JG (v2)

Graphics demo by Arthur Rakhteenko features interactive 3D scene which is rendered using Impressionist painterly strokes as particles (in the video below, the effect appears three minutes into it):

The “painted” effect wasn’t planned. Originally I only had an idea to render a natural scenery of a certain kind, and I wasn’t ready to spend a whole lot of time on it. It became clear to me, a “realistic” approach won’t work, resulting in either very mediocre visuals (due to engine limitations and the complexity of real-time vegetation modeling), or a whole year of trying to catch up with Crysis. So it wasn’t the way.

What I really wanted is to preserve the atmosphere, the feeling, avoiding ruining it with technical limitations.

A demo for PC can be downloaded here

More background on how this was technically done can be found here

[H/T: @fluate]

Scientists identify main component of brain repair after stroke

Looking at brain tissue from mice, monkeys and humans, scientists have found that a molecule known as growth and differentiation factor 10 (GDF10) is a key player in repair mechanisms following stroke. The findings suggest that GDF10 may be a potential therapy for recovery after stroke. The study, published in Nature Neuroscience, was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health.

“These findings help to elucidate the mechanisms of repair following stroke. Identifying this key protein further advances our knowledge of how the brain heals itself from the devastating effects of stroke, and may help to develop new therapeutic strategies to promote recovery,” said Francesca Bosetti, Ph.D., stroke program director at NINDS.

Stroke can occur when a brain blood vessel becomes blocked, preventing nearby tissue from getting essential nutrients. When brain tissue is deprived of oxygen and nutrients, it begins to die. Once this occurs, repair mechanisms, such as axonal sprouting, are activated as the brain attempts to overcome the damage. During axonal sprouting, healthy neurons send out new projections (“sprouts”) that re-establish some of the connections lost or damaged during the stroke and form new ones, resulting in partial recovery. Before this study, it was unknown what triggered axonal sprouting.

Previous studies suggested that GDF10 was involved in the early stages of axonal sprouting, but its exact role in the process was unclear. S. Thomas Carmichael, M.D., Ph.D., and his colleagues at the David Geffen School of Medicine at the University of California Los Angeles took a closer look at GDF10 to identify how it may contribute to axonal sprouting.

Examining animal models of stroke as well as human autopsy tissue, Dr. Carmichael’s team found that GDF10 was activated very early after stroke. Then, using rodent and human neurons in a dish, the researchers tested the effect of GDF10 on the length of axons, the neuronal projections that carry messages between brain cells. They discovered that GDF10 stimulated axonal growth and increased the length of the axons.
“We found that GDF10 caused many different neurons in a dish to grow, including human neurons that were derived from stem cells,” said Dr. Carmichael.

His group also found that GDF10 may be important for functional recovery after stroke. They treated mouse models of stroke with GDF10 and had the animals perform various motor tasks to test recovery. The results suggested that increasing levels of GDF10 were associated with significantly faster recovery after stroke. When the researchers blocked GDF10, the animals did not perform as well on the motor tasks, suggesting the repair mechanisms were impaired — and that the natural levels of GDF10 in the brain represent a signal for recovery.

“We were surprised by how consistently GDF10 caused new connections to form across all of the levels of analysis. We looked at rodent cortical neurons and human neurons in dish as well as in live animals. It’s a demanding gauntlet to run, but the effects of GDF10 held up in all of the levels that we tested,” said Dr. Carmichael.

It has been widely believed that mechanisms of brain repair are similar to those that occur during development. Dr. Carmichael’s team conducted comprehensive analyses to compare the effects of GDF10 on genes related to stroke repair with genes involved in development and learning and memory, processes that result in connections forming between neurons.

Surprisingly, there was little similarity. The findings revealed that GDF10 affected entirely different genes following stroke than those involved in development or learning and memory.

“We found that regeneration is a unique program in the brain that occurs after injury. It is not simply Development 2.0, using the same mechanisms that take place when the nervous system is forming,” said Dr. Carmichael.

More research is necessary to determine whether GDF10 can be a potential treatment for stroke recovery.


My mother had a stroke last night. Thanks to my dad who recognised the signs and acted fast, she is alive and well. But others are not so lucky.
Please share this, it means so much.

(Image caption: In research performed in the laboratory of Raghu Vemuganti in the Department of Neurological Surgery at the University of Wisconsin-Madison, brain damage is outlined in red for rats that were treated to block one type of RNA (right), compared to controls. Credit: Raghu Vemuganti, Suresh Mehta and TaeHee Kim, University of Wisconsin-Madison)

Not ‘junk’ anymore: Obscure DNA has key role in stroke damage

A study of rats shows that blocking a type of RNA produced by what used to be called “junk DNA” can prevent a significant portion of the neural destruction that follows a stroke. The research points toward a future treatment for post-stroke damage, which is often more extensive than the initial destruction that results when blood to the brain is temporarily shut off.

The research also links two mysteries: Why does the majority of damage follow the restoration of blood supply? And what is the role of the vast majority of the human genome, which was once considered junk because it does not pattern for the RNA that makes proteins?

“Less than 2 percent of the RNAs formed from the genome code for proteins, leaving 98 percent that we call 'noncoding RNA,’” says senior author Raghu Vemuganti, a professor of neurological surgery at the University of Wisconsin-Madison.

In the study published in the Journal of Neuroscience, Vemuganti and colleagues blocked one variety of long noncoding RNA (lncRNA), which exists in at least 40,000 unique varieties – possibly as many as 100,000.

“This lncRNA can bind to other RNA, to a protein, or to a protein on one side and DNA on the other,” says first author Suresh Mehta, a scientist in the Department of Neurological Surgery. “Among many other jobs, lncRNAs can regulate gene activity.”

“Stroke influences the expression of all types of RNA, and this RNA has a broad influence throughout the cell after the blood supply is restored, in what we call reperfusion injury” says Vemuganti. “A few years ago, our lab started to look at how stroke affects noncoding RNA. Two years ago, we identified about 200 types of various lncRNAs that greatly increase or decrease after stroke, and zeroed in on one that we named FosDT.

"We knew that the level of FosDT went up more than tenfold in the rat brain within three hours after the stroke,” adds Vemuganti. “We thought, if we block FosDT after the stroke, would it make any difference in the amount of structural damage or behavioral disability?”

Vemuganti and his colleagues designed three custom-made strands of RNA to silence FosDT, injected them into the rats, and deliberately shut off one artery in the brain for one hour. Tests performed within the first week showed that the treated rats regained motor skills much faster and more completely than control animals. Brain scans showed a significant reduction in the total volume of brain that was destroyed by the stroke.

These studies were partially funded by the American Heart Association, National Institutes of Health, U.S. Department of Veterans Affairs and the Department of Neurological Surgery.

Further investigation showed that FosDT stimulates a pathway to cell death, while also impairing cell-survival pathways. Interfering with both mechanisms could explain the benefits, says Mehta.

“We did not change the initial insult, caused by lack of oxygen,” says Vemuganti, “but this targeted approach greatly reduced the damage after one week. We cannot completely reverse the post-stroke damage, but the total damage decreased by one-third. If we can protect this much brain tissue from stroke, that would be an enormous improvement.”

Because post-stroke damage (the “reperfusion injury”) can be even more disabling than harm caused by the initial loss of blood flow, Vemuganti says he is pursuing several lines of research. “We are further exploring the mechanism, and we are preparing to see what happens after a stroke in rats that have no gene for FosDT.”

Although rates of stroke have fallen in recent decades, about 795,000 Americans have a stroke each year, and stroke remains among the leading causes of disability.

“We intend to vigorously pursue this finding,” Vemuganti said.

‘Window of Recovery’ Can Reopen after Stroke

Using mice whose front paws were still partly disabled after an initial induced stroke, Johns Hopkins researchers report that inducing a second stroke nearby in their brains let them “rehab” the animals to successfully grab food pellets with those paws at pre-stroke efficiency.

The findings, described online Dec. 31, 2015, in Neurorehabilitation and Neural Repair, show that the “window of opportunity” for recovering motor function after a stroke isn’t permanently closed after brain damage from an earlier stroke and can reopen under certain conditions, in conjunction with rapid rehabilitation efforts.

(Image caption: A cross-section of a mouse brain with the initial stroke showing as a gray region on the right. The second stroke was given in the region on the left labeled AGm. Credit: Courtesy of Neurorehabilitation and Neural Repair)

The investigators strongly emphasize that their experiments do not and will never make a case for inducing strokes as a therapy in people with stroke disability. But they do suggest the mammalian brain may be far more “plastic” in such patients, and that safe and ethical ways might be found to better exploit that plasticity and reopen the recovery window for people who have never fully regained control of their motor movements.

“If we can better understand how to reopen or extend the optimal recovery period after a stroke, then we might indeed change how we treat patients for the better,” says Steven Zeiler, M.D., Ph.D., assistant professor of neurology at the Johns Hopkins University School of Medicine. “Our study adds new strong and convincing evidence that there is a sensitive period following stroke where it’s easiest to relearn motor movements — a topic that is still debated among stroke researchers.”

The new mouse experiments build on a previous study at Johns Hopkins, which found that the window of optimal recovery following a stroke in mice was within the first seven days, but this time period could be extended by giving mice the common antidepressant fluoxetine immediately after the stroke. The investigators suspected that the antidepressant increased the brain’s response to learning. Until now, however, the researchers say, there was no evidence that once the optimal period was over — with or without fluoxetine — the potential for recovery could be reopened.

For the new research, which did not involve the use of the antidepressant, the researchers — as in their first experiments — taught mice to reach through a slit in their cage with their front paw to grasp food pellets affixed to a bar, a task that four-legged animals don’t naturally perform.

Once the mice became efficient at the task — it took about 10 days of training — the researchers measured their individual success rates. On average, they found the mice successfully grabbed pellets just over 50 percent of the time.

The researchers then induced a stroke in the motor cortex of the mice’s brains, making them unable to perform the task. After waiting a week — well beyond the known “optimal” window during which rehab training will work — they put the mice through almost three weeks of task training, during which the mice successfully grabbed the pellets again, but only about 30 percent of the time.

For the next phase of the experiment, the scientists built on previous research and observations in mice that brain ischemia — the cutoff or reduction of oxygen to the brain during a stroke or other insult to the cortex — under certain conditions increased brain plasticity, the ability of the brain to compensate for injury and form new connections.

To that end, the scientists induced a second stroke in the lab mice either in the secondary motor cortex near the first stroke site or, for purposes of a control group, in the visual cortex, located far from the original site.

Instead of waiting days, the investigators began retraining these mice the next day and found that mice with the follow-up stroke in the motor cortex relearned to grasp the food pellets just as well as they did before the first stroke, with success more than 50 percent of the time.

Mice in the control group never did any better, even with extended training, suggesting that the motor cortex may be the only part of the brain with this type of “reopening” capability for motor movements, the investigators say.

Zeiler plans to investigate other ways to reopen the window of recovery and make use of the optimal recovery window. The lead investigator of the study, John Krakauer, M.D., M.A., professor of neurology, directs the Brain, Learning, Animation and Movement Lab, which uses basic science data, like that in this study, to develop new patient therapies. Currently, the lab is investigating the importance of early and intense rehabilitation in patients to enhance brain plasticity after stroke.

According to the Centers for Disease Control and Prevention, in the U.S., stroke is the No. 1 cause of disability and costs $34 billion each year in in health care, medications and missed days of work.

(Image caption: The image of a cell’s DNA taken with the new super-resolution microscopy technique developed at the Institute of Molecular Biology shows the DNA in crisp detail (left). By contrast, a conventional microscopy image is blurry, making it impossible to see the striking changes in DNA discovered by the scientists at IMB (right). Credit: Aleksander Szczurek, Ina Kirmes)

Cells starved of oxygen and nutrients condense their DNA

Scientists at the Institute of Molecular Biology (IMB) at Johannes Gutenberg University Mainz (JGU) have been able to see, for the first time, the dramatic changes that occur in the DNA of cells that are starved of oxygen and nutrients. This starved state is typical in some of today’s most common diseases, particularly heart attack, stroke, and cancer. The findings provide new insight into the damage these diseases cause and may help researchers to discover new ways of treating them.

When a person has a heart attack or a stroke, the blood supply to part of their heart or brain is blocked. This deprives affected cells there of oxygen and nutrients, a condition known as ischaemia, and can cause long-term damage, meaning that the person may never fully recover. Ina Kirmes, a PhD student in the group of Dr. George Reid at IMB, investigated what happens to the DNA in cells that are cut off from their oxygen and nutrient supply.

In a healthy cell, large parts of the DNA are open and accessible. This means that genes can be easily read and translated into proteins, so that the cell can function normally. However, the researchers showed that, in ischaemia, DNA changes dramatically: it compacts into tight clusters. The genes in this clumped DNA cannot be read as easily anymore by the cell, their activity is substantially reduced, and the cell effectively shuts down. If cells in a person’s heart stop working properly, this part of the heart stops beating and they will have a heart attack. Similarly, when blood supply is blocked to cells in someone’s brain and their cells there are starved of oxygen and nutrients, they have a stroke.

Dr. George Reid is excited about the implications of this finding. “When you have a stroke, when you have a heart attack, this is likely to be what’s happening to your DNA,” he explained. “Now we know that this is what’s going on, we can start to look at ways of preventing this compaction of DNA.”

The key to this discovery was a close collaboration with Aleksander Szczurek, joint first author on this publication, who is part of the group of Professor Christoph Cremer at IMB. They developed a new method that made it possible to see DNA inside the cell at a level of detail never achieved before. Their technique is a further development of super-resolution light microscopy, which uses blinking dyes that bind to DNA to enable the researchers to define the location of individual molecules in cells. This novel technology has been described in a separate paper, published in Experimental Cell Research in September 2015.

I’m Dying and I Need Money

The important information here is that my wife and I need money, for food and for meds, and that you can donate either through the donate button on my blog (which Paypal takes a cut from for using their button), or else by sending money directly through Paypal to mrsmctanuki@gmail.com

The less important details are that I am a physically and mentally disabled trans former sex worker with a terminal illness (it’s complicated, but in short: my brain strokes out very easily). I have a whole host of brain disorders, a broken back, and a bunch of other physical maladies. I’m severely agoraphobic and I can hardly walk. I get $124 from disability each month from the state, and about $150 in food stamps. This has to go to cover everything - food, bills, medications, soap, toilet paper - everything. I have Medicaid, but they specifically do not cover HRT meds or Schedule 1 medications, such as the ones I take to keep myself from stroking out again. Last year, I was bashed by the local police. You can read the full story of my assault and subsequent treatment at the hospital here.

My wife is also disabled. We don’t get our food stamps until the 7th. We need donations, from you, the person reading this. A dollar, 10 cents, whatever you can spare, it’s a literal life-saver.

Righting a wrong? Right side of brain can compensate for post-stroke loss of speech

After a debate that has lasted more than 130 years, researchers at Georgetown University Medical Center have found that loss of speech from a stroke in the left hemisphere of the brain can be recovered on the back, right side of the brain. This contradicts recent notions that the right hemisphere interferes with recovery.

While the findings will likely not put an immediate end to the debate, they suggest a new direction in treatment.

The study, published online in Brain, is the first to look at brain structure and grey matter volume when trying to understand how speech is recovered after a stroke. Results show that patients who have regained their voice have increased grey matter volume in the back of their right hemisphere – mirroring the location of one of the two left hemisphere speech areas.

“Over the past decade, researchers have increasingly suggested that the right hemisphere interferes with good recovery of language after left hemisphere strokes,” says the study’s senior author, Peter Turkeltaub, MD, PhD., an assistant professor of neurology at Georgetown University Medical Center and director of the aphasia clinic at MedStar National Rehabilitation Network. “Our results suggest the opposite – that right hemisphere compensation improves recovery.”

Approximately one-third of stroke survivors lose speech and language – a disorder called aphasia – and most never fully regain it. Turkeltaub says loss of speech occurs almost exclusively in patients with a left hemisphere stroke – roughly 70 percent of people with left hemisphere strokes have language problems.

In a group of 32 left-hemisphere stroke survivors, the researchers determined whether increased grey matter volume in the right hemisphere related to better than expected speech abilities, given the individual features of each person’s stroke. The researchers enrolled an additional 30 individuals who had not experienced a stroke as a control group.

The investigators found that stroke participants who had better than expected speech abilities after their stroke had more grey matter in the back of the right hemisphere compared to stroke patients with worse speech. Those areas of the right hemisphere were also larger in the stroke survivors than in the control group, Turkeltaub says. “This indicates growth in these brain areas that relates to better speech production after a stroke.”