Knowledge Update

London, July 26 (IANS) Using a novel technique, scientists have demonstrated for the first time that it is possible to selectively sequence fragments of DNA in real time, thus greatly reducing the period needed to analyse biological samples.

"This is the first time that direct selection of specific DNA molecules has been shown on any device. We hope that it will enable many future novel applications, especially for portable sequencing," said Matt Loose from University of Nottingham.

Called MinION, the new device was used with real-time nanopore sequencing to enable the user analyse only DNA strands that contain pre-determined signatures of interest. 

"This makes sequencing as efficient as possible and will provide a viable, informatics based alternative to traditional wet lab enrichment techniques. The application of this approach to a wide number of problems from pathogen detection to sequencing targeted regions of the human genome is now within reach," Loose added in a paper described in the journal Nature Methods.

The pocket-sized device -- the same technology which NASA recently sent to the International Space Station (ISS) in an effort to investigate whether DNA sequencing is possible in microgravity - employs tiny molecular pores in a membrane that 'sense' the sequence of DNA fragments passing through these nanopores, producing minute fluctuations in a current trace. 

These current traces, termed "squiggles" then need to be converted to DNA bases using base caller software, often located in the cloud. The team used signal processing techniques to map these squiggles to reference sequences, by passing this step.

The researchers showed that this "real-time selective sequencing", or as some have called it "DNA testing", can reduce the time needed to sequence key DNA fragments or enable the analysis of pathogen samples where there is host and other DNA present in the sample.​

New York, July 22 (IANS) Borrowing an idea from metalsmiths and pastry chefs, researchers have created composite materials containing hundreds of layers that are just atoms thick but span the full width of the material -- a feat that could open new vistas in materials science.

The work, described recently in the journal Science, could open up wide-ranging possibilities for designing new, easy-to-manufacture composites for optical devices, electronic systems, and high-tech materials. 

Materials such as graphene, a two-dimensional form of pure carbon, and carbon nanotubes, tiny cylinders that are essentially rolled-up graphene, are "some of the strongest, hardest materials we have available," said Michael Strano from the Massachusetts Institute of Technology (MIT) .

Therefore, researchers have been searching for ways of using these nanomaterials to add great strength to composite materials, much the way steel bars are used to reinforce concrete.

However, the biggest obstacle has been finding ways to embed these materials within a matrix of another material in an orderly way. 

These tiny sheets and tubes have a strong tendency to clump together, so just stirring them into a batch of liquid resin before it sets doesn't work at all. The MIT team's insight was in finding a way to create large numbers of layers, stacked in a perfectly orderly way, without having to stack each layer individually.

They used a technique similar to that used to make ultrastrong steel sword blades, as well as puff pastries. 

A layer of material -- be it steel, dough, or graphene -- is spread out flat. Then, the material is doubled over on itself, pounded or rolled out, and then doubled over and over again.

With each fold, the number of layers doubles, thus producing an exponential increase in the layering. Just 20 simple folds would produce more than a million perfectly aligned layers.

The MIT team produced composites with up to 320 layers of graphene embedded in them. They were able to demonstrate that even though the total amount of the graphene added to the material was minuscule -- less than 1/10 of a percent by weight -- it led to a clear-cut improvement in overall strength.

The team also found a way to make structured fibres from graphene, potentially enabling the creation of yarns and fabrics with embedded electronic functions, as well as yet another class of composites.​

London, July 25 (IANS) Diabetes may be due to the failure of a privileged few cells, rather than the behaviour of all cells, suggests new research.

"This study is interesting as it suggests that failure of a handful of cells may lead to diabetes," said co-lead researcher Guy Rutter from Imperial College London.

Type-2 diabetes occurs when the pancreas fails to produce enough insulin to function properly, meaning that glucose stays in the blood rather than being converted into energy.

Beta cells make up around 65-80 per cent of the cells in the islets of the pancreas. Their primary function is to store and release insulin and, when functioning correctly, can respond quickly to fluctuations in blood glucose concentrations by secreting some of their stored insulin.

The new findings showed that just one to ten per cent of beta cells control islet responses to glucose.

"These specialised beta cells appear to serve as pacemakers for insulin secretion. We found that when their activity was silenced, islets were no longer able to properly respond to glucose," David Hodson from the University of Birmingham explained.

Studies were conducted on islet samples from both murine and human models. 

The researchers used optogenetic and photopharmacological targeting to precisely map the role of the cells required for the secretion of insulin.

The team believes that the findings, published in the journal Cell Metabolism, could pave the way for therapies that target these handful of specialised cells.

"It has long been suspected that ‘not all cells are equal’ when it comes to insulin secretion. These findings provide a revised blueprint for how our pancreatic islets function, whereby these hubs dictate the behaviour of other cells in response to glucose," Hodson noted.​

Toronto, July 22 (IANS) Students from the lower-income groups have less working memory capacity than their peers from higher-income brackets, says a study.

The researchers have discovered important differences between children from lower and higher-income groups in their ability to use "working memory" -- a key brain function responsible for everything from remembering a phone number to doing math in your head.

The team used fMRI (functional magnetic resonance imaging) to measure and map the brain activity of a group of middle-schoolers.

"It has never been shown before that lower-income (group) children have this qualitatively different brain response for this very basic ability that is essential to almost all cognition," said Amy Finn from the University of Toronto in the study published in the journal Developmental Science.

For the study, 67 students were enrolled in either seventh or eighth grades in schools who were ethnically diverse and with a roughly equal number of boys and girls.

In the study, researchers focused on regions of the brain, such as the prefrontal cortex, which are important for high-level functions.

The researchers observed that students from the high-income groups largely kept this region of the brain in reserve until the tasks began to get more difficult. But the lower-income group children relied on brain more often and to a greater extent than chilkdren from higher-income groups even for relatively simple problems.

This suggested that there is a difference in how lower-income background children tap into their working memory -- which is how the brain organises and holds information in mind that it can't immediately see, revealed the study.

"We knew that there were differences in the neural structure of children from lower-income versus higher-income families, but we didn't know if that really mattered for solving problems," added Finn.

Most cognitive neural science is conducted on people who are from middle and upper-middle class backgrounds because it's less expensive to study populations near the university than to reach out to lower-income communities.​

​London, July 22 (IANS) The failure of a handful of beta cell "hubs" in the pancreas are the likely reason for developing diabetes, rather than the behaviour of all cells, says a study.

Type 2 diabetes occurs when the pancreas fail to produce enough insulin to function properly, meaning that glucose stays in the blood rather than being converted into energy.

Beta cells that produce insulin -- a hormone that can reduce blood glucose concentration -- make up around 65-80 per cent of the cells in the islets of the pancreas, with the primary function of storing and releasing insulin.

However, the findings revealed that just 1-10 per cent of beta cells control islet responses to glucose.

"These specialised beta cells appear to serve as pacemakers for insulin secretion. The study found that when their activity was silenced, islets were no longer able to properly respond to glucose," said David Hodson from the University of Birmingham in Britain.

"It has long been suspected that 'not all cells are equal' when it comes to insulin secretion. These findings provide a revised blueprint for how our pancreatic islets function, whereby these hubs dictate the behaviour of other cells in response to glucose," Hodson explained, adding that the results could pave the way for therapies that target the "hubs".

In the study, published in the journal Cell Metabolism, the team used optogenetic and photopharmacological targeting to precisely map the role of the cells required for the secretion of insulin.​

​London, July 22 (IANS) Paving the way for the next-generation storage revolution, scientists have pioneered a novel effect arising from the relativistic physics of Albert Einstein that allows the fabrication of a new type of magnet that behaves like cats.

Similar to a cat's ability to flip itself in the air by twisting different parts of her body in different directions and land on its feet, these magnets can flip themselves through the internal motion of their own electrons, the researchers claimed.

"In these new magnetic materials, a current running through the magnet can turn around the direction of the magnetisation depending on the direction of the current," said Jairo Sinova of the Johannes Gutenberg University in Mainz. 

Sinova's group worked together with theoretical and experimental collaborators on this novel effect. 

"This novel phenomenon in physics, dubflipbed spin-orbit torques, links the spin-degree of freedom of magnets which gives rise to the magnetisation to the charge degree of freedom that allows for current-charge motion inside the material," Sinova added.

This effect occurs in magnetic materials that have broken-inversion symmetry. The researchers first observed spin-orbit torques in the artificial bulk diluted magnetic semiconductor GaMnAs. 

GaMnAs is the diluted counterpart of crystalline zincblende structures of Silicon and Gallium arsenide, which are the pillars of modern electronics. However, in GaMnAs, spin-orbit torques were demonstrated only at very low temperatures.

The discovery can pave the way for using spin-orbit torques in technological applications, said the study appeared in the journal Nature Physics.

New York, July 22 (IANS) Feeding babies avocados, which has a neutral flavour, soft consistency and nutrient density, can help in boosting their growth and development, says a study, suggesting that the fruit can be used as a first food for infants.

Babies' ideal first foods should have a low to moderate sweet and salty flavour profile to avoid early preferences for sweet foods.

The findings showed that avocados are unique among complementary and transitional foods and they provide an ideal source of calories to meet the increasing energy and growth demands of weaning infants and toddlers.

"It's important that infants experience a wide variety of tastes, textures, colours and combinations, in their first foods," said Robert Murray, Professor at the Ohio State University, in the US.

Avocados were found to contain less than 1 gram of sugar per serving (0.09g) -- the least amount of any other fresh fruit. 

Avocados' soft and smooth textures can also help infants to develop the ability to chew and swallow.

Infants should consume moderately energy-dense foods that are low in sugar and rich in multiple nutrients, said the paper published in the journal Nutrients.

Avocados were found to be higher in key developmental nutrients per one once serving, such as folate, Vitamin E, and lutein, compared to a serving of the most popular complementary and transitional fruits served in many households.

Avocados also help significantly enhance the absorption of lipid-soluble vitamins from foods eaten with them, the researchers concluded.​

​New York, July 22 (IANS) Researchers, including one of Indian-origin, have identified a new way that tuberculosis bacteria get into the body, revealing a novel potential therapeutic angle to explore.

The bacterium that causes tuberculosis, Mycobacterium tuberculosis, or Mtb, previously was thought to infect the body only through inhalation and subsequent infection of cells in the lungs.

The new research found that microfold cell (M-cell) translocation is a new and previously unknown mechanism by which Mtb enters the body.

Vidhya Nair, postdoctoral researcher at The University of Texas Southwestern Medical Center, is the lead author of the study published online in the journal Cell Reports.

"The current model of disease is that when Mtb bacteria are inhaled, they reach the end of the lung - the alveolus - and then are ingested by a macrophage, a type of white blood cell that swallows and kills invading bacteria," Michael Shiloh, Assistant Professor of Internal Medicine and Microbiology at UT Southwestern said.

"Our study shows that once Mtb bacteria are inhaled, they also can enter the body directly through M-cells that line the airway tissue, and then travel to the lymph nodes and beyond," Shiloh explained.

M-cells are specialised epithelial cells that transport particles from the airway or mucosal surface to the compartment below the cell.

"This is a key finding that suggests disease onset outside of alveolar macrophages is not only possible, but also important in the pathogenesis of tuberculosis infection," Shiloh noted.

Although further studies are necessary, potential clinical applications of the team's finding would involve developing methods or drugs that prevent Mtb from entering M-cells.

For example, preventing Mtb from attaching to receptors on the M-cell surface - such as by vaccinating against a bacterial protein - could block the bacteria's entry, infection, and spread to other organs, Shiloh said.

One of the world's most deadly diseases, tuberculosis - primarily a lung disease - infects more than eight million people and is responsible for 1.5 million deaths each year.

According to the US Centers for Disease Control and Prevention, approximately one-third of the world's population is infected with tuberculosis. ​

London, July 21 (IANS) Why do people help those in distress or the needy when there is no direct benefit involved? Why do some people not like bribing or cheating the system? The answer may not lie in genes but elsewhere.

An international team of researchers has found that altruism is favoured by random fluctuations in nature -- offering an explanation to the mystery as to why this seemingly disadvantageous trait has evolved.

The team from the Universities of Bath, Manchester and Princeton (US), developed a mathematical model to predict the path of evolution when altruistic "cooperators" live alongside "cheats" who use up resources but do not themselves contribute.

Humans are not the only organisms to cooperate with one another.

The scientists used the example of Brewer's yeast, which can produce an enzyme called invertase that breaks down complex sugars in the environment, creating more food for all.

However, those that make this enzyme use energy that could instead have been used for reproduction, meaning that a mutant "cheating" strain that waits for others to do the hard work would be able to breed faster as a result.

Darwinian evolution suggests that their ability to breed faster will allow the cheats (and their cheating offspring) to proliferate and eventually take over the whole population.

This problem is common to all altruistic populations, raising the difficult question of how cooperation evolved.

"Scientists have been puzzled by this for a long time. What we are lacking is an explanation of how these behaviours could have evolved in organisms as basic as yeast. Our research proposes a simple answer - it turns out that cooperation is favoured by chance," said Dr Tim Rogers, Royal Society University Research Fellow at University of Bath..

The key insight is that the total size of population that can be supported depends on the proportion of cooperators: more cooperation means more food for all and a larger population.

If, due to chance, there is a random increase in the number of cheats then there is not enough food to go around and total population size will decrease.

Conversely, a random decrease in the number of cheats will allow the population to grow to a larger size, disproportionally benefitting the cooperators.

Dr George Constable, soon to join the University of Bath from Princeton, uses the analogy of flipping a coin, where heads wins ?20 but tails loses ?10.

"Although the odds winning or losing are the same, winning is more good than losing is bad. Random fluctuations in cheat numbers are exploited by the cooperators, who benefit more then they lose out," he noted in a paper appeared in the journal the Proceedings of the National Academy of Sciences.​

​New York, July 21 (IANS) Researchers, including one of Indian-origin, have found that long-term antibiotic treatment in mice decreases levels of amyloid plaques, a hallmark of Alzheimer's disease.

The study, published in the journal Scientific Reports, also showed significant changes in the gut microbiome after antibiotic treatment, suggesting the composition and diversity of bacteria in the gut play an important role in regulating immune system activity that impacts progression of Alzheimer's disease.

"We're exploring very new territory in how the gut influences brain health," said senior author of the study Sangram Sisodia, Professor of Neurosciences at the University of Chicago. 

Two of the key features of Alzheimer's disease are the development of amyloidosis, accumulation of amyloid-beta peptides in the brain, and inflammation of the microglia, brain cells that perform immune system functions in the central nervous system. 

For this study, Sisodia and his team administered high doses of broad-spectrum antibiotics to mice over five to six months. 

At the end of this period, genetic analysis of gut bacteria from the antibiotic-treated mice showed that while the total mass of microbes present was roughly the same as in controls, the diversity of the community changed dramatically. 

The antibiotic-treated mice also showed more than a two-fold decrease in amyloid-beta plaques compared to controls.

While the mechanisms linking these changes is unclear, the study points to the potential in further research on the gut microbiome's influence on the brain and nervous system.

Sisodia cautioned that while the current study opens new possibilities for understanding the role of the gut microbiome in Alzheimer's disease, it iss just a beginning step.

"There's probably not going to be a cure for Alzheimer's disease for several generations, because we know there are changes occurring in the brain and central nervous system 15 to 20 years before clinical onset," he said. 

"We have to find ways to intervene when a patient starts showing clinical signs, and if we learn how changes in gut bacteria affect onset or progression, or how the molecules they produce interact with the nervous system, we could use that to create a new kind of personalized medicine," he noted.​