Mass Relay

neurosciencestuff:

No Two People Smell the Same
A difference at the smallest level of DNA — one amino acid on one gene —  can determine whether you find a given smell pleasant. A different amino acid on the same gene in your friend’s body could mean he finds the same odor offensive, according to researchers at Duke University.
There are about 400 genes coding for the receptors in our noses, and according to the 1000 Genomes Project, there are more than 900,000 variations of those genes. These receptors control the sensors that determine how we smell odors. A given odor will activate a suite of receptors in the nose, creating a specific signal for the brain. 
But the receptors don’t work the same for all of us, said Hiroaki Matsunami, Ph.D., associate professor of molecular genetics and microbiology at the Duke University School of Medicine. In fact, when comparing the receptors in any two people, they should be about 30 percent different, said Matsunami, who is also a member of the Neurobiology Graduate Program and the Duke Institute for Brain Sciences. 
"There are many cases when you say you like the way something smells and other people don’t. That’s very common," Matsunami said. But what the researchers found is that no two people smell things the same way. "We found that individuals can be very different at the receptor levels, meaning that when we smell something, the receptors that are activated can be very different (from one person to the next) depending on your genome."
The study didn’t look at the promoter regions of the genes, which are highly variable, or gene copy number variation, which is very high in odor receptors, so the 30 percent figure for the difference between individuals is probably conservative, Matsunami said.
While researchers had earlier identified the genes that encode for odor receptors, it has been a mystery how the receptors are activated, Matsunami said. To determine what turns the receptors on, his team cloned more than 500 receptors each from 20 people that had slight variations of only one or two amino acids and systematically exposed them to odor molecules that might excite the receptors. 
By exposing each receptor to a very small concentration — 1, 10, or 100 micromoles — of 73 odorants, such as vanillin or guaiacol, the group was able to identify 27 receptors that had a significant response to at least one odorant. This finding, published in the December issue of Nature Neuroscience, doubles the number of known odorant-activated receptors, bringing the number to 40.
Matsunami said this research could have a big impact for the flavors, fragrance, and food industries.
"These manufacturers all want to know a rational way to produce new chemicals of interest, whether it’s a new perfume or new-flavored ingredient, and right now there’s no scientific basis for doing that," he said. "To do that, we need to know which receptors are being activated by certain chemicals and the consequences of those activations in terms of how we feel and smell."

Slight variations in amino acid sequence can determine what smells we find pleasant or offensive.

neurosciencestuff:

No Two People Smell the Same

A difference at the smallest level of DNA — one amino acid on one gene —  can determine whether you find a given smell pleasant. A different amino acid on the same gene in your friend’s body could mean he finds the same odor offensive, according to researchers at Duke University.

There are about 400 genes coding for the receptors in our noses, and according to the 1000 Genomes Project, there are more than 900,000 variations of those genes. These receptors control the sensors that determine how we smell odors. A given odor will activate a suite of receptors in the nose, creating a specific signal for the brain. 

But the receptors don’t work the same for all of us, said Hiroaki Matsunami, Ph.D., associate professor of molecular genetics and microbiology at the Duke University School of Medicine. In fact, when comparing the receptors in any two people, they should be about 30 percent different, said Matsunami, who is also a member of the Neurobiology Graduate Program and the Duke Institute for Brain Sciences. 

"There are many cases when you say you like the way something smells and other people don’t. That’s very common," Matsunami said. But what the researchers found is that no two people smell things the same way. "We found that individuals can be very different at the receptor levels, meaning that when we smell something, the receptors that are activated can be very different (from one person to the next) depending on your genome."

The study didn’t look at the promoter regions of the genes, which are highly variable, or gene copy number variation, which is very high in odor receptors, so the 30 percent figure for the difference between individuals is probably conservative, Matsunami said.

While researchers had earlier identified the genes that encode for odor receptors, it has been a mystery how the receptors are activated, Matsunami said. To determine what turns the receptors on, his team cloned more than 500 receptors each from 20 people that had slight variations of only one or two amino acids and systematically exposed them to odor molecules that might excite the receptors. 

By exposing each receptor to a very small concentration — 1, 10, or 100 micromoles — of 73 odorants, such as vanillin or guaiacol, the group was able to identify 27 receptors that had a significant response to at least one odorant. This finding, published in the December issue of Nature Neuroscience, doubles the number of known odorant-activated receptors, bringing the number to 40.

Matsunami said this research could have a big impact for the flavors, fragrance, and food industries.

"These manufacturers all want to know a rational way to produce new chemicals of interest, whether it’s a new perfume or new-flavored ingredient, and right now there’s no scientific basis for doing that," he said. "To do that, we need to know which receptors are being activated by certain chemicals and the consequences of those activations in terms of how we feel and smell."

Slight variations in amino acid sequence can determine what smells we find pleasant or offensive.

400,000 year old early-human DNA sequenced

8bitfuture:

image The DNA sequenced from the fossilized femur bone found in an underground cave in Northern Spain has revealed a surprising discovery for scientists.

Read More

File under evolution and genetics.

(Source: blogs.smithsonianmag.com, via 8bitfuture)

logikblok-science:

Tardigrades - Microscopic Water Bears

They may look cute but Tardigrades are one of the hardiest creatures on the planet. They are considered under a distinction of life as an extremophile, meaning they can survive in a hostile environment examples include the arctic, deserts, hydrothermal vents and more.

However Tardigrades have a gained a further fame of their own as a polyextremophile by being able to survive not only intense heat, but cold, radiation, desiccation and even the vacuum of space! It’s important to remember that we are considering extreme measured against human abilities, nevertheless these abilities make Tardigrades of great scientific interest.

What researchers believe allows Tardigrades these extreme abilities is their ability to effectively shutdown internally going into stasis and their remarkable repair mechanisms when in this state. Overall they can dehydrate themselves completely known as an anhydrobiotic state a form of Cryptobiosis and survive without a metabolism for months.

Why Tardigrades can do this might be due to how their environments have shaped them. Being less than 1mm in size exposes these organisms to a dynamic and harsh environment. Meaning they have been selected to be able to cope with sudden drastic changes such as loss of water, extreme changes in temperature, similar to the conditions of space. In fact these organisms have multiple forms of existence further refining their abilities to survive in extreme environments. Although eventually every organism needs to eat and when they do their preferred diet consists of algae perhaps filling stores to survive future conditions. Researchers have ongoing research into these creatures in Italy & NASA

More about Tardigrades. More Microorganisms here & here. Logikblok

Cutest bear ever!

(via scinerds)

neurosciencestuff:

Gene expression changes with meditation
With evidence growing that meditation can have beneficial health effects, scientists have sought to understand how these practices physically affect the body.
A new study by researchers in Wisconsin, Spain, and France reports the first evidence of specific molecular changes in the body following a period of mindfulness meditation.
The study investigated the effects of a day of intensive mindfulness practice in a group of experienced meditators, compared to a group of untrained control subjects who engaged in quiet non-meditative activities. After eight hours of mindfulness practice, the meditators showed a range of genetic and molecular differences, including altered levels of gene-regulating machinery and reduced levels of pro-inflammatory genes, which in turn correlated with faster physical recovery from a stressful situation.
"To the best of our knowledge, this is the first paper that shows rapid alterations in gene expression within subjects associated with mindfulness meditation practice," says study author Richard J. Davidson, founder of the Center for Investigating Healthy Minds and the William James and Vilas Professor of Psychology and Psychiatry at the University of Wisconsin-Madison.
"Most interestingly, the changes were observed in genes that are the current targets of anti-inflammatory and analgesic drugs," says Perla Kaliman, first author of the article and a researcher at the Institute of Biomedical Research of Barcelona, Spain (IIBB-CSIC-IDIBAPS), where the molecular analyses were conducted.
The study was published in the journal Psychoneuroendocrinology.
Mindfulness-based trainings have shown beneficial effects on inflammatory disorders in prior clinical studies and are endorsed by the American Heart Association as a preventative intervention. The new results provide a possible biological mechanism for therapeutic effects.
The results show a down-regulation of genes that have been implicated in inflammation. The affected genes include the pro-inflammatory genes RIPK2 and COX2 as well as several histone deacetylase (HDAC) genes, which regulate the activity of other genes epigenetically by removing a type of chemical tag. What’s more, the extent to which some of those genes were downregulated was associated with faster cortisol recovery to a social stress test involving an impromptu speech and tasks requiring mental calculations performed in front of an audience and video camera.
Perhaps surprisingly, the researchers say, there was no difference in the tested genes between the two groups of people at the start of the study. The observed effects were seen only in the meditators following mindfulness practice. In addition, several other DNA-modifying genes showed no differences between groups, suggesting that the mindfulness practice specifically affected certain regulatory pathways.
However, it is important to note that the study was not designed to distinguish any effects of long-term meditation training from those of a single day of practice. Instead, the key result is that meditators experienced genetic changes following mindfulness practice that were not seen in the non-meditating group after other quiet activities — an outcome providing proof of principle that mindfulness practice can lead to epigenetic alterations of the genome.
Previous studies in rodents and in people have shown dynamic epigenetic responses to physical stimuli such as stress, diet, or exercise within just a few hours.
"Our genes are quite dynamic in their expression and these results suggest that the calmness of our mind can actually have a potential influence on their expression," Davidson says.
"The regulation of HDACs and inflammatory pathways may represent some of the mechanisms underlying the therapeutic potential of mindfulness-based interventions," Kaliman says. "Our findings set the foundation for future studies to further assess meditation strategies for the treatment of chronic inflammatory conditions."

Interesting.  Need to analyze this paper ASAP.

neurosciencestuff:

Gene expression changes with meditation

With evidence growing that meditation can have beneficial health effects, scientists have sought to understand how these practices physically affect the body.

A new study by researchers in Wisconsin, Spain, and France reports the first evidence of specific molecular changes in the body following a period of mindfulness meditation.

The study investigated the effects of a day of intensive mindfulness practice in a group of experienced meditators, compared to a group of untrained control subjects who engaged in quiet non-meditative activities. After eight hours of mindfulness practice, the meditators showed a range of genetic and molecular differences, including altered levels of gene-regulating machinery and reduced levels of pro-inflammatory genes, which in turn correlated with faster physical recovery from a stressful situation.

"To the best of our knowledge, this is the first paper that shows rapid alterations in gene expression within subjects associated with mindfulness meditation practice," says study author Richard J. Davidson, founder of the Center for Investigating Healthy Minds and the William James and Vilas Professor of Psychology and Psychiatry at the University of Wisconsin-Madison.

"Most interestingly, the changes were observed in genes that are the current targets of anti-inflammatory and analgesic drugs," says Perla Kaliman, first author of the article and a researcher at the Institute of Biomedical Research of Barcelona, Spain (IIBB-CSIC-IDIBAPS), where the molecular analyses were conducted.

The study was published in the journal Psychoneuroendocrinology.

Mindfulness-based trainings have shown beneficial effects on inflammatory disorders in prior clinical studies and are endorsed by the American Heart Association as a preventative intervention. The new results provide a possible biological mechanism for therapeutic effects.

The results show a down-regulation of genes that have been implicated in inflammation. The affected genes include the pro-inflammatory genes RIPK2 and COX2 as well as several histone deacetylase (HDAC) genes, which regulate the activity of other genes epigenetically by removing a type of chemical tag. What’s more, the extent to which some of those genes were downregulated was associated with faster cortisol recovery to a social stress test involving an impromptu speech and tasks requiring mental calculations performed in front of an audience and video camera.

Perhaps surprisingly, the researchers say, there was no difference in the tested genes between the two groups of people at the start of the study. The observed effects were seen only in the meditators following mindfulness practice. In addition, several other DNA-modifying genes showed no differences between groups, suggesting that the mindfulness practice specifically affected certain regulatory pathways.

However, it is important to note that the study was not designed to distinguish any effects of long-term meditation training from those of a single day of practice. Instead, the key result is that meditators experienced genetic changes following mindfulness practice that were not seen in the non-meditating group after other quiet activities — an outcome providing proof of principle that mindfulness practice can lead to epigenetic alterations of the genome.

Previous studies in rodents and in people have shown dynamic epigenetic responses to physical stimuli such as stress, diet, or exercise within just a few hours.

"Our genes are quite dynamic in their expression and these results suggest that the calmness of our mind can actually have a potential influence on their expression," Davidson says.

"The regulation of HDACs and inflammatory pathways may represent some of the mechanisms underlying the therapeutic potential of mindfulness-based interventions," Kaliman says. "Our findings set the foundation for future studies to further assess meditation strategies for the treatment of chronic inflammatory conditions."

Interesting. Need to analyze this paper ASAP.

neurosciencestuff:

Splice this: End-to-end annealing demonstrated in neuronal neurofilaments
While popularly publicized neuroscience research focuses on structural and functional connectomes, timing patterns of axonal spikes, neural plasticity, and other areas of inquiry, the intraneuronal environment also receives a great deal of investigative attention.
One example is the study of cytoskeletal polymers called neurofilaments –intermediate filaments of nerve cells that and a major component of the neuronal cytoskeleton believed to provide the axon with structural support. Neurofilaments are transported into axons where they accumulate during development, causing the axons to expand in girth. This is important because the cross-sectional area of an axon influences the rate of propagation of the nerve impulse. The space-filling properties of these polymers are maximized by spoke-like projection domains called side-arms that function to space the polymers apart. Once in the axons these polymers (which are barely 10 nm in diameter) can grow to reach remarkably long lengths – 100,000 nm (0.1 mm) or more – but how they attain such lengths and how their length is regulated is not known. Recently, scientists at The Ohio State University – who previously showed that neurofilaments and vimentin filaments expressed in nonneuronal cell lines can lengthen by joining ends in a process known as end-to-end annealing – demonstrated robust and efficient end-to-end annealing of neurofilaments in nerve cells. In additions, the researchers reported evidence for a neurofilament-severing mechanism.
Read more

neurosciencestuff:

Splice this: End-to-end annealing demonstrated in neuronal neurofilaments

While popularly publicized neuroscience research focuses on structural and functional connectomes, timing patterns of axonal spikes, neural plasticity, and other areas of inquiry, the intraneuronal environment also receives a great deal of investigative attention.

One example is the study of cytoskeletal polymers called neurofilaments –intermediate filaments of nerve cells that and a major component of the neuronal cytoskeleton believed to provide the axon with structural support. Neurofilaments are transported into axons where they accumulate during development, causing the axons to expand in girth. This is important because the cross-sectional area of an axon influences the rate of propagation of the nerve impulse. The space-filling properties of these polymers are maximized by spoke-like projection domains called side-arms that function to space the polymers apart. Once in the axons these polymers (which are barely 10 nm in diameter) can grow to reach remarkably long lengths – 100,000 nm (0.1 mm) or more – but how they attain such lengths and how their length is regulated is not known. Recently, scientists at The Ohio State University – who previously showed that neurofilaments and vimentin filaments expressed in nonneuronal cell lines can lengthen by joining ends in a process known as end-to-end annealing – demonstrated robust and efficient end-to-end annealing of neurofilaments in nerve cells. In additions, the researchers reported evidence for a neurofilament-severing mechanism.

Read more

kotakucom:

Iron Man vs Assassin’s Creed vs Dragonball vs Daft Punk vs Gundam. By BossLogic.

More here.

Sick!

(via fuckyeahattackoftheshow)

neurosciencestuff:

FYI: Do Lobotomies Work?
Surprisingly, yes.
The modern lobotomy originated in the 1930s, when doctors realized that by severing fiber tracts connected to the frontal lobe, they could help patients overcome certain psychiatric problems, such as intractable depression and anxiety. Over the next two decades, the procedure would become simple and popular, completed by poking a sharpened tool above the eyeball. According to one study, about two thirds of patients showed improvement after surgery.
Unfortunately, not all lobotomy practition-ers were responsible, and the technique left some patients with severe side effects, including seizures, lethargy, changes in personality, and incontinence. In response, doctors refined their techniques. They replaced the lobotomy with more specialized approaches: the cingulotomy, the anterior capsulotomy, and the subcaudate tractotomy. Studies of these procedures found evidence of benefit for at least one fourth of patients suffering from problems such as OCD and depression.
Even with the risk of side effects, those in the field still say the procedures were by and large successful. “I feel that the principle behind ablative surgery was somewhat exonerated by the research findings, which showed that it worked for very specific indications,” says Konstantin Slavin, president of the American Society for Stereotactic and Functional Neurosurgery, and professor at the Uni­versity of Illinois at Chicago.
By the 1980s, lobotomies had fallen out of fashion. “In general, the entire functional neurosurgery field moved away from destruction—from ablative surgery,” Slavin says. A then-new technique called deep-brain stimulation made ablative surgery obsolete. In the procedure, a surgeon drills holes in the head and inserts electrodes into the neural tissue. When current passes through the leads, they activate or inactivate patches of the brain. “The attractive part is that we don’t destroy the tissue,” Slavin says. Doctors can also adjust treatment if a patient suffers side effects. They can turn the current down or suspend it altogether—so as to “give the brain a holiday,” as Slavin calls it.
Most deep-brain stimulation is now used to treat movement disorders such as Parkinson’s Disease. The surgical treatment of patients with OCD is FDA-approved but reserved only for extreme cases. Slavin and his colleagues have been examining broader uses in an ongoing study. “Within the next five years, we hope we’ll have a definitive answer of whether or not it works.”

Interesting.

neurosciencestuff:

FYI: Do Lobotomies Work?

Surprisingly, yes.

The modern lobotomy originated in the 1930s, when doctors realized that by severing fiber tracts connected to the frontal lobe, they could help patients overcome certain psychiatric problems, such as intractable depression and anxiety. Over the next two decades, the procedure would become simple and popular, completed by poking a sharpened tool above the eyeball. According to one study, about two thirds of patients showed improvement after surgery.

Unfortunately, not all lobotomy practition-ers were responsible, and the technique left some patients with severe side effects, including seizures, lethargy, changes in personality, and incontinence. In response, doctors refined their techniques. They replaced the lobotomy with more specialized approaches: the cingulotomy, the anterior capsulotomy, and the subcaudate tractotomy. Studies of these procedures found evidence of benefit for at least one fourth of patients suffering from problems such as OCD and depression.

Even with the risk of side effects, those in the field still say the procedures were by and large successful. “I feel that the principle behind ablative surgery was somewhat exonerated by the research findings, which showed that it worked for very specific indications,” says Konstantin Slavin, president of the American Society for Stereotactic and Functional Neurosurgery, and professor at the Uni­versity of Illinois at Chicago.

By the 1980s, lobotomies had fallen out of fashion. “In general, the entire functional neurosurgery field moved away from destruction—from ablative surgery,” Slavin says. A then-new technique called deep-brain stimulation made ablative surgery obsolete. In the procedure, a surgeon drills holes in the head and inserts electrodes into the neural tissue. When current passes through the leads, they activate or inactivate patches of the brain. “The attractive part is that we don’t destroy the tissue,” Slavin says. Doctors can also adjust treatment if a patient suffers side effects. They can turn the current down or suspend it altogether—so as to “give the brain a holiday,” as Slavin calls it.

Most deep-brain stimulation is now used to treat movement disorders such as Parkinson’s Disease. The surgical treatment of patients with OCD is FDA-approved but reserved only for extreme cases. Slavin and his colleagues have been examining broader uses in an ongoing study. “Within the next five years, we hope we’ll have a definitive answer of whether or not it works.”

Interesting.

Yup!  So true.  Found this in Mathematics for Physical Chemistry by Donald A. McQaurrie.

Yup! So true. Found this in Mathematics for Physical Chemistry by Donald A. McQaurrie.

laboratoryequipment:

Bacteria, Iron Cooperate to Clean Uranium from WaterSince 2009, SLAC scientist John Bargar has led a team using synchrotron-based X-ray techniques to study bacteria that help clean uranium from groundwater in a process called bioremediation. Their initial goal was to discover how the bacteria do it and determine the best way to help, but during the course of their research the team made an even more important discovery: nature thinks bigger than that.The researchers discovered that bacteria don’t necessarily go straight for the uranium, as was often thought to be the case. The bacteria make their own, even tinier allies – nanoparticles of a common mineral called iron sulfide. Then, working together, the bacteria and the iron sulfide grab molecules of a highly soluble form of uranium known as U(VI), or hexavalent uranium, and transform them into U(IV), a less-soluble form that’s much less likely to spread through the water table. According to Barger, this newly discovered partnership may be the basis of a global geochemical process that forms deposits of uranium ore.Read more: http://www.laboratoryequipment.com/news/2013/03/bacteria-iron-cooperate-clean-uranium-water-0

And it’s stuff like this made have an interest in microbiology.

laboratoryequipment:

Bacteria, Iron Cooperate to Clean Uranium from Water

Since 2009, SLAC scientist John Bargar has led a team using synchrotron-based X-ray techniques to study bacteria that help clean uranium from groundwater in a process called bioremediation. Their initial goal was to discover how the bacteria do it and determine the best way to help, but during the course of their research the team made an even more important discovery: nature thinks bigger than that.

The researchers discovered that bacteria don’t necessarily go straight for the uranium, as was often thought to be the case. The bacteria make their own, even tinier allies – nanoparticles of a common mineral called iron sulfide. Then, working together, the bacteria and the iron sulfide grab molecules of a highly soluble form of uranium known as U(VI), or hexavalent uranium, and transform them into U(IV), a less-soluble form that’s much less likely to spread through the water table. According to Barger, this newly discovered partnership may be the basis of a global geochemical process that forms deposits of uranium ore.

Read more: http://www.laboratoryequipment.com/news/2013/03/bacteria-iron-cooperate-clean-uranium-water-0

And it’s stuff like this made have an interest in microbiology.