The enzyme that manufactures melatonin - hormone which regulates the body's internal clock - originated 500 million years ago, according to a new study which may hold clues to treating jet lag and 'winter blues'.

The research by an international team of scientists led by National Institutes of Health (NIH) indicates that this crucial enzyme likely began its role in timekeeping when vertebrates diverged from their non-vertebrate ancestors.

An understanding of the enzyme's function before and after the divergence may contribute to an understanding of such melatonin-related conditions as seasonal affective disorder, jet lag, and disorders involving vision.

The findings provide strong support for the theory that the time-keeping enzyme originated to remove toxic compounds from the eye and then gradually morphed into the master switch for controlling the body's 24-hour cyclic changes in function.

The researchers isolated a second, non-vertebrate form of the enzyme from sharks and other contemporary animals thought to resemble the prototypical early vertebrates that lived 500 million years ago.

The study was conducted by senior author David C Klein and colleagues at NIH, and at institutions in France, Norway, and Japan.

Melatonin is a key hormone that regulates the body's day and night cycle.

Klein explained that it is manufactured in the brain's pineal gland and is found in small amounts in the retina of the

Melatonin is produced from the hormone serotonin, the end result of a multi-step sequence of chemical reactions. The next-to-last step in the assembly process consists of attaching a small molecule the acetyl group to the nearly finished melatonin molecule.

This step is performed by an enzyme called arylalkylamine N-acetyltransferase, or AANAT.

Because melatonin accumulated at night, the ancestors of today's vertebrates became dependent on melatonin as a signal of darkness, researchers said.

As the need for greater quantities of melatonin grew, the pineal gland developed as a structure separate from the eyes, to keep serotonin and other toxic substances needed to make melatonin away from sensitive eye tissue.

The first evidence of how the vertebrate form of the enzyme originated came when study co-author Steven L Coon, discovered genes for the non-vertebrate and vertebrate forms of AANAT in genomic sequences from the elephant shark, considered to be a living representative of early vertebrates.

This finding indicated that the vertebrate form of AANAT may have resulted after a phenomenon known as gene duplication which is thought to be a major factor influencing evolutionary change, Klein said.

The study was published in the journal PNAS.

There is good news for those seeking a cure to the Kawasaki Disease (KD) - a rare childhood affliction that involves inflammation of the blood vessels.

A team of scientists at Sanford Children's Health Research Centre in South Dakota, US, has discovered a molecule called 'THRIL' that helps regulate the immune response in children suffering from KD.

"THRIL could be a novel biomarker for immune activation and a potential target for inflammatory diseases like KD, rheumatoid arthritis and inflammatory bowel disease," said Tariq Rana, senior author and professor at Sanford Children's Health Research Centre.

According to the study, findings if which appeared in the journal Proceedings of the National Academy of Sciences, the new molecule is formed when certain white blood cells - macrophages - are stimulated in response to pathogens.

The team of scientists measured 'THRIL' levels in KD samples at different stages and found that levels were at their lowest during the acute stage of the disease when TNF-alpha - a potent cytokine that promotes inflammation - levels are at their highest.

"For some time, we have known that non-coding regions of RNA play important roles in regulating the immune response to microbial pathogens," added Rana.

"When we realised that THRIL functioned to control the TNF-alpha gene, we wanted to see if it mirrors the progression in inflammatory diseases," he added.

KD usually occurs in children between ages 1-5, and its cause is still unknown. It is extremely important that an accurate diagnosis be made at the earliest to prevent fatality. However, symptoms of the disease only manifest after about five days of its onset. By that time, the damage to the coronary vessel might have already been done.

Symptoms of the disease include red eyes, red lips, and redness on the palm of their hands and soles of their feet - all signs of inflamed blood vessels.

Kawasaki syndrome was first described by Tomisaku Kawasaki in Japan in 1967. Various reports published in international journals showed that the prevalence of the disease had been on the rise in almost all countries.

A new study has revealed that walking just 20 minutes extra every day could cuts the risk of cardiovascular episodes such as heart attacks by eight per cent.

According to experts, increasing daily exercise by just 2,000 steps may be good for older people who may struggle to exercise regularly and is recommended for the overweight and those with a family history of diabetes, the Daily express reported.

Study's lead author Dr Thomas Yates, of Leicester University, said their results provide novel evidence that changing physical activity levels through simply increasing the number of steps taken can substantially reduce the risk of cardiovascular disease.

The study looked at 9,306 adults from 40 countries with impaired glucose tolerance (IGT), a precursor to diabetes.

It found an extra 2,000 steps a day over one year - 20 minutes of moderate walking daily - cuts the risk of cardiovascular -episodes such as heart attacks by eight per cent.

The study is published in journal The Lancet.

MIT researchers have developed a new hand-held device that scans a patient's entire retina in seconds to detect a host of retinal diseases including diabetic retinopathy, glaucoma and macular degeneration.

Researchers at the Massachusetts Institute of Technology (MIT) developed the new instrument which is the first to combine cutting-edge technologies such as ultrahigh-speed 3-D imaging, a tiny micro-electro-mechanical systems (MEMS) mirror for scanning, and a technique to correct for unintentional movement by the patient.

These innovations, researchers said, would allow collection of comprehensive data with just one measurement.

Normally, to diagnose retinal diseases, an ophthalmologist must examine the patient in his or her office, typically with table-top instruments.

The MIT group, in collaboration with the University of Erlangen and Praevium/Thorlabs, has developed a portable instrument that can be taken outside a specialist's office.

The instrument uses a technique called optical coherence tomography (OCT), which the MIT group and collaborators helped pioneer in the early 1990s.

The technology sends beams of infrared light into the eye and onto the retina. Echoes of this light return to the instrument, which uses interferometry to measures changes in the time delay and magnitude of the returning light echoes, revealing the cross sectional tissue structure of the retina - similar to radar or ultrasound imaging.

Tabletop OCT imagers have become a standard of care in ophthalmology, and current generation hand-held scanners are used for imaging infants and monitoring retinal surgery.

The researchers were able to shrink what has been typically a large instrument into a portable size by using a MEMS mirror to scan the OCT imaging beam.

They tested two designs, one of which is similar to a hand-held video camera with a flat-screen display. In their tests, the researchers found that their device can acquire images comparable in quality to conventional table-top OCT instruments used by ophthalmologists.

To deal with the motion instability of a hand-held device, the instrument takes multiple 3-D images at high speeds, scanning a particular volume of the eye many times but with different scanning directions.

By using multiple 3-D images of the same part of the retina, it is possible to correct for distortions due to motion of the operator's hand or the subject's own eye.

According to study author James Fujimoto of MIT, the next step is to evaluate the technology in a clinical setting.

But the device is still relatively expensive, he added, and before this technology finds its way into doctors' offices or in the field, manufacturers will have to find a way to support or lower its cost.

The study appears in the journal Biomedical Optics Express, published by The Optical Society (OSA).

In view of increasing cases of malaria treatment failures reported across the globe, scientists have now identified a way to stop malaria parasites from multiplying, raising hope for a new malaria treatment.

A team of scientists led by Ed Tate, of the Department of Chemistry at Imperial College, London, have shown that blocking the activity of an enzyme called NMT in plasmodium falciparum, the most common malaria parasite, prevents mice from showing malaria symptoms and also extends their lifespan.

NMT is involved in a wide range of essential processes in the parasite cell, including the production of proteins that enable malaria to be transmitted between humans and mosquitoes, and proteins that enable malaria to cause long-term infection, said the study.

"Finding an enzyme that can be targeted effectively in malaria can be a big challenge. Here, we've shown not only why NMT is essential for a wide range of important processes in the parasite, but also that we can design molecules that stop it from working during infection," Tate said.

"It has so many functions that we think blocking it could be effective at preventing long-term disease and transmission, in addition to treating acute malaria," he added.

The scientists expect the treatment to work not just on plasmodium falciparum but on other malaria parasites as well.

However, although the researchers have tested a handful of molecules that block the activity of NMT in the parasite living inside human red blood cells, and in mice, the treatment is not yet refined enough to be tested in humans.

"We need to do some more work in the lab to find the best candidate molecule to take into clinical trials, but hopefully we'll be ready to do that within a few years," Tate said.

The findings of the study appeared in the latest edition of the journal Nature Chemistry.