22 fevereiro 2015

timfitzgeraldstudio:Myasthenia gravis infographicThis...


Myasthenia gravis infographic

This infographic compares the normal condition of neuron-muscle communication, and the clinical condition of myasthenia gravis. The images show the molecular and cellular components involved with each circumstance.

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The Dark River to Antares

Connecting the Pipe Nebula to the colorful region near bright star Antares is a dark cloud dubbed the Dark River, flowing from the picture's left edge. Murky looking, the Dark River's appearance is caused by dust obscuring background starlight, although the dark nebula contains mostly hydrogen and molecular gas. Surrounded by dust, Antares, a red supergiant star, creates an unusual bright yellowish reflection nebula. Above it, bright blue double star Rho Ophiuchi is embedded in one of the more typical bluish reflection nebulae, while red emission nebulae are also scattered around the region. Globular star cluster M4 is just seen above and right of Antares, though it lies far behind the colorful clouds, at a distance of some 7,000 light-years. The Dark River itself is about 500 light years away. The colorful skyscape is a mosaic of telescopic images spanning nearly 10 degrees (20 Full Moons) across the sky in the constellation of the Scorpion (Scorpius).

from NASA http://ift.tt/1B3A4ZG

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Panel Says Chronic Fatigue Syndrome Is A Disease, And Renames...

Panel Says Chronic Fatigue Syndrome Is A Disease, And Renames It

The mysterious and complicated illness that has been called chronic fatigue syndrome has a new definition and a new name: Systemic Exertion Intolerance Disease, or SEID for short.

The name change is big news because many patients and experts in the field hate the name chronic fatigue syndrome; they feel that it trivializes the condition. Another name, myalgic encephalomyelitis, has been used in Canada, the United Kingdom and elsewhere, but it doesn’t accurately describe the illness, either.

The condition, which can render people housebound or bedridden and unable to work or go to school, is believed to affect between 860,000 and 2.5 million Americans. Because there is no specific test for SEID, many people who have it haven’t been diagnosed, and health care professionals often have viewed patients as complainers whose symptoms are psychological, not physical.

But a 15-member panel of the Institute of Medicine, an independent (IOM) government advisory body with a lot of clout, says otherwise. In a report released, the panel writes that the condition “is real” and admonishes clinicians, “It is not appropriate to dismiss these patients by saying ‘I am chronically fatigued, too.’ “

The new definition, for use in adults and children, focuses on the disease’s core symptoms:

  • Profound fatigue lasting at least six months;

  • Total exhaustion after even minor physical or mental exertion that patients sometimes describe as a “crash” and is known medically as post-exertional malaise;

  • Unrefreshing sleep;

  • Cognitive impairment (aka “brain fog”) or a worsening of symptoms upon standing.

This definition is much simpler than some previous ones for chronic fatigue syndrome and myalgic encephalomyelitis. And it doesn’t require doctors to run a bunch of expensive and time-consuming tests to rule out other causes for the patient’s symptoms before making the diagnosis.

In the 235-page report, the panel summarizes the scientific evidence it used to come up with the new definition, as well as for other aspects of the condition, including links to viruses such as Epstein-Barr (the cause of mononucleosis), and studies showing that people with the disorder have abnormal immune systems.

The condition has had all sorts of other names in the past, including epidemic neuromyasthenia, myalgia nervosa, and Royal Free Disease, after the British hospital where an outbreak reportedly occurred in 1955.

Systemic exertion intolerance disease might not roll off the tongue, but the panel chose it very purposefully, says Dr. Lucinda Bateman, a panel member who runs a fatigue specialty clinic in Salt Lake City.

"For years, nobody has been able to come up with an alternate name. We struggled, but we tried to pack each word with meaning," she said.

Rather than use a name that presumes a cause, the IOM committee decided to name the disease by focusing on post-exertional malaise, the core symptom. “Systemic” indicates that the reaction to exertion involves the entire body, while “intolerance” implies impairment. “Glucose intolerance,” for example, is a medical term used in relation to diabetes.

And, Bateman told Shots, the panel chose “disease” rather than “disorder” because “it’s a stronger word.”

Beyond encouraging physicians to take the condition seriously, diagnose patients and treat their symptoms, the panel also intends for the document to spur more research funding. As more information becomes available, both the diagnostic criteria and the name are expected to evolve. The goal is to identify markers in the patient’s blood or body tissues that can be used both to diagnose the illness and as targets for treatment. Indeed, the report calls for a re-evaluation of both the definition and the name in “no more than five years.”

"Change is not easy in any system, especially complex systems," Bateman says. "But I think we have about as good a foundation as we possibly could have to jump-start this process."

Patient advocates — some of whom were concerned about the IOM endeavor when it began over a year ago — are now cautiously optimistic. Jennie Spotila, a patient and former attorney who writes a widely read blog about the illness, tells Shots, “I think the IOM panel got a lot of things right with the new criteria. They focused on the central feature of the disease, post-exertional malaise, and limited the required symptoms to a short list.”

Spotila praised the new name both for focusing on post-exertional malaise and for using the word “disease,” although she also predicted that “SEID will be controversial, especially for the advocates like myself who argued for use of the term myalgic encephalomyelitis. … I would like to see data that support SEID as a better name.”

Asked whether she believes the IOM report will help patients, she responded, “That all depends on how widely and how accurately the criteria are implemented.”

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taggedgross: soulful-tree: mousathe14: upallnightogetloki: rac...








Language Maps of the US.

Why wasn’t this the first one I saw!? This is so much more interesting!!


This is ten times better than the initial one. I love it.

I buy that, I’ve known tons and tons of Korean folks growing up in Northern Virginia.

Here’s to all ignorant people who say “this is America, speak English”

I love this so much, languages are so cool though, languages, maps, facts, america

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"In winter, they hang about them simply an undressed deer or bear or panther skin; or they take some..."

In winter, they hang about them simply an undressed deer or bear or panther skin; or they take some beaver and otter skins, wild cat, raccoon, martin, otter, mink, squirrel or such like skins, which are plenty in this country, and sew some of them to others, until it is a square piece, and that is then a garment for them… They make themselves stockings and also shoes of deer skin, or they take leaves of their corn, and plait [braid] them together and use them for shoes.

They generally live without marriage; and if any of them have wives, the marriage continues no longer than seems good to one of the parties, and then they separate, and each takes another partner. I have seen those who had parted, and afterwards lived a long time with others, leave these again, seek their former partners, and again be one pair.

- Johannes Megapolensis’ descriptions of the Mohawk. He was a thirty-nine-year-old Dutch minister who made his way to Fort Orange with his wife and four children in 1642. The fort, built north of New Amsterdam (New York City) along the Hudson River, was very important for the Dutch fur trade. Megapolensis had a six-year contract with the West India Company, the Dutch company that monopolized the Netherlands’ North American trade, and so the fur trade. He was send to Fort Orange as a pastor, to fill the spiritual needs of the inhabitants of the area. Megapolensis described his experience in a series of letters that were later published as a book.
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Meet your other brainFor years, changes in the brain –whether...

Meet your other brain

For years, changes in the brain –whether from learning to ridea bike, taking a Prozac, or sinking into Alzheimer’s disease – have been attributedto the activity of neurons and the small chemical junctions between them,called synapses. Targeting synapses is like fiddling with the connections ateither end or calling the cable company. But ignoring the wiring in between maybe a mistake.

“All ideas about communication and plasticity in thenervous system were focused on the synapse,” says Douglas Fields at the NationalInstitutes of Health in Bethesda, Maryland. That’s starting to change, as he and other neuroscientists realise that neurons alone are not enough to explain our brain’s plasticity – its ability to learn, adapt, and form new memories.

“All ideas about communication and plasticity in the nervous system were focused on the synapse,” says Douglas Fields at the National Institutes of Health in Bethesda, Maryland. That’s starting to change, as he and other neuroscientists realise that neurons alone are not enough to explain our brain’s plasticity – its ability to learn, adapt, and form new memories. What it comes down to is myelin, the fatty sheath that envelops most neurons. We are used to thinking of it like insulation along a cable – allowing electrical impulses to zip along faster. But we are learning that this fatty layer is not like a wire’s insulation, installed uniformly and left unattended. Instead, it is dynamic and autonomous, customising itself to match the brain’s demands. The cells that produce it respond in real time to our cognitive needs: new insulation is laid down to help the brain master a skill; a frayed section can be replaced. What’s more, these additions and renovations continue well into adulthood.

This new kind of plasticity has come as a shock to many researchers. Bill Rebeck at Georgetown University in Washington DC has been a professor of neuroscience for over a decade, but when he heard about it last year, he was gobsmacked. “Wait, really?” was all he could mutter. And plasticity is just the start. Because they are not nerve cells, which are notoriously hard to tinker with, we might be able to tweak them manually to give the brain an extra boost when needed, or to help mend the damage behind conditions such as multiple sclerosis. It turns out a most vital part of our cognitive potential has been hiding in plain sight.

To better understand why myelin is so important, you need to look at how information travels around the brain. A neuron sends electrical impulses zipping down long projections called axons to the synapse, a small gap that chemicals called neurotransmitters travel across. These relay the signal to neighbouring neurons. Myelin keeps the information tightly confined within the axon, allowing a speedy trip.

Wired for learning

The substance is thought to have evolved to allow animals to react quickly. But myelin does more than just speed up our reflexes, it is also crucial to learning, development and behaviour. “Ultimately it allows us to have clever brains,” says William Richardson, who studies neuronal plasticity at University College London.

Hints about the role of myelination in cognitive abilities come from the way it is produced during our lifetime. A small amount is made as we develop in the womb, but after birth it takes off, and we see surges as infants learn to crawl, walk and talk. By about age 4, the rate of myelination slows, and teenagers still have the prefrontal cortex left to myelinate – an area crucial for planning and consideration of consequences. Until then, processing in the prefrontal cortex is slow and inefficient and teens remain precariously impulsive. The finer circuitry is complete by the time we reach our 40s, but from the 60s onwards the coverings start to fray and degenerate, which fits with the common experience of cognitive decline as we age. As myelin degenerates, the signals get fuzzier.

Until recently, scientists thought insulating the prefrontal cortex was the final hurrah for myelin. Plasticity was then down to the neurons, and synapses between them. For instance, the number of neurotransmitter receptors increase in a synapse the more that pathway is used, which enables the brain to adapt according to learning or experience. As a result, our quest to understand cognitive decline, and the potential for activities that boost brain power, has focused on grey matter, the part of the brain and spinal cord packed with the neuron cell bodies and synapses.

But Heidi Johansen-Berg at the University of Oxford began to wonder about white matter, the area of our brain that is rich in myelincovered axons. “It seemed like an overlooked but obviously very important structure in the central nervous system,” she says. It wasn’t until 2009 that she could investigate, with the help of a new neuroimaging method called diffusion MRI, which accurately measures human white matter in the living brain.

To test her idea, Johansen-Berg turned to a 2004 study, which had found that learning a new skill such as juggling changed the density of grey matter – an example of classic synaptic plasticity. Johansen-Berg decided to recreate the study, and measure changes in white matter too. A group of volunteers agreed to learn how to juggle, and after six weeks, brain scans showed that their myelin had increased more than that of a control group who had no training (Nature Neuroscience, vol 12, p 1370).

“We saw a change not only in the grey matter but also in the underlying white matter pathways, suggesting that these pathways strengthen in some way as a result of experience,” says Johansen-Berg. The changes to white and grey matter took place over different timescales, suggesting two separate processes. Johansen-Berg thinks the increase in white matter would have enabled faster conduction along the circuits coordinating juggling. What’s more, the effect was seen in everyone who learned to juggle, regardless of how good they became, which means it is the learning process itself that is responsible.

This was the first study to reveal that training can alter white matter in healthy adults, and it opened the door to a plethora of similar findings. Since then, numerous activities have been linked to extra myelin, from learning to read, to meditating, and learning a new skill like playing the piano or another language.

To investigate these changes more closely, Richardson turned to rodents. Rather than juggle, he made mice run on a complicated wheel, with rungs removed in a random pattern. Watching the struggling mice is a pitiful sight – their legs slip through the bars, their paws feel desperately into empty space. But after just a few days, they look like they’ve been doing it forever. So was myelin the key?

Myelin is formed by oligodendrocytes, octopus-shaped cells with long arms that wrap thin layers of fat 50 to 100 times around the axon, preventing electrical signals from slipping out, and expediting the conversation between brain regions. The cells are made throughout life by oligodendrocyte precursor cells (OPCs), which tile the brain, ready to morph when needed. When Richardson bred mice that couldn’t produce oligodendrocytes – or new myelin – in adulthood, the mice weren’t able to get used to the wheel, even after a week of practice.

Further proof of the essential role of myelin in learning complex skills came last year. Michelle Monje at Stanford University in California turned to another relatively new technology, optogenetics, which involves breeding mice with light-sensitive genes. This allows unprecedented control over neurons using pulses of light. Monje used it to activate a particular set of neurons that made the mice run in anticlockwise circles. After a while, they became slightly more efficient with the left paw, and when Monje inspected the brains of the mice, she found that new myelin had been laid down in these circuits. Crucially, she was able to show that repeatedly activating specific neurons led to changes in the surrounding myelin rather than changes within neurons, so it was this that was critical to making the circuits more efficient.

Richardson and Monje’s papers, both published in 2014, distinguish myelin plasticity as a second type of plasticity – distinct from the better-known synaptic version. Although more studies will be needed in humans, the findings have important implications for learning and memory. Well-used pathways get more myelin, as shown in the juggling study, speeding up the signals and making the brain more efficient. Being more efficient, these pathways are also more likely to be used next time around. “It’s not only that information is stored in the plasticity of synapses, but actually in the myelin as well,” says Gabriel Corfas at the University of Michigan in Ann Arbor. If you are learning Mandarin, for instance, myelination would help you remember the right character faster and more intuitively. “This gives a new dimension to the amount of information and the types of information the nervous system can store,” Corfas says. The importance of these and other non-neuronal cells has led Fields to term them our “other brain”.

While we now know that stimulating the brain in various ways can boost myelin production, so too can the insulation be lost, emphasising that the brain is a “use it or lose it” organ. If electricity isn’t flowing, the myelin can degrade, and this can lead to psychological and social problems. If the brain were a city, and myelin the insulation on wires connecting the buildings, some parts would end up in the dark. A lack of myelin is implicated in conditions like autism, in mental illnesses such as schizophrenia, and in spinal cord and traumatic brain injuries.

And there is a further twist. It turns out that myelin production is in part controlled by packets of messenger chemicals that are relayed through the blood. Could we use these messengers to give struggling brains a boost, rather than trying to manipulate brain cells directly, which is notoriously hard?

That’s the thinking behind the work of Richard Kraig, at the University of Chicago. His team discovered that small packets of proteins and RNA in the blood known as exosomes influence myelin production.

Many types of cell release exosomes as a way of delivering specific messages to other cells: they are part of the body’s vast communication network. Kraig began to wonder about the roles of exosomes on brain function after reading that transferring the blood of young mice into old mice can reverse their cognitive decline.

He has now shown that exosomes produced in the blood are taken up by OPCs in the brain. Their message is the “trigger to make the myelination go”, says Kraig. That raises the exciting possibility that a blood transfusion packed with the right exosomes could help treat multiple sclerosis (MS), in which myelin is attacked by the immune system.

OPC-regulating exosomes are dispensed whenever the brain is stimulated in new ways, such as during exercise and learning. They may be one reason why physical and mental activity help ward off diseases like Alzheimer’s. But while advice to exercise the body and mind is not new, for many people it is not that simple – if you have MS, for instance. Kraig hopes that treating people with donor exosomes might improve myelination enough to enable them to exercise, and thus boost exosomes and myelination themselves.

Another disease, amyotrophic lateral sclerosis (ALS), is not normally associated with myelin. It is characterised by the death of neurons that control muscles. But in 2013, Dwight Bergles at Johns Hopkins University in Baltimore, Maryland, showed in mice that oligodendrocytes die before the neurons. Late in the disease, more than half of them had died. “This is a massive reorganisation of myelin. It is very stressful for neurons and can induce them to degenerate,” Bergles says.

He has now found that in people with ALS, OPCs seem to have difficulty converting to oligodendrocytes. The key to an ALS cure may lie in preventing the initial oligodendrocyte loss, or helping OPCs to morph properly.

There is still much to be worked out, and many of the animal studies need to be confirmed in humans. But as Corfas said at the Society for Neuroscience conference in Washington DC last November, “it’s an exciting time. The way we think about myelin is changing.” Indeed, if we can uncover enough, this type of research might even yield an actual wonder drug, says Richardson, one that makes us smarter, speeding up the rate of learning.

In the meantime, the message is clear. “Keep learning, keep your mind active,” Richardson says. Kraig recommends learning new things, like a new piano piece, as well as keeping up with ordinary activities like taking a walk. If it’s an unfamiliar route, with changing scenery and the requirement to memorise the way home, that’s all to the good. So embrace a new hobby. And then another. It should help keep the electricity flowing a little better, a little longer.


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ppaction:Submitted without comment.h/t NARAL Pro-Choice America


Submitted without comment.

h/t NARAL Pro-Choice America

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Did The Buddha Eat Wisdom?

What did Siddhartha do to eat after he left his family? I mean, he was rich and noble, and then one day he decided to leave — presumably he did not have any real-life skills at that point. According to the traditional narrative, Siddhartha Gautama started off his life of asceticism by becoming a beggar. Then and now, it was a common way for religious ascetics to survive. After a while, he went off to live in the woods, where he ate nuts and leaves. And he almost starved. He then decided that such extreme asceticism was not the path to enlightenment and instead focused on the Middle Way. It is the middle way between the extremes of asceticism and sensual indulgence (and between starving and eating to obesity).

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February 22nd 1837: Jackson’s cheese receptionOn this day...

Andrew Jackson (1767 - 1845)

'The Cheese Levee' of 1837

February 22nd 1837: Jackson’s cheese reception

On this day in 1837, U.S. President Andrew Jackson held a reception at the White House where he served a 1,400-pound block of cheese to members of the public. Elected in 1828, Jackson was the embodiment of a new kind of American governance based on the vote of the common man - Jacksonian Democracy. Many of his supporters saw his brand of politics, which was focused on an ideal agrarian republic of small farmers, as an inheritor of the nation’s third President - Thomas Jefferson. During Jefferson’s term, one of his admirers from Cheshire, MA. resolved to make the President the largest cheese imaginable. The cow-owners of the town joined together to create a 1,600-pound block of cheese, which was bought to Washington D.C. and presented to Jefferson in the White House East Room. Several years later, Jackson’s supporters decided to award him with his own block of cheese. A prosperous New York farmer named Thomas Meacham led the project, and the giant cheese was exhibited around Northern cities including New York, Philadelphia, and Baltimore, before being presented at the White House. During an 1837 reception on Washington’s birthday Jackson, in desperation with what to do with such a mammoth cheese, invited thousands of citizens to come and eat the cheese. Two weeks later, the increasingly feeble Jackson stepped down as President upon the inauguration of his successor, Martin Van Buren. The event resurfaced in national attention when it was mentioned in political drama The West Wing, which has inspired an annual event held by the White House where they invite members of the public to send questions to the administration via social media.

"The air was redolent with cheese, the carpet was slippery with cheese, and nothing else was talked about at Washington that day"

- Benjamin Perley Poore in Perley’s Reminiscences of Sixty Years in the National Metropolis (1886)

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plannedparenthood: 10,000 years of condom history and 10...


10,000 years of condom history and 10 dioramas in 2 minutes. Watch this awesome video from Planned Parenthood of the Great Northwest.

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Walter Mischel was born.

GO HERE —> http://ift.tt/1eWNk1f For Free Psychology Information & Resources.

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