Knowledge Update

Melbourne, May 16 (IANS) Using space dust, researchers from Monash University here have made a surprising discovery about the chemistry of Earth's atmosphere 2.7 billion years ago, thus challenging the accepted view that Earth's ancient atmosphere was oxygen-poor.

The ancient Earth's upper atmosphere contained about the same amount of oxygen as today and that a methane haze layer separated this oxygen-rich upper layer from the oxygen-starved lower atmosphere, the team noted.

“Using cutting-edge microscopes, we found that most of the micrometeorites (space dust) had once been particles of metallic iron - common in meteorites - that had been turned into iron oxide minerals in the upper atmosphere, indicating higher concentrations of oxygen than expected," explained Andrew Tomkins from Monash University.

He explained how the team extracted micrometeorites from samples of ancient limestone collected in the Pilbara region in western Australia and examined them at the Monash Centre for Electron Microscopy (MCEM) and the Australian Synchrotron.

“This was an exciting result because it is the first time anyone has found a way to sample the chemistry of the ancient Earth's upper atmosphere,” Tomkins noted in a paper appeared in the journal Nature.

Co-researcher Matthew Genge from Imperial College London performed calculations that showed oxygen concentrations in the upper atmosphere would need to be close to modern day levels to explain the observations.

“This was a surprise because it has been firmly established that the Earth's lower atmosphere was very poor in oxygen 2.7 billion years ago. How the upper atmosphere could contain so much oxygen before the appearance of photosynthetic organisms was a real puzzle," Genge noted.

The results suggest the Earth at this time may have had a layered atmosphere with little vertical mixing, and higher levels of oxygen in the upper atmosphere produced by the breakdown of carbon dioxide by ultraviolet (UV) light.

A possible explanation for this layered atmosphere might have involved a methane haze layer at middle levels of the atmosphere.

The methane in such a layer would absorb UV light, releasing heat and creating a warm zone in the atmosphere that would inhibit vertical mixing.

“By studying fossilised particles of space dust the width of a human hair, we can gain new insights into the chemical makeup of Earth's upper atmosphere, billions of years ago,” Tomkins pointed out.

The next stage for the team will be to extract micrometeorites from a series of rocks covering over a billion years of Earth's history in order to learn more about changes in atmospheric chemistry and structure across geological time.

“We will focus particularly on the great oxidation event, which happened 2.4 billion years ago when there was a sudden jump in oxygen concentration in the lower atmosphere,” the authors noted.

Sydney, May 17 (IANS) A study released on Tuesday has found that a high concentration of coal dust can quickly kill coral on Australia's Great Barrier Reef.

The research by the Australian Institute of Marine Science discovered coal dust could also slow the growth rate of seagrasses and fish, Xinhua news agency reported.

"Corals exposed to the highest concentrations of coal dust died within two weeks," author Kathryn Berry said.

"Corals exposed to lower concentrations of coal lasted longer, but most of them also died after four weeks of exposure."

She noted that while some fish and seagrass died from coal dust exposure, it mostly stunted their growth by half compared to clean water.

The study found coal dust entered the marine environment at loading and storage facilities, or when it is blown into the sea during transport.

Researches also noted a shipping disaster as a possible risk to the reef.

"Risks to the Great Barrier Reef posed by large coal spills depend on the probability of an accident and the potential impacts to marine life," author Andrew Negri said.

"While the likelihood of a major spill on a coral reef or seagrass meadow is low, we are now beginning to understand the likely consequences."

Researchers hope the results will send a message to coal shipping companies in Australia and across the world.​

​New York, May 17 (IANS) The mother's voice can lighten up and engage the child's brain far more than the voices of women they do not know, say researchers including an Indian-origin scientist.

The findings showed that brain regions that respond more strongly to the mother's voice extend beyond regions of hearing.

It included regions of emotion and reward processing, social functions, detection of what is personally relevant and face recognition.

Also, the strength of connections between the brain regions activated by the voice of own mother predicted the child's social communication abilities.

"Many of our social, language and emotional processes are learned by listening to our mom's voice," said lead author Daniel Abrams from Stanford University in the US. 

"But surprisingly little is known about how the brain organises itself around this very important sound source. We didn't realise that a mother's voice would have such quick access to so many different brain systems," Abrams said.

"We wanted to know: Is it just auditory and voice-selective areas that respond differently, or is it more broad in terms of engagement, emotional reactivity and detection of salient stimuli," added Vinod Menon, professor at Stanford University.

For the study, published in the journal Proceedings of the National Academy of Sciences, the team examined 24 children ages 7 to 12. None had any developmental disorders, and were raised by their biological mothers. 

Each child's mother was recorded saying three nonsense words and two other women also were recorded saying the three nonsense words. The children's brains were then scanned using MRIs.

The results revealed that the children could identify their own mother with 97 percent accuracy, even after listening to recordings less than 1 second long.

"The study can be an important new template for investigating social communication deficits in children with disorders such as autism," Menon noted. ​

​Toronto, May 17 (IANS) Researchers have uncovered a new molecular mechanism for stimulating the body to burn fat -- a discovery that could lead to new medications to fight obesity, diabetes and heart diseases.

By knocking out the gene that produces a protein, known as folliculin, in fat cells in mice, the researchers triggered a series of biomolecular signals that switched the cells from storing fat to burning it.

This process is known as the 'browning' of fat cells. The principal role of brown fat is to burn energy to produce heat, which helps keep our body temperature constant. White fat serves as an energy-storage tissue.

Scientists recently discovered a new type of fat tissue with characteristics somewhere between healthy brown fat and the not-so-healthy white kind. The so-called beige fat is capable of behaving like brown fat in response to certain stimuli such as exposure to cold. 

"Conversion from white fat cells to beige or brown fat cells is a very desirable effect in the obesity, diabetes, and metabolic syndrome indications, since excess energy in the body is not stored in fat tissue but is burned in brown or beige fat tissue," said the study's senior author Arnim Pause, professor at McGill University in Montreal, Canada.

For the study, published in the journal Genes & Development, the team bred mice to have fat cells that did not produce folliculin. They then fed normal mice and folliculin-deficient mice with a high-fat, junk food-like diet over 14 weeks. 

Normal mice gained weight rapidly, whereas folliculin-deficient mice remained slim.

By measuring rates of oxygen consumption and CO2 production, the researchers found the folliculin-deficient mice were burning more fat. 

At the end of the trial, these mice had smaller white fat cells and less white fat tissue overall.

The extra energy they were producing made them better at tolerating cold temperatures, too, the researchers said.

The research could open the way for new medications to be developed that will stimulate the 'browning' process.

"One implication (of the study) is that a drug could be developed to stimulate the activity of beige/brown fat cells and thus help manage obesity and other metabolic disorders," Vincent Giguere from the University in Montreal noted.​

​New York, May 17 (IANS) Researchers have discovered a biological mechanism that could lead to a potential way to "tune up" the immune system's ability to kill cancer cells.

In the study, published in the journal Proceedings of the National Academy of Sciences, they reported that a protein called Kruppel-like factor 2 (KFL2) is critical for expansion and survival of natural killer (NK) cells, a type of white blood cell that specifically recognise and destroy tumour cells.

NK cell-mediated tumor therapy -- essentially, injections of NK cells -- is a cutting-edge technique currently used clinically. 

It can sweep the blood clean of cancer cells in leukemia patients. However, the remission is often short-lived.

The protein reported in this study both limits immature NK cell proliferation and helps mature NK cells to be rich in interleukin 15 (IL-15), which is necessary for their continued survival.

"This is the same process likely used by cancer cells to avoid destruction by NK cells," said one of the researchers Eric Sebzda from Vanderbilt University Medical Centre in Tennessee, US.

In particular, tumours may avoid immune clearance by promoting the destruction of the protein within the NK cell population, thereby starving these cells of IL-15.

The researchers believe that the findings could lead to new cancer therapy.​

London, May 16 (IANS) Researchers have identified a biomarker that can not only predict the progression of a deadly lung diseased called chronic obstructive pulmonary disease (COPD) but also lead to better treatment.

COPD is a group of lung diseases that block airflow and make it difficult to breathe.

According to researchers, a process initiated in neutrophils -- the most common type of white blood cells found in mammals and important for fighting infection -- may lead to worse outcomes for some patients with COPD.

"The study found that a recently identified form of neutrophil behaviour called neutrophil extracellular trap (NET) formation is present in the lungs of COPD patients and may weaken their ability to eat and kill bacteria," said lead author James D Chalmers from the University of Dundee in Scotland. 

For the study, the team recruited 141 patients with stable COPD. 

The findings showed that during neutrophilic airway inflammation -- when NET formation weakens neutrophils' bacteria-fighting capability -- patients experience more frequent chest infections, worse lung function and quality of life.

Further, the amount of NET complexes in the lungs of patients was directly related to the severity of their COPD and the risk of exacerbations. 

NETs increased significantly during exacerbations that did not respond to corticosteroid treatment.

The marker may also help in identifying patients at higher risk of the disease deterioration as well as those who may need treatments other than corticosteroids like anti-inflammatory medicine (steroids).

"The study stressed the need to identify new COPD treatments and further discover whether inhibiting NET formation will result in improved clinical outcomes for patients with COPD," the researchers concluded.

The results were presented at the ATS 2016 International Conference in California recently.​

London, May 15 (IANS) An international team of scientists has developed a new bio-glass material that can mimic and potentially encourage cartilage to repair or regrow.

This material developed by the researchers from Imperial College London and the University of Milano-Bicocca can be formulated to exhibit different properties and the researhers are now hoping to use it to develop implants for replacing damaged cartilage discs between vertebrae.

They believe that it also has the potential to encourage cartilage (a flexible connective tissue found in places such as in joints and between vertebrae in the spine) cells to grow in knees, which has previously not been possible with conventional methods.

"Our research shows that a new flexible version of this material could be used as cartilage-like material," said professor Julian Jones, one of the developers of the bio-glass from the department of materials at Imperial College.

"Patients will readily attest to loss of mobility that is associated with degraded cartilage and the lengths they will go to try and alleviate often excruciating pain. We still have a long way to go before this technology reaches patients," Jones added in a university statement.

The bio-glass consists of silica and a plastic or polymer called polycaprolactone. It displays cartilage-like properties such as flexibility, strength, durability and resilience.

It can be made in a biodegradable ink form, enabling the researchers to 3D print it into structures that encourage cartilage cells in the knee to form and grow -- a process that they have demonstrated in test tubes.

It also displays self-healing properties when it gets damaged, which could make it a more resilient and reliable implant and easier to 3D print when it is in ink form.​

London, May 15 (IANS) Researchers have found new evidence that humans were living in southern Arabia 10,000 years earlier than initially perceived.

The last Ice Age made much of the globe uninhabitable, but there were oases where people were able to cluster together and survive.

The findings, based on the study of a rare DNA lineage, showed that one of the oases existed in southern Arabia and modern humans dwelt in this territory during the last Ice Age also, known as the Pleistocene glaciation.

R0a -- the rare mitochondrial DNA lineage -- was found to be most frequent in Arabia and the Horn of Africa, said lead author Francesca Gandini, research fellow at the University of Huddersfield in Britain.

Also found was evidence for the movement of people in the R0a descent through the Middle East and into Europe indicating a likely trading network and a "gene flow" from Arabia into the territories that are now Iran, Pakistan and India.

Nearly 15,000 years ago when the Ice Age had receded, the people in this region disappeared.​

​London, May 15 (IANS) Researchers have identified a gene which causes inherited high cholesterol in the blood that can lead to premature heart disease, including cardiac attacks, strokes, narrowing heart valves and sudden death.

Familial hypercholesterolemia is a genetic condition that is associated with very high levels of low-density lipoprotein cholesterol (LDL-C) or "bad" cholesterol.

The findings showed that cholesterol-containing lipoprotein is the cause of a quarter of all diagnoses of familial hypercholesterolemia.

"Individuals diagnosed with familial hypercholesterolemia have higher levels of lipoprotein(a) in their blood than individuals without the diagnosis," said lead researcher Anne Langsted from the University of Copenhagen's Herlev Hospital in Denmark.

High levels of lipoprotein(a) in the blood add to the already very high risk of suffering a heart attack for people with familial hypercholesterolemia.

Also, individuals with familial hypercholesterolemia and high levels of lipoprotein(a) are five times more likely to suffer a heart attack than individuals without these two conditions.

"All individuals with familial hypercholesterolemia should have their lipoprotein(a) concentrations measured in order to identify those with the highest concentrations and, therefore, also the highest risk of suffering a heart attack," added one of the researchers Borge G. Nordestgaard, clinical professor at the University of Copenhagen.

The study will help identify the individuals with the highest risk of suffering a heart attack and hopefully facilitate better preventive treatment for these extremely high risk individuals," the researchers said in the paper published in the journal The Lancet Diabetes and Endocrinology​

New York, May 15 (IANS) Scientists have identified two statistically significant genetic variants that may lead to an increased risk of post-traumatic stress disorder (PTSD).

Post-traumatic stress disorder is a mental health condition triggered by experiencing or seeing a terrifying event.

"We found two notable genetic variants," said Murray.B.Stein, professor at University of California in the US.

"The first was in a gene (ANKRD55) on chromosome 5 and the other variant was found on chromosome 19," he added.

In previous research, this gene was also found to be associated with various autoimmune and inflammatory disorders, including multiple sclerosis, type II diabetes, celiac disease, and rheumatoid arthritis.

Also, a genetic overlap was observed between PTSD and rheumatoid arthritis and psoriasis, the researchers said.

The study, published online in JAMA Psychiatry, was conducted in a massive analysis of DNA samples from more than 13,000 US soldiers.

"Further research will be needed to replicate the genome-wide significant association we found with the gene ANKRD55 and clarify the nature of the added another researcher Robert.J.Ursano, professor at Uniformed Services University in the US.​