affiliate marketing Erwin's Blog

neurosciencestuff:

Our Brains are Hardwired for Language

People blog, they don’t lbog, and they schmooze, not mshooze. But why is this? Why are human languages so constrained? Can such restrictions unveil the basis of the uniquely human capacity for language?

A groundbreaking study published in PLOS ONE by Prof. Iris Berent of Northeastern University and researchers at Harvard Medical School shows the brains of individual speakers are sensitive to language universals. Syllables that are frequent across languages are recognized more readily than infrequent syllables. Simply put, this study shows that language universals are hardwired in the human brain.

LANGUAGE UNIVERSALS

Language universals have been the subject of intense research, but their basis remains elusive. Indeed, the similarities between human languages could result from a host of reasons that are tangential to the language system itself. Syllables like lbog, for instance, might be rare due to sheer historical forces, or because they are just harder to hear and articulate. A more interesting possibility, however, is that these facts could stem from the biology of the language system. Could the unpopularity of lbogs result from universal linguistic principles that are active in every human brain?

THE EXPERIMENT

To address this question, Dr. Berent and her colleagues examined the response of human brains to distinct syllable types—either ones that are frequent across languages (e.g., blif, bnif), or infrequent (e.g., bdif, lbif). In the experiment, participants heard one auditory stimulus at a time (e.g., lbif), and were then asked to determine whether the stimulus includes one syllable or two while their brain was simultaneously imaged.

Results showed the syllables that were infrequent and ill-formed, as determined by their linguistic structure, were harder for people to process. Remarkably, a similar pattern emerged in participants’ brain responses: worse-formed syllables (e.g., lbif) exerted different demands on the brain than syllables that are well-formed (e.g., blif).

UNIVERSALLY HARDWIRED BRAINS

The localization of these patterns in the brain further sheds light on their origin. If the difficulty in processing syllables like lbif were solely due to unfamiliarity, failure in their acoustic processing, and articulation, then such syllables are expected to only exact cost on regions of the brain associated with memory for familiar words, audition, and motor control. In contrast, if the dislike of lbif reflects its linguistic structure, then the syllable hierarchy is expected to engage traditional language areas in the brain.

While syllables like lbif did, in fact, tax auditory brain areas, they exerted no measurable costs with respect to either articulation or lexical processing. Instead, it was Broca’s area—a primary language center of the brain—that was sensitive to the syllable hierarchy.

These results show for the first time that the brains of individual speakers are sensitive to language universals: the brain responds differently to syllables that are frequent across languages (e.g., bnif) relative to syllables that are infrequent (e.g., lbif). This is a remarkable finding given that participants (English speakers) have never encountered most of those syllables before, and it shows that language universals are encoded in human brains.

The fact that the brain activity engaged Broca’s area—a traditional language area—suggests that this brain response might be due to a linguistic principle. This result opens up the possibility that human brains share common linguistic restrictions on the sound pattern of language.

FURTHER EVIDENCE

This proposal is further supported by a second study that recently appeared in the Proceedings of the National Academy of Science, also co-authored by Dr. Berent. This study shows that, like their adult counterparts, newborns are sensitive to the universal syllable hierarchy.

The findings from newborns are particularly striking because they have little to no experience with any such syllable. Together, these results demonstrate that the sound patterns of human language reflect shared linguistic constraints that are hardwired in the human brain already at birth.

(Reblogged from neurosciencestuff)
neurosciencestuff:

Study Connects Sleep Deficits Among Young Fruitflies to Disruption in Mating Later in Life
Mom always said you need your sleep, and it turns out, she was right. According to a new study published in Science this week from researchers at the Perelman School of Medicine at the University of Pennsylvania, lack of sleep in young fruit flies profoundly diminishes their ability to do one thing they do really, really well – make more flies.
The study, led by Amita Sehgal PhD, professor of Neuroscience and a Howard Hughes Medical Institute (HHMI) Investigator, links sleep disruption in newborn fruit flies with a critical adult behavior: courtship and mating.
The team, addressed sleep in the very youngest of flies. “These flies sleep considerably more than adults and that behavior repeats across the animal kingdom,” Sehgal says. “Infant humans, rats, and flies, they all sleep a lot.”
Co-author Matthew Kayser, MD, PhD, in the Department of Psychiatry and Center for Sleep and Circadian Neurobiology, whose research centers on the link between sleep disruption and human neuropsychiatric diseases, used the fly – which is far more genetically pliant than mammals — to ask two basic questions: Why do young animals sleep so much? And, what is the implication of altering those patterns?
The team used genetically manipulated flies to show that young flies normally produce relatively little dopamine – a wake-promoting neurotransmitter — in certain neural circuits that feed into the sleep-promoting brain region called the dorsal fan-shaped body (dFSB). Premature activation of those circuits profoundly inhibits the dFSB, reducing sleep.
That answers the first question, Sehgal explains: Young flies make less dopamine, which keeps the dFSB active and sleep levels high. These animals sleep more than adults and are harder to rouse from sleep.
Some clues to the second question – what is the consequence of sleep loss – came from Kayser’s finding that increased dopamine in young flies not only causes sleep loss, but also affects their ability to court when they’re older. “The flies spend less time courting, and those that do usually don’t make it all the way to the end,” Sehgal says.
To address whether sleep loss in young flies affects development of courtship circuits, the team investigated a group of neurons implicated in courtship. One particular subset of those neurons, localized in a specific brain region called VA1v, was smaller in sleep-deprived animals than normal flies, suggesting a possible mechanism for how sleep deprivation can lead to altered courting behavior.
That sleep-deprived flies have altered behavior is not itself a novel finding, Sehgal notes. Earlier studies from her lab and others used mechanical disruption to alter sleep patterns, but in the current study, Sehgal’s team was able to drill down to the specific neural network that is affected. “We identified the circuit that is less active in young flies. If you activate that circuit, you disrupt courtship by impairing the development of a different, courtship-relevant circuit.”
The question now is how these findings relate to human behavior – Kayser’s original question. Though no direct lines can be drawn, the study “does provide the first mechanistic link between sleep in early life and adult behavior,” says Sehgal.

neurosciencestuff:

Study Connects Sleep Deficits Among Young Fruitflies to Disruption in Mating Later in Life

Mom always said you need your sleep, and it turns out, she was right. According to a new study published in Science this week from researchers at the Perelman School of Medicine at the University of Pennsylvania, lack of sleep in young fruit flies profoundly diminishes their ability to do one thing they do really, really well – make more flies.

The study, led by Amita Sehgal PhD, professor of Neuroscience and a Howard Hughes Medical Institute (HHMI) Investigator, links sleep disruption in newborn fruit flies with a critical adult behavior: courtship and mating.

The team, addressed sleep in the very youngest of flies. “These flies sleep considerably more than adults and that behavior repeats across the animal kingdom,” Sehgal says. “Infant humans, rats, and flies, they all sleep a lot.”

Co-author Matthew Kayser, MD, PhD, in the Department of Psychiatry and Center for Sleep and Circadian Neurobiology, whose research centers on the link between sleep disruption and human neuropsychiatric diseases, used the fly – which is far more genetically pliant than mammals — to ask two basic questions: Why do young animals sleep so much? And, what is the implication of altering those patterns?

The team used genetically manipulated flies to show that young flies normally produce relatively little dopamine – a wake-promoting neurotransmitter — in certain neural circuits that feed into the sleep-promoting brain region called the dorsal fan-shaped body (dFSB). Premature activation of those circuits profoundly inhibits the dFSB, reducing sleep.

That answers the first question, Sehgal explains: Young flies make less dopamine, which keeps the dFSB active and sleep levels high. These animals sleep more than adults and are harder to rouse from sleep.

Some clues to the second question – what is the consequence of sleep loss – came from Kayser’s finding that increased dopamine in young flies not only causes sleep loss, but also affects their ability to court when they’re older. “The flies spend less time courting, and those that do usually don’t make it all the way to the end,” Sehgal says.

To address whether sleep loss in young flies affects development of courtship circuits, the team investigated a group of neurons implicated in courtship. One particular subset of those neurons, localized in a specific brain region called VA1v, was smaller in sleep-deprived animals than normal flies, suggesting a possible mechanism for how sleep deprivation can lead to altered courting behavior.

That sleep-deprived flies have altered behavior is not itself a novel finding, Sehgal notes. Earlier studies from her lab and others used mechanical disruption to alter sleep patterns, but in the current study, Sehgal’s team was able to drill down to the specific neural network that is affected. “We identified the circuit that is less active in young flies. If you activate that circuit, you disrupt courtship by impairing the development of a different, courtship-relevant circuit.”

The question now is how these findings relate to human behavior – Kayser’s original question. Though no direct lines can be drawn, the study “does provide the first mechanistic link between sleep in early life and adult behavior,” says Sehgal.

(Reblogged from neurosciencestuff)
jtotheizzoe:

Tripedal to the Metal
That’s some loco motion, huh? Found this neat little GIF showing how an ant’s legs move at a full gallop. While calmly strolling though the picnic grounds, ants have five of their six legs at a time in contact with the ground. But when it’s time to put the (tiny) pedal to the metal, they change their gait to this alternating tripod motion.
This pattern isn’t controlled by the insect’s brain, but rather by bundles of neurons in the leg called central pattern generators. While moving at such a clip, it just so happens that three legs is the minimum number it needs on the ground at a time to balance its rigid exoskeleton without toppling over.
Is that part of the reason that insects have six legs and not another number like four or eight? Or did the gait evolve to match the hardware? My guess is the latter, but I am not sure. What say you, insect folks? 
(GIF via NC State University)

jtotheizzoe:

Tripedal to the Metal

That’s some loco motion, huh? Found this neat little GIF showing how an ant’s legs move at a full gallop. While calmly strolling though the picnic grounds, ants have five of their six legs at a time in contact with the ground. But when it’s time to put the (tiny) pedal to the metal, they change their gait to this alternating tripod motion.

This pattern isn’t controlled by the insect’s brain, but rather by bundles of neurons in the leg called central pattern generators. While moving at such a clip, it just so happens that three legs is the minimum number it needs on the ground at a time to balance its rigid exoskeleton without toppling over.

Is that part of the reason that insects have six legs and not another number like four or eight? Or did the gait evolve to match the hardware? My guess is the latter, but I am not sure. What say you, insect folks? 

(GIF via NC State University)

(Reblogged from jtotheizzoe)

In Old Age, Lack of Emotion and Interest May Signal Your Brain Is Shrinking

neurosciencestuff:

Older people who have apathy but not depression may have smaller brain volumes than those without apathy, according to a new study published in the April 16, 2014, online issue of Neurology®, the medical journal of the American Academy of Neurology. Apathy is a lack of interest or emotion.

image

“Just as signs of memory loss may signal brain changes related to brain disease, apathy may indicate underlying changes,” said Lenore J. Launer, PhD, with the National Institute on Aging at the National Institutes of Health (NIH) in Bethesda, MD, and a member of the American Academy of Neurology. “Apathy symptoms are common in older people without dementia. And the fact that participants in our study had apathy without depression should turn our attention to how apathy alone could indicate brain disease.”

Launer’s team used brain volume as a measure of accelerated brain aging. Brain volume losses occur during normal aging, but in this study, larger amounts of brain volume loss could indicate brain diseases.

For the study, 4,354 people without dementia and with an average age of 76 underwent an MRI scan. They were also asked questions that measure apathy symptoms, which include lack of interest, lack of emotion, dropping activities and interests, preferring to stay at home and having a lack of energy.

The study found that people with two or more apathy symptoms had 1.4 percent smaller gray matter volume and 1.6 percent less white matter volume compared to those who had less than two symptoms of apathy. Excluding people with depression symptoms did not change the results.

Gray matter is where learning takes place and memories are stored in the brain. White matter acts as the communication cables that connect different parts of the brain.

“If these findings are confirmed, identifying people with apathy earlier may be one way to target an at-risk group,” Launer said.

(Reblogged from neurosciencestuff)

neurosciencestuff:

Neurons in the Brain Tune into Different Frequencies for Different Spatial Memory Tasks

Your brain transmits information about your current location and memories of past locations over the same neural pathways using different frequencies of a rhythmic electrical activity called gamma waves, report neuroscientists at The University of Texas at Austin.

The research, published in the journal Neuron on April 17, may provide insight into the cognitive and memory disruptions seen in diseases such as schizophrenia and Alzheimer’s, in which gamma waves are disturbed.

Previous research has shown that the same brain region is activated whether we’re storing memories of a new place or recalling past places we’ve been.

“Many of us leave our cars in a parking garage on a daily basis. Every morning, we create a memory of where we parked our car, which we retrieve in the evening when we pick it up,” said Laura Colgin, assistant professor of neuroscience and member of the Center for Learning and Memory in The University of Texas at Austin’s College of Natural Sciences. “How then do our brains distinguish between current location and the memory of a location? Our new findings suggest a mechanism for distinguishing these different representations.”

Memory involving location is stored in an area of the brain called the hippocampus. The neurons in the hippocampus that store spatial memories (such as the location where you parked your car) are called place cells. The same set of place cells are activated both when a new memory of a location is stored and, later, when the memory of that location is recalled or retrieved.

When the hippocampus forms a new spatial memory, it receives sensory information about your current location from a brain region called the entorhinal cortex. When the hippocampus recalls a past location, it retrieves the stored spatial memory from a subregion of the hippocampus called CA3.

The entorhinal cortex and CA3 transmit these different types of information using different frequencies of gamma waves. The entorhinal cortex uses fast gamma waves, which have a frequency of about 80 Hz (about the same frequency as a bass E note played on a piano). In contrast, CA3 sends its signals on slow gamma waves, which have a frequency of about 40 Hz.

Colgin and her colleagues hypothesized that fast gamma waves promote encoding of recent experiences, while slow gamma waves support memory retrieval.

They tested these hypotheses by recording gamma waves in the hippocampus, together with electrical signals from place cells, in rats navigating through a simple environment. They found that place cells represented the rat’s current location when cells were active on fast gamma waves. When cells were active on slow gamma waves, place cells represented locations in the direction that the rat was heading.

“These findings suggest that fast gamma waves promote current memory encoding, such as the memory of where we just parked,” said Colgin. “However, when we need to remember where we are going, like when finding our parked car later in the day, the hippocampus tunes into slow gamma waves.”

Because gamma waves are seen in many areas of the brain besides the hippocampus, Colgin’s findings may generalize beyond spatial memory. The ability for neurons to tune into different frequencies of gamma waves provides a way for the brain to traffic different types of information across the same neuronal circuits.

Colgin said one of the next steps in her team’s research will be to apply technologies that induce different types of gamma waves in rats performing memory tasks. She imagines that they will be able to improve new memory encoding by inducing fast gamma waves. Conversely, she expects that inducing slow gamma waves will be detrimental to the encoding of new memories. Those slow gamma waves should trigger old memories, which would interfere with new learning.

(Reblogged from neurosciencestuff)

neurosciencestuff:

Brain Anatomy Differences Between Deaf, Hearing Depend on First Language Learned

In the first known study of its kind, researchers have shown that the language we learn as children affects brain structure, as does hearing status. The findings are reported in The Journal of Neuroscience.

While research has shown that people who are deaf and hearing differ in brain anatomy, these studies have been limited to studies of individuals who are deaf and use American Sign Language (ASL) from birth. But 95 percent of the deaf population in America is born to hearing parents and use English or another spoken language as their first language, usually through lip-reading. Since both language and audition are housed in nearby locations in the brain, understanding which differences are attributed to hearing and which to language is critical in understanding the mechanisms by which experience shapes the brain.

“What we’ve learned to date about differences in brain anatomy in hearing and deaf populations hasn’t taken into account the diverse language experiences among people who are deaf,” says senior author Guinevere Eden, DPhil, director for the Center for the Study of Learning at Georgetown University Medical Center (GUMC).

Eden and her colleagues report on a new structural brain imaging study that shows, in addition to deafness, early language experience – English versus ASL – impacts brain structure. Half of the adult hearing and half of the deaf participants in the study had learned ASL as children from their deaf parents, while the other half had grown up using English with their hearing parents.

“We found that our deaf and hearing participants, irrespective of language experience, differed in the volume of brain white matter in their auditory cortex. But, we also found differences in left hemisphere language areas, and these differences were specific to those whose native language was ASL,” Eden explains.

The research team, which includes Daniel S. Koo, PhD, and Carol J. LaSasso, PhD, of Gallaudet University in Washington, say their findings should impact studies of brain differences in deaf and hearing people going forward.

“Prior research studies comparing brain structure in individuals who are deaf and hearing attempted to control for language experience by only focusing on those who grew up using sign language,” explains Olumide Olulade, PhD, the study’s lead author and post-doctoral fellow at GUMC. “However, restricting the investigation to a small minority of the deaf population means the results can’t be applied to all deaf people.”

(Image: iStockphoto)

(Reblogged from neurosciencestuff)

neurosciencestuff:

Loneliness impacts DNA repair: The long and the short of telomeres

Telomeres are DNA-protein complexes that function as protective caps at the ends of chromosomes. Biologists and veterinarians at the Vetmeduni Vienna recently examined the telomere length of captive African grey parrots. They found that the telomere lengths of single parrots were shorter than those housed with a companion parrot, which supports the hypothesis that social stress can interfere with cellular aging and a particular type of DNA repair. It suggests that telomeres may provide a biomarker for assessing exposure to social stress. The findings have been published in the open access journal PLOS ONE.

In captivity, grey parrots are often kept in social isolation, which can have detrimental effects on their health and wellbeing. So far there have not been any studies on the effects of long term social isolation from conspecifics on cellular aging. Telomeres shorten with each cell division, and once a critical length is reached, cells are unable to divide further (a stage known as ‘replicative senescence’). Although cellular senescence is a useful mechanism to eliminate worn-out cells, it appears to contribute to aging and mortality. Several studies suggest that telomere shortening is accelerated by stress, but until now, no studies have examined the effects of social isolation on telomere shortening.

Using molecular genetics to assess exposure to stress

To test whether social isolation accelerates telomere shortening, Denise Aydinonat, a doctorate student at the Vetmeduni Vienna, conducted a study using DNA samples that she collected from African grey parrots during routine check-ups. African greys are highly social birds, but they are often reared and kept in isolation from other parrots (even though such conditions are illegal in Austria). She and her collaborators compared the telomere lengths of single birds versus pair-housed individuals with a broad range of ages (from 1 to 45 years). Not surprisingly, the telomere lengths of older birds were shorter compared to younger birds, regardless of their housing. However, the important finding of the study was that single-housed birds had shorter telomeres than pair-housed individuals of the same age group.

Reading signs of stress by erosion of DNA

“Studies on humans suggest that people who have experienced high levels of social stress and deprivation have shorter telomeres,” says Dustin Penn from the Konrad Lorenz Institute of Ethology at the Vetmeduni Vienna. “But this study is the first to examine the effects of social isolation on telomere length in any species.” Penn and his team previously conducted experiments on mice, which were the first to show that exposure to crowding stress causes telomere shortening. He points out that this new finding suggests that both extremes of social conditions affect telomere attrition. However, he also cautions “further ‘longitudinal’ studies, in which changes in telomeres of the same individuals over time, are needed to investigate the consequences of stress on telomere shortening and the subsequent effects on health and longevity.”

(Reblogged from neurosciencestuff)

Is Parkinson’s an Autoimmune Disease?

neurosciencestuff:

The cause of neuronal death in Parkinson’s disease is still unknown, but a new study proposes that neurons may be mistaken for foreign invaders and killed by the person’s own immune system, similar to the way autoimmune diseases like type I diabetes, celiac disease, and multiple sclerosis attack the body’s cells. The study was published April 16, 2014, in Nature Communications.

image

(Image caption: Four images of a neuron from a human brain show that neurons produce a protein (in red) that can direct an immune attack against the neuron (green). Credit: Carolina Cebrian.)

“This is a new, and likely controversial, idea in Parkinson’s disease; but if true, it could lead to new ways to prevent neuronal death in Parkinson’s that resemble treatments for autoimmune diseases,” said the study’s senior author, David Sulzer, PhD, professor of neurobiology in the departments of psychiatry, neurology, and pharmacology at Columbia University College of Physicians & Surgeons.

The new hypothesis about Parkinson’s emerges from other findings in the study that overturn a deep-seated assumption about neurons and the immune system.

For decades, neurobiologists have thought that neurons are protected from attacks from the immune system, in part, because they do not display antigens on their cell surfaces. Most cells, if infected by virus or bacteria, will display bits of the microbe (antigens) on their outer surface. When the immune system recognizes the foreign antigens, T cells attack and kill the cells. Because scientists thought that neurons did not display antigens, they also thought that the neurons were exempt from T-cell attacks.

“That idea made sense because, except in rare circumstances, our brains cannot make new neurons to replenish ones killed by the immune system,” Dr. Sulzer says. “But, unexpectedly, we found that some types of neurons can display antigens.”

Cells display antigens with special proteins called MHCs. Using postmortem brain tissue donated to the Columbia Brain Bank by healthy donors, Dr. Sulzer and his postdoc Carolina Cebrián, PhD, first noticed—to their surprise—that MHC-1 proteins were present in two types of neurons. These two types of neurons—one of which is dopamine neurons in a brain region called the substantia nigra—degenerate during Parkinson’s disease.

To see if living neurons use MHC-1 to display antigens (and not for some other purpose), Drs. Sulzer and Cebrián conducted in vitro experiments with mouse neurons and human neurons created from embryonic stem cells. The studies showed that under certain circumstances—including conditions known to occur in Parkinson’s—the neurons use MHC-1 to display antigens. Among the different types of neurons tested, the two types affected in Parkinson’s were far more responsive than other neurons to signals that triggered antigen display.

The researchers then confirmed that T cells recognized and attacked neurons displaying specific antigens.

The results raise the possibility that Parkinson’s is partly an autoimmune disease, Dr. Sulzer says, but more research is needed to confirm the idea.

“Right now, we’ve showed that certain neurons display antigens and that T cells can recognize these antigens and kill neurons,” Dr. Sulzer says, “but we still need to determine whether this is actually happening in people. We need to show that there are certain T cells in Parkinson’s patients that can attack their neurons.”

If the immune system does kill neurons in Parkinson’s disease, Dr. Sulzer cautions that it is not the only thing going awry in the disease. “This idea may explain the final step,” he says. “We don’t know if preventing the death of neurons at this point will leave people with sick cells and no change in their symptoms, or not.”

(Reblogged from neurosciencestuff)

neurosciencestuff:

Brain Cancer: Hunger for Amino Acids Makes It More Aggressive

An enzyme that facilitates the breakdown of specific amino acids makes brain cancers particularly aggressive. Scientists from the German Cancer Research Center (DKFZ) discovered this in an attempt to find new targets for therapies against this dangerous disease. They have reported their findings in the journal “Nature Medicine”.

To fuel phases of fast and aggressive growth, tumors need higher-than-normal amounts of energy and the molecular building blocks needed to build new cellular components. Cancer cells therefore consume a lot of sugar (glucose A number of tumors are also able to catabolize the amino acid glutamine, an important building block of proteins. A key enzyme in amino acid decomposition is isocitrate dehydrogenase (IDH). Several years ago, scientists discovered mutations in the gene coding for IDH in numerous types of brain cancer. Very malignant brain tumors called primary glioblastomas carry an intact IDH gene, whereas those that grow more slowly usually have a defective form.

“The study of the IDH gene currently is one of the most important diagnostic criteria for differentiating glioblastomas from other brain cancers that grow more slowly,” says Dr. Bernhard Radlwimmer from the German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ). “We wanted to find out what spurs the aggressive growth of glioblastomas.” In collaboration with scientists from other institutes including Heidelberg University Hospital, Dr. Martje Tönjes and Dr. Sebastian Barbus from Radlwimmer’s team compared gene activity profiles from several hundred brain tumors. They aimed to find out whether either altered or intact IDH show further, specific genetic characteristics that might help explain the aggressiveness of the disease.

The researchers found a significant difference between the two groups in the highly increased activity of the gene for the BCAT1 enzyme, which in normal brain tissue is responsible for breaking down so-called branched-chain amino acids. However, Radlwimmer’s team discovered, only those tumor cells whose IDH gene is not mutated produce BCAT1. “This is not surprising, because as IDH breaks down amino acids, it produces ketoglutarate – a molecule which BCAT1 needs. This explains why BCAT1 is produced only in tumor cells carrying intact IDH. The two enzymes seem to form a kind of functional unit in amino acid catabolism,” says Bernhard Radlwimmer.

Glioblastomas are particularly dreaded because they aggressively invade the healthy brain tissue that surrounds them. When the researchers used a pharmacological substance to block BCAT1’s effects, the tumor cells lost their invasive capacity. In addition, the cells released less of the glutamate neurotransmitter. High glutamate release is responsible for severe neurological symptoms such as epileptic seizures, which are frequently associated with the disease. When transferred to mice, glioblastoma cells in which the BCAT1 gene had been blocked no longer grew into tumors.

“Altogether, we can see that overexpression of BCAT1 contributes to the aggressiveness of glioblastoma cells,” Radlwimmer says. The study suggests that the two enzymes, BCAT1 and IDH, cooperate in the decomposition of branched-chain amino acids. These protein building blocks appear to act as a “food source” that increases the cancer cells’ aggressiveness. Branched-chain amino acids also play a significant role in metabolic diseases such as diabetes. This is the first time that scientists have been able to show the role of these amino acids in the growth of malignant tumors.

“The good news,” sums up Radlwimmer, “is that we have found another target for therapies in BCAT1. In collaboration with Bayer Healthcare, we have already started searching for agents that might be specifically directed against this enzyme.” The researchers also plan to investigate whether BCAT1 expression may serve as an additional marker to diagnose the malignancy of brain cancer.

(Reblogged from neurosciencestuff)

theedgeofscience:

Saturn’s Beautiful Rings

The Cassini spacecraft was a project launched by NASA, the European Space Agency and the Italian Space Agency that has yielded large amounts of useful data and many beautiful pictures. This one in particular shows the C ring on the right, and the B on the left. The red hues indicate dirty particles and blue the cleaner ice. The rings of Saturn are labelled from the inside out with rings, D, C, B, and A, followed by F, G, and E. In order to image the rings in such quality the Cassini spacecraft used its Ultraviolet Imaging Spectrograph in resolution some 100 times that of the Voyager 2 spacecraft.

(Reblogged from outreachscience)