Daily Archives: January 16, 2015

Astronaut to spend one year in space

Posted: January 16, 2015 at 4:46 pm

Story highlights Astronaut Scott Kelly to live in space one year Kelly's twin brother, Mark, will take part in a "twins study" from the ground

A year is a long time to stay anyplace. But staying a year in space has some special challenges.

There's what to pack: How many changes of clothes do you bring?

Kelly says NASA supplies most of what he needs but he's taking his own tool pouch, some sweatshirts and special shoes to use when he's lifting weights.

"I bought a special kind of shoes I thought would be better for that," Kelly said at a NASA briefing on Thursday.

Then there's what to do for a year in space. You get a great view of Earth, so the scenery is amazing. But the space station orbits Earth about every 90 minutes, or about 16 times a day. Could get a little repetitive. So how do you keep from getting bored?

Experiments. Lots and lots of experiments. NASA says space station crews normally work on about 200 experiments over six months, but Kelly will be doing many more. He says he's actually fascinated with the space station itself as a giant experiment in living in space.

"Building this facility that allows us to understand how to operate for long periods of time in space to allow us someday to go to Mars."

In his free time Kelly says he'll spend a lot of time talking to people on Earth, messaging on social media, reading email, watching TV and writing.

"I'm going to keep a personal journal of the experience," Kelly said. He also will share some of his journal with researchers studying the psychological impacts of long-term space flight. Will he tell all?

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1-Year Space Station Mission May Pave NASA's Way to Mars

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The first crew to embark on a yearlong International Space Station mission could help NASA get to Mars.

NASA astronaut Scott Kelly and Russian cosmonaut Mikhail Kornienko will launch to the space station in March with cosmonaut Gennady Padalka. Kornienko and Kelly will remain on the orbiting outpost performing research until March 2016. This mission will mark the first time a crew has spent a continuous year on the space station, and researchers are planning to take advantage of it. Scientists and doctors on the ground will monitor the way Kelly and Kornienko's bodies change throughout the year in order to understand the potential effects of long-term spaceflight (like a mission to Mars) more fully.

"As a test pilot and as an engineer, what fascinates me is the space station as a whole experiment," Kelly said during a news conference yesterday (Jan. 15). "Traveling around Earth at 17,500 mph in a vacuum, extremes of temperature and pressure, building this facility that allows us to understand how to operate for long periods of time in space to allow us someday to go to Mars." [Most Extreme Human Spaceflight Records]

Astronauts will likely need to spend more than a year in weightlessness if flying to Mars. The kind of research that Kornienko and Kelly are expected to perform in orbit could be a first step toward understanding how to mitigate any harmful changes the body might go through during a long trip in space.

NASA officials have a good sense of how the body behaves when exposed to the rigors of spaceflight for up to six months, but after that, the data is a little hazy.

Kelly will be the first American to spend a full year in space, however, Kornienko will not be the first cosmonaut to do so. A number of Russians spent a continuous year on the Mir space station in the 1980s and 1990s.

"We know a lot about six months, but we know almost nothing about what happens between six and 12 months in space," Julie Robinson, a space station program scientist, said during the news conference yesterday. Kelly and Kornienko's one-year mission is designed to help fill in the gaps between what the body experiences after six months versus what it experiences after one year.

Kornienko and Kelly's eyes will be monitored for any changes to their eyesight or ocular health during the mission, NASA officials said. Astronauts have noticed changes in intracranial pressure due to fluid shifts that can result in possibly negative changes to the eyes, scientists have said.

Scientists are also interested in monitoring the microbial environment (microbiome) inside the crewmembers, keeping tabs on their physical performance, fine motor skills, metabolism and other health factors throughout the mission.

Cosmic Quiz: Do You Know the International Space St...

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As Musk goes to Mars, Bezos heads to Hollywood

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Nothing feeds Wall Streets appetite like the prospect of conquering China or Mars.

That is why Teslas TSLA, +0.63% Elon Musk, who hums with electric cars and eclectic daydreams, had such a strange week. Teslas China sales were down, but Mars is looking up.

Like Marco Polo, lets write about China first.

Without offering much in the way of numbers or reasons, Musk said Teslas business in China had declined significantly. He dismissed the country, which holds the hope of business everywhere, as little more than wild card. That was about as detailed as Musk, who incidentally fancies himself a mythic visionary, got on the future of China. How bad is that? Marco Polo spoke with more nuanced characterization about China and that was eight hundred years ago.

In terms of Mars, though, Musk is full of ... specifics.

This week we learned that Musks portal to his intended colonization of Mars will run through the cradle of pretentious coffee. To settle Mars, Musk will first send a drove of engineers in Seattle, home of Starbucks SBUX, +1.29%

What in the wide, wide world of narcissism is it about entrepreneurs and space?

On this note, lets give Musk a break. With oil prices falling, average Americans are about as likely to buy electric cars as they are to swear off Cheez Whiz. Instead, lets talk Virgins VA, +0.56% entrepreneurial whiz Richard Branson Sir Richard to you.

But first, speaking of oil, lets give Mikhail Prokhorov a moment. Reacting to oil-driven currency issues in his home country, the Russian oligarch decided to put the Brooklyn Nets up for sale. What could this lead to? If oil drops any further, Vladimir Putin may be forced to list the Ural Mountains on eBay EBAY, +1.22%

Now back to space. Branson is currently peddling the concept of space tourism hard, despite the November death of one of his test pilots.

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UN message to Israelis, Palestinians: Stop downward spiral

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United Nations UN Secretary-General Ban Ki-moon is alarmed that Israelis and Palestinians are engaged in a downward spiral of actions and counter actions and calls on both sides not to exacerbate existing divisions, a senior UN official said Thursday.

Israel is withholding critical tax revenue and seeking ways to prosecute Palestinian leaders for war crimes in retaliation for Palestinian moves to join the International Criminal Court (ICC).

"We call on Israel to immediately resume the transfer of tax revenues," UN deputy political affairs chief Jens Anders Toyberg-Frandzen told the Security Council. "The Israeli-Palestinian conflict is now entering unchartered territory, which, lamentably, seems to have dashed any immediate hope for a return to peace talks."

The council's monthly meeting on the Middle East was the first on the Israeli-Palestinian conflict since the failure last month of a Palestinian statehood bid at the United Nations Security Council.

Chief Palestinian delegate Riyad Mansour said his government was undeterred.

"In spite of this setback, we will continue to approach the Security Council," he said without elaborating. The Palestinians will become full ICC members on April 1.

Mansour called the withholding of Palestinian tax revenues a "blatant act of reprisal and theft of Palestinian funds" and condemned Israel's "rabid settlement colonization."

Israel has condemned Palestinian moves, with Ambassador Ron Prosor accusing Palestinians of "running away from negotiations" and obstructing the peace process.

The ICC move paves the way for the court to take jurisdiction over alleged crimes committed in Palestinian lands and investigate the conduct of Israeli and Palestinian leaders. Neither Israel nor the United States is an ICC member.

The United States has suggested some $400 million in aid could now be in jeopardy.

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Genetic Engineering Process – Video

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Genetic Engineering Process
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What drives killers like the Ottawa or Paris attackers?

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IMAGE:Violence and Gender is the only peer-reviewed journal focusing on the understanding, prediction, and prevention of acts of violence. Through research papers, roundtable discussions, case studies, and other... view more

Credit: Mary Ann Liebert, Inc., publishers

New Rochelle, NY, January 15, 2015-Zehaf-Bibeau, the Islamist convert who recently killed a Canadian military reservist on duty in Ottawa, Canada, represents a type of attacker rarely discussed--a person so obsessed with an overvalued idea that it defines their identity and leads them to commit violence without regard for the consequences. Although it appears that the assailants in Paris had more ties with terrorist organizations, the individuals still fit the description of people acting on overvalued ideas. This emerging, and likely growing phenomenon is explored in the article, published in the Perspectives section of the journal, "Lone Wolf Killers: A Perspective on Overvalued Ideas," published in the peer-reviewed journal Violence and Gender, from Mary Ann Liebert, Inc., publishers.

The article is available free on the Violence and Gender website.

Author Matthew H. Logan, PhD, a 28-year veteran officer with the Royal Canadian Mounted Police (RCMP), as well as an RCMP Criminal Investigative Psychologist (ret.), Ontario, Canada, explains that these killers do not always work alone, stating that "in the future I believe we will see more 'packs' of these wolves as they unite on common beliefs and themes."

"The violence we witnessed in Paris just days ago shook the world," says Violence and Gender Editor-in-Chief Mary Ellen O'Toole, PhD, Forensic Behavioral Consultant and Senior FBI Profiler/Criminal Investigative Analyst (ret.). "It was coldblooded, purposeful, and seemingly without remorse, driven by a unique self-righteous ideation of the killers. Dr. Matt Logan explains the 'motivating mindset' of young male offenders, sometimes loners and sometimes part of a group, whose 'overvalued ideas' combined with their own psychopathology is what motivates them to engage in this type of terror. 'Overvalued ideas do not constitute mental illness,' according to Dr. Logan, which makes this senseless, savage violence seem even more chilling and despicable."

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About the Journal

Violence and Gender is the only peer-reviewed journal focusing on the understanding, prediction, and prevention of acts of violence. Through research papers, roundtable discussions, case studies, and other original content, the Journal critically examines biological, genetic, behavioral, psychological, racial, ethnic, and cultural factors as they relate to the gender of perpetrators of violence. Led by Editor-in-Chief Mary Ellen O'Toole, PhD, Forensic Behavioral Consultant and Senior FBI Profiler/Criminal Investigative Analyst (ret.), Violence and Gender explores the difficult issues that are vital to threat assessment and prevention of the epidemic of violence. Violence and Gender is published quarterly online with Open Access options and in print, and is the official journal of The Avielle Foundation. Tables of content and a sample issue may be viewed on the Violence and Gender website.

About the Publisher

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What drives killers like the Ottawa or Paris attackers?

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New genetic clues found in fragile X syndrome

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Scientists have gained new insight into fragile X syndrome -- the most common cause of inherited intellectual disability -- by studying the case of a person without the disorder, but with two of its classic symptoms.

In patients with fragile X, a key gene is completely disabled, eliminating a protein that regulates electrical signals in the brain and causing a host of behavioral, neurological and physical symptoms. This patient, in contrast, had only a single error in this gene and exhibited only two classic traits of fragile X -- intellectual disability and seizures -- allowing the researchers to parse out a previously unknown role for the gene.

"This individual case has allowed us to separate two independent functions of the fragile X protein in the brain," said co-senior author Vitaly A. Klyachko, PhD, associate professor of cell biology and physiology at Washington University School of Medicine in St. Louis. "By finding the mutation, even in just one patient, and linking it to a partial set of traits, we have identified a distinct function that this gene is responsible for and that is likely impaired in all people with fragile X."

The research, appearing in the Proceedings of the National Academy of Sciences (PNAS) Online Early Edition in December and in the print issue Jan. 5, is by investigators at Washington University and Emory University School of Medicine in Atlanta.

In studying fragile X, researchers' focus long has been on the problems that occur when brain cells receive signals. Like radio transmitters and receivers, brain cells send and receive transmissions in fine tuned ways that separate the signals from the noise. Until recently, most fragile X research has focused on problems with overly sensitive receivers, those that allow in too much information. The new study suggests that fragile X likely also causes overactive transmitters that send out too much information.

"The mechanisms that researchers have long thought were the entirety of the problem with fragile X are obviously still very much in play," Klyachko said. "But this unique case has allowed us to see that something else is going on."

The finding also raises the possibility that drugs recently tested as treatments for fragile X may be ineffective, at least in part, because they only dialed down the brain's receivers, presumably leaving transmitters on overdrive.

Fragile X syndrome results from an inherited genetic error in a gene called FMR1. The error prevents the manufacture of a protein called FMRP. Loss of FMRP is known to affect how cells in the brain receive signals, dialing up the amount of information allowed in. The gene is on the X chromosome, so the syndrome affects males more often and more severely than females, who may be able to compensate for the genetic error if their second copy of FMR1 is normal.

Patients with fragile X have a range of symptoms. One of the mysteries of the syndrome is how loss of a single gene can lead to such a variety of effects in different patients. Some patients are profoundly intellectually disabled, unable to talk or communicate. Others are only mildly affected. Patients often experience seizures, anxiety and impulsive behavior. Typical physical symptoms include enlarged heads, flat feet and distinctive facial features. Almost one-third of patients with fragile X also show symptoms of autism spectrum disorders.

To gain insight into what else FMRP might do, the researchers plumbed genetic sequencing data from more than 900 males with intellectual disabilities but without classic fragile X syndrome. They looked for mutations in the FMR1 gene that might impair the protein but not eliminate it entirely. Even in this relatively large sample size, they only found one patient with abnormal FMRP, resulting from a change in a single letter of the gene's DNA code.

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Baylor College of Medicine scientist identify a novel precursor to neurodegeneration

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HOUSTON -- (Jan. 15, 2015) - Alteration of lipid metabolism in brain cells promotes the formation of lipid droplets that presage the loss of neurons, said researchers from Baylor College of Medicine and the Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital in a report that appears online in the journal Cell.

Neuroscience graduate student Lucy Liu, and Dr. Hugo Bellen, professor of molecular and human genetics, neuroscience, a Howard Hughes Medical Institute investigator and director of the Graduate Program in Developmental Biology at Baylor connected the presence of lipid droplet accumulation in the glia of specific mutants as a harbinger of neurodegeneration.

Fruit fly genetics

The Bellen lab uses fruit fly mutants of evolutionarily conserved genes that lead to neurodegeneration in human patients to dissect the molecular mechanisms that underlie the demise of neurons. The fruit flies carry mutations in genes that have human homologs that cause Leigh syndrome, Charcot-Marie-Tooth type 2A2 and ARSAL (autosomal recessive spastic ataxia with leukoencephalopathy). All of these mutations affect the function of the mitochondria, the powerhouse of the cell.

Lipid droplets and energy

Lipid droplets are organelles that serve as energy storage depots. They accumulate in the brain support cells (glia) when defects in the mitochondria of neurons lead to elevated levels of reactive oxygen species (ROS). Working with three independent fruit fly models and a mouse model, Liu et al., revealed a novel pathway leading to this accumulation through the inappropriate activation of two proteins: c-Jun-N-terminal Kinase (JNK) and Sterol Regulatory Element Binding Protein (SREBP). These lipid droplets accumulate in glial cells before signs of neurodegeneration appeared.

"This is the first documentation of lipid droplet accumulation in glial cell" said Liu, first author of the study. The authors show that elevated reactive oxygen species in the neurons promotes synthesis of lipids leading to the formation of lipid droplets in glia. This accumulation affects the glia's ability to support the neurons when the lipid droplets become peroxidated, completing a negative feedback loop.

Not enough for neurodegeneration

"ROS or lipid droplets alone do not lead to the rapid onset of neurodegeneration," said Bellen, senior author on the study. "The synergism of ROS with lipid droplets is key. Reducing one or the other delays neurodegeneration."

Upon further investigation, Liu and her colleagues showed that reducing many of the components of this pathway can delay neurodegeneration. For example, treatments with a blood-brain-barrier penetrating antioxidant delay the onset of neurodegeneration in flies and mice developed by their collaborator Dr. Albert Quintana at University of Washington in Seattle.

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Rare mutations do not explain 'missing heritability' in asthma

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Largest study to date of rare genetic variants and asthma risk finds few associations

Despite a strong suspected link between genetics and asthma, commonly found genetic mutations account for only a small part of the risk for developing the disease - a problem known as missing heritability.

Rare and low frequency genetic mutations have been thought to explain missing heritability, but it appears they are unlikely to play a major role, according to a new study led by scientists from the University of Chicago. Analyzing the coding regions of genomes of more than 11,000 individuals, they identified mutations in just three genes that were associated with asthma risk. Each was associated with risk in specific ethnicities. Their findings, published in Nature Communications on Jan. 16, suggest gaps in the current understanding of asthma genetics.

"Previous studies have likely overestimated the heritability of asthma," said study senior author Carole Ober, PhD, Blum-Riese Professor and chair of the Department of Human Genetics at the University of Chicago. "This could be because those estimates are based on correlations between family members that share environment as well as genes, which could inflate the heritability. Gene-environment interactions are not considered in these large scale association studies, and we know that these are particularly important in establishing individual risks for asthma."

Asthma affects more than 25 million adults and children of all ages and ethnicities in the US. Due to the widespread nature of the disease, most studies of its genetic underpinnings have focused on commonly occurring mutations, referred to as genetic variants. However, while numerous such variants have been identified, they are able to account for only a small proportion of the risk for inheriting or developing asthma. Rare mutations, found in less than five percent of the population, have been hypothesized to explain this disparity.

Graduate student Catherine Igartua led the analysis under the supervision of co-senior author Dan Nicolae, PhD, Professor in the Departments of Medicine, Statistics and Human Genetics. She evaluated nearly 33,000 rare or low frequency mutations in more than 11,000 individuals of a variety of ethnicities representing European, African and Latino backgrounds. She analyzed mutations jointly across subjects, using a technique that allowed them to study mutations common in one ethnicity, but rare in others.

Only mutations in the genes GRASP, GSDMB and MTHFR showed a statistical link to asthma risk. Mutations in the first two genes were found primarily in Latino individuals, and mutations in the last gene in those with African ancestry. These genes, involved in protein scaffolding, apoptosis regulation and vitamin B9 metabolism respectively, have as yet unknown roles in asthma. The rarity and ethnic-specificity of these genes is insufficient to account for the widespread prevalence of asthma.

Although rare mutations might not contribute much to population asthma risk, these genes still have the potential to serve as targets for therapeutic development. Ober points to the discovery of rare mutations in the LDL receptor that eventually led to the development of statins to treat high cholesterol. She also notes that it is possible, but unlikely, that there are mutations with large effects on asthma risk outside of their screen as it looked at approximate 60 percent of mutations in coding regions of the genome.

"It was assumed that there would be rare mutations with larger effect sizes than the common variants we have been studying," Ober said. "Surprisingly, we found that low frequency mutations explain only a very small amount of asthma risk."

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AW: *SOLO* Double DNA | FAQ Niki und Aveex – Video

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