Matters of Taste

Compounds we perceive as sweet or bitter in the mouth trigger similar receptors and signaling pathways elsewhere in the body, helping to regulate digestion, respiration, and other systems.

By Thomas E. Finger and Sue C. Kinnamon | 

Shift Foto / Corbis

In the choice of what to ingest, the sense of taste is both a guardian and a guide. The sensations of bitter and sour keep us from eating potentially toxic substances and strong acids, while the preferred qualities of sweet, umami (the “savory” taste of glutamate), and salty drive intake of carbohydrates, amino acids, and sodium, respectively. Taste sensations are mediated by taste buds—small clusters of specialized epithelial cells on the tongue, soft palate, and larynx. Over the last two decades, as scientists have uncovered the array of G protein–coupled receptor (GPCR) cascades and ion channels that underlie taste signaling, they have also discovered, to their surprise, that the expression of these receptors and channels is not limited to taste buds. Indeed, elements of the taste transduction cascade occur in many chemoresponsive epithelial cells scattered throughout the stomach, the intestines, and even the airways. Despite the similarities in receptor molecules and signaling cascades, however, only the chemoreceptive systems in the mouth evoke a sensation of taste. The others, researchers are learning, serve different functions depending on their location.

The taste transduction story

The sensations of taste are divisible into five distinct qualities: salty, sour, bitter, sweet, and umami. Salty and sour sensory perceptions rely on ion channels, which are expressed in a variety of tissues, such as kidney, as well as in taste buds. Bitter, sweet, and umami qualities rely predominantly on two distinct families of GPCRs, Tas1R and Tas2R (T1R and T2R), first identified in taste tissues in 1999, but subsequently identified in other tissues, including gut and airway epithelia. Despite the difference in the qualities detected by the two families of taste receptors, both utilize similar, if not identical, downstream signaling effectors, including the taste receptor-associated G protein α-gustducin, one of the first identified proteins of a GPCR taste transduction cascade.

In 1996, researchers at the University of Würzburg reported that α-gustducin is expressed by brush cells of the stomach and intestine.¹

 

 Brush cells are tall, columnar epithelial cells that display a distinctive tuft of stiff microvilli at their apex. Based on morphological features, researchers had suspected that these cells were chemosensory, but the findings of gustducin, taste receptors,2

 

 and the ion channel TrpM5, another taste transduction element,3

 

 confirmed this early speculation, and suggested that brush cells detect nutrients in the gut. In the last 15 years, researchers have uncovered more and more taste cascade elements throughout the digestive tract, and even in the airways, suggesting a widespread distribution of complete taste transduction cascades—from taste receptor to transduction channel.

These seemingly misplaced taste-like pathways do not, however, give rise to sensations of taste, though they appear to detect compounds known to elicit a taste response in the mouth. Instead, these compounds initiate the taste transduction cascade with the end result of inducing particular physiological changes. For example, the pancreatic release of insulin in response to glucose is partially mediated by the binding of glucose to sweet-taste receptors on cells of the intestine and subsequent activation of the signaling cascade.⁴

 

 Similarly, accidental inhalation of a beverage into the airways triggers taste receptors there, but rather than evoking a sensation of taste, the substance is irritating and provokes choking or coughing. (Although we use the phrases “taste transduction” and “taste receptors” below, we do not mean to imply that these equate to a perception of taste.)

Indeed, for every taste transduction cascade discovered outside the oral cavity, researchers seek to uncover the functional significance of the chemoresponsive cells in those areas. Taken together, the findings suggest that the taste transduction cascade is not restricted to the sensation of taste per se, or even to systems regulating food intake. In fact, the receptors mediating taste transduction appear to have evolved early in the vertebrate lineage, and to have since been widely adopted as a chemodetection system in a variety of organ systems.

“Taste” in the gut

In taste buds, receptors of the T1R family combine to form either a sweet receptor (T1R2 + T1R3) or an umami receptor (T1R1 + T1R3), and signal the presence of macronutrients necessary for survival: a carbohydrate energy source or amino acids, respectively. In the gut, the presence of sweet substances is detected by hormone-producing cells known as enteroendocrine cells that respond by secreting the glucagon-like peptide GLP-1, which in turn stimulates the release of insulin from pancreatic β-cells. The presence of circulating insulin results in the uptake of glucose from the bloodstream by diverse tissues. In addition, activation of the sweet receptors in the gut drives the insertion of the glucose transporters SGLT-1 and GLUT2 into the membranes of cells lining the intestines, thereby facilitating uptake of glucose.⁵

 

^,6

 

While the presence of T1R-class receptors for macronutrients in the gut is an obvious means to regulate digestive functions, the function of widespread T2R bitter receptors throughout the GI tract is less clear. Researchers have shown in vitro that activation of T2R receptors in an enteroendocrine cell line results in release of the peptide hormone cholecystokinin (CCK), which can reduce gut motility. Thus, intake of a potential toxin that activates the T2R pathway should decrease the rate at which food passes through the stomach and lower the drive for continued eating.⁷

 

 Nonetheless, a recent study suggests that the lowered gut motility following intake of bitter substances is not dependent on T2R signaling, nor on CCK, leading researchers to reconsider the function of the receptors in this context.8

 

One possibility is that the CCK-secreting enteroendocrine cells are involved in a local epithelial signaling system that reduces transfer of toxic substances from gut into circulation. The CCK released from T2R-expressing enteroendocrine cells in response to stimulation by some bitter-tasting ligands may act on CCK2 receptors located on nearby intestinal epithelial cells, called enterocytes, which regulate the absorption of molecules from the intestinal lumen into the bloodstream.⁹

 

 In vitro studies show that activating CCK2 receptors on these cells increases expression of the transporter ABCB1, which pumps out toxins or unwanted substances from the cytoplasm, allowing the toxins to be excreted rather than absorbed into the blood. Thus, activation of T2R signaling in the intestines indirectly results in increased elimination of absorbed toxins from gut epithelium before the toxins can enter circulation.

Lower in the gut, activation of T2R receptors similarly appears to combat toxins, though via a different mechanism. When some bitter-tasting ligands bind to epithelial cells in the colon, they induce the secretion of anions, which leads to fluid secretion into the intestine.¹⁰

 

 This induced efflux of fluids is likely to flush out any noxious irritant from the colon, resulting in diarrhea.

“Taste” in the airways

Three years after taste-related signaling components were discovered in the gut, Zancanaro and colleagues at the University of Verona described the presence of gustducin-expressing cells in the airway. Specifically, the researchers examined mice and identified gustducin-expressing cells scattered in the epithelium lining the incoming ducts of the vomeronasal organ, a specialized part of the olfactory system found in many vertebrates, but not in adult humans. Such cells were also identified in the nasal respiratory epithelium. The morphology of these cells is similar to chemosensory cells scattered within the epidermis of fishes, first described by Mary Whitear in the 1970s. In a series of elegant ultrastructural studies, she identified a distinctive type of epithelial cell that extends through the height of the epithelium with microvillous extensions at its apical end. Since these cells also form extensive synapses at their base with local nerve fibers, Whitear suggested they must be a sensory cell type. Furthermore, since the apical specializations were not rigid, she deduced that the cells could not be mechanosensory, and therefore were likely chemosensory elements. Later, two physiological studies on fish with specialized appendages rich in solitary chemosensory cells confirmed the chemoresponsiveness of this system, although the identity of the natural stimulus remains controversial.

Subsequently, we and others showed that morphologically and molecularly similar solitary chemosensory cells (SCCs) are present throughout the upper respiratory systems of alligators, mice, and rats; and in the rodents, the cells express the entire panoply of taste-related signaling molecules, including T2R receptors, gustducin, PLCb2, and the transduction channel TrpM5.^3,

 

11

 

 In 2003, we confirmed that the taste signaling cascade is necessary for activation of the SCCs of the nasal cavity.11

 

 These SCCs synapse onto polymodal pain fibers of the trigeminal nerve, which produce a sensation of irritation and pain when activated. In addition, activation of these fibers evokes protective airway reflexes such as apnea (to prevent further inhalation) and sneezing (to remove the irritant). Thus, inhalation of a toxin that activates T2R receptors will be irritating and will provoke changes in respiration,12

 

 but will not, of course, produce the sensation of a bitter taste.

More recently, we showed that even some bacterial metabolites and signal molecules can activate the nasal SCCs and the trigeminal nerve.¹²

 

 Upon activation, the trigeminal nerve fibers not only transmit the information towards the brain, but also release peptide modulators (such as substance P and calcitonin gene-related peptide) into the local tissue, including around nearby blood vessels. These modulators bind to receptors on mast cells and blood vessels, causing a local, neurally mediated inflammation of the airway lining. In this way, SCCs not only act as sentinels warning against inhalation of irritants, but also serve as guardians capable of activating the innate immune system to respond to the presence of potentially damaging toxins or pathogens.

In all of the examples described so far, the taste signaling cascade is used to detect molecules in the lumen of an organ (oral cavity, gut, respiratory passages), and to generate an intracellular cascade to effect release of a neurotransmitter or hormone to signal to other cells in the body. Two recent reports on the expression of taste receptors in the airways indicate that taste-receptor signaling may directly affect the function of the cell that actually detects the stimulus (i.e., a cell-autonomous effect). Last year, Deshpande and colleagues reported that human airway smooth muscle cells express T2R (bitter) taste receptors along with α-gustducin and some components of the taste-associated phospholipase C (PLC) arm of the signaling cascade.¹³

 

 Application of various bitter-tasting substances to cultured human airway smooth muscle cells shows the same PLC-dependent increases in intracellular Ca²⁺ typical of taste cells or solitary chemosensory cells. Surprisingly, however, these increases in intracellular Ca²⁺ caused relaxation, rather than contraction, of the muscle cells. This paradoxical effect is attributed to the proximity of the T2R receptor complex to calcium-activated potassium channels (BK_Ca channels), which open in response to increased intracellular Ca²⁺, causing the hyperpolarization and subsequent relaxation of the muscle cells. In contrast, in taste cells of the mouth and solitary chemosensory cells of the upper airways, the increase in intracellular Ca²⁺ as a result of T2R activation triggers the transduction channel TrpM5 to depolarize the cell and evoke transmitter release to stimulate other cells. Thus, in different signaling contexts, activation of the same receptor can produce opposite cellular-level effects. However, two recent letters to the editor call Deshpande’s results into question, so the resolution of this remains controversial.

T2R activation has also been reported to have a cell-autonomous effect in ciliated cells of human lower airways.¹⁴

 

 Cultured human airway epithelium expresses some T2Rs along with associated downstream elements. Curiously, these are the first cells with motile cilia known to express sensory signaling elements. In these cells, the T2Rs are present on the cilia, while PLCb2 is associated with the cell membrane where the cilia insert into the cell body. Binding of the T2R receptor by a bitter ligand initiates a transduction cascade to activate PLCb2 at the base of the cilium, generating a Ca²⁺ response. The resulting T2R-mediated increase in intracellular Ca²⁺ causes an increase in ciliary beat frequency, which the researchers suggest could serve to sweep irritants away from the surface of the cell. But while T2Rs can be detected in cultured human airway cells, they are not detected in the lower airways of mice.12

 

 Whether this represents a species difference or the difference between in vivo and in vitro states remains to be determined.

Remaining taste mysteries

It is evident that taste receptors and their associated downstream signaling components are widely dispersed in diverse organ systems, and in many cases serve to help with digestion or to protect cells from potential toxins. But taste receptors have also been identified in other organs and tissues, such as the bile ducts, where their functions are still unclear. The composition of the fluid in the bile ducts is dictated by secretions of the pancreas, liver, and gall bladder. Why should it be necessary to diligently monitor the composition of biliary fluids as they move from gall bladder to intestine?

Similarly enigmatic are the reported effects of T2R (bitter receptor) agonists on contractile elements of both the airway and the gut. In the trachea, T2R agonists cause muscle relaxation (see above), but it is not clear how a bitter substance would have access to the smooth muscle cells of the trachea under normal conditions. The smooth muscle of the trachea is buried beneath a relatively tight airway epithelium, and so it seems unlikely that an inhaled bitter substance would penetrate the epithelium to access T2R receptors on the muscle. Similarly, the inhibition of smooth muscle contractility by T2R agonists in the stomach is not mediated by any of the peptides released by dispersed endocrine (enteroendocrine) cells of the gut, and may not even be mediated by T2R receptors. These and other nonspecific effects of bitter ligands emphasize the need to utilize either well-defined pharmacological agents or, better still, knockout animals to establish the specificity of receptors and transduction pathways and the consequences of their activation. Though they may not be for tasting per se, the taste-family receptors are surely doing something to affect the physiology of the organs in which they reside.

Thomas E. Finger is a professor of Cellular & Developmental Biology at the University of Colorado Medical School and codirector of the Rocky Mountain Taste & Smell Center. Sue C. Kinnamon is a professor of Otolaryngology at the University of Colorado Medical School and a core director of the Rocky Mountain Taste & Smell Center. 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

References

1. D. Höfer et al., “Taste receptor-like cells in the rat gut identified by expression of alpha-gustducin,” PNAS
    
   , 93:6631-34, 1996. ↩
    
2. S.V. Wu et al., “Expression of bitter taste receptors of the T2R family in the gastrointestinal tract and enteroendocrine STC-1 cells,” PNAS
    
   , 99:2392-97, 2002. ↩
    
3. S. Kaske et al., “TRPM5, a taste-signaling transient receptor potential ion-channel, is a ubiquitous signaling component in chemosensory cells,” BMC Neurosci
    
   , 8:49, 2007. ↩
    
4. H.J. Jang et al., “Gut-expressed gustducin and taste receptors regulate secretion of glucagon-like peptide-1,” PNAS
    
   , 104:15069-74, 2007. ↩
    
5. O.J. Mace et al., “Sweet taste receptors in rat small intestine stimulate glucose absorption through apical GLUT2,” J Physiol
    
   , 582:379-92, 2007. ↩
    
6. R.F. Margolskee et al., “T1R3 and gustducin in gut sense sugars to regulate expression of Na+-glucose cotransporter 1,” PNAS
    
   , 104:15075-80, 2007. ↩
    
7. J.I. Glendinning et al., “Intragastric infusion of denatonium conditions flavor aversions and delays gastric emptying in rodents,” Physiol Behav
    
   , 93:757-65, 2008. ↩
    
8. S. Janssen et al., “Bitter taste receptors and α-gustducin regulate the secretion of ghrelin with functional effects on food intake and gastric emptying,” PNAS
    
   , 108:2094-99, 2011. ↩
    
9. T.I. Jeon et al., “Gut bitter taste receptor signaling induces ABCB1 through a mechanism involving CCK,” Biochem J
    
   , 438:33-37, 2011. ↩
    
10. I. Kaji et al. “Secretory effects of a luminal bitter tastant and expressions of bitter taste receptors, T2Rs, in the human and rat large intestine,” Am J Physiol Gastrointest Liver Physiol
     
    , 296:G971-81, 2009. ↩
     
11. T. E. Finger et al., “Solitary chemoreceptor cells in the nasal cavity serve as sentinels of respiration,” PNAS
     
    , 100:8981-86, 2003. ↩
     
12. M. Tizzano et al., “Nasal chemosensory cells use bitter taste signaling to detect irritants and bacterial signals,” PNAS
     
    , 107:3210-15, 2010. ↩
     
13. D.A. Deshpande et al., “Bitter taste receptors on airway smooth muscle bronchodilate by localized calcium signaling and reverse obstruction,” Nat Med
     
    , 16:1299-304, 2010. ↩
     
14. A. S. Shah et al., “Motile cilia of human airway epithelia are chemosensory,” Science
     
    , 325:1131-34, 2009. ↩
     

Source: The Scientist
http://the-scientist.com/2011/12/01/matters-of-taste/

 

 

Posted by
Robert Karl Stonjek

FOUR BEST MONEY MAKING TIPS

Wealth building is not always about making it big, with outrageously innovative ideas. Sometimes it is simply about saving and actively maintaining financial security. Here are some great tips to help you get started on this path.

Intobiz Tripod recommends…

Amazing Money Tip #1:

The great scientist Albert Einstein once said, “It takes a genius to see the obvious.” What he meant by that is that sometimes the simplest things in life are the most powerful … but because they are so simple, we tend to ignore them, and not let them work for us.

One of the simplest but most powerful money making ideas is this: Keep a daily log of everything you spend. Go to the dime store and buy a little notebook. Carry it with you wherever you go. Write down every penny – every single penny – you spend every day. It’s as simple as that.

If you do this, you will find something magic happening in your financial life in just a few weeks.

There is something incredibly powerful about writing down all your expenditures. It makes the flow of money through your life more real and exact. It shows you simply and clearly just where you are spending your money, on what and why. Once you know that, it becomes much easier to control your spending.

Many people who have taken up this practice have not only learned something about themselves which they never knew before, but they are often astounded.

For example, one woman realized through examining her notebook that she actually spent nearly $2,000 per year on diet soft drinks, snacks and candy bars! Since her job as a office clerk brought her a scant $12,000 per year, she realized that one-sixth of her entire income was being frittered away on something entirely frivolous. The woman gave up the snacks and drinks, and found she had enough money to afford health insurance – plus has $400 left over. If you could choose snacks or health insurance, which would you choose?

The point is, it was her daily expense log that helped her achieve the insight and clarity she needed to get control of her finances. That’s what a simple spending record will do for you – it will give you control over your spending, and thus your financial life. There may be nothing but a 75-cent notebook and a ballpoint pen between your life of financial struggle and financial freedom.

Amazing Money Tip #2:

Stop deficit spending! We all know how much trouble Uncle Sam has been creating spending more money than our country takes in. It’s called deficit spending. Well, don’t fool yourself. The same rules apply to you. Using those evil little plastic cards may be the “American Way,” but it’s a damn poor way.

Today, the average credit card holder is carrying $7,000 in plastic debt!

Spending yourself into debt with a credit card is unbelievably easy, as many of you already know. The reason is psychological. When you give that clerk a credit card, it’s just not the same as handing over a stack of green dollar bills. Would you as readily hand over a fistful of ten dollar bills as flip a credit card across a counter? Probably not.

Credit cards put you in the hole and keep you there. Even for people with good incomes, paying your credit card debt down to zero is amazingly difficult. And make no bones about it, credit card debt will sap your financial strength just as readily as an open vein will deplete your physical body of its very life force. Using a credit card by choice can quickly turn to using it for need. Once you get to that point, you are already in trouble.

There is no secret to freeing yourself from the credit card game. You must take out a pair of scissors TODAY, cut your cards in half, and begin paying them back, slowly but surely. Once you stop adding to the debt, even small payment will eventually add up. You can get out of debt if you are patient and disciplined. Once your cards are history, you must adopt a strict pay-as-you go policy. Instead of buying now and paying later, save now and buy when you have the full amount.

Once again, this is not rocket science, but stopping credit-oriented consuming is one of the most powerful financial tools available to anyone today. Why not pick up this tool and use it?

Amazing Tip #3:

Sell your junk. That’s right, it’s high past time for a major garage sale. If you don’t have a garage, it’s time to search through your house or apartment for every single item you don’t need, and could convert quickly to cash at a flea market or garage sale.

Take an inventory. The truth is, most people are astounded by what they own – and how much money they have tied up in useless stuff. Why let it collect dust in your attic while it could collect interest in a savings account.

You could easily be $500, $1,000 … even $3,000 richer by the end of the week. As an added bonus, you’d have your place cleaned up, and you will have a fresh feeling of starting over. A garage sale is an excellent way to not only clean out your house, but it often gives a psychological boost that helps people get control of their life and money.

Amazing Tip #4

Ben Franklin said it long ago: “A penny saved is a penny earned.” Yes, It’s still true, and still one of the most powerful money-making tips inall history.

Implied within Franklin’s famous statement is the difficulty of saving. It’s tough to save and easy to spend! You know that! That’s why every penny saved truly is earned – because it takes so much effort to hold on to that cash! But if you can do it, it will work magic in your life. Having a savings account will de-stress your life. Imagine being ahead of your bills, rather than behind. When you are ahead of your bills, you entire life comes under your control. You sleep better at night. Your mind is freer to come up with new ways to make more money and save more. Saving is contagious – once you let it get started!

Here are some tips to help you save:

* Don’t settle for interest checking. Have a separate savings account that can’t be as easily accessed as a checking account.

* Keep your savings in another bank – one that’s off your regular route, or perhaps even in another town. That way you won’t be tempted to dip into it every time you visit the bank to make a checking deposit.

* Buy short-term savings bonds, which have 6-month to one-year maturity dates. That way you will get a higher rate, while at the same time keeping your money close in case of real emergencies.

* If you can, open the account under two names and require that both signatures be required to make a withdrawal. Two people can debate each withdrawal and keep each other in line.

Get more tips at Intobiz Tripod!

Even unconsciously, sound helps us see

 

“Imagine you are playing ping-pong with a friend. Your friend makes a serve. Information about where and when the ball hit the table is provided by both vision and hearing. Scientists have believed that each of the senses produces an estimate relevant for the task (in this example, about the location or time of the ball’s impact) and then these votes get combined subconsciously according to rules that take into account which sense is more reliable. And this is how the senses interact in how we perceive the world. However, our findings show that the senses of hearing and vision can also interact at a more basic level, before they each even produce an estimate,” says Ladan Shams, a UCLA professor of psychology, and the senior author of a new study appearing in the December issue of Psychological Science, a journal published by the Association for Psychological Science. “If we think of the perceptual system as a democracy where each sense is like a person casting a vote and all votes are counted (albeit with different weights) to reach a decision, what our study shows is that the voters talk to one another and influence one another even before each casts a vote.”

“The senses affect each other in many ways,” says cognitive neuroscientist Robyn Kim. There are connections between the auditory and visual portions of the brain and at the cognitive level. When the information from one sense is ambiguous, another sense can step in and clarify or ratify the perception. Now, for the first time, Kim, Megan Peters, and Ladan Shams, working at the University of California Los Angeles, have shown behavioral evidence that this interplay happens in the earliest workings of perception—not just before that logical decision-making stage, but before the pre-conscious combination of sensory information.

To demonstrate that one sense can affect another even before perception, the researchers showed 63 participants a bunch of dots on a screen, in two phases with a pause between them. In one phase, the dots moved around at random; in the other, some proportion moved together from right to left. The participants had to indicate in which phase the dots moved together horizontally. In experiment 1, the subjects were divided into three groups. While they looked at the dots, one group heard sound moving in the same direction as the right-to-left dots, and stationary sound in the random phase. A second group heard the same right-to-left sound in both phases. The third group heard the identical sound in both phases, but it moved in the opposite direction of the dots. In the second and third conditions, because the sound was exactly the same in both phases, it added no cognitively useful information about which phase had the leftward-moving dots. In experiment 2, each participant experienced trials in all three conditions.

The results: All did best under the first condition—when the sound moved only in the leftward-motion phase. The opposite-moving sound neither enhanced nor worsened the visual perception. But surprisingly, the uninformative sound—the one that traveled leftward both with the leftward-moving dots and also when the dots moved randomly—helped people correctly perceive when the dots were moving from one side to the other. Hearing enhanced seeing, even though the added sense couldn’t help them make the choice.

The study, says Kim, should add to our appreciation of the complexity of our senses. “Most of us understand that smell affects taste. But people tend to think that what they see is what they see and what they hear is what they hear.” The findings of this study offer “further evidence that, even at a non-conscious level, visual and auditory processes are not so straightforward,” she says. “Perception is actually a very complex thing affected by many factors.”

“This study shows that at least in regards to perception of moving objects, hearing and sight are deeply intertwined, to the degree that even when sound is completely irrelevant to the task, it still influences the way we see the world,” Shams says.

Provided by Association for Psychological Science

"Even unconsciously, sound helps us see." December 2nd, 2011. http://medicalxpress.com/news/2011-12-unconsciously.html

 

Posted by
Robert Karl Stonjek

How do we learn to speak and read?

Image of brain renderings highlighting various parts of the brain.

Do you remember how you learned to speak? Most people do not recall learning how to talk, or know how it is that they can understand others. The process involves a complex coordination of moving air from our lungs in coordination with the larynx, palate, jaw, tongue, and lips to form vowels and consonants that express a thought originating in the neural network of the brain.

You may recall the difficult process of learning how to read – associating a letter of the alphabet with a sound and then putting letters together to form words and sentences. In comparison, learning to speak may seem to come to us more naturally.

Ultimately, finding the answers behind how we learn to speak and read could help those who have an impaired ability to speak or understand others, as well as assist those who have difficulty learning to read and write.

UConn’s Experts

UConn faculty and alumni associated with world-renowned Haskins Laboratories in New Haven, Conn., have been working on the science of the spoken and written word for more than four decades. Founded in 1935 by Caryl Haskins and Franklin Cooper, Haskins is an independent, interdisciplinary research center affiliated with UConn and Yale University.

“We have a literacy crisis in this country,” says Philip Rubin ’73 MA, ’75 Ph.D., Haskins chief executive officer and former director of the Division of Behavioral and Cognitive Sciences at the National Science Foundation. “Many of our kids struggle with reading. At the heart, what we do is address those that are struggling. What makes them different than kids who don’t struggle … is the kind of work that we’re doing.”

The National Center for Educational Statistics says about 22 percent of adults in the United States have “minimal literacy skills,” meaning that they can read some words but cannot understand simple forms, such as a job application, or instructions, such as how to operate a computer.

Haskins researchers have been responsible for major scientific advances in speech and reading, including the development of the first reading machine for the blind, which ultimately led to the synthesis of artificial speech in computers. One of the scientists who conducted early research on the device was the late Alvin Liberman, a psychologist who served as director of Haskins for a decade and helped create the Department of Linguistics in the College of Liberal Arts and Sciences (CLAS) in Storrs. Liberman and Donald Shankweiler, professor emeritus of psychology in CLAS, collaborated with other Haskins colleagues in 1967 to produce “Perception of the Speech Code,” a landmark study published in Psychological Review that remains among the most cited papers in the literature of psychology.

“Haskins Labs in the 1950s was beginning to ask the question: What are the bits of sound, physical sound, that are conveying consonants and vowels?” says Shankweiler. “That was not an easy question to answer. Speech recognition is still less than perfect, but it depended very much on the research done at Haskins Labs over the past 40 to 50 years.”

Shankweiler says the link between speech and reading results in literacy, which provides the key to unlocking the ability to learn. “One of the main advantages of reading is that we are not limited by the speech we hear,” he says. “We extend our knowledge through print. A scholar will learn more through print than the spoken word. It’s a way to expand our use of language to increase knowledge.”

Talking Shop

With speech and reading research at the core of Haskins, its scientists have expanded their investigations to include the neural basis of reading development, examination of “birth-to-five” development through a Child Language Studies Laboratory, and increased attention to the cognitive and neurobiological foundations of bilingualism.

“You can do things in this place that you can’t do elsewhere; it’s really an interdisciplinary model,” says Kenneth Pugh, president and director of research, who also serves as a psychology professor in CLAS. “It provides an opportunity for researchers to be involved with really good technology. It’s a very good resource for UConn graduate students and faculty.”

The strength of the connection between the University and Haskins is evident by the cadre of graduate students who have been drawn to Storrs by the opportunity to associate with pioneering faculty researchers that include the late Isabelle Liberman, professor of educational psychology and an authority on reading disabilities, and the late Ignatius Mattingly, professor of linguistics who conducted groundbreaking research on speech synthesis; as well as Michael T. Turvey, Board of Trustees Distinguished Professor of Psychology Emeritus and director of the Center for the Ecological Study of Perception and Action, and Leonard Katz, professor of psychology emeritus in the Department of Psychology.

“It’s tremendously energizing,” says Turvey of the collegial discussions between faculty and students focused on their research. “It’s not just happening when we’re in the laboratories. We’re doing this on Friday night in the pub. The most important graduate students tend to come from UConn.”

Additional audio:

For many of those graduate students, Haskins is where they were mentored and encouraged to continue their research, leading to their own independent research and careers as scientists. While a graduate student in Storrs, Julia Irwin ’98 Ph.D. was nominated to become a Haskins research assistant. She and other UConn students would carpool from Storrs to New Haven each week to work on their projects, a tradition that continues today.

This video is not supported by your browser at this time.

This video is not supported by your browser at this time.

“I came here as a very low-level research assistant and was mentored by a number of UConn faculty and Haskins scientists,” says Irwin, now an assistant professor of psychology at Southern Connecticut State University and senior scientist at Haskins, whose research focuses on the role of the face in audiovisual speech perception. “I’m getting at the very fundamental level of speech sound. When there is a face that accompanies a voice, it’s pretty heavily used. What I’ve argued is that when people are speaking, there’s tons of information on the face.”

Carol Fowler ’73 MA, ’77 Ph.D. first learned of Alvin Liberman’s work as an undergraduate at Brown and became interested in the relation of speech production to speech perception and how phonemes – the smallest segments of speech that distinguish one word from another in a given language – work. Her 1983 paper published in the Journal of Experimental Psychology on how vowels are produced as part of the rhythm of speech, broke new ground in the field.

“We need to understand what it is about the language system that gives it the power that it has,” says Fowler, a former president and director of research at Haskins. “Why can we talk about anything we can think about? Why can we understand sentences we have never heard before in our lives? Why can we generate sentences we’ve never said before in our lives and expect others to understand them?”

Provided by University of Connecticut

"How do we learn to speak and read?." December 2nd, 2011. http://medicalxpress.com/news/2011-12-how-do-we-learn-to.html

 

Posted by
Robert Karl Stonjek

Punch Drunk

After a concussion forces him to retire, a former pro-wrestler starts an institute to study the neurological effects of repeated brain injuries.

By Jef Akst |

Chris “Harvard” Nowinski (right) wrestling Jeff Hardy in 2002. WWE

In the middle of a July night in 2003, Chris Nowinski woke up on the floor of his hotel room in Terre Haute, Indiana. The lamp on the bedside table was broken, as was the table itself, and he had no idea what had happened. According to his girlfriend, he had stood up on the bed, tried to climb the wall, and then jumped off the bed, taking out the nightstand on the way down. All he could remember was trying to catch something that was falling, but apparently it had all been just a bad dream.

Though he had never sleepwalked before, Nowinski, a professional wrestler, had an idea why the strange episode had occurred. About a month earlier, he had taken a blow to the head during a match. “Bubba gave me a boot to the chin that I was too close to,” Nowinski recalls. “It was just like a real kick to the head.” Since then, he had been dealing with daily headaches, memory problems, nausea, and other symptoms typically associated with severe concussions. Having played football in high school and then at Harvard, Nowinski had been hit in the head before, but the symptoms had always been short-lived. This time, they were worse—and they were lingering. It didn’t take him long to decide it was time to quit wrestling.

Over the next few years, Nowinski started digging into the scientific literature on repeated concussions. He even wrote a book, Head Games, on the topic. “I realized that if everybody knew what I was learning about brain trauma and sports, we would change how we played the games,” he says. Then, in 2007, he teamed up with Robert Cantu, a neurosurgeon at Emerson Hospital in Massachusetts, to launch the Sports Legacy Institute to study the treatment and prevention of brain trauma in athletes. In 2008, the Institute joined forces with Boston University School of Medicine, forming the Center for the Study of Traumatic Encephalopathy, to which more than 350 current and former athletes, including 60 retired NFL players, have pledged to donate their brains for study. Many of the athletes have also agreed to be monitored over the years for mental and physical changes.

 

Nowinski pointing to scan of a 50-year-old former NFL player’s brain (yellow) next to a control (blue). Acquired Brain Injury Ireland

Blows to the head are a common occurrence in contact sports, including football, hockey, and boxing, among others. Concussions can result in headaches and transient neurological impairment, but the effects are usually short-lived, and the vast majority of patients recover within a week or two. Some individuals, however, particularly those who have suffered repeated blows, may appear to have recovered but later suffer more serious, progressively worsening effects, including personality changes, memory problems, difficulty processing information, and even full-blown dementia. (See “Vital Signs

 

,” The Scientist, April 2011 and “Personalized Athletics

 

,” The Scientist, August 2011.)

In 1928, Essex County, New Jersey, medical examiner Harrison  Martland first described the symptoms associated with repeated head trauma, dubbing the condition “punch drunk.” Until recently, it was almost exclusively studied among professional boxers, and in 1937 was given a new name: dementia pugilistica. The disease now goes by the name of chronic traumatic encephalopathy (CTE), and the symptoms and neurological characteristics that define it are finally coming into focus.

After reviewing documented autopsies of CTE patients, Nowinski and his colleagues found that several of their brain regions had degenerated, including the frontal lobes, medial temporal lobes, hippocampus, amygdala, and brainstem. The researchers also noted the accumulation of abnormal protein deposits known as tau-immunoreactive neurofibrillary tangles—similar to those found in Alzheimer’s patients, but with a distinct distribution in the brain—and other microscopic abnormalities.

Daniel Amen, founder of Amen Clinics, Inc., which specializes in brain health, uses two different tests to measure blood flow and electrical activity in the brains of living head-trauma patients. In more than 100 active and retired NFL players, Amen’s team found consistent decreases in brain activity in the prefrontal cortex, both temporal lobe poles, and the cerebellum.

This August, neurosurgeons Joe Maroon and Russell Blaylock published the first comprehensive theory regarding CTE’s pathogenesis (Surgical Neurology International

 

, 2:107, 2011). The pair proposed that CTE results from the body’s innate immune response working in overdrive. “If you get a splinter under your fingernail, within seconds it becomes red, hot, swollen, and painful,” says Maroon, a clinician and lecturer at the University of Pittsburgh Medical Center and the Pittsburgh Steelers’ team neurosurgeon. “We believe there’s a similar inflammatory response in the brain with a traumatic insult.” Specifically, neuronal support cells called microglia release cytokines, chemokines, and other agents that cause neural inflammation. Normally, this response is neuroprotective, Maroon says, but “if you get repetitive blows to the head before the brain has healed, this normal repair process gets stuck in the accelerated mode and continues to pour out inflammatory agents, which leads to neurodegeneration and CTE.”

But the mechanism of CTE is not the only unanswered question, Nowinski says: “We don’t have diagnostic criteria in living people, so we don’t have a test and we don’t have treatment.”  As a result, the disease is grossly underdiagnosed, often confused with Alzheimer’s disease or ALS. But “there’s a certain pattern of atrophy with CTE,” he says. “In theory, we should be able to diagnosis it off imaging.”

Source: TheScientist
http://the-scientist.com/2011/12/01/punch-drunk/

 

Posted by
Robert Karl Stonjek

Flying robots, the builders of tomorrow

                                            A team of scientists has demonstrated that a coordinated group of pre-programmed, autonomous robots can do the job of building workers, constructing a six meter high tower without any human intervention. Architects say this new technology paves the way for new methods of engineering buildings of the future. Georgina Cooper reports.    

Facebookஇன் நிறுவுனர் மார்க் சக்கர்பேக்கின் வாழ்க்கையில் இடம்பெற்ற முக்கிய சில சம்பவங்கள்

ஹவாட் பல்கலைக்கழகத்தில் கல்விபயின்ற Facebook நிறுவுனர் மார்க் சக்கர்பேர்க்கின் சொத்துக்கள் 17.5 பில்லியன்கள் எனக் கணக்கிடப்படுகின்றது.

அத்துடன் இவரது வாழ்வுபற்றிப் படமெடுப்பதற்கும் ஹொலிவூட் தயாராவதாகக் கதைகள் உலாவுகின்றன. தற்போது இவரது வாழ்நாள் ஆவணமொன்று வெளியிடப்பட்டுள்ளது.

1984 – நியூயோர்க்கின் White Plains இல் பல்வைத்தியர் மற்றும் மனோதத்துவ நிபுணராகப் பணியாற்றிய ஒருவரின் ஒரே மகனாகப் பிறந்தார். இவருக்கு 3 சகோதரிகள் உள்ளனர்.

2002- நியூ ஹம்ஸயரிலுள்ள தனியார் பள்ளியொன்றான Phillips Exeter Academy என்ற பள்ளியில் ஆரம்பக்கல்வியைக் கற்றார். பின்னர் ஹவாட் பல்கலைக்கழகத்தில் மனோதத்துவம் மற்றும் கணினி அறிவியல் பற்றிய துறையில் இணைந்து கற்றார்.

2003 – Facemash என்ற இணையத்தள நிகழ்ச்சிநிரலை வெளியிட்டார். இதனை ஹவாட் மாணவர்களிடையே ஒரே பால் மாணவர்களின் படங்களை ஒப்பிட்டு யார் கவர்ச்சியானவர்கள் எனத் தரம்பிரிக்கும் செயற்பாட்டை மேற்கொள்ள உருவாக்கினார்.

இதன் உடனடியான புகழினால் பல்கலைக்கழக நிர்வாகிகளின் கவனத்தை ஈர்த்து உடனடியாகவே நிறுத்தப்பட்டது.

2004 – பெப்ரவரியில் Thefacebook.com என்ற இணையத்தளத்தினை ஆரம்பித்தார்.

2004 – தனது இரண்டாம் வருடப் படிப்பின் இறுதியில் ஹவாட் பல்கலைக்கழகத்திலிருந்து விலகி Palo Alto என்ற இடத்திற்குச் சென்று ஒரு வீட்டை வாங்கினார். இவ்வீட்டிலுள்ள ஒரு நீச்சல் தடாகம் தற்போது மிகவும் புகழ்பெற்றுவிட்டது.

2004 – 200,000 பயனாளர்களைத் தொட்டது Facebook. கணினி உலகின் திட்டவல்லுநர்களுடன் தொடர்புகொண்டு அரைமில்லியன் டொலர்களை ஆரம்ப இலாபமாகப் பெறுகின்றார். இதில் சிறிதளவை சீன உணவுவிடுதிக்கு மேலே சிறியதொரு அலுவலகத்தினை உருவாக்கப் பயன்படுத்தினார்.

2004 - புதியதொரு சமூக வலைத்தளமான HarvardConnection (பின்னர் ConnectU) என்ற தமது எண்ணத்தினைக் களவெடுத்துவிட்டதாக சக்கர்பேர்க் மீது Winklevoss இரட்டையளர்கள் வழக்கொன்றை மேற்கொண்டனர்.

2005 – 5 மில்லியன் பயனாளர்களை Facebook தொட்டது.

2006 – 22 வயதில் சக்கர்பேக், Yahoo விடமிருந்து Facebook இற்காக 1 பில்லியன் உதவியைப் பெற்றார். 

2007 – பல்கலைக்கழகத்திற்கும் அப்பால் மின்னஞ்சல் உள்ளவர்கள் எவரும் பயன்படுத்தலாமென்ற முறையை Facebook இல் திறந்தார். இதற்காக மைக்ரோசொப்ற்ரிலிருந்து 15பில். உதவி கிடைத்தது. இதனால் அவருக்குத் தனிப்பட்ட ரீதியில் மட்டும் 4பில். டொலர் கிடைத்தது.

2007 – சுயமாக மென்பொருள் எழுதுபவர்களை Facebook இல் அனுமதித்தார். ஆனால் Beacon என்ற மென்பொருள் வெளிவந்தபோது தமது நண்பர்கள் எவற்றை ஒன்லைனில் வாங்குகின்றார்கள் என்பதை மற்றவர்களால் பார்க்கக்கூடியதாயிருந்த நிலையை இது தந்ததால் தனிநபர் விடயங்களில் தலையிடுவதாகக் கூறி பெரும் எதிர்ப்பைச் சந்தித்தது.

2008 – 65மில். டொலர் பெறுமதியான Winklevoss வழக்கினை முடிவுக்குக் கொண்டுவந்தார். எனினும் இன்னமும் தான் எந்தவொரு சொத்துத்திருட்டினையும் செய்யவில்லையென்றே மறுத்துவருகின்றார்.

2009 –வீட்டுப் பாவனையில் Facebook இனை சீனா தடுத்தது.

2010 – இவ்வருடத்தின் Time சஞ்சிகையின் நபராக இவரைத் தெரிவுசெய்தது.

2010 – The Social Network என்ற ஆவணப்படத்தினை ஹொலிவூட் திரையுலகம் வெளியிட்டது. இதில் சக்கர்பேர்க்கின் ஹாவட் பல்கலைக்கழக வாழ்க்கை மற்றும் Facebook இன் ஆரம்பகாலங்கள்பற்றிக் காட்டப்படுகின்றன.

2011 – Saturday Night Live என்ற நிகழ்ச்சியில் விவரணத்தில் நடிகராக நடித்த ஜெசி ஈசின்பேர்க்கினால் பேட்டிகாணப்பட்டார்.

2011 - ஒரு நாளில் Facebook அரைமில்லியன் பயனாளர்களைத் தொட்டது. இதற்கு வரியாக 4பில். டொலர் எதிர்பார்க்கப்பட்டது. இது முந்தைய வருடத்தை விடவும் இரண்டு மடங்காகும்.

2012 – ஒரு பில். பயனாளர்களை அடைந்தது. 100பில். டொலர்களைப் பெறலாமென பங்குச்சந்தை நிலைவரம் எதிர்பார்க்கப்படுகிறது.

Sharing Shree Shirdi Sai Baba Of South San Francisco: Divine Touch