Scientists are using memristors- electronic microcomponents that imitate natural nerves- as key components in a blueprint for an artificial brain.

Scientists have long been dreaming about building a computer that would work like a brain. This is because a brain is far more energy-saving than a computer, it can learn by itself, and it doesn`t need any programming.

Dr. Andy Thomas from Bielefeld University`s Faculty of Physics and his colleagues constructed a memristor that is capable of learning a year ago.

He is now is experimenting with his memristors for building an artificial brain.

A nanocomponent that is capable of learning: The Bielefeld memristor built into a chip here is 600 times thinner than a human hair. Memristors are made of fine nanolayers and can be used to connect electric circuits.

For several years now, the memristor has been considered to be the electronic equivalent of the synapse. Synapses are, so to speak, the bridges across which nerve cells (neurons) contact each other. Their connections increase in strength the more often they are used. Usually, one nerve cell is connected to other nerve cells across thousands of synapses.

Like synapses, memristors learn from earlier impulses. In their case, these are electrical impulses that (as yet) do not come from nerve cells but from the electric circuits to which they are connected. The amount of current a memristor allows to pass depends on how strong the current was that flowed through it in the past and how long it was exposed to it.

Thomas said that because of their similarity to synapses, memristors are particularly suitable for building an artificial brain - a new generation of computers.

"They allow us to construct extremely energy-efficient and robust processors that are able to learn by themselves," he stated.

Dr. Thomas has summarized the technological principles that need to be met when constructing a processor based on the brain.

Thanks to these properties, synapses can be used to reconstruct the brain process responsible for learning, said Thomas.

He will be presenting his results at the beginning of March in the print edition of the prestigious Journal of Physics published by the Institute of Physics in London.

Mild maternal hypertension early in pregnancy actually benefits the fetus, but that late-pregnancy hypertension has negative health consequences for the child, a new study has found.

The study, conducted by researchers from the Centre for Social Evolution at the Department of Biology, University of Copenhagen, is based on more than 750,000 births in Denmark, with follow-up data on children`s hospital diagnoses for up to 27 years.

"It has been known for some time now that pregnancy-induced hypertension can lead to more serious toxic conditions ( preeclampsia ), but it has puzzled biologists why such a medical condition that can be quite dangerous for both mother and child has not previously been removed by natural selection in our stoneage ancestors," said Professor Jacobus Boomsma, Director of the Centre for Social Evolution and coordinator of the study.

"However, evolutionary theory also emphasizes that paradoxes of this kind can be due to genetic parent-offspring conflicts, so we set out to test whether we could find statistical evidence for that type of explanation," he stated.

The results clearly indicate that mothers with minor increases in blood pressure in the first trimester of pregnancy have babies that enjoy generally better health than children of mothers who never get a hypertension diagnosis during pregnancy.

The difference was between 10 and 40 percent fewer diagnoses across all disease categories during the 27 years of available follow-up data, a result that has never been documented before.

However, when hypertension continues or starts later in pregnancy, this advantage shifts to a ca. 10 percent disadvantage in terms of an increased risk of acquiring a diagnosis in the Danish public health data bases.

Child mortality during the first year of life showed the same trend. In spite of this risk being very low in Denmark, no children of mothers with early pregnancy-induced hypertension died, whereas the mortality risk of children born to mothers with hypertension late in pregnancy was above average.

Parent-offspring-conflict theory maintains that father-genes in the placenta will have a tendency to `demand` a somewhat higher level of nutrition for the fetus than serves the interests of mother-genes. It argues that father genes that somehow manage to enhance maternal blood pressure will likely be met by maternal genes compensating this challenge.

Both types of genes are 50/50 represented and thus likely to find a `negotiated` balance while creating an optimally functioning placenta. However, when the pull of paternal genes cannot quite be managed by maternal counterbalances, there is a risk of elevated blood pressure to develop and persist, leading to late occurring pregnancy complications and compromised offspring health.

The results obtained are consistent with the idea that some deep fundamental conflicts lay buried in our genes right from the moment of conception. Imprinted genes are prime suspects for mediating such conflicts as they `remember` which parent they come from.

"Molecular biologists have recently found many such genes in mice and man, and they are particularly expressed in the placenta as the theory predicts. Our study therefore suggests that further research to test whether different patterns of pregnancy-induced hypertension are indeed related to paternal or maternal imprints would be highly worthwhile," said PhD student Birgitte Hollegaard, who did the analyses together with EU Marie Curie Postdoctoral Fellow Sean Byars.

The authors of the study hope these results will help build bridges between their evolutionary inspired public health analyses and established clinical praxis.

"Ultimately we are not only interested in the fundamental science aspects of genome level reproductive conflicts, but also in seeing some of these findings being made more directly useful, for example by adjusting pregnancy monitoring schemes to take long term risks for offspring health into account," Jacobus Boomsma concluded.

Scientists have for the first time explained mechanisms behind the brain`s ability to protect itself from damage due to stroke.

The Oxford University researchers hope that harnessing this inbuilt biological mechanism, identified in rats, could help in treating stroke and preventing other neurodegenerative diseases in the future.

"We have shown for the first time that the brain has mechanisms that it can use to protect itself and keep brain cells alive," said lead researcher Professor Alastair Buchan in a statement.

Stroke occurs when the blood supply to part of the brain is cut off. When this happens, brain cells are deprived of the oxygen and nutrients they need to function properly, and they begin to die.

This explains why treatment for stroke is so dependent on speed. The faster someone can reach hospital, be scanned and have drugs administered to dissolve any blood clot and get the blood flow re-started, the less damage to brain cells there will be.

The Oxford University research group have now identified the first example of the brain having its own built-in form of neuroprotection, so-called `endogenous neuroprotection`.

They did this by going back to an observation first made over 85 years ago. It has been known since 1926 that neurons in one area of the hippocampus, the part of the brain that controls memory, are able to survive being starved of oxygen, while others in a different area of the hippocampus die.

However, what protected that one set of cells from damage had remained a puzzle until now.

"Previous studies have focused on understanding how cells die after being depleted of oxygen and glucose. We considered a more direct approach by investigating the endogenous mechanisms that have evolved to make these cells in the hippocampus resistant," explained first author Dr Michalis Papadakis.

Working in rats, the researchers found that production of a specific protein called hamartin allowed the cells to survive being starved of oxygen and glucose, as would happen after a stroke.

They showed that the neurons die in the other part of the hippocampus because of a lack of the hamartin response. The team was then able to show that stimulating production of hamartin offered greater protection for the neurons.

The researchers were also able to identify the biological pathway through which hamartin acts to enable the nerve cells to cope with damage when starved of energy and oxygen.

The group pointed out that knowing the natural biological mechanism that leads to neuroprotection opens up the possibility of developing drugs that mimic hamartin`s effect.

The study was published in the journal Nature Medicine.

A combination of fish oil and aspirin could be the key to beating a host of devastating chronic diseases including arthritis, a new breakthrough study has found.

Researchers found that the two work together to combat the inflammation responsible for a host of illnesses, including heart disease, cancer and arthritis.
Experts have always touted the health benefits of low-dose aspirin and omega-3 fatty acids found in foods like flax seeds and salmon, but the detailed mechanisms involved in their effects were not fully known.

Now a new study published in the Cell Press journal Chemistry and Biology shows that aspirin helps trigger the production of molecules called resolvins that are naturally made by the body from omega-3 fatty acids.

These resolvins shut off, or "resolve," the inflammation that underlies destructive conditions such as inflammatory lung disease, heart disease, and arthritis.

"In this report, we found that one resolvin, termed resolvin D3 from the omega-3 fatty acid DHA, persists longer at sites of inflammation than either resolvin D1 or resolvin D2 in the natural resolution of inflammation in mice," said senior study author Dr Charles Serhan of Brigham and Women`s Hospital and Harvard Medical School.

"This finding suggests that this late resolution phase resolvin D3 might display unique properties in fighting uncontrolled inflammation," Serhan said in a statement.

The researchers also confirmed that aspirin treatment triggered the production of a longer acting form of resolvin D3 through a different pathway.

"Aspirin is able to modify an inflammatory enzyme to stop forming molecules that propagate inflammation and instead produce molecules from omega-3 fatty acids, like resolvin D3, that help inflammation to end," said co-author Dr Nicos Petasis of the University of Southern California.

"We were able to produce by chemical synthesis both resolvin D3 and aspirin-triggered resolvin D3 in pure form, which allowed us to establish their complete structures and biological activities," said Petasis.

When administered to human cells, both of these resolvins demonstrated potent anti-inflammatory actions. When given to mice, the compounds also stimulated the resolution of inflammation in the body.

"We also identified the human receptor that is activated by resolvin D3, which is critical in understanding how resolvin D3 works in the body to resolve inflammation," said Serhan.

A lifelong diet that is rich in omega-3 fatty acids - found in fish oils - can decrease growth of breast cancer tumours by 30 percent, a new research has revealed.

Study authors David Ma, a professor in Guelph`s Department of Human Health and Nutritional Sciences, said that their study shows that lifelong exposure to omega-3s had a beneficial role in disease prevention - in this case, breast cancer prevention.

Ma said that health advocates have long believed that diet may significantly help in preventing cancer but epidemiological and experimental studies to back up such claims have been lacking, and human studies have been inconsistent.

For their research, they created a novel transgenic mouse that produced both omega-3 fatty acids and develops aggressive mammary tumours. The team compared those animals to mice genetically engineered only to develop the same tumours.

Mice producing omega-3s developed only two-thirds as many tumours - and tumours were also 30-per-cent smaller - as compared to the control mice.

"The difference can be solely attributed to the presence of omega-3s in the transgenic mice - that`s significant," Ma said.

"The fact that a food nutrient can have a significant effect on tumour development and growth is remarkable and has considerable implications in breast cancer prevention," he added.

The study has been published in the Journal of Nutritional Biochemistry.