The thousands of aromas humans can smell can be sorted into 10 basic categories, US scientists say.

Prof Jason Castro, of Bates College, and Prof Chakra Chennubhotla, of the University of Pittsburgh, used a computerised technique to whittle down smells to their most basic essence.

They told the PLoS One journal they had then tested 144 of these and found they could be grouped into 10 categories.

The findings are contentious - some say there are thousands of permutations.

Prof Castro said: "You have these 10 basic categories because they reflect important attributes about the world - danger, food and so on.

"If you know these basic categories, then you can start to think about building smells.

"We have not solved the problem of predicting a smell based on its chemical structure, but that's something we hope to do."

He said it would be important to start testing the theory on more complex aromas, such as perfumes and everyday smells.

In reality, any natural scent was likely to be a complex mix - a blend of the 10 different categories, he said.

Prof Tim Jacob, a UK expert in smell science at Cardiff University, said: "In the 1950s a scientist called John Amoore proposed a theory which involved seven smell categories based upon molecular shape and size.

"He eventually withdrew it, to the poorly suppressed glee of his rival R W Moncrieff, who said there was 'never much solid evidence to support it, and there were difficulties all along the line, but it did stimulate a lot of useful thought'.

"I'm sure that Castro et al's paper will 'stimulate a lot of useful thought'."

Scientists have devised a completely new way in which they can identify good fat.

Researchers at The University of Texas Health Science Center at Houston (UTHealth) Medical School are studying brown fat with a goal of fighting obesity.

Mikhail Kolonin, Ph.D., the study's senior author and associate professor at the UTHealth Center for Stem Cell and Regenerative Medicine, said that brown adipose tissue, responsible for heat generation, has high importance in the context of metabolic diseases.

He said that brown fat is more common in kids but has recently been discovered in adult humans.

Kolonin asserted that however, measurement of its body distribution has remained technically challenging.

He said that they are reporting a peptide probe that zeroes in on brown fat and can be used for localization of this tissue in mice by whole body imaging.

Kolonin teamed up with UTHealth medical imaging researcher Eva Sevick-Muraca , Ph.D., to develop a near-infrared fluorescence imaging probe that binds to brown adipose vasculature and emits tiny amounts of skin-penetrating light that can be picked up by highly sensitive cameras.

Kolonin's team tested numerous combinations before finding one that selectively localizes to brown fat when administered intravenously. Sevick-Muraca's team coupled the peptide with a dye that could be picked up during whole body scans.

This study has been published in Nature Communications.

Scientists have successfully grown stem cells, which have the ability to develop into two different types of cells that make up a healthy pancreas.

The research team led by Dr. Hans Clevers of the Hubrecht Institute, The Netherlands, have isolated and grown stem cells from the pancreases of mice using a 3-D culture system previously developed by the scientists.

The results could eventually lead to ways to repair damaged insulin-producing beta cells or pancreatic duct cells.

Cell signalling molecules known as Wnts and a protein called Lgr5 are essential to produce adult stem cells that can be coaxed to grow and divide rapidly.

Clevers said that they have found a way to activate the Wnt pathway to produce an unlimited expansion of pancreatic stem cells isolated from mice.

He said that by changing the growth conditions we can select two different fates for the stem cells and generate large numbers of either hormone-producing beta cells or pancreatic duct cells.

In the study, the pancreases of mice were altered in a way that makes duct cells proliferate and differentiate. Some cells in this new population were stem cells that were capable of self-renewal.

The scientists were able to culture these cells to give rise to large numbers of pancreatic cells or tiny clumps of tissue referred to as organoids.

The results have been published in The EMBO Journal.

Indulging in fatty foods could destroy stomach's signals to the brain, according to a new study which gives insight why many dieters tend to regain the weight after losing it.

New University of Adelaide research has found the nerves in the stomach which signal fullness to the brain appeared to be desensitised after long-term consumption of a high-fat diet.

The findings could explain why many dieters tend to regain the weight they have lost.

PhD student Stephen Kentish investigated the impact of high-fat diets on the ability of the gut to signal its fullness, and whether those changes revert back to normal by losing weight.

Study leader Associate Professor Amanda Page said laboratory studies showed the stomach's nerve response does not return to normal upon a return to a normal diet.

"This means you would need to eat more food before you felt the same degree of fullness as a healthy individual," she said.

"A hormone in the body, leptin, known to regulate food intake, can also change the sensitivity of the nerves in the stomach that signal fullness.

"In normal conditions, leptin acts to stop food intake. However, in the stomach in high-fat diet induced obesity, leptin further desensitises the nerves that detect fullness."

Associate Professor Page said the two mechanisms combined meant that obese people needed to eat more to feel full, which fuels their obesity cycle.

She said the results had "very strong implications for obese people, those trying to lose weight, and those who are trying to maintain their weight loss".

"Unfortunately, our results show that the nerves in the stomach remain desensitised to fullness after weight loss has been achieved," she said.

Associate Professor Page says the researchers were not yet sure whether the effect was permanent or just long-lasting.

Contrary to popular belief, alcohol does not cause depression, Australian scientists have found.

Researchers also debunk the view that mild to moderate alcohol consumption may reduce the risk of depression.

Until now it was believed that alcohol caused people to become depressed, particularly if consumed at excessive levels, according to Professor Osvaldo Almeida, from The University of Western Australia.

"Even one of the diagnoses we have for depressive disorders - Substance Induced Mood Disorder - is a diagnosis where alcohol plays a role," Almeida said.

"However, because of the observational nature of the association between alcohol and depression, and the risk of confounding and bias that comes with observational studies, it is difficult to be entirely certain that the relationship is causal.

"For example, people who drink too much may also smoke, have poor diets and other diseases that could explain the excess number of people with depression among heavy drinkers," he said.

Almeida and fellow researchers with the Health in Men Study (HIMS), including 12,201 men aged 65-83 when recruited in 1996, decided to search for a causal link via physiological pathways instead: specifically the genetic polymorphism, or mutation, most closely associated with alcohol metabolism.

"We now know that certain genetic variations affect the amount of alcohol people consume. There is one particular genetic variation that affects the enzyme responsible for the metabolism of alcohol," Almeida said.

"This variation produces an enzyme that is up to 80 times less competent at breaking down alcohol. Consequently, people who carry this variation are much less tolerant to alcohol. In fact, there is now evidence that alcohol-related disorders are very uncommon in this group.

"Now, if alcohol causes depression, then a genetic variation that reduces alcohol use and alcohol-related disorders, should reduce the risk of depression.

"The great advantage of looking at the gene is that this association is not confounded by any other factors - people are born like that," he said.

The researchers analysed the triangular association between the genetic mutation, alcohol and depression in 3,873 elderly male participants of the study, using data collected over three to eight years.

"We found (as expected) that this particular genetic variant was associated with reduced alcohol use, but it had no association with depression whatsoever," Almeida said.

"The conclusion is that alcohol use neither causes nor prevents depression in older men. Our results also debunk the view that mild to moderate alcohol consumption may reduce the risk of depression," he added.