Knowledge Update

​New York, Dec 26 (IANS) Scientists have identified a link between Huntington's disease and dysfunction in a section of brain structures that are critical for movement and impulse control.

Huntington's disease is characterised by the progressive loss of nerve cells in the brain and affects approximately one in 10,000 people. This fatal disorder is caused by a hereditary defect in a single gene.

According to the study, led by researchers at the Northwestern University in Illinois, the disease is caused by a dysfunction in the subthalamic nucleus -- a component of the basal ganglia which is a group of brain structures critical for movement and impulse control.

The findings may explain the causes of the debilitating symptoms such as as loss of motor and cognitive function, depression and personality changes that typically manifest in adulthood, as well as loss of brain tissue as the disease progresses.

For the study, the researchers used genetically engineered mice to carry the Huntington's disease gene. They discovered that the electrical activity of the subthalamic nucleus was lost. 

Impaired subthalamic activity was caused by anomalous receptor signalling, leading to defective energy metabolism and accumulation of damaging oxidants. 

In addition, the abnormalities in the subthalamic nucleus was found to occur earlier than in other brain regions and that subthalamic nucleus nerve cells progressively degenerate as the mice age, mirroring the human pathology of Huntington's disease.

"Our findings suggest early problems in the subthalamic nucleus not only contribute to the symptoms of Huntington's disease, but are also likely to impair the processing capacity and health of other brain structures, more traditionally associated with the disease," said Mark Bevan, professor at Northwestern University. 

A better understanding of aberrant brain receptor signaling that leads to nerve cell dysfunction could reveal a target for therapy, the researchers said.

The study was published in the journal eLife.

London, Dec 26 (IANS) Listening to sounds such as music and noise has a significant effect on an individuals' moods and emotions, possibly as a result of brain dopamine regulation -- a neurotransmitter strongly involved in emotional behaviour and mood regulation, researchers have found.

However, the differences in dopamine receptors may drive the differences between individuals, the researchers said.

The study revealed that a functional variation in dopamine D2 receptor (DRD2) gene modulates the impact of music as opposed to noise on mood states and emotion-related prefrontal and striatal brain activity.

"Our results suggest that even a non-pharmacological intervention such as music might regulate mood and emotional responses at both the behavioural and neuronal level," said Elvira Brattico, Professor at Aarhus University in Denmark.

For the study, 38 healthy participants were recruited, with 26 of them having a specific "GG variant" of DRD2 and 12 a "GT variant". They underwent functional magnetic resonance imaging (fMRI) during performance of an implicit emotion-processing task while listening to music or noise.

The results showed that in participants with DRD2GG receptors the mood improved after music exposure, whereas in GT partipants mood deteriorated after noise exposure.

Moreover, the music, as opposed to noise environment, decreased the striatal activity of GT subjects as well as the prefrontal activity of GG subjects while processing emotional faces. 

These findings suggest that genetic variability of dopamine receptors affects sound environment modulations of mood and emotion processing, the researchers suggested. 

Importantly, these study encourages the search for personalised music-based interventions for the treatment of brain disorders associated with aberrant dopaminergic neurotransmission as well as abnormal mood and emotion-related brain activity, Brattico said, in the paper published in the journal Neuroscience.

​London, Dec 26 (IANS) If a recently proposed combination of three particular drugs is used, the devastating elephantiasis disease can be prevented or treated rapidly using fewer rounds of drugs, a new research has found.

Lymphatic filariasis -- commonly known as elephantiasis -- is a neglected tropical disease, which causes serious damage to the lymphatic system. 

A large proportion of the billion people living with the threat of transmission of this disabling parasitic disease is in India, Indonesia and Myanmar where the triple drug combination could be used, the researchers said.

"Our results show that this regimen could potentially overcome important issues plagued by elimination campaigns, by making elimination as a public health problem achievable in a few years," said first author of the study Mike Irvine from the University of British Columbia in Canada.

Lymphatic filariasis is caused by parasitic worms, and is transmitted to humans by mosquitoes.

Many people with the disease develop elephantiasis causing pain and profound disfigurement -- such as large swelling of the arms, legs or genitals -- and leading to permanent disability. 

These patients are not only physically disabled, but suffer mental, social and financial losses, contributing to stigma and poverty.

Currently, people with Lymphatic filariasis require multiple rounds of treatment -- but if the drugs ivermectin, diethylcarbamazine, and albendazole are used together recent clinical studies have shown that the drugs are more effective at killing the worms. 

The new modelling work - published in the journal The Lancet Infectious Diseases - showed that this meant that the number of rounds of mass drug administration needed to treat the disease may fall from many rounds to only two or three.

The models were developed at the University of Warwick in Britain, Erasmus Medical Centre in the Netherlands, and Notre Dame University in the US. 

All three models were in agreement in the effectiveness of the regimen in reducing the prevalence of disease. The researchers noted that more effective treatment with fewer drugs rounds is crucial in poorer countries where transmission is high but resources are low.

The World Health Organisation (WHO) has targeted the disease for elimination as a public health problem by the year 2020.

​London, Dec 26 (IANS) Your kid is most likely to exhibit fear or phobia about things or ideas, if his or her 'buddy' fears the same, a study has found.

The findings showed that children in close friends exhibit shared patterns of fear-related thoughts and they influence each other when discussing them together.

Apart from transmitting fears, friends also impart ideas about how to behave in fear-provoking situations.

"Our findings indicate that close friends may share negative thoughts and to some extent may maintain these thoughts," said lead author Jinnie Ooi, research associate at University of East Anglia (UEA) in Britain.

Further, children's fear-related thoughts do not necessarily become more negative when children discuss their fears with close friends who are more anxious, the study said. 

This supports the use of group therapy and may be useful information for parents concerned that exposure to more anxious children within group-based therapy may increase their child's anxiety, the researchers said.

School-based interventions aiming to reduce anxiety in primary school-aged children could instruct pairs of close friends to discuss and resolve their worries in a positive manner among each other.

"It may also be beneficial to ask children being treated for anxiety disorders to identify whether they have friends who may be influencing or maintaining their negative thoughts.

"It may subsequently be useful for them to be given strategies for how to discuss these thoughts with peers in an adaptive way," Ooi added.

In addition, gender pair type predicted change in children's fear responses over time. 

Boys together became more afraid after discussing threatening animals, while girls appeared to make each other feel better when talking, the researchers noted. 

The study was published in the journal Behaviour Research and Therapy.

​Dubai, Dec 25 (IANS/WAM) A new council has been formed to reinforce the United Arab Emirates policies and strategies on climate change, and environmental and sustainable development.

London, Dec 25 (IANS) Using ultrafast imaging of moving energy, scientists have determined the speed of photosynthesis.

The study said the imaging could help scientists better understand the process and how it could be copied for producing fuels.

Earlier, it was believed that the process of charge separation in the reaction was the slowest step in the process. But scientists have shown that the slowest step is in fact the process through which the plants harvest light and transfer its energy through the antennae to the reaction centre.

"We can now see how nature has optimised the physics of converting light energy to fuel, and can probe this process using our new technique of ultrafast crystal measurements," said Jasper van Thor from Imperial College, London.

"For example, is it important that the bottleneck occurs at this stage, in order to preserve overall efficiency? Can we mimic it or tune it to make artificial photosynthesis more efficient? These questions, and many others, can now be explored," Thor added.

Scientists used lasers to cause reactions in crystals of Photosystem II -- enzyme that uses the light energy to split water into oxygen and hydrogen -- and then measured in space and time the movement of excitations of electrons.

"The resulting movie of the movement of excited electrons across minute sections of the system revealed where energy is held and when it is passed along," the study noted.

The study was published in the journal Nature Communications.

​New York, Dec 25 (IANS) US researchers claim to have found the risk factors associated with adults having mental illness becoming victims or perpetrators of violence.

Previous study found that almost one-third of adults with mental illness were likely to be victims of violence within a six-month period.

The study found that factors such as homelessness, in-patient mental-health treatment, psychological symptoms of mental illness, substance use and as victims or perpetrators of violence are both indicators and outcomes -- that is, they can act as both causes and effects.

"We found that all of these indicators mattered, but often in different ways," said Sarah Desmarais, Associate Professor at North Carolina State University in the US.

"For example, drug use was a leading indicator of committing violence, while alcohol use was a leading indicator of being a victim of violence," Desmarais added.

However, the researchers also found that affective symptoms -- category of psychological symptoms -- were also closely associated with violence.

"By affect, we mean symptoms including anxiety, depressive symptoms and poor impulse control. The more pronounced affective symptoms were, the more likely someone was to both commit violence and be a victim of violence," Desmarais noted.

The study highlights the importance of interventions to treat mental-health problems in order to reduce community violence and instances of mental-health crises.

"By treating people who are exhibiting these symptoms, we could reduce violence. Just treating drug or alcohol use - which is what happens in many cases - isn't enough. We need to treat the underlying mental illness that is associated with these affective symptoms," Desmarais said, in the paper appearing in the journal Psychological Medicine.

New York, Dec 25 (IANS) Driverless cars can save fuel if they trail each other in large platoons, as they will experience less aerodynamic drag when they drive close together, researchers have found.

But formation of a vehicle platoon could be time consuming.

The study by the researchers at Massachusetts Institute of Technology (MIT) that was recently presented at the International Workshop on the Algorithmic Foundations of Robotics suggested that relatively simple, straightforward schedules may be the optimal approach for saving fuel and minimising delays for autonomous vehicle fleets.

The findings may also apply to conventional long-distance trucking and even ride-sharing services.

"Ride-sharing and truck platooning and even flocking birds and formation flight, are similar problems from a systems point of view," said Sertac Karaman, Associate Professor at MIT.

"People who study these systems only look at efficiency metrics like delay and throughput. We look at those same metrics, versus sustainability such as cost, energy, and environmental impact. This line of research might really turn transportation on its head," Karaman added.

The research noted that for truck-driving -- particularly over long distances -- most of a truck's fuel is spent on trying to overcome aerodynamic drag, that is, to push the truck through the surrounding air.

"Scientists have previously calculated that if several trucks were to drive just a few metres apart, one behind the other, those in the middle should experience less drag, saving fuel by as much as 20 per cent, while the last truck should save 15 per cent -- slightly less, due to air currents that drag behind," the study found.

As the number of vehicles are increased in the platoon, more energy can be collectively saved but it may cost in terms of time it takes to form a platoon.

The study found that the simplest policies resulted in least delays in platoon formation while saving most fuel.

"Time tables set to deploy platoons at regular intervals were more sustainable and efficient than those that deployed at more staggered times," the study mentioned.

​London, Dec 25 (IANS) British researchers have discovered a new genetic disease which results in neuro-degeneration and help find treatments for brain ageing conditions, such as Alzheimer's, Huntington's and Parkinson's.

The study revealed that the disease -- ataxia oculomotor apraxia type XRCC1 -- is caused by a genetic mutation that disrupts the repair of our DNA.

The study showed that when single strands of our DNA are damaged, a genetic mutation in a gene called XRCC1 causes a vital DNA-repairing enzyme (known as PARP1) in our bodies to over-activate.

In people suffering from the new disease, the speeding up of this key enzyme actually triggers the death of brain cells, the researchers said.

"Discovering this new disease and its cause is a huge step towards developing drug-based therapies for other rare neurodegenerative conditions," said lead author Keith Caldecott, Professor at University of Sussex.

"Drugs which target this key DNA repairing enzyme in the right way, could prove vital for treating people suffering from diseases caused by the over-activation of this protein - it is now crucial we determine what diseases these are.

Single strand breaks are one of the most common types of DNA damage and the researchers believe it's possible the discovery of this new genetic disease could be important for scientists researching other rare DNA repair related diseases.

The details appeared in the journal Nature.

​New York, Dec 25 (IANS) Researchers have identified a genetic immune disorder characterised by increased susceptibility and poor immune control of Epstein-Barr virus (EBV) and, in some cases, an EBV-associated cancer called Hodgkin's lymphoma.

The researchers studied two unrelated sets of siblings with similar immune problems and determined their symptoms were likely caused by a lack of CD70, a protein found on the surface of several types of immune cells.

Scientists at the US National Institute of Allergy and Infectious Diseases (NIAID), part of the US National Institutes of Health (NIH), conducted the research with an international team of collaborators.

Both sets of siblings had evidence of uncontrolled infection with EBV, a common and usually mild virus, which resulted in the development of Hodgkin's lymphoma in three of these children.

Each child also had other immune symptoms, such as reduced activity of pathogen-fighting T cells, low production of antibodies and poor activation of antibody-producing B cells.

The researchers analysed the genomes of all four children and found that each had two mutated copies of the CD70 gene, resulting in nonfunctioning or nonexistent CD70 proteins.

All four parents, who had healthy immune systems, had only one copy of the mutation--indicating that CD70 deficiency follows an autosomal recessive pattern of inheritance.

This means affected individuals receive a flawed gene from each parent in order to have symptoms.

While no specific treatment for CD70 deficiency currently exists, each of the four children has recovered from Hodgkin's lymphoma and is receiving antibody infusions to help bolster the immune system, the researchers recently reported in the Journal of Experimental Medicine.