University of Utah biologists found new evidence why mice, people and other vertebrate animals carry thousands of varieties of genes to make immune-system proteins named MHCs – even though some of those genes make us susceptible to infections and to autoimmune diseases.

“Major histocompatibility complex” (MHC) proteins are found on the surface of most cells in vertebrate animals. They distinguish self from foreign, and trigger an immune response against foreign invaders. MHCs recognize invading germs, reject or accept transplanted organs and play a role in helping us smell compatible mates.

“This study explains why there are so many versions of the MHC genes, and why the ones that cause susceptibility to diseases are being maintained and not eliminated,” says biology Professor Wayne Potts. “They are involved in a never-ending arms race that causes them, at any point in time, to be good against some infections but bad against other infections and autoimmune diseases.”

By allowing a disease virus to evolve rapidly in mice, the study produced new experimental evidence for the arms race between genes and germs – known technically as “antagonistic coevolution.” The findings will be published online the week of Feb. 6, 2012, in the journal Proceedings of the National Academy of Sciences.

Potts, the senior author, ran the study with first author and former doctoral student Jason Kubinak, now a postdoctoral fellow in pathology. Other co-authors were biology doctoral student James Ruff, biology undergraduate C. Whitney Hyzer and Patricia Slev, a clinical assistant professor of pathology. The research was funded by the National Science Foundation and the National Institute of Allergy and Infectious Diseases.

Theories for the Diversity of Immune-System MHC Genes

Most genes in humans and other vertebrate have only one or two “alleles,” which are varieties or variants of a single gene. Although any given person carries no more than 12 varieties of the six human MHC genes, the human population has anywhere from hundreds to 2,300 varieties of each of the six human genes that produce MHC proteins.

“The mystery is why there are so many different versions of the same [MHC] genes in the human population,” Kubinak says, especially because many people carry MHCs that make them susceptible to many pathogens (including the AIDS virus, malaria and hepatitis B and C) and autoimmune diseases (including type I diabetes, rheumatoid arthritis, lupus, multiple sclerosis, irritable bowel disease and ankylosing spondylitis).

Scientists have proposed three theories for why so many MHC gene variants exist in vertebrate animal populations (invertebrates don’t have MHCs), and say all three likely are involved in maintaining the tremendous diversity of MHCs:

– An organism with more MHC varieties has a better immune response than organisms with fewer varieties, so over time, organisms with more MHCs are more likely to survive. However, this theory cannot explain the full extent of MHC diversity.

– Previous research indicates people and other animals are attracted to the smell of potential mates with MHCs that are “foreign” rather than “self.” Parents with different MHC variants produce children with more MHCs and thus stronger immune systems.

– Antagonistic coevolution between an organism and its pathogens. Kubinak says: “We have an organism and the microbes that infect it. Microbes evolve to better exploit the organism, and the organism evolves better defenses to fight off the infection. One theory to explain this great diversity in MHC genes is that those competing interests over time favor retaining more diversity.”

The Arms Race between Germs and MHC Genes

“You naturally keep genes that fight disease,” Kubinak says. “They help you survive, so those MHC genes become more common in the population over time because the people who carry them live to have offspring.”

Pathogens – disease-causing viruses, bacteria or parasites – infect animals, which defend themselves with MHCs that recognize the invader and trigger an immune response to destroy the invading pathogen.

But over time, some pathogens mutate and evolve to become less recognizable by the MHCs and thus evade an immune response. As a result, the pathogens thrive. MHCs that lose the battle to germs become less common because they now predispose people who carry them to get sick and maybe die. It was thought such disease-susceptibility MHC genes eventually should vanish from the population, but they usually don’t.

Why? While some of those MHCs do go extinct, others can persist, for two reasons. First, some of the now-rare MHCs gain an advantage because they no longer are targeted by evolving microbes, so they regain an ability to detect and fight the same germ that earlier defeated them – after that germ mutates yet again. Second, some of the rare MHCs can mount an effective immune response against completely different microbes.

How the Study was Performed; Implications of the Findings

The researchers studied 60 mice that were genetically identical, except the mice were divided into three groups, each with a different variety of MHC genes known as b, d and k, respectively.

A mouse leukemia virus named the Friend virus was grown in tissue culture and used to infect two mice from each of the three MHC types. The fast-evolving retrovirus grew within the mice for 12 days, attacking, enlarging and replicating within the spleen and liver. Virus particles in the spleen were collected, and the severity of illness was measured by weighing the enlarged spleen.

Then, virus taken from each of the first three pairs of mice (b, d and k) was used to infect another three pair of mice with the same MHC types. The process was repeated until 10 pairs of mice in each MHC type were infected, allowing the virus time to mutate.

In this first experiment, the biologists showed they could get the Friend virus to adapt to and thus evade the MHC variants (b, d or k) in the mouse cells it attacked.

Next, the researchers showed that the virus adapted only to specific MHC proteins. For example, viruses that adapted to and sickened mice with the MHC type b protein still were attacked effectively in mice that had the type d and k MHCs.

In the third experiment, the researchers showed that pathogen fitness (measured by the number of virus particles in the spleen) correlated with pathogen virulence (as measured by spleen enlargement and thus weight). So the virus that evaded MHC type b made mice with that MHC sicker.

Together, the experiments demonstrate “the first step in the antagonistic coevolutionary dance” between a virus and MHC genes, Potts says.

Potts says the findings have some important implications:

– The use of antibiotics to boost productivity in dairy herds and other livestock is a major reason human diseases increasingly resist antibiotics. Selective breeding for more milk and beef has reduced genetic diversity in livestock, including their MHCs. So breeding more MHCs back into herds could enhance their resistance to disease and thus reduce the need for antibiotics.

– Because their populations are diminished, endangered species have less genetic diversity, making them an easier target for germs. Potts says it would be desirable to breed protective MHCs back into endangered species to bolster their disease defenses.

– Genetic variation of MHCs in people and other organisms is important for limiting the evolution and spread of emerging diseases. In effect, Potts and colleagues created emerging diseases by making a virus evolve in mice. “It’s a model to identify what things change in viruses to make them more virulent and thus an emerging disease.”

Source: University of Utah
Photo: This electron microscope image shows yellow particles of a mouse leukemia virus named Friend virus emerging or “budding” out of an infected white blood cell known as a T-cell. ~ Elizabeth Fischer and Kim Hasenkrug, NIH.

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The famed “corpse flower” plant – known for its giant size, rotten-meat odor and phallic shape – has a new, smaller relative: A University of Utah botanist discovered a new species of Amorphophallus that is one-fourth as tall but just as stinky.

The new species, collected on two small islands off Madagascar, brings to about 170 the number of species in the genus Amorphophallus, which is Greek for “misshapen penis” because of the shape of the plants’ flower-covered shaft, called the inflorescence or the spadix, says Greg Wahlert, a postdoctoral researcher in biology.

The 4.5-foot-tall plant, Amorphophallus perrieri, began reeking Friday, Feb. 3 as it approached the peak of its bloom in a campus greenhouse. A day later, Wahlert began cutting down the plant in stages so the spadix, the surrounding leafy spathe and other parts could be pressed, mounted and submitted to the National Museum of Natural History in Paris as part of the process of designating the plant a new species.

That won’t be official until about a year from now after Wahlert publishes a scientific paper formally describing the species, which can grow to 5 feet high, and how it differs from relatives in the genus, including Amorphophallus titanum – also known as the “corpse plant,” “corpse flower” and “titan arum” – which grows to 20 feet high.

After Wahlert first collected specimens of the new plant in 2006 and 2007 and discovered it was a new species, he found the Paris museum’s herbarium held a dried specimen collected from one of the same islands by French botanist-geologist Joseph Marie Henri Perrier de la Bâthie (1873-1958), who didn’t realize it was a new species. So Wahlert is naming it for Perrier.

“Perrier collected it in 1932, and it sat in the museum until we dug it up and compared it to the other specimens and the plants that I had collected,” Wahlert says. “Perrier spent years working on scores of other plant groups [and describing hundreds of other new species] and just never got around to it.”

The corpse flower smells like rotting meat to attract the flies and beetles that pollinate it. Wahlert had expected the new species would smell like cheese, which it did briefly when it began blooming Feb. 3. But the odor soon grew worse – much worse – and more like its giant relative.

“I smelled rotting roadkill out in the sun reeking,” says University of Utah biology Professor Lynn Bohs, in whose lab Wahlert works. “There’s also a note of public restroom – a Porta Potty smell.”

Wahlert added: “I would say carrion and feces. When you get right up to it, it’s really foul and disgusting.”

Another Utah researcher collected volatile gases emitted by the plant “and will identify the components of the smell,” Wahlert says. Only a small group of Amorphophallus species have been tested for odors, but the known aromas range from rotting meat to anise, cheese, dung, fish, urine, spice and chocolate, he adds.

Two weeks before the plant began to bloom, “it was just a little bud sticking out of the dirt,” he says. When it bloomed, the stalk was almost 4 feet tall and the inflorescence or spadix was about 10 inches long. It was yellow, with pollen on the top part. The lower part, hidden by the reddish, leafy spathe, was covered by hundreds of tiny flowers, each a fraction of an inch wide. (Sometimes the entire spadix is referred to informally as the flower.)

“They are just so rude – their appearance and smell,” Bohs says. “Everybody I’ve talked to says they almost started puking when they smelled it. It’s horrid.”

In the Same Family as Philodendrons and Skunk Cabbage

Some thought the plants’ suggestive genus name was horrid. In 2008, Sir David Attenborough said he invented the name “titan arum” for the corpse flower for his BBC series “The Private Life of Plants” because he thought it would be inappropriate to repeatedly refer to Amorphophallus.

Bohs says the genus belongs to the family Araceae, commonly known as the arum or aroid family. The family includes philodendrons, taro root (from which Hawaiians make poi), skunk cabbage and anthurium, a plant common in floral arrangements, with a yellow spadix surrounded by a leafy, red, heart-shaped spathe.

Wahlert says plants in the genus Amorphophallus are found in southern Asia, the South Pacific, Australia and Africa, including Madagascar. Of the 170 or so species in the genus, which first was discovered in 1834, “a lot have been known for 150 years, but one, two or three new species are described every year,” he adds.

A. titanum grows naturally only in Sumatra in Indonesia, although it is found around the world in greenhouses that compete for the largest corpse flower plant. The Guinness Book of Records title currently is held by a New Hampshire specimen that had a spadix measuring 10-feet-2.25-inches tall in 2010. Counting the stem and spadix, A. titanum can reach 20 feet tall, compared with a 5-foot maximum for A. perrieri, which has a longer stem and shorter spadix – about 10 inches long in the case of the one that bloomed on campus.

New Species Collected from a Burial Island

Wahlert collected the new species from Nosy Mitsio and Nosy Ankarea – two islands northwest of Madagascar, which is off the east coast of Africa. “Nosy” means island in the Malagasy language. The plant since has been found on Madagascar.

He had to obtain permission from a local village to visit Nosy Ankarea, an uninhabited, half-mile-wide island where the Sakalava people buried their rulers. Unlike Ankarea, which is still vegetated, Mitsio is heavily deforested. A. perrieri was found there in low scrub behind beach dunes.

“I went there in 2006 to collect tree violets, and when I got there I discovered these Amorphophallus in full bloom on the first day in the field,” cutting and collecting four or five specimens, Wahlert says. “That night I got malaria. I stayed there a week but was so sick I couldn’t do much collecting.”

After the trip, Wahlert showed the specimens to Dutch botanist Wilbert Hetterscheid of Wageningen University. Hetterscheid, an expert on Amorphophallus, said they were a new species, and is co-authoring the descriptive paper with Wahlert.

In October 2007, Wahlert went back to the islands at the end of the dry season, and once again the new species were in full bloom. He collected 15 tubers – the roots – so he could grow the plants.

Wahlert kept the live plants at various institutions where he worked and gave others away, ending up with one left when he moved to Utah last fall.

Why should anyone care about a stinking plant with a suggestive shape?

“It’s not high-tech, but it’s still important to describe new species, to document biodiversity, particularly in a place like Madagascar, which is one of the world’s great biodiversity hotspots,” Wahlert says. “It’s been severely deforested and is continuing to be deforested. So it’s important to document new species before they go extinct.”

Source: University of Utah
Photo 1: Close-up of the reddish-purplish, leafy “spathe” surrounding the central “spadix” of the newly discovered plant species Amorphophallus perrieri, which grows to 5 feet tall. ~ Cameron McIntire, University of Utah.
Photo 2: University of Utah botanist Greg Wahlert stands next to a new plant species he discovered — Amorphophallus perrieri. ~ Lee J. Siegel, University of Utah

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The University of Haifa is hosting an international conference of leading brain researchers from around the world next week, where the participants will be attempting to answer the question of where and how memory is stored; or in less ordinary terms: “Cell and molecular mechanisms of memory formation”. “The more we know about where and how memory is formed, the better we will be able to treat diseases that are related to the brain’s memory mechanisms, such as Alzheimer’s and Parkinson’s,” says Prof. Kobi Rosenblum, Head of the Department of Neurobiology at the University of Haifa, who is organizing the conference with Dr. Raphael Lamprecht (for more information and a detailed program, visit http://neuro.haifa.ac.il ).

About 30 brain researchers from around the world will be joining another 30 researchers from Israel at the conference, which is taking place on 5-7 February, 2012. All of the participating experts have a background in researching various aspects of memory formation, from the most basic molecular mechanisms to advanced brain imaging. The conference is being organized by the University of Haifa’s Department of Neurobiology, the University’s Haifa Forum for Brain and Behavior, and the international Molecular and Cellular Cognition Society. More than 100 of the latest studies in the field will be presented at the conference.

A special feature will be an open discussion, where Israel Prize winner and faculty member of the University of Haifa’s Department of Psychology Prof. Asher Koriat will argue that describing cognition and describing material mechanisms are two different and distant fields. In other words, he claims that molecular and electrophysiology brain researchers cannot really find explanations for cognitive processes. Dozens of brain researchers will contend with this claim at the open discussion.

“The fact that such a large international conference is being held at the University of Haifa is an indicator of the outstanding basic neurobiology research being conducted at the university and of the significance we assign to this field. I am confident that the conference will bring us another step closer to solving the most complex puzzle of all – the human brain,” says Prof. Rosenblum.

Source: University of Haifa
Photo: Prof. Kobi Rosenblum, Head of the Department of Neurobiology at the University of Haifa, who is organizing the conference with Dr. Raphael Lamprecht. Courtesy of the University of Haifa (photo: Gil Nehushtan)

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Many infections, even those caused by antibiotic-sensitive bacteria, resist treatment. This paradox has vexedphysicians for decades, and makes some infections impossible to cure.

A key cause of this resistance is that bacteria become starved for nutrients during infection. Starved bacteria resist killing by nearly every type of antibiotic, even ones they have never been exposed to before.

What produces starvation-induced antibiotic resistance, and how can it be overcome? In a paper appearing this week in Science, researchers report some surprising answers.

“Bacteria become starved when they exhaust nutrient supplies in the body, or if they live clustered together in groups known as biofilms,” said the lead author of the paper, Dr. Dao Nguyen, an assistant professor of medicine at McGill University.

Biofilms are clusters of bacteria encased in a slimy coating, and can be found both in the natural environment as well as in human tissues where they cause disease. For example, biofilm bacteria grow in the scabs of chronic wounds, and the lungs of patients with cystic fibrosis. Bacteria in biofilms tolerate high levels of antibiotics without being killed.

“A chief cause of the resistance of biofilms is that bacteria on the outside of the clusters have the first shot at the nutrients that diffuse in,” said Dr. Pradeep Singh, associate professor of medicine and microbiology at the University of Washington, the senior author of the study. “This produces starvation of the bacteria inside clusters, and severe resistance to killing.”

Starvation was previously thought to produce resistance because most antibiotics target cellular functions needed for growth. When starved cells stop growing, these targets are no longer active. This effect could reduce the effectiveness of many drugs.

“While this idea is appealing, it presents a major dilemma,” Nguyen noted. “Sensitizing starved bacteria to antibiotics could require stimulating their growth, and this could be dangerous during human infections.”

Nguyen and Singh explored an alternative mechanism. Microbiologists have long known that when bacteria sense that their nutrient supply is running low, they issue a chemical alarm signal. The alarm tells the bacteria to adjust their metabolism to prepare for starvation. Could this alarm also turn on functions that produce antibiotic resistance?

To test this idea, the team engineered bacteria in which the starvation alarm was inactivated, and then measured antibiotic resistance in experimental conditions in which bacteria were starved. To their amazement, bacteria unable to sense starvation were thousands of times more sensitive to killing than those that could, even though starvation arrested growth and the activity of antibiotic targets.

“That experiment was a turning point,” Singh said. “It told us that the resistance of starved bacteria was an active response that could be blocked. It also indicated that starvation-induced protection only occurred if bacteria were aware that nutrients were running low.”

With the exciting result in hand, the researchers turned to two key questions. First does the starvation alarm produce resistance during actual infections? To test this the team examined naturally starved bacteria, biofilms, isolates taken from patients, and bacterial infections in mice. Sure enough, in all cases the bacteria unable to sense starvation were far easier to kill.

The second question was about the mechanism of the effect. How does starvation sensing produce such profound antibiotic resistance? Again, the results were surprising.

Instead of well-described resistance mechanisms, like pumps that expel antibiotics from bacterial cells, the researchers found that the bacteria’s protective mechanism defended them against toxic forms of oxygen, called radicals. This mechanism jives with new findings showing that antibiotics kill by generating these toxic radicals.

The findings suggest new approaches to improve treatment for a wide range of infections.

“Discovering new antibiotics has been challenging,” Nguyen said. “One way to improve infection treatment is to make the drugs we already have work better. Our experiments suggest that antibiotic efficacy could be increased by disrupting key bacterial functions that have no obvious connection to antibiotic activity.”

The work also highlights the critical advantage of being able to sense environmental conditions, even for single-celled organisms like bacteria. Cells unaware of their starvation were not protected, even though they ran out of nutrients and stopped growth. This proves again that, even for bacteria, “what you don’t know can hurt you.”

The Burroughs Welcome Fund, the Cystic Fibrosis Foundation, the National Institutes of Health, and the Canadian Institutes for Health Research supported this research.

The results are contained in the Science article, “Active starvation responses mediate antibiotic tolerance in biofilms and nutrient-limited bacteria.”

In addition to Nguyen and Singh, the researchers on the study were Amruta Joshi-Datar, Elizabeth Bauerle, Karlyn Beer, and Richard Siehnel of the Departments of Medicine and of Microbiology at the UW, James Schafhauser of McGill University, Francois Lepine of INRS Armand Frappier in Canada, Oyebode Olakanmi and Bradley E. Britigan of the University of Cincinnati, and Yun Wang of Northwestern University.

Source: University of Washington
Photo: Bacterial clusters living in the lungs of a cystic fibrosis patient are highly resistant to killing by antibiotics. Credit: Singh lab

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“Neuroscientists have long known that some people have a better sense of touch than others, but the reasons for this difference have been mysterious,” said Daniel Goldreich, PhD, of McMaster University in Ontario, one of the study’s authors. “Our discovery reveals that one important factor in the sense of touch is finger size.”

To learn why the sexes have different finger sensitivity, the authors first measured index fingertip size in 100 university students. Each student’s tactile acuity was then tested by pressing progressively narrower parallel grooves against a stationary fingertip — the tactile equivalent of the optometrist’s eye chart. The authors found that people with smaller fingers could discern tighter grooves.

“The difference between the sexes appears to be entirely due to the relative size of the person’s fingertips,” said Ethan Lerner, MD, PhD, of Massachusetts General Hospital, who is unaffiliated with the study. “So, a man with fingertips that are smaller than a woman’s will be more sensitive to touch than the woman.”

The authors also explored why more petite fingers are more acute. Tinier digits likely have more closely spaced sensory receptors, the authors concluded. Several types of sensory receptors line the skin’s interior and each detect a specific kind of outside stimulation. Some receptors, named Merkel cells, respond to static indentations (like pressing parallel grooves), while others capture vibrations or movement.

When the skin is stimulated, activated receptors signal the central nervous system, where the brain processes the information and generates a picture of what a surface “feels” like. Much like pixels in a photograph, each skin receptor sends an aspect of the tactile image to the brain — more receptors per inch supply a clearer image.

To find out whether receptors are more densely packed in smaller fingers, the authors measured the distance between sweat pores in some of the students, because Merkel cells cluster around the bases of sweat pores. People with smaller fingers had greater sweat pore density, which means their receptors are probably more closely spaced.

“Previous studies from other laboratories suggested that individuals of the same age have about the same number of vibration receptors in their fingertips. Smaller fingers would then have more closely spaced vibration receptors,” Goldreich said. “Our results suggest that this same relationship between finger size and receptor spacing occurs for the Merkel cells.”

Whether the total number of Merkel cell clusters remains fixed in adults and how the sense of touch fluctuates in children as they age is still unknown. Goldreich and his colleagues plan to determine how tactile acuity changes as a finger grows and receptors grow farther apart.

The research was supported by the National Eye Institute and the Natural Sciences and Engineering Research Council in Canada.

_____
Source: Society for Neuroscience
Photo: nesharm / iStockphoto

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The findings appeared in the Nov. 9 issue of the Archives of Ophthalmology.

The macula, located within the retina, is an area of high-resolution central vision that is needed to read or drive, for example. This area is damaged in more common retinal conditions such as macular degeneration and can be damaged by diabetes.

“It is rare to find a new inherited eye disease that affects the macula. We thought we had seen them all,” said the study’s lead author Vinit Mahajan, M.D., Ph.D., assistant professor of ophthalmology and visual sciences at the UI Roy J. and Lucille A. Carver College of Medicine.

“This newly found retinal disease causes abnormal blood vessels in the macula, and these vessels are prone to bleeding. This causes swelling or scars that ‘black out’ or blur parts of the field of vision,” said Mahajan, who also is a retinal specialist with UI Hospitals and Clinics.

The finding came about when one person in a family in the United States sought care for eye problems. “If a doctor saw just one family member, they would probably call this macular degeneration. We knew there was something different, and we had to examine the rest of the family,” Mahajan said.

The team assessed 20 extended family members who were not blind but had visual problems of different severities. Some family members also had areas of central vision loss, and some family members had strabismus, a disorder in which the eyes are not aligned.

The UI researchers have presented their findings at international meetings of retinal specialists in Arizona, Florida and London. The investigators are now working with researchers worldwide to determine if other people have this particular disease.

“Through our paper and by sharing pictures of what the affected eye looks like, we hope to find more people affected,” Mahajan said. “We also will work to find the gene that causes the condition. This information could be very useful in eventually preventing or treating this and other diseases that affect the macula.”

The advanced genetics research capabilities at the UI Carver Family Center for Macular Degeneration increase the likelihood of finding a gene, Mahajan said.

The study’s senior author was Edwin Stone, M.D., Ph.D., Howard Hughes Medical Institute investigator and UI professor of ophthalmology and visual sciences. Stephen Russell, M.D., UI professor of ophthalmology and visual sciences, also contributed to the study.

The study was supported in part by grants from the Foundation Fighting Blindness and Research to Prevent Blindness.

Source: The University of Iowa

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The team of researchers discovered that influenza virus’ contain a protein called M2, which destroys or damages the epithelial cells of our lungs by removing liquid from inside, promoting the early stages of pneumonia as well as other lung problems.

The research was carried out in four steps. First, the lung protein was injected into frog eggs to measure its function. Second, the M2 protein from H1N1 virus and the lung protein were injected into frog eggs and the researchers discovered that the M2 protein caused the lung protein function to decrease significantly.

The team then isolated the segment of the virus M2 protein responsible for the damage to the lung protein and were able to demonstrate that without this segment, the virus was unable to damage the lung protein. Lastly, an intact virus M2 protein and the lung protein were then re-injected into frog eggs along with antioxidant drugs. The antioxidants prevented the virus M2 protein from damaging the lung protein. When these experiments were repeated using human lung cells, the results were exactly the same.

“Although vaccines will remain the first line of intervention against the flu for a long time to come, this study opens the door for entirely new treatments geared toward stopping the virus after you’re sick,” said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal, “and this discovery is another reason to drink red wine to your health.”

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Unfortunately it would not allow for non-invasive brain stimulation. However it could potentially be used in deep brain stimulation devices. Current deep brain stimulation devices are basically brain implants that use electricity to alter the surrounding brain tissue. A person requires brain surgery to get a deep brain stimulation implant. The deep brain stimulation device is hooked up to a battery that is inserted into a person’s chest. In the future scientists may be able to use infrared light for deep brain stimulation implants in place of the electricity that is used now. This would allow a better targeting accuracy and higher efficacy for those types of brain implants.

Infrared brain stimulation may be used for a variety of other therapeutic indications. Researchers may use it for those who have traumatic brain injuries. It could potentially be a useful tool for brain rehabilitation. Infrared nerve stimulation would allow for a more precise mapping of the brain’s cortex. It would enable scientists to better understand the functioning of the brain by selectively activating for deactivating specific brain regions.

Researchers have recently used infrared to stimulate nerve cells that are located in a person’s ear. An ear implant based on this technology would allow a deaf person to hear again. It would also allow for much better sound than current hearing implants provide.

Scientists are currently not quite sure how infrared light actually excites brain cells. They believe that it may have something to due with the increase in heat that comes along with the infrared light. Other types of electromagnetic radiation such as radio waves also have the ability to affect the functioning of the brain. Scientists still have a lot of research to perform to better understand this mechanism of brain stimulation. In the future, though, these new brain manipulation tools should increasingly find more and more use.

__________
About the Author:
Robert Webb has a blog that focuses on new neurotechnology methods of brain stimulation, brain-computer interfaces, neuroscience, brain emulation, altering consciousness and miscellaneous futurism at http://brainstimulant.blogspot.com.

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One proof that right-handed people are “right-eared” is when we talk on the phone. In most cases, right-handed people use their right ear to talk on the phone. This does not only apply to hands and ears. The main point of it all is that we all have a dominant hand, dominant ear, dominant foot and other parts of the body that we prefer using. Some of us may have noticed that even when we are chewing food, we prefer chewing using one side of the jaw only.

So, which ear can people hear best with? Are we convinced that if we are right-handed, then we are also right-eared? This is true based on the results of some studies. However, there are also results of studies indicating that it does not follow that right-handed people are also right-eared but then, it has been proven that the right and the left ear work differently. In a research conducted using infants as subjects, it was concluded that voice-like sounds are better heard by the right ear and singing-like sounds are better heard by the left ear.. This conclusion may also be the answer as to why most people use the right ear to talk on a telephone.

Several studies have been conducted by researchers in order to know which ear can people hear best with. So far, the most popular research ever conducted is the one where infants were used as subjects. To discuss further the singing-like sounds that are better heard by the left ear, it was also found outer that emotional talks, including sweet nothings, are better heard using the left ear.

The findings of studies on which ear can people hear best with actually have a relation to the results of the studies conducted on brain functions. Conclusions on studies on brain functions include that prolonged sound vibrations or speech are processed via the brain’s left hemisphere while tones are processed via the brain’s right hemisphere. The cross connections of such hemispheres then allow the left ear to hear singing-like sounds while the right ear hears voice-like vibrations.

This means that the answer to the question which ear can people hear best with is “it depends.” We may notice ourselves using our right ear more often than our left ear but this may be because of the fact that we are talking to someone on the phone. We may also notice ourselves using our left ear more often than our right ear but that is probably because we are listening to music.

So, is it important to know which ear can people hear best with? Well, it’s interesting to know the results of the studies conducted but what’s more important is the fact that we are blessed to have useful ears.

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So how do cold-blooded creatures cope with this season, anyway? First of all, let’s be clear on what, “cold-blooded” means. This is actually an inaccurate and outdated word. We’re talking about animals that get their heat from their environment, like amphibians, reptiles, insects and other arthropods, and fish. We call them “ectothermic”, meaning literally, “outside heat”. These creatures seek out warm places or cooler places in order to stay just the right temperature. The benefit of being ectothermic is food. They don’t need to eat nearly as much as mammals and birds who need to fuel that fire within. Going without eating for a few months therefore works for them; winter’s cold though is a challenge.

I’ve compiled a few ectothermic animals and their amazing adaptations for surviving winter. These over-wintering strategies have developed over a long period of time enabling generation after generation to carry on from year to year.

Yellow-jackets and Hornets: During summer months, a whole colony of sterile female workers are busy hunting for insects, raising young and caring for the colony while the queen lays eggs. Toward the end of the season, the queen lays eggs that develop into fertile females and males, who, once mature, mate. The fertilized females are the only ones who over-winter; every other colony member dies. Each female may find a bark crevice, rotten log, or pile of leaves to hide in. These queens single-handedly start a new colony next spring.

Mosquitoes: Mosquitoes from temperate regions have varying winter strategies. The adults of some species die, after leaving cold-hardy eggs that over-winter under ice. When the water warms in spring, the eggs will hatch. In other species, females who have mated in the fall will hibernate in a hollow log, your basement, or other secure place. This location does not have to stay above freezing, as the insect produces glycerol, which infuses its body and acts as a natural anti-freeze. Amazing.

Aquatic Frogs: Aquatic frogs, like leopard frogs, green frogs or American bullfrogs, spend the winter underwater in a low energy state. During this time, they have to breathe through their skin, so they cannot be buried deep in the mud where the oxygen content is low. They need to be where the water still has plenty of oxygen, so incoming streams and rivulets may be good places for them to be.

Terrestrial Frogs (Toads): The American toad is a good digger. It digs itself a deep burrow in which to over-winter below the frost line. Spring peepers and wood frogs cannot dig so well, and find themselves a crevice in which to sleep away the winter. The amazing thing is, the fluid in their bodies can freeze – without doing harm to the animal. Again, a natural antifreeze – glucose – infuses the vital organs, preventing ice crystals from piercing cells and body organs, and dropping the freezing point of water. A partially frozen frog wakes up in the spring none-the-worse for wear.

Snakes: Snakes spend the winter in a rock crevice, animal burrow, or deep hole under a root ball. It is necessary that this den be below frost level. Since there may not be many of these locations, many snakes oftentimes den together. Some garter snakes may number in the hundreds – or thousands – in a single hibernaculum, or winter den. Copperheads, black rat snakes and rattlesnakes commonly den together.

Each organism has a way of coping with winter’s challenges. During this time, life is certainly on-the-edge. Cold snaps can be disastrous. Still, amazingly, there are those who survive. The next time you are snuggled in your hibernaculum, think about some of those creatures outside who are awaiting the warming rays of spring sunshine..

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About the Author:
Nancy Condon is an award-winning Environmental Educator, cross-country canoeist, hike leader, fan of National Parks, and co-founder of NaturePods, Guides for the Nature Traveler. For unique programs to download to your iPod before you travel or explore the outdoors, visit NaturePods.

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