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Comment by Dr. Krishna Kumari Challa on December 18, 2015 at 8:12am

Here is some good news for science communicators:

Stephen Hawking launches medal for science communication

Renowned British cosmologist Stephen Hawking on Wednesday launched an award for science communication that will bear his name.

The "Stephen Hawking Medal for Science Communication" will be awarded to those who help promote science to the public through media such as cinema, music, writing and art.

"People worldwide display an incredible appetite of scientific information... The public want to know, they want to understand."

The first medals will be awarded next summer in three different categories: the scientific, artistic and film communities.

The winners will be announced at the Starmus Festival, a gathering celebrating art and science in Spain's Canary Islands that will take place from June 27 to July 2 next year.

Comment by Dr. Krishna Kumari Challa on December 18, 2015 at 7:54am

This year's top science stories:

7. The discovery that Alzheimer's protein behaves like a prion; Why?

Under some conditions, an Alzheimer’s-related protein may have jumped between people, scientists reported this year. If true, that observation, the first of its kind, could recast the way scientists view the disease.

Scientists already had hints that the protein in question, amyloid-beta, behaves like an infectious prion, a misshapen protein that coaxes other proteins to misfold and spread from cell to cell. In a study reported in Nature, Collinge and colleagues found A-beta buildup in four of eight postmortem brains from people who had received growth hormone injections derived from cadavers. Because A-beta buildup is rare in relatively young people — all were between the ages of 36 and 51 — the finding suggests that the buildup might have been seeded by growth hormone contaminated with A-beta.

This result adds to evidence that prions may be behind Alzheimer’s disease as well as other neurodegenerative disorders such as Parkinson’s and Huntington’s. But some scientists caution that it’s too soon to label these disorders as prion diseases.

8. The genetics of cancer; Why?

Personalized genomics has been heralded as the next big weapon in the war on cancer. But researchers analyzing various tissue types this year, looking for mutations linked to the disease, have found that not all genetic alterations should be targeted equally.

Genetic profiles of tumors offer unprecedented opportunities for both cancer diagnostics and for doctors planning treatment. Bowel cancer tumors with mutations in the KRAS gene, for example, respond poorly to the drug cetuximab; the skin cancer drug vemurafenib works only if melanomas have a particular mutation in the BRAF gene.

But such genetic testing can be misleading if it isn’t conducted alongside tests of healthy cells from the same person. A vast analysis comparing the genetic profiles of tumors and normal tissue of more than 800 cancer patients  found that nearly two-thirds of mutations in the studied tumors — many of which might be used to guide treatment — also showed up in patients’ healthy tissues . For those patients, the mutations were probably just benign variants unrelated to the cancer. Analyzing healthy tissue can also reveal whether mutations found in tumors are heritable or not, scientists say, which is important for deciding whether a cancer patient’s family should receive genetic counseling.

Complicating matters further is the fact that even mutations that have been linked to cancer will not always manifest as cancer. A study published in May examining eyelid skin discovered numerous cancer-associated mutations in normal, healthy patches of the skin . Detecting these mutations might lead to great anxiety and unnecessary, sometimes invasive treatments.As genetic testing of tumors becomes more widespread, best practices will emerge, as will a better understanding of the disease. Therefore, scientists working in the field are trying to change the way we look at cancer.

Comment by Dr. Krishna Kumari Challa on December 18, 2015 at 7:27am

This year's top science stories:

4. Understanding why life got so complicated; why?

Microbes discovered in Arctic mud could be the closest relatives yet found to the single-celled ancestor that swallowed a bacterium and made life so complicated. Biologists have proposed that this swallowing event, perhaps 1.8 billion years ago, led to complex cells with membrane-wrapped organelles, the hallmark of all eukaryotes from amoebas to zebras.

Researchers discovered the new phylum of microbes, dubbed Lokiarchaeota, by screening DNA from sediment . Though no one has identified an actual cell yet, the new phylum appears to mingle genes similar to those in modern eukaryotes and genes from archaea, the sister group to bacteria. Analyses suggest the cells have dynamic structures that could have engulfed bacteria long ago. (Biologists have proposed representing that merger as a ring of life, rather than a tree.) What happened next in the tale is clearer but still a puzzle.

5. New light on Quantum Spookiness; Why?

Some loopholes no longer plague a crucial test for assessing the weirdness of quantum mechanics. Experiments reported in 2015 definitively demonstrate that the quantum world violates locality, the principle that events sufficiently separated in spacetime must be independent.

European researchers this year performed an experiment with electrons on opposite sides of a university campus, nearly 1.3 kilometers apart. In trials lasting 18 days, the team coaxed the electrons into an entangled state 245 times, reliably measuring the electrons’ spins every time. The results showed a clear nonlocal connection.

6. Epigenome effect; Why?

This yea,r Researchers cataloged how chemical modifications fold, compress and unwind the static DNA over time and how those modifications control when genes are on or off. The researchers cataloged epigenetic marks — chemical modifications either of DNA itself or proteins called histones — in more than 100 types of human cells. The epic effort revealed that gene variants associated with Alzheimer’s disease are more active in immune cells in the brain than in nerve cells as researchers had assumed. Another interesting aspect of this research:Tightly packed areas of the genome are more vulnerable to cancer-causing mutations.

Researchers using data from this project and other efforts to view the genome in 3-D have made startling discoveries . For instance, researchers found that a gene called FTO, thought to be a major genetic contributor to obesity, isn’t involved in fat production. Instead, a genetic variant hiding in the gene’s vicinity actually determines what type of fat the body builds . Disorganized DNA may be a cause of aging, researchers also discovered .

Comment by Dr. Krishna Kumari Challa on December 18, 2015 at 7:23am

This year's top science stories:

1. Gene-editing; why? Read it here:

http://kkartlab.in/group/some-science/forum/topics/crispr-cas9-gene...

2. Biological aging; why?

A study, out of Duke University, analyzed the health of nearly one thousand 38-year-olds and found that some resembled people a decade older while others appeared years younger. Researchers determined this “biological age” based on health indicators such as body mass index, blood pressure and cholesterol level. The finding tapped into a mystery that has long captivated scientists and the public alike — “why some people can live to 120 with no disease, and others are already in bad shape at age 70”.

3. Irreproducibility problem; why?

Because scientists understood the problem and are trying to rectify it.

Experimental results that don’t hold up to replication have caused consternation among scientists for years, especially in the life and social sciences. In 2015 several research groups examining the issue reported on the magnitude of the irreproducibility problem. The news was not good.

Results from only 35 of 97 psychology experiments published in three major journals in 2008 could be replicated, researchers reported in August. The tumor-shrinking ability of the cancer drug sunitinib was overestimated by 45 percent on average, an analysis published in October showed . And a report in June found that, in the United States alone, an estimated $28 billion is spent annually on life sciences research that can’t be reproduced .

There are many possible reasons for the problem, including pressure to publish, data omission and contamination of cell cultures. Faulty statistics are another major source of irreproducibility, and several prominent scientific journals have set guidelines for how statistical analyses should be conducted. Very large datasets, which have become common in genetics and other fields, present their own challenges: Different analytic methods can produce widely different results, and the sheer size of big data studies makes replication difficult.

Perfect reproductions might never be possible in biology and psychology, where variability among and between people, lab animals and cells, as well as unknown variables, influences the results. But several groups, including the Science Exchange and the Center for Open Science, are leading efforts to replicate psychology and cancer studies to pinpoint major sources of irreproducibility.

Although there is no consensus on how to solve the problem, suggestions include improving training for young scientists, describing methods more completely in published papers and making all data and reagents available for repeat experiments.

Comment by Dr. Krishna Kumari Challa on December 17, 2015 at 6:41am

Confirmation bias is bad for science. For example consider this conversation between an alchemist and  a scientist:

Alchemist: "Hoo doo woodoo doo!" (Mixes an element to form a compound while waving his hands mystically)

Scientist: "What're you doing?"

Alchemist: "I'm making a healing salve."

Scientist: "You don't need to wave your arms about, mixing those chemicals is all you need to do to make a local anaesthetic."

Alchemist: "But I waved my arms and it worked!"

Scientist: "Really?"

Alchemist: "Yes, my waving hands has magical influence that makes the drug work!"

Scientist: This is ignorance at its best!

This is what we call confirmation bias. We look for the things that fit our idea of how things work.

Comment by Dr. Krishna Kumari Challa on December 17, 2015 at 6:01am

What causes changes in speed of Earth's rotation? Rising sea levels!

The connection is through the change in the speed of Earth’s rotation. Meltwater from glaciers not only causes sea levels to rise, but also shifts mass from the pole to the equator, which slows down the rotation. (Picture the Earth as a spinning figure skater. The skater moves his or her arms in to spin more quickly or out to slow down.) The gravity pull from the Moon also contributes to the slowdown, acting a little like a lever brake. However, the combination of these effects is not enough to explain the observations of the slowing down of Earth’s rotation: a contribution from Earth’s core must be added.

Over the past 3,000 years, the core of the Earth has been speeding up a little, and the mantle-crust on which we stand is slowing down. As a consequence of Earth rotating more slowly, the length of our days is slowly increasing. In fact, a century from now, the length of a day will have increased by 1.7 milliseconds. This may not seem like much, but  note that this is a cumulative effect that adds up over time.

Based on their work reconciling these discrepancies, the scientists involved in the study are confident in predicting sea levels to the end of the 21^st century. This can help to better prepare coastal towns, for example, to cope with climate change.

The findings, “Reconciling past changes in Earth’s rotation with 20^th century global sea-level rise: Resolving Munk’s enigma,” were published in the Dec. 11 issue of the journal Science Advances.

The lead author of the study is Mathieu Dumberry, a professor in the Dept. of Physics  at the University of Alberta.

Comment by Dr. Krishna Kumari Challa on December 16, 2015 at 10:05am

Dead people tell no tales — but dead people’s microbes do.

Bacteria, fungi and worms living in the soil beneath a decomposing body can help reveal the time — and place — of death, scientists report December 10 in Science.

Researchers have tracked the comings and goings of cadaver microbes before, but the new study is the most comprehensive survey yet. For months, microbial ecologist Jessica Metcalf of the University of Colorado Boulder and colleagues tallied up microbes on and near dead mice and humans.

As bodies decayed, similar microbes cropped up like clockwork, even on different soil types and during different seasons of the year, the team found. The microbes were so predictable that researchers could estimate the time of death (within a few days) of a body that had been dead for about a month.

And because telltale microbes stayed in the soil long after a body had been moved, they could offer investigators clues about potential crime scenes, the team suggests.

 http://www.sciencemag.org/content/early/2015/12/09/science.aad2646

Comment by Dr. Krishna Kumari Challa on December 16, 2015 at 9:47am

The route followed by Hepatitis C to escape our Immune System :
A high proportion of hepatitis C-infected individuals develop chronic infections, suggesting that hepatitis C can subvert host antiviral responses.
The innate immune system, the body's first line of defence, is known to depend on the transcription factor nuclear factor κB (NF-κB). Its activation requires the ubiquitylation of upstream proteins including the adaptor protein NEMO (NF-κB essential modulator). Hepatitis C is one of many infectious pathogens that survive by inhibiting NF-κB signaling in host cells. Normally, the inflammatory cytokine tumor necrosis factor-α (TNF-α) induces antiviral innate immune responses by stimulating NF-κB through a cascade of signaling events. However patients with chronic hepatitis C infections have increased serum amounts of TNF-α, but have ineffective immune responses due to the inhibited NF-κB activation. The researchers hypothesized that the inhibition of TNF-α–induced NF-κB activation might be mediated by a viral protein expressed during hepatitis C infection. They used a luciferase reporter assay to screen which viral protein suppresses TNF-α–induced NF-κB activation and found that NS3 was sufficient to block NF-κB signaling in cells. Co-immunoprecipitation and immunofluorescence staining experiments showed that NS3 directly interacted with the linear ubiquitin chain assembly complex (LUBAC). More detailed domain mapping experiments showed that NS3 is bound to the ZnF-RBZ domain of HOIP (HOIL-1L–interacting protein; also known as RNF31), which is the same domain in LUBAC that binds to NEMO. To investigate the role of NS3 binding to HOIP, the researchers performed competitive coimmunoprecipitation experiments. They found that overexpression NS3 disrupted the interaction between HOIP and NEMO in a concentration-dependent manner. NS3 directly interacted with LUBAC, competed with NEMO for binding to LUBAC, and inhibited the LUBAC-mediated linear ubiquitylation of NEMO as well as the subsequent activation of NF-κB. The results highlight a novel immune evasion strategy adopted by hepatitis C to modulate host antiviral responses and enhance virus survival and persistence.
http://stke.sciencemag.org/content/8/403/ra118

Comment by Dr. Krishna Kumari Challa on December 16, 2015 at 9:38am

Arsenic release metabolically limited to permanently water-saturated soil
Scientists have solved the mystery of where the microbes responsible for releasing dangerous arsenic into groundwater in Southeast Asia get their food. Their findings, published Nature Geosciences, could guide future land management and future development. Groundwater in South and Southeast Asia commonly contains concentrations of arsenic 20 to 100 times greater than the World Health Organization's recommended limit, resulting in more than 100 million people being poisoned by drinking arsenic-laced water in Bangladesh, Cambodia, India, Myanmar, Vietnam and China. Arsenic is bound to iron oxide compounds in rocks from the Himalayas, and gets washed down the major rivers and deposited in the lowland basins and deltas. Scientists know that in the absence of oxygen, some bacteria living in those deposited sediments can use arsenic and iron oxide particles as an alternative means of respiration. When they do this, however, the microbes separate the arsenic and iron oxides and transfer the toxin into underlying groundwater. The mystery in this system, though, is an obvious source of energy that the microbes can tap to fuel the separation process.
The scientists hypothesized that bacteria residing in the shallow layers of seasonal wetlands were eating all of the digestible plant material during dry periods, when sediments are exposed to air and the microbes have access to oxygen. As a result, no food is left for the microbes when the floods returned, rendering them unable to cleave arsenic particles from iron oxides.
The same experiment repeated with samples taken from about 100 feet underground—the depth of most drinking wells in Asia—showed that bacteria living deep beneath permanent and seasonal wetlands are similarly limited and and do not release arsenic into groundwater under normal conditions. The careful sleuthing has identified the bacteria in the permanent wetlands as the primary culprit of arsenic release. The work suggests that, under normal conditions, microbes in seasonal wetlands don't pose a significant threat for adding arsenic to groundwater. But what if the conditions changed ?
To answer this question, the team conducted a second type of experiment, in which they simulated the conversion of a small, remote seasonal wetland into a permanent one by digging out a seasonal wetland plot and keeping it permanently filled with water. As predicted, this resulted in the release of arsenic. (The amount was small and transient and people were never threatened by the experiment.) The findings have large-scale implications for projecting changes in arsenic concentrations with land development in South and Southeast Asia and for the terrestrial carbon cycle.
http://www.nature.com/ngeo/journal/vaop/ncurrent/full/ngeo2589.html

Comment by Dr. Krishna Kumari Challa on December 16, 2015 at 9:32am

Pesticide In Milk Associated With Parkinson’s Disease: Exposure to a pineapple pesticide via milk intake has been linked to an increased incidence of Parkinson’s in Japanese men.
A pesticide used prior to the early 1980s and found in milk at that time may be associated with signs of Parkinson's disease in the brain, according to a study published in Neurology.
For the study, 449 Japanese-American men with an average age of 54 who participated in the Honolulu-Asia Aging Study were followed for more than 30 years and until death, after which autopsies were performed. Tests looked at whether participants had lost brain cells in the substantia nigra area of the brain, which occurs in Parkinson's disease and can start decades before any symptoms begin. Researchers also measured in 116 brains the amount of residue of a pesticide called heptachlor epoxide. The pesticide was found at very high levels in the milk supply in the early 1980s in Hawaii, where it was used in the pineapple industry. It was used to kill insects and was removed from use in the US around that time. The pesticide may also be found in well water. The study found that non-smokers who drank more than two cups of milk per day had 40 percent fewer brain cells in that area of the brain than people who drank less than two cups of milk per day. For those who were smokers at any point, there was no association between milk intake and loss of brain cells. Previous studies have shown that people who smoke have a lower risk of developing Parkinson's disease. Residues of heptachlor epoxide were found in 90 percent of people who drank the most milk, compared to 63 percent of those who did not drink any milk. Abbott noted that the researchers do not have evidence that the milk participants drank contained heptachlor epoxide. He also stated that the study does not show that the pesticide or milk intake cause Parkinson's disease; it only shows an association.
http://www.neurology.org/content/early/2015/12/09/WNL.0000000000002254

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