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
What I really wanted is to preserve the atmosphere, the feeling, avoiding ruining it with technical limitations.
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
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
“We found that GDF10 caused many different neurons in a dish to grow,
including human neurons that were derived from stem cells,” said Dr.
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
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.
More research is necessary to determine whether GDF10 can be a potential treatment for stroke recovery.
concern of an explosion of dementia cases in an aging population over
the next few decades, a new study, based on data from the Framingham
Heart Study (FHS), suggests that the rate of new cases of dementia
actually may be decreasing.These findings, which appear in the New England Journal of Medicine,
provide hope that some cases of dementia might be preventable or
delayed and encourages funding agencies and the scientific community to
further explore demographic, lifestyle and environmental factors
underlying this positive trend.
The decline was more
pronounced with a subtype of dementia caused by vascular diseases, such
as stroke. There also was a decreasing impact of heart diseases, which
suggests the importance of effective stroke treatment and prevention of
heart disease. Interestingly, the decline in dementia incidence was
observed only in persons with high school education and above.
“Incidence of Dementia
over Three Decades in the Framingham Heart Study” by Claudia L.
Satizabal, Ph.D., Alexa S. Beiser, Ph.D., Vincent Chouraki, M.D., Ph.D.,
Geneviève Chêne, M.D., Ph.D., Carole Dufouil, Ph.D., and Sudha
Seshadri, M.D. in New England Journal of Medicine. Published online February 11 2016 doi:10.1056/NEJMoa1504327
(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)
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
"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
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.
(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)
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.
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.
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
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
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
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
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.
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.”
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 email@example.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.