The design of this protocol allowed the isolation of the effect of the internal circadian timing system on platelet function, independent of effects of the sleep/wake cycle and other behavioral or environmental changes. Platelet function was assessed by flow cytometry and whole blood platelet aggregability.

Advancing the understanding of the underlying mechanisms for this morning peak is expected to have important clinical relevance. “We believe it’s likely that there are many other factors that contribute to the peak in adverse cardiovascular events in the morning,” said Dr. Scheer. “The next steps in addressing this issue are to further investigate control mechanisms involved in the circadian rhythm in platelet function, the role of the circadian system in other cardiovascular risk factors, and the changes in circadian control of cardiovascular risk factors in vulnerable populations.”

Source: Holly Brown-Ayers, Brigham and Women’s Hospital, via EurekAlert

Circadian rhythms — the natural cycle that dictates our biological processes over a 24-hour day — does more than tell us when to sleep or wake. Disruptions in the cycle are also associated with depression, problems with weight control, jet lag and more. Now Prof. Yoav Gothilf of Tel Aviv University’s Department of Neurobiology at the George S. Wise Faculty of Life Sciences is looking to the common zebrafish to learn more about how the human circadian system functions.

Prof. Gothilf and his Ph.D. student Gad Vatine, in collaboration with Prof. Nicholas Foulkes of the Karlsruhe Institute for Technology in Germany and Dr. David Klein of the National Institute of Health in Maryland, has discovered that a mechanism that regulates the circadian system in zebrafish also has a hand in running its human counterpart.

The zebrafish discovery provides an excellent model for research that may help to develop new treatments for human ailments such as mental illness, metabolic diseases or sleep disorders. The research appears in the journals PLoS Biology and FEBS Letters.

A miniature model

Zebrafish may be small, but their circadian system is similar to those of human beings. And as test subjects, says Prof. Gothilf, zebrafish also have several distinct advantages: their embryos are transparent, allowing researchers to watch as they develop; their genetics can be easily manipulated; and their development is quick — eggs hatch in two days and the fish become sexually mature at three months old.

Previous research on zebrafish revealed that a gene called Period2, also present in humans, is associated with the fish’s circadian system and is activated by light. “When we knocked down the gene in our zebrafish models,” says Prof. Gothilf, “the circadian system was lost.” This identified the importance of the gene to the system, but the researchers had yet to discover how light triggered gene activity.

The team subsequently identified a region called LRM (Light Responsive Model) within Period2 that explains the phenomenon. Within this region, there are short genetic sequences called Ebox, which mediate clock activity, and Dbox, which confer light-driven expression — the interplay between the two sequences is responsible for light activation. Based on this information, they identified the proteins which bind the Ebox and Dbox and trigger the light-induction of the Period2 gene, a process that is important for synchronization of the circadian system.

To determine whether a similar mechanism may exist in humans, Prof. Gothilf and his fellow researchers isolated and tested the human LRM and inserted it into zebrafish cells. In these fish cells, the human LRM behaved in exactly the same way, activating Period2 when exposed to light — and unveiling a fascinating connection between humans and the two-inch-long fish.

Shedding new light on circadian systems and the brain

Zebrafish and humans could have much more in common, Prof. Gothilf says, leading to breakthroughs in human medicine. Unlike rats and mice but like human beings, zebrafish are diurnal — awake during the day and asleep at night — and they have circadian systems that are active as early as two days after fertilization. This provides an opportunity to manipulate the circadian clock, testing different therapies and medications to advance our understanding of the circadian system and how disruptions, whether caused by biology or lifestyle, can best be treated.

Prof. Gothilf believes this model has further application to brain and biomedical research. Researchers can already manipulate the genetic makeup of zebrafish, for example, to make specific neurons and their synapses (the junctions between neurons in the brain) fluorescent — easy to see and track. “Synapses can be actually counted. This kind of accessible model can be used in research into degenerative brain disorders,” he notes, adding that several additional research groups at TAU are now using zebrafish to advance their work.

Source: George Hunka, American Friends of Tel Aviv University, via EurekAlert

A new study of the brain’s master circadian clock — known as the suprachiasmatic nucleus, or SCN — reveals that a key pattern of rhythmic neural activity begins to decline by middle age. The study, whose senior author is UCLA Chancellor Gene Block, may have implications for the large number of older people who have difficulty sleeping and adjusting to time changes.

“Aging has a profound effect on circadian timing,” said Block, a professor of psychiatry and biobehavioral sciences and of physiological science. “It is very clear that animals’ circadian systems begin to deteriorate as they age, and humans have enormous problems with the quality of their sleep as they age, difficulty adjusting to time-zone changes and difficulty performing shift-work, as well as less alertness when awake. There is a real change in the sleep–wake cycle.

“The question is, what changes in the nervous system underlie all of that? This paper suggests a primary cause of at least some of these changes is a reduction in the amplitude of the rhythmic signals from the SCN.”

The SCN, located in the hypothalamus, is the central circadian clock in humans and other mammals and controls not only the timing of the sleep–wake cycle but also many other rhythmic and non-rhythmic processes in the body.

The UCLA research team examined the SCN in mice and found that while critical neural activity rhythms were already disrupted in middle age, the molecular mechanisms that generate these rhythms were not significantly altered.

“These results indicate that the outputs of the central circadian clock start to decline in middle age and suggest that the same may be true in humans,” said study co-author Christopher Colwell, a UCLA professor of psychiatry and biobehavioral sciences who has conducted research with Block for many years. “Before this study, we did not know that the SCN was the site where the decline occurs.”

In a technical tour de force, the research team successfully recorded electrical activity from the brain’s SCN — not in a Petri dish but in living animals. The research marks the first time this has been achieved in middle-aged animals and the first time scientists have watched the central biological clock of aging animals in action. The study was published July 13 in the Journal of Neuroscience, the journal of the Society for Neuroscience.

The scientists studied young mice, which were just a few months old, and middle-aged mice, which were more than a year old. SCN brain cells are electrically active during the day and electrically silent during the night in younger animals and younger people, the researchers said, but that difference is reduced with aging.

“The changes we observed in the electrical rhythm between the young and middle-aged animals, which are quite dramatic, occur even though we do not see significant changes in the underlying molecular rhythm,” Block said. “Our hypothesis is that the age-related changes in the circadian timing system are primarily occurring, at least initially, at the level of the electrical output signaling, perhaps mediated by changes in the cell-membrane properties of SCN clock cells. This is good news, because it points where in the cell to look for the age-related ‘lesion’ and thus helps inform what type of measures may be available to reduce these age-related deficits.”

Block and Colwell suspect the process is similar in humans.

The SCN keeps the system of multiple distributed circadian oscillators in synchrony, but disruptions in the SCN lead to disrupted sleep, as well as dysfunction in memory, the cardiovascular system, and the body’s immune response and metabolism.

The SCN, Block said, can be imagined as a heavy pendulum that controls many light pendulums (oscillators), with rubber bands between them.

“If the central clock weakens, it’s effectively like making those rubber bands thinner and weaker,” Block said. “When the SCN ages and those rubber bands become weaker, it becomes hard for the SCN to synchronize all of these other oscillators.”

In the young mice, the scientists found high levels of activity during the day and much lower activity levels during the night. In middle-aged mice, there was not nearly as large a difference in activity between the day and the night.

“In the middle-aged mice, they still have a circadian rhythm, but the amplitude is reduced,” Block said. “During the nighttime, when electrical impulse activity levels are usually fairly low, the levels have increased. Thus, the difference between the highest levels of activity during the daytime and the lowest levels of activity during the nighttime is much smaller in the middle-aged mice.”

Large numbers of people over the age of 65 regularly take sleeping pills, but the effects of taking such pills over many years is not known, said Colwell, who hopes the new research will lead to other options for getting a good night’s sleep.

Colwell, Block and their team plan to pursue follow-up research on treatment options that could enhance the function of the circadian system with aging. They are studying the specific membrane channel changes in the SCN that are responsible for the electrical rhythm and also are looking at the circadian regulation of the heart and the mechanisms underlying neural activity rhythms in the SCN.

Their research could potentially lead to new ways of boosting the circadian output. It is possible, Colwell and Block said, that relatively simple approaches could be beneficial, such as exercising early in the morning, getting regular exposure to bright light, eating meals at consistent times and, when traveling, eating meals at the appropriate local time, regardless of whether one is hungry then.

Possible interventions may involve discovering ways to improve the sleep cycle of aging people and their ability to better handle time-zone changes, perhaps by boosting the amplitude of the SCN. New pharmaceutical approaches may be developed, the scientists said. Future research may reveal which approaches are likely to be most effective.

Co-authors of the study included lead scientist Takahiro Nakamura, a former UCLA postdoctoral scholar in Colwell and Block’s laboratory, who is currently on the faculty of Japan’s Teikyo Heisei University; Takashi Kudo, a UCLA postdoctoral scholar; and Tamara Cutler, a UCLA undergraduate student who works in Colwell and Block’s lab.

The research was funded by the National Institutes of Health and by UCLA.

Implications for patients with neurological disorders such as Parkinson’s

In related research, Colwell and his colleagues have documented that changes similar to those that occur as we age also occur in mouse models of neurodegenerative disorders like Huntington’s disease and Parkinson’s disease.

“With many neurological disorders, patients have a hard time sleeping during the night and staying awake during the day,” said Colwell, who was a postdoctoral fellow in Block’s lab in the early 1990s at the University of Virginia. “One of the main clinical complaints of patients with Huntington’s disease and Parkinson’s disease is they cannot sleep and do not respond well to sleeping pills. We think the same dysfunction we see with normal aging occurs much earlier and more severely with these patients, and we hope that the treatment strategies we develop for aging can be applied to help patients with neurodegenerative diseases as well. If we learn what is going wrong, then we may be able to develop treatments.”

Colwell’s research on Huntington’s disease was published earlier this year in the journal Experimental Neurology, and his research on Parkinson’s has been accepted for publication in the same journal.

Undergraduate works in laboratory of Colwell and Block

Tamara Cutler, a UCLA senior majoring in neuroscience and physiological science, co-authored the new SCN research. So what is it like for an undergraduate to conduct research with distinguished scientists, including the university’s chancellor?

“Working in the laboratory of Professor Colwell and Chancellor Block has been rewarding, demanding and priceless,” Cutler said. “I joined the lab with the usual book knowledge of a life sciences student, a nearly boundless enthusiasm for research and a love for solving puzzles of every kind. Professor Colwell, Chancellor Block, the postdocs (Dawn Loh and Takshi Kudo) and the graduate students all invested time in my training and provided me with many fantastic opportunities to develop a strong set of skills.

“Since joining the lab, I have learned numerous techniques and been allowed to perform my own experiments from start to finish while working on my honors thesis. I have been treated as a valuable member of the lab and have been encouraged to make intellectual contributions to our research, which I am certain has greatly accelerated my growth as a scientist. Being granted a co-authorship on this manuscript as an undergraduate is very meaningful to me because it is not handed out lightly here.

“Dr. Colwell and Chancellor Block are really extraordinary scientists and renowned figures in the circadian research community, and it has been my great privilege to learn from them. I know my time here in the Colwell–Block lab has transformed me from someone who merely learns science into someone who can actually do science. I still have years of training ahead, but the journey thus far has been priceless.”

UCLA is California’s largest university, with an enrollment of more than 38,000 undergraduate and graduate students. The UCLA College of Letters and Science and the university’s 11 professional schools feature renowned faculty and offer 328 degree programs and majors. UCLA is a national and international leader in the breadth and quality of its academic, research, health care, cultural, continuing education and athletic programs. Six alumni and five faculty have been awarded the Nobel Prize.

Source: Stuart Wolpert, University of California – Los Angeles, via EurekAlert

Women who often work at night may face higher odds of developing type 2 diabetes, a new study suggests.

The study, which focused only on women, found that the effect got stronger as the number of years spent in shift work rose, and remained even after researchers accounted for obesity.

“Our results suggest that women have a modestly increased risk of type 2 diabetes mellitus after extended period of shift work, and this association appears to be largely mediated through BMI [weight],” concluded a team led by An Pan, a researcher in nutrition at the Harvard School of Public Health in Boston.

His team was slated to present its findings Sunday in San Diego at the annual meeting of the American Diabetes Association.

Prior studies have suggested that working nights disrupts circadian (day/night) rhythms, and such work has long been associated with obesity, the cluster of cardiovascular risk factors known as the “metabolic syndrome,” and dysregulation of blood sugar.

In the new study, researchers looked at data on more than 69,000 U.S. women tracked from 1988 to 2008 as part of the Nurses Health Study. Almost 6,200 women developed type 2 diabetes over the course of the study.

Beginning at their entry into the study, women were asked how long they had worked rotating night shifts (including at least three nights of work per month).

The researchers found that the risk of developing type 2 diabetes rose with increasing duration of shift work. After adjusting for obesity, women who’d worked night shifts regularly for three to nine years faced a 6 percent rise in risk, while women who had done so for 10 to 19 years saw their risk rise by 9 percent, and those who had worked such shifts for 20 years or more faced a 20 percent increase in risk.

Weight gain accounted for some, but not all, of the night shift-linked rise in diabetes risk, the team noted.

Experts note that research presented at meetings is typically considered preliminary until published in a peer-reviewed journal.

Source: HealthDay News

I wasn’t controlling the device; the device was controlling me. Something similar seems to be happening with today’s tablet computers. The portability of Apple’s iPad and Research in Motion’s PlayBook encourages us to take the tablet with us to bed. Many of us have replaced a good book with the iPad as the last media our eyes meet before dark. A U.S. poll released in March by the National Sleep Foundation estimated that 61% of people used some form of computer a few nights a week in the hour before bed. In fact, nearly half of adults in their twenties surfed the Internet every night, or almost every night, within the hour they went to sleep.

All that computer use may be harming our ability to perform the mental switch-off sleep requires – which could make us less productive and more irritable during the day.

Dr. Michael Gradisar is a psychology professor at Australia’s Flinders University and an expert on the sleep effects of interactive media. His research indicates that passive media – classically, books – are good for lulling us to sleep. But Gradisar says more interactive media, such as video games, cellphones or Web-browsing devices, “are more alerting and disrupt the sleep-onset process.”

One of the most comprehensive studies I was able to find about this was a Belgian study published in 2006 in the Journal of Paediatrics and Child Health. Based on a survey of 2,546 children in Grades 7 and 10, the study investigated media use as a sleep aid and how it related to fatigue. Respondents who said they used as sleep aids such activities as television-watching, computer-gaming and music-listening each reported decreased number of hours of sleep per week and increased self-reported levels of tiredness.

Disturbed sleep patterns may lead to daytime sleepiness, poor school results and behaviour problems for children. Other studies have shown children’s poor sleep patterns can carry over into adulthood. Interestingly, reading books in bed did not negatively affect sleep. “Although the respondents report using television, computer games and music as a sleeping aid,” the researchers noted, “the results suggest that there is no reason to assume that these media are really helping them sleep.”

Several theories attempt to explain how bedroom media use affects sleep patterns. The “displacement” hypothesis suggests that time spent consuming media displaces time spent conducting other activities, such as sleeping. Another theory suggests interactive media creates a state of hyper-arousal and cognitive stimulation just as we’re supposed to be winding down. Dealing with work-related email before bed, or in bed, also can lead to sleep-delaying cognitive stimulation. Finally, lying in bed with a multimedia device can cause such ergonomic challenges as neck and arm strain if the activity is not conducted in a comfortable position.

“Ah,” says the diehard iPad user. “At night, I only use the iPad to read e-books. That’s OK, right?” Maybe not. Darkness is an important component in the circadian rhythm that sees us transition from sleep to wakefulness and back again. That’s because darkness triggers the pineal gland’s production of melatonin, a hormone that suppresses body temperature and heart rate and in general promotes sleep. A growing body of research indicates the sort of light projected from backlit computer screens could be enough to suppress melatonin production, in turn disrupting our natural circadian rhythms.

The effect may be strengthened when the computer display is held as close to the face as iPads and PlayBooks tend to be. For example, a Swiss-German study published in March in the Journal of Applied Physiology established that exposure to light from a backlit LED computer screen prolonged wakefulness even over non-LED screens. (The test was conducted with a Hewlett-Packard screen. Apple’s iPad also has an LED screen.) Interestingly, dedicated e-book readers such as the Kobo or the Kindle, which are not backlit and do not function as light sources, probably wouldn’t create this effect.

I’m not criticizing the use of tablet computers. I think mine is great. Studies have shown the media they store can promote health – from humorous TV shows and clips that help people deal with stress and depression to video games helping children deal with the pain of severe burns. They’ve also been shown to assist in stroke rehabilitation.

But we’re fooling ourselves if we think tablet computers work as sleep aids. The general rule? If you’re serious about your night’s sleep, leave technology outside the bedroom. No TV, no video games, certainly no tablet computer. Instead, protect the bedroom as a sanctuary. Treat it as your space to restore, relax and recharge the old-fashioned way, with soothing bedtime activities, such as a great book, which can ease the body’s transition into a long night of calm and rejuvenating sleep.

Source: Dr. James Aw, National Post

Northwestern University scientists have discovered a new mechanism in the core gears of the circadian clock. They found the loss of a certain gene, dubbed “twenty-four,” messes up the rhythm of the common fruit fly’s sleep-wake cycle, making it harder for the flies to awaken.

The circadian clock drives, among other things, when an organism wakes up and when it sleeps. While the Northwestern study was done using the fly Drosophila melanogaster, the findings have implications for humans.

The research will be published Feb. 17 in the journal Nature.

“The function of a clock is to tell your system to be prepared, that the sun is rising, and it’s time to get up,” said Ravi Allada, M.D., who led the research at Northwestern. “The flies without the twenty-four gene did not become much more active before dawn. The equivalent in humans would be someone who has trouble getting out of bed in the morning.”

Allada is professor of neurobiology and physiology in the Weinberg College of Arts and Sciences and associate director for the Center for Sleep and Circadian Biology.

Period (per) is a gene in fruit flies that encodes a protein, called PER, which regulates circadian rhythm. Allada and his colleagues found that twenty-four is critically important to producing this key clock protein. When twenty-four is not present very little PER protein is found in the neurons of the brain, and the fly’s sleep-wake rhythm is disturbed.

It seems it was fate that the gene Allada and his team pinpointed would be important in regulating the 24-hour sleep-wake cycle. The gene’s generic name is CG4857, and the numbers add up to 24, earning it the twenty-four nickname. (The fruit fly’s genome was sequenced in 2000, but until now the function of this gene was unknown.)

The known core mechanisms of the circadian clock, both in flies and humans, involve the process of transcription, where RNA is produced from DNA. A portion of the control system called a transcriptional feedback loop also is important. (The word circadian comes from the Latin phrase “circa diem,” meaning “about a day.”)

In trying to identify new clock components, the researchers identified a new player in the system, the gene twenty-four. Instead of operating in the process of transcription, they found twenty-four operates in the process of translation: translating proteins from RNA.

Twenty-four appears to be a protein that promotes translation of period RNA to protein. “This really defines a new mechanism by which circadian clocks are functioning,” Allada said. “We found that twenty-four has a really strong and critical role in translating a key clock protein. Translation really wasn’t appreciated before as having such an important role in the process.”

The researchers believe it is likely that a mechanism similar to that described for the fly gene twenty-four will be evolutionarily conserved and found in humans.

Allada and his Northwestern team worked with scientists at the Korea Advanced Institute of Science and Technology (KAIST). Using a Drosophila library at KAIST, the researchers first screened the behavior of 4,000 different flies looking for flies whose sleep-wake cycles were awry. (Each fly had a different overexpressed gene and thus different behavior.) The fly with the most dramatic change was one with a longer cycle than normal, 26 hours instead of 24.

The overexpressed gene in this fly was CG4857. The researchers next removed, or knocked out, this gene in the flies. These flies had very poor sleep-wake rhythm and would sleep and wake at all times of day. The researchers found very little of the critical PER protein in the brain neurons despite the fact that per RNA is likely produced in the neurons. Without twenty-four the RNA was not translated into the PER protein, leading to dysfunction.

Source: Megan Fellman, Northwestern University via EurekAlert