Torchwood 99

Out of Body Experience

2009-01-08T09:26:00.000-08:00

An out-of-body experience is defined as the experience in which a person who is awake sees his or her own body from a location outside the physical body.

OBEs have been reported in clinical conditions where brain function is compromised, such as stroke, epilepsy and drug abuse. They have also been reported in association with traumatic experiences such as car accidents. Around one in ten people claim to have had an OBE at some time in their lives.

OBEs have fascinated mankind for millennia. Their existence has raised fundamental questions about the relationship between human consciousness and the body, and has been much discussed in theology, philosophy and psychology. Although out-of-body experiences have been reported in a number of clinical conditions, the neuro-scientific basis of this phenomenon remains unclear.

Dr Henrik Ehrsson, a neuroscientist working at the Institute of Neurology University College London (UCL) has devised the first experimental method to induce an out-of-body experience in healthy participants. In a paper published in Science, he outlines the unique method by which the illusion is created and the implications of its discovery.

The set-up of the illusion is as follows: the study participant sits in a chair wearing a pair of head-mounted video displays. These have two small screens over each eye, which show a live film recorded by two video cameras placed beside each other two metres behind the participant's head. The image from the left video camera is presented on the left-eye display and the image from the right camera on the right-eye display. The participant sees these as one 'stereoscopic' (3D) image, so they see their own back displayed from the perspective of someone sitting behind them.

The researcher then stands just beside the participant (in their view) and uses two plastic rods to simultaneously touch the participant's actual chest out-of-view and the chest of the illusory body, moving this second rod towards where the illusory chest would be located, just below the camera's view.

The participants confirmed that they had experienced sitting behind their physical body and looking at it from that location. Dr Ehrsson said: "This was a bizarre, fascinating experience for the participants - it felt absolutely real for them and was not scary. Many of them giggled and said 'Wow, this is so weird!'".

"The invention of this illusion is important because it reveals the basic mechanism that produces the feeling of being inside the physical body. This represents a significant advance because the experience of one's own body as the centre of awareness is a fundamental aspect of self-consciousness."

Discovering this means of inducing an OBE could also have industrial applications. Dr Ehrsson explains:

"This is essentially a means of projecting yourself, a form of teleportation. If we can project people into a virtual character, so they feel and respond as if they were really in a virtual version of themselves, just imagine the implications. The experience of playing video games could reach a whole new level, but it could go much beyond that. For example, a surgeon could perform remote surgery, by controlling their virtual self from a different location."

To test the illusion further and provide objective evidence, Dr Ehrsson then performed an additional experiment to measure the participants' physiological response - specifically the level of perspiration on the skin - in a scenario where they felt the illusory body was threatened. Their bodily response strongly indicated that they thought the threat was real.

The creation of this perceptual illusion stems from an idea Dr Ehrsson had as a medical student, when he wondered what would happen to the 'self' if you could effectively move your eyes to another part of the room, just a few metres away, so you could observe yourself from an outside perspective. Would the self 'follow' the eyes or stay in the body"

The illusion is different from anything published previously. It is the first to involve a change in the perceived location of the self, relative to the physical body. It is also different from any virtual reality set-up because it examines what happens when you look at yourself, and there is also multisensory information that triggers the illusion. There has been no way of inducing an OBE in healthy people before, apart from unsubstantiated reports in occult literature. It's a very exciting development, and has implications for a range of disciplines from neuroscience to theology.

Article: 'The experimental induction of out-of-body experiences' published in the advance online edition of Science on Thursday 23rd August.
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Non-Critical String Theory Formulation of Microtubule Dynamics and Quantum Aspects of Brain Function arxiv hep-ph/9505401v3
Beyond Virtual Reality: "Out of Body Experiences" @ The Daily Galaxy
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The Colour Purple

2009-01-04T08:30:00.000-08:00

Compounds that colour fruits may protect against cancer

Understanding the molecular structures of compounds that give certain fruits and vegetables their rich colours may help researchers find even more powerful cancer fighters.

Anthocyanins, the compounds that give colour to purple, red and blue fruits and vegetables—some of which are also commonly used as dyes—can significantly slow the growth of cancer cells.

“These foods contain many compounds, and we're just starting to figure out what they are and which ones provide the best health benefits,” said Monica Giusti, the lead author of the study and an assistant professor of food science at Ohio State University.

Giusti and her colleagues found that in some cases, slight alterations to the structure of anthocyanin molecules made these compounds more potent anti-cancer agents. The finding brings scientists a step closer to figuring out exactly what properties in fruits and vegetables give them their cancer-fighting capacity.

The anti-cancer effects of anthocyanin-rich extracts from a variety of produce were tested. They retrieved these anthocyanins from some relatively exotic fruits and other plants, including grapes, radishes, purple corn, bilberries, purple carrots and elderberries.

The plants were chosen due to their extremely deep colours, and therefore high anthocyanin content. The researchers added different extracts to flasks that contained colon cancer cells. They used an analytical technique called high-performance liquid chromatography – mass spectrometry in order to determine the exact chemical structure of each compound. They used biological tests to determine the number of cancer cells left after anthocyanin treatment.

Researchers found that the amount of anthocyanin extract needed to reduce cancer cell growth by 50 percent varied among the plants. Extract derived from purple corn was the most potent, in that it took the least amount of extract to cut cell numbers in half.

In additional laboratory studies, she and her colleagues found that anthocyanin pigments from radish and black carrots slowed the growth of cancer cells anywhere from 50 to 80 percent. But pigments from purple corn and chokeberries not only completely stopped the growth of cancer cells, but also killed roughly 20 percent of the cancer cells while having little effect on healthy cells.

“All fruits and vegetables that are rich in anthocyanins have compounds that can slow down the growth of colon cancer cells, whether in experiments in laboratory dishes or inside the body,” Giusti said. There may be relatively simple ways to implement these new findings.

“There are more than 600 different anthocyanins found in nature,” Giusti said. “While we know that the concentration of anthocyanins in the GI tract is ultimately affected by their chemical structures, we're just beginning to scratch the surface of understanding how the body absorbs and uses these different structures.”

“It is possible to use natural, anthocyanin-based food colourants instead of synthetic dyes,” Giusti said. “Doing so still maintains the wonderful colours of foods while enhancing their health-promoting properties.”

Previous research at Ohio State found that black raspberries appear to reduce the growth of esophageal and colon cancers tumors.

The team is also evaluating how these pigments interact with other compounds in foods – such interactions could ultimately affect the health benefits of the food or the anthocyanin itself.
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Essence of Being

2009-01-02T08:12:00.000-08:00

neuron from cimion @ digitalblasphemy dotcom

The Essence of Being.

Are we riding the camel or is the camel riding us.

We all know about the origin of cells, the origin of biological 'life' on earth, and the evolution of organisms into species.

We even know about the cataclysmic demise or extinction of the dynosaurs.

The cell is the structural and functional unit of all known living organisms, and is sometimes called the "building block of life."

The origin of cells has to do with the origin of life, and was one of the most important steps in evolution of biological life as we know it. The birth of the cell marked the passage from prebiotic chemistry to biological life.

In a gene-centered view of evolution, life is regarded in terms of replicators—that is DNA molecules in the organism. In this paradigm, cells satisfy two fundamental conditions: protection from the outside environment and confinement of biochemical activity. The former condition is needed to maintain the stability of fragile DNA chains in a varying and sometimes aggressive environment, and may have been the main reason for which cells evolved. The latter is fundamental for the evolution of complexity.

The eukaryotic cell seems to have evolved from a symbiotic community of prokaryotic cells. It is almost certain that DNA-bearing organelles like the mitochondria and the chloroplasts are what remains of ancient symbiotic oxygen-breathing proteobacteria and cyanobacteria, respectively, where the rest of the cell seems to be derived from an ancestral archaean prokaryote cell – a theory termed the endosymbiotic theory.

There is still considerable debate about whether organelles like the hydrogenosome predated the origin of mitochondria, or viceversa: see the hydrogen hypothesis for the origin of eukaryotic cells.

Some organisms, such as bacteria, are unicellular (consist of a single cell). Other organisms, such as humans, are multicellular. (Humans have an estimated 100 trillion cells; a typical cell size is 10 µm; a typical cell mass is 1 nanogram.) The largest known cell is an ostrich egg.

Sex, as the stereotyped choreography of meiosis and syngamy that persists in nearly all extant eukaryotes, may have played a role in the transition from prokaryotes to eukaryotes. An 'origin of sex as vaccination' theory suggests that the eukaryote genome accreted from prokaryan parasite genomes in numerous rounds of lateral gene transfer. Sex-as-syngamy (fusion sex) arose when infected hosts began swapping nuclearized genomes containing coevolved, vertically transmitted symbionts that conveyed protection against horizontal infection by more virulent symbionts.

Why do people have sex?

2009-01-01T12:34:00.000-08:00

Research at The University of Texas at Austin reveals hundreds of varied and complex motivations why people have sex, that range from the spiritual to the vengeful.

People's motivations ranged from the mundane "I was bored", to the spiritual "I wanted to feel closer to God"
and from the altruistic "I wanted the person to feel good about himself/herself" to the manipulative "I wanted to get a promotion".

Some said they had sex to feel powerful, others to debase themselves. Some wanted to impress their friends, others to harm their enemies "I wanted to break up a rival's relationship".

Buss and Meston conducted two studies. In the first, they asked more than 400 men and women to identify reasons people have sex. In the second, the researchers asked more than 1,500 undergraduate students about their experiences and attitudes.
The Texas psychologists identified four major factors and 13 sub-factors for why people have sex:

Physical reasons
such as to reduce stress "It seemed like good exercise", feel pleasure "It's exciting", improve or expand experiences "I was curious about sex", and the physical desirability of their partner "The person was a good dancer".
Goal-based reasons,
including utilitarian or practical considerations "I wanted to have a baby", social status "I wanted to be popular" and revenge "I wanted to give someone else a sexually transmitted disease".
Emotional reasons
such as love and commitment "I wanted to feel connected" and expression "I wanted to say 'thank you'". Insecurity-based reasons, including self-esteem "I wanted the attention", a feeling of duty or pressure "My partner kept insisting" and to guard a mate "I wanted to keep my partner from straying".

So here's the golden question, what motivates YOU ?
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From couch potatoes to world-class athletes,
Fitness Institute of Texas helps them achieve their fitness goals
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Is it for Real?

2008-12-29T01:00:00.000-08:00

We live in an age where we can create computer software and sequencing, and hardware to build robot car makers and even manufacture smaller & smaller chips for ever more powerful computers - even to the point of presuming to simulate the big bang and the universe, but god forbid that we should conceive of a higher being or 'creator' of the universe.

We live in an age where dna sequencing is almost complete, where we presume to be able to manipulate genes to create new species and/or beings thru genetic modification, but god forbid we should dare presume that man (humanity) is the product of anything other than 'evolution' and natural selection.

It seems the only thing that truly defines some large brains, is their inability to accept there could be anything greater than themselves - and this in the age when we can communicate via mobile phone with unseen beings on the remotest corners of the earth (the other side of the planet) or even on the ISS International Space Station, if not quite on other planets yet, and we are on the verge of showing that other worlds in other dimensions may actually 'exist' even if we are still far from communicating with them, or travelling there.

But hey, some people whilst busy insisting that imagination and fiction are not 'real' - fail to realise they are very much a part of the 'real' world.

What is clear is that the human species has evolved in the last 50 years. By and large the females of the species can now choose, if, when & where they wish to procreate, and organ transplants mean that many who would by 'natural selection' be dead, can now hope to live a little longer. But no matter how far we try to be masters of our own destiny, we still have no choice in whether we are born, where & when. By and large we have no say on where, when, and how we die.

Ultimately, perhaps the only difference between humans & turkeys, is that turkeys get 'plucked' before they get stuffed at xmas.
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Chronic Pain

2008-12-24T01:00:00.000-08:00

Why Don't Painkillers Work For People With Fibromyalgia?

People who have the common chronic pain condition fibromyalgia often report that they don't respond to the types of medication that relieve other people's pain.

New research from the University of Michigan Health System helps to explain why that might be: Patients with fibromyalgia were found to have reduced binding ability of a type of receptor in the brain that is the target of opioid painkiller drugs such as morphine.

The study included positron emission tomography (PET) scans of the brains of patients with fibromyalgia, and of an equal number of sex- and age-matched people without the often-debilitating condition. Results showed that the fibromyalgia patients had reduced mu-opioid receptor (MOR) availability within regions of the brain that normally process and dampen pain signals -- specifically, the nucleus accumbens, the anterior cingulate and the amygdala.

"The reduced availability of the receptor was associated with greater pain among people with fibromyalgia," says lead author Richard E. Harris, Ph.D., research investigator in the Division of Rheumatology at the U-M Medical School's Department of Internal Medicine and a researcher at the U-M Chronic Pain and Fatigue Research Center.

"These findings could explain why opioids are anecdotally thought to be ineffective in people with fibromyalgia," he notes. The findings appear in The Journal of Neuroscience. "The finding is significant because it has been difficult to determine the causes of pain in patients with fibromyalgia, to the point that acceptance of the condition by medical practitioners has been slow."

Opioid pain killers work by binding to opioid receptors in the brain and spinal cord. In addition to morphine, they include codeine, propoxyphene-containing medications such as Darvocet, hydrocodone-containing medications such as Vicodin, and oxycodone-containing medications such as Oxycontin.

The researchers theorize based on their findings that, with the lower availability of the MORs in three regions of the brains of people with fibromyalgia, such painkillers may not be able to bind as well to the receptors as they can in the brains of people without the condition.

Put more simply: When the painkillers cannot bind to the receptors, they cannot alleviate the patient's pain as effectively, Harris says. The reduced availability of the receptors could result from a reduced number of opioid receptors, enhanced release of endogenous opioids (opioids, such as endorphins, that are produced naturally by the body), or both, Harris says.

The research team also found a possible link with depression. The PET scans showed that the fibromyalgia patients with more depressive symptoms had reductions of MOR binding potential in the amygdala, a region of the brain thought to modulate mood and the emotional dimension of pain.
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7 Medical Misconceptions

2008-12-20T01:21:00.000-08:00

Popular culture is loaded with myths and half-truths.
Most are harmless. But when doctors start believing medical myths, perhaps it's time to worry. In the British Medical Journal this week, researchers looked into several common misconceptions, from the belief that a person should drink eight glasses of water per day to the notion that reading in low light ruins your eyesight.

Myth: We use only 10 percent of our brains.

Fact: Physicians and comedians alike, including Jerry Seinfeld, love to cite this one. It's sometimes erroneously credited to Albert Einstein. But MRI scans, PET scans and other imaging studies show no dormant areas of the brain, and even viewing individual neurons or cells reveals no inactive areas, the new paper points out. Metabolic studies of how brain cells process chemicals show no nonfunctioning areas. The myth probably originated with self-improvement hucksters in the early 1900s who wanted to convince people that they had yet not reached their full potential. Our other organs run at full tilt.

Myth: You should drink at least eight glasses of water a day.

Fact: There is no medical evidence to suggest that you need that much water. This myth can be traced back to a 1945 recommendation from the Nutrition Council that a person consume the equivalent of 8 glasses (64 ounces) of fluid a day. Over the years, "fluid" turned to water. But fruits and vegetables, plus coffee and other liquids, count.

Myth: Fingernails and hair grow after death.

Fact: Most physicians queried on this one initially thought it was true. Upon further reflection, they realized it's impossible. As the body’s skin is drying out, soft tissue, especially skin, is retracting. The nails appear much more prominent as the skin dries out. The same is true, but less obvious, with hair. As the skin is shrinking back, the hair looks more prominent or sticks up a bit.

Myth: Shaved hair grows back faster, coarser and darker.

Fact: A 1928 clinical trial compared hair growth in shaved patches to growth in non-shaved patches. The hair which replaced the shaved hair was no darker or thicker, and did not grow in faster. More recent studies have confirmed that one. Here's the deal: When hair first comes in after being shaved, it grows with a blunt edge on top. Over time, the blunt edge gets worn so it may seem thicker than it actually is. Hair that's just emerging can be darker too, because it hasn't been bleached by the sun.

Myth: Reading in dim light ruins your eyesight.

Fact: The researchers found no evidence that reading in dim light causes permanent eye damage. It can cause eye strain and temporarily decreased acuity, which subsides after rest.

Myth: Eating turkey makes you drowsy.

Fact: A chemical in turkey called tryptophan is known to cause drowsiness. But turkey doesn't contain any more of it than does chicken or beef. This myth is fueled by the fact that turkey is often eaten with a colossal holiday meal, often accompanied by alcohol — both things that will make you sleepy.

Myth: Mobile phones are dangerous in hospitals.

Fact: There are no known cases of death related to this one. Cases of less-serious interference with hospital devices seem to be largely anecdotal, the researchers found. In one real study, mobile phones were found to interfere with 4 percent of devices, but only when the phone was within 3 feet of the device. A more recent study, this year, found no interference in 300 tests in 75 treatment rooms. To the contrary, when doctors use mobile phones, the improved communication means they make fewer mistakes.

"Whenever we talk about this work, doctors at first express disbelief that these things are not true," said Vreeman. "But after we carefully lay out medical evidence, they are very willing to accept that these beliefs are actually false."
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Natural Chemo-prevention

2008-12-09T10:57:00.000-08:00

The next cancer-fighting therapeutic could be growing in your garden. For example, a black raspberry-based gel might offer a means of stopping oral lesions from turning into a particularly dangerous and disfiguring form of cancer.

And new studies show that cancer prevention might come in drinkable form: green tea extract, a powerful antioxidant, shows efficacy against colorectal cancer; and a new berry-rich beverage, made from a combination of known plant-based antioxidants, could prevent or slow the growth of prostate cancer.

That is, according to research presented December 6, at the American Association for Cancer Research's Sixth Annual International Conference on Frontiers in Cancer Prevention Research, being held in Philadelphia, Pennsylvania.

Topically applied black raspberry gel applied on oral premalignant tumors

Oral squamous cell carcinoma is a deadly cancer that, even when treated successfully, often leaves patients permanently disfigured. Other than radical surgery, there are few known treatments. Researchers at Ohio State University, however, report a Phase I/II trial demonstrating that a gel made from black raspberries shows promise in preventing or slowing the malignant transformation of precancerous oral lesions.

"Black raspberries are full of anthocyanins, potent antioxidants that give the berries their rich, dark colour, and our findings show these compounds have a role in silencing cancerous cells," said Susan Mallery, professor in the Department of Oral Maxillofacial Surgery and Pathology at Ohio State University's College of Dentistry. "This gel appears to be a valid means of delivering anthocyanins and other cancer-preventing compounds directly to precancerous cells, since it slowed or reduced lesion progression in about two-thirds of study participants."

According to American Cancer Society statistics, oral cancer is one of the deadliest of all cancers, with about 35,000 new cases each year in the United States and 7,500 deaths annually. These cancers generally begin as small, often unnoticed, lesions inside the mouth. "More than a third of untreated precancerous oral lesions will undergo malignant transformation into squamous cell cancer, but we do not have the capability to predict which lesions will progress," Mallery said.

The National Cancer Institute-funded trial included 30 participants, 20 of whom had identifiable precancerous lesions, and 10 normal controls. Each of the participants was instructed to gently dry the lesion sites (or a pre-selected control site for the normal participants) and rub the gel into the area four times a day, once after each meal and at bedtime.

After six weeks, about 35 percent of the trial participants' lesions showed an improvement in their microscopic diagnosis, while another 45 percent showed that their lesions had stabilized. About 20 percent showed an increase in their lesional microscopic diagnoses. Importantly, none of the participants experienced any side effects from the gel.

"The trial was designed to test the safety of the gel and detect any possible toxicity, but the next obvious step is a multicenter, double-blind, placebo-controlled Phase II study," Mallery said. "Such a study would enable us to determine that the black raspberries are the active factor and not just the gel base or the act of drying and rubbing the lesions."

The researchers also collected cell samples from the lesion sites of each participant before and after treatment in order to study the genetics and biology of the lesions. The majority of patients with precancerous lesions at the start of the trial showed elevated levels of COX-2 and iNOS, two proteins closely correlated with inflammation and malignant progression. Following treatment, Mallery says, levels of those proteins in the treated lesional epithelial cells decreased dramatically.

Mallery and her colleagues also examined samples for three tumor suppressor genes in order to determine what researchers call "loss of heterozygosity," whether or not a cancer cell has lost one of its two copies of the gene. Such loss greatly increases a cell's chances of losing the benefit of the tumor suppressor genes due to a second mutation or gene silencing event. Following the trial, the researchers noted that many lesions returned to normal, retaining both copies of each tumor suppressor gene. "We speculate that the chemopreventive compounds in black raspberries assist in modulating cell growth by promoting programmed cell death or terminal differentiation, two mechanisms that help "reeducate" precancerous cells," Mallery said.

"Oral cancer is a debilitating disease and there is a desperate need for early detection and management of precancerous lesions," Mallery said. "While screening can help detect the disease early -- and survival rates are definitely improved the earlier the disease is caught -- many of these precancerous lesions recur despite complete surgical removal. There are currently no effective chemopreventive treatments which could conceivably serve as either adjunctive or alternative approaches to surgery."

According to Mallery, the development of black raspberries as potential cancer-fighters is the result of decades of research into identification of naturally derived chemopreventive compounds by Ohio State researcher Gary D. Stoner, Ph.D., an emeritus professor at Ohio State University's College of Medicine and Public Health. Clinical studies stemming from his research are currently underway for oral, esophageal and colorectal cancer.

The gel looks deceptively like black raspberry jam, but it certainly does not taste like something you would want to spread on toast, Mallery says. The bioadhesive gel, which contains 10 percent freeze dried black raspberries, is devoid of many of the tasty sugars found in native berries.

The black raspberry gel was manufactured by the University of Kentucky's Good Manufacturing Production (GMP) facility. NanoMed Pharmaceuticals is partnering with OSU investigators Mallery, Stoner and Peter E. Larsen and Russell J. Mumper, of the University of North Carolina, in product development.

Suppressive effects of a phytochemical cocktail on prostate cancer growth in vitro and in vivo

A commercially available nutrition drink reduces the growth of tumors in a mouse model of human prostate cancer by 25 percent in two weeks, according to researchers from the University of Sydney. The drink, Blueberry Punch, is a mixture of plant-based chemicals - phytochemicals - known to have anti-cancer properties.

In particular, Blueberry Punch consists of a combination of fruit concentrates (blueberry, red grape, raspberry and elderberry), grape seed and skin extract, citrus skin extracts, green tea extract (EGCG), olive leaf and olive pulp extracts, tarragon, turmeric and ginger.

"We have undertaken efficacy studies on individual components of Blueberry Punch, such as curcumin, resveratrol and EGCG, in the same laboratory setting and found these effective in suppressing cell growth in culture," said Jas Singh, research fellow at the University of Sydney.

"While individual phytochemicals are successful in killing cancer cells, we reasoned that synergistic or additive effects are likely to be achieved when they are combined."

Singh and her colleagues studied the effect of the beverage on both cancer cell cultures and in mouse models that mimic human prostate cancer. After 72 hours of exposure to increasing concentrations of Blueberry Punch, prostate cancer cells showed a dose-dependent reduction in size and viability when compared with untreated cells, Singh says. After feeding mice a 10 percent solution of the punch for two weeks, the tumors in the test mice were 25 percent smaller than those found in mice that drank only tap water.

Because Blueberry Punch is a combination of several ingredients, it could have multiple mechanisms of action, Singh says. "Based on our initial findings, the mechanisms include, at least, the inhibition of the inflammation-related pathways, which is similar to the action of non-steroidal anti-inflammatory drugs; and inhibition of cyclin D1, which is similar to green tea action."

Based on these results, the researchers believe Blueberry Punch is now ready for human prostate cancer trials. Because Blueberry Punch is a food product rather than a drug, it is unlikely to have adverse reactions or side effects assuming that the individual is tolerant to all ingredients, Singh says. "The evidence we have provided suggests that this product could be therapeutic, although it requires clinical validation," Singh said.

The study was partially funded by the makers of Blueberry Punch, Dr. Red Nutraceuticals, a firm located near Brisbane, Australia, but the experiments were designed and conducted independently in the University of Sydney.

Read More
Chemoprevention, Naturally: Findings On Plant-derived Cancer Medicines
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Making Sense of what We See

2008-11-21T07:04:00.000-08:00

In a situation where the visual information provided is ambiguous — whether we are looking at Escher's art or looking at, say, a forest — how do our brains settle on just one interpretation?

In a study published this month in Nature Neuroscience, researchers at The Johns Hopkins University demonstrate that brains do so by way of a mechanism in a region of the visual cortex called V2.

Researchers say that mechanism, identifies "figure & background" regions of an image, provides a structure for paying attention to only one of those two regions at a time and assigns shapes to the collections of foreground "figure" lines that we see.

"What we found is that V2 generates a foreground-background map for each image registered by the eyes," said Rudiger von der Heydt, a neuroscientist, professor in the university's Zanvyl Krieger Mind/Brain Institute and lead author on the paper. "Contours are assigned to the foreground regions, and V2 does this automatically within a tenth of a second."

The study was based on recordings of the activity of nerve cells in the V2 region in the brain of macaques, whose visual systems are much like that of humans. V2 is roughly the size of a microcassette and is located in the very back of the brain. Von der Heydt said the foreground- background "map" generated by V2 also provides the structure for conscious perception in humans.

"Because of their complexity, images of natural scenes generally have many possible interpretations, not just two, like in Escher's drawings," he said. "In most cases, they contain a variety of cues that could be used to identify fore- and background, but oftentimes, these cues contradict each other. The V2 mechanism combines these cues efficiently and provides us immediately with a rough sketch of the scene."

Von der Heydt called the mechanism "primitive" but generally reliable. It can also, he said, be overridden by decision of the conscious mind.

"Our experiments show that the brain can also command the V2 mechanism to interpret the image in another way," he said. "This explains why, in Escher's drawings, we can switch deliberately" to see either the white birds or the dark birds, or to see either side of the staircase as facing "up."

The mechanism revealed by this study is part of a system that enables us to search for objects in cluttered scenes, so we can attend to the object of our choice and even reach out and grasp it.

"We can do all of this without effort, thanks to a neural machine that generates visual object representations in the brain," von der Heydt said. "Better yet, we can access these representations in the way we need for each specific task. Unfortunately, how this machine' works is still a mystery to us. But discovering this mechanism that so efficiently links our attention to figure-ground organization is a step toward understanding this amazing machine."

Understanding how this brain function works is more than just interesting: It also could assist researchers in unraveling the causes of — and perhaps identifying treatment for — visual disorders such as dyslexia.
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Can 3D movies like Beowulf save the World of Cinema
Surrogate Memory - Back Up your Brain @ The Galactic Emporium
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Mirror in the Brain

2008-11-08T06:10:00.000-08:00

Recent findings are rapidly expanding researchers' understanding of a new class of brain cells -- mirror neurons -- which are active both when people perform an action and when they watch it being performed.

Some scientists speculate that a mirror system in people forms the basis for social behavior, for our ability to imitate, acquire language, and show empathy and understanding. It also may have played a role in the evolution of speech. Mirror neurons were so named because, by firing both when an animal acts and when it simply watches the same action, they were thought to "mirror" movement, as though the observer itself were acting.

Advances in the past few years have newly defined different types of mirror neurons in monkeys and shown how finely tuned these subsets of mirror neurons can be. New studies also have further characterized abnormal-as well as normal-mirror activity in the brains of children with the social communication disorder known as autism, suggesting new approaches to treatment.

"The tremendous excitement that has been generated in the field by the study of mirror neurons stems from the implications of the findings, which have led to numerous new hypotheses about behavior, human evolution, and neurodevelopmental disorders," says Mahlon DeLong, MD, of Emory University School of Medicine.

Mirror neurons, a class of nerve cells in areas of the brain relaying signals for planning movement and carrying it out, were discovered 11 years ago, an offshoot of studies examining hand and mouth movements in monkeys. Mirror neuron research in the intervening years has expanded into a diverse array of fields. And the implications have been enormous, encompassing evolutionary development, theories of self and mind, and treatments for schizophrenia and stroke.

Findings being presented at Neuroscience 2007 include new research based on work in monkeys, showing that subsets of mirror neurons distinguish between observed actions carried out within hand's reach and those beyond the animal's personal space.

In his study, Peter Thier, PhD, at Tübingen University, first identified a group of mirror neurons by recording single nerve cell activity from electrodes when a monkey gripped different objects and when the monkey watched a person grasp the same objects, both nearby and farther away. About half of the nerve cells that were active when the monkey picked up the objects also sprung into action when it watched a person do so. Thier was assisted by research fellow Antonio Casile and PhD student Vittorio Caggiano, and worked closely with the lab of Giacomo Rizzolatti, MD, at the University of Parma.

They also noticed that some of these confirmed mirror neurons were active only when the monkey was watching activity within its personal space, defined as within reaching distance; others responded only to actions performed in a place outside the monkey's grasp. Thier and colleagues recorded this preferential activity in 22 nerve cells, or together half of the mirror neurons. The other half of the mirror neurons showed activity that did not depend on how close the grasping action was to the monkey.

Although at this stage assigning a functional role is still speculation, Thier suggests this proximity-specific activity in mirror neurons may play an important role when we monitor what goes on around us, or serve as the basis for inferring the intentions of others and for cooperative behavior. "These neurons might encode actions of others that the observers might directly influence, or with which he or she can interact," he says.

Other findings show that mirror neuron activity is instrumental for interpreting the facial expressions and actions of others but may not be sufficient for decoding their thoughts and intentions.

The studies examined changes in certain electroencephalograms (EEG) or brain wave patterns known as mu rhythms, which have a frequency of 8-13 hertz, or oscillations per second. Previous findings based on EEG recordings from the part of the brain that is directly involved in relaying signals for movement and sensing stimuli, known as the sensorimotor cortex, indicate that mu rhythms typically are suppressed by mirror activity in premotor areas of the brain. However, this does not happen in children with autism. As a result, the new work suggests, alternative strategies for reading faces and understanding others develop in the brains of these children.

Pursuing two parallel studies, Jaime Pineda, PhD, at the University of California, San Diego, aimed to contribute evidence supporting one of two theories about the ways we evaluate the actions and intentions of other people-either implicitly or through language-based theoretical concepts.

Using EEG recordings to examine patterns of brain wave activity, Pineda first worked with 23 adults, who were asked to look at photos showing just the eye region of people making various facial expressions. In three separate trials, the subjects were asked to identify either the emotion, race, or gender of the people in the photographs. In a subsequent task, subjects looked at three-panel cartoon strips and were asked to choose a fourth panel that completed the strip-either the conclusion of a series of physical actions or the result of a person interacting with an object. A sequence of a prisoner removing the window of his cell, then looking at his bed, for example, could be followed by a frame of the prisoner asleep, yawning, or using the bedsheet to make a rope. Answering correctly depended on interpreting the cartoon character's intentions appropriately or understanding how physical objects interact.

Pineda repeated the studies with 28 children, 7 to 17 years old, half of whom had autism. The other half were typically developing children.

Recordings from the studies with adults showed a correlation between mu suppression, or mirror neuron activity, and accuracy for both tasks. In fact, the suppression of mu rhythms during the facial expression task also correlated with accuracy in the exercise with the cartoons, suggesting that reading people's expressions and interpreting their intentions may draw from similar activity in the brain.

Recordings from the typically developing children showed similar patterns of suppression during the two tasks, indicating that mirror neuron activity is fully developed by age 7.

In contrast, recordings from the children with autism showed that mu rhythms were enhanced during both tasks. Enhancement is an indication that the mirror neuron system is disengaged. However, because the children still were able to perform the task, Pineda says, "we propose that children with autism develop alternative, non-mirror neuron-based coping strategies for understanding facial expressions and interpreting others' mental states." He suggests that "these compensatory strategies involve inhibition of residual mirror neuron functioning."

These results could be applied to the development of treatments for autism. Pineda and his group have been using neurofeedback training to successfully renormalize functioning in this system. That is, they see mu suppression that is more characteristic of the typically developing brain following such training. "Our findings are consistent with the idea that mirror neurons are not absent in autism," Pineda says, "but rather are abnormally responsive to stimuli and abnormally integrated into wider social-cognitive brain circuits.

"This idea implies that a retraining of mirror neurons to respond appropriately to stimuli and integrate normally into wider circuits may reduce the social symptoms of autism."

Advances in recording brain activity also have made possible findings showing that mirror systems are active even when we are not observing an action with an eye to repeating it.

Suresh Muthukumaraswamy, PhD, at Cardiff University, found that the mirror system is activated when we watch specific actions, even when we are concentrating on a separate task.

The results are based on previous research showing that motor systems in the brain are activated when a person observes an action being performed and on interpretations suggesting that we understand and learn to imitate the actions of others through these brain mechanisms.

Working with 13 adults with an average age of 29, Muthukumaraswamy compared brain activity recorded via magnetoencephalography (MEG). This monitoring technique measures the weak magnetic fields emitted by nerve cells, and, recording from 275 locations, Muthukumaraswamy was able to monitor changes in activity every 600th of a second.

"Although MEG has been in existence for more than 20 years, recent advances in hardware, computing technology, and the algorithms used to analyze the data allow much more detailed analysis of brain function than was previously possible," he says.

Brain activity was recorded as the subjects passively watched a sequence of finger movements, watched the movements knowing they would be asked to repeat them, added up the number of fingers moved as they watched, and performed the sequence of movements themselves.

Results from these recordings showed similar activity when the subjects performed the movement sequence and when they watched someone else do it. In addition, Muthukumaraswamy noted increased activity in areas of the brain regulating motor activity when subjects observed the movements knowing they would later do them, and when they added up the number of fingers used, compared with passive watching.

"These data suggest that activity of human mirror neuron systems is generally increased by attention relative to passive observation, even if that attention is not directed toward a specific motor activity," says Muthukumaraswamy. "Our results suggest that the mirror system remains active regardless of any concurrent task and hence is probably an automatic system.

"A good scientific understanding of the properties of the mirror system in normal humans is important," he adds, "because this may help to understand clinical disorders such as autism where the mirror system may not be functioning normally."

Other findings based on EEG recordings provide the first evidence of normal mirror activity in children with autism: People familiar to children with autism may activate mirror areas of the brain in normal patterns when unfamiliar people do not.

Previous research has shown that mu rhythms are suppressed when a subject identifies with an active person being observed. Based on this work, Lindsay Oberman, PhD, at the University of California, San Diego, examined the role of two separate factors in the mirror system response of children with autism.

Six videos were shown to a group of 26 boys, 8 to 12 years old; half had autism. Three videos showed images representing varying degrees of social interaction: two bouncing balls (the baseline measurement), three people tossing a ball to themselves, and three people throwing the ball to each other and off the screen to the viewer. The other set of videos showed people with varying degrees of familiarity to the subjects: strangers opening and closing their hand, family members making the same hand movement, and the subjects themselves doing the same.

EEG recordings from 13 electrodes in a cap showed that mu activity was suppressed most when subjects watched videos of themselves, indicating the greatest mirror neuron activity. For both groups, the measurements showed a slightly lower level of suppression when subjects watched familiar people in the video and the least when watching strangers. This indicates that normal mirror neuron activity was evoked when children with autism watched family members, but not strangers.

"Thus, to say that the mirror neuron system is nonfunctional may only be partially correct," says Oberman. "Perhaps individuals with autism have fewer mirror neurons and/or less functional mirror neurons that require a greater degree of activation than a typical child's system in order to respond."

The mirror neuron system may react to stimuli that the observer sees as "like me." If this is the case, suggests Oberman, "perhaps typical individuals apply this identification to all people (both familiar and unfamiliar), resulting in activation of these areas in response to the observed stimuli, while individuals on the autism spectrum only consider familiar individuals (including themselves) as 'like me,' " she says.

This evidence for normal mirror neuron activity in autistic children may indicate that mirror system dysfunction in these cases reflects an impairment in identifying with and assigning personal significance to unfamiliar people and things, Oberman suggests. Whether deficits in relating to unfamiliar people that are characteristic of autism are the cause or the result of a dysfunctional mirror neuron system is unclear.

Mirror, Mirror In The Brain: Mirror Neurons, Self-understanding And Autism Research
Adapted from Society for Neuroscience findings (2007, November 7)
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Autism A Dysfunctional Mirror-neuron System?
Autism Linked To Mirror Neuron Dysfunction from Science Daily
Humans Do Not Understand Mirror Reflections, Say Researchers
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Reboot Your Brain

2008-10-31T14:56:00.000-07:00

Contrary to popular belief, recent studies have found that there are probably ways to regenerate brain matter.

Animal studies conducted at the National Institute on Aging Gerontology Research Center and the Johns Hopkins University School of Medicine, for example, have shown that both calorie restriction and intermittent fasting along with vitamin and mineral intake, increase resistance to disease, extend lifespan, and stimulate production of neurons from stem cells.

In addition, fasting has been shown to enhance synaptic elasticity, possibly increasing the ability for successful re-wiring following brain injury. These benefits appear to result from a cellular stress response, similar in concept to the greater muscular regeneration that results from the stress of regular exercise.

Additional research suggests that increasing time intervals between meals might be a better choice than chronic calorie restriction, because the resultant decline in sex hormones may adversely affect both sexual and brain performance. Sex steroid hormones testosterone and estrogen are positively impacted by an abundant food supply. In other words, you might get smarter that way, but it might adversely affect your fun in the bedroom, among other drawbacks.

But if your not keen on starving yourself, there are other options. Another recent finding, stemming from the Burnham Institute for Medical Research and Iwate University in Japan, reports that the herb rosemary contains an ingredient that fights off free radical damage in the brain. The active ingredient, known as carnosic acid (CA), can protect the brain from stroke and neurodegeneration such as Alzheimer’s and from the effects of normal aging.

Although researchers are patenting more potent forms of isolated compounds in this herb, unlike most new drugs, simply using the rosemary in its natural state may be the most safe and clinically tolerated because it is known to get into the brain and has been consumed by people for over a thousand years. The herb was used in European folk medicine to help the nervous system.

Another brain booster that Bruce N. Ames, Ph.D., a professor of biochemistry and molecular biology at the University of California, Berkeley, swears by his daily 800 mg of alpha-lipoic acid and 2,000 mg of acetyl-L-carnitine, chemicals which boost the energy output of mitochondria that power our cells. Mitochondrial decay is a major factor in aging and diseases such as Alzheimer's and diabetes. Elderly rats on these supplements had more energy and ran mazes better.

Omega-3s fatty acids DHA and EPA found in walnuts and fatty fish (such as salmon, sardines, and lake trout) are thought to help ward off Alzheimer's disease. (In addition, they likely help prevent depression and have been shown to help prevent sudden death from heart attack).

Turmeric, typically found in curry, contains curcumin, a chemical with potent antioxidant and anti-inflammatory properties. In India, it is even used as a salve to help heal wounds. East Asians also eat it, which might explain their lower rates (compared to the United States) of Parkinson's disease and Alzheimer's disease, in addition to various cancers. If curry isn’t part of your favorite cuisines, you might try a daily curcumin supplement of 500 to 1,000 mg.

Physical exercise may also have beneficial effects on neuron regeneration by stimulating regeneration of brain and muscle cells via activation of stress proteins and the production of growth factors. But again, additional research suggests that not all exercise is equal. Interestingly, some researchers found that exercise considered drudgery was not beneficial in neuronal regeneration, but physical activity that was engaged in purely for fun, even if equal time was spent and equal calories were burned, resulted in neuronal regeneration.

Exercise can also help reduce stress, but any stress-reducing activity, such as meditation and lifestyle changes, can help the brain. There is some evidence that chronic stress shrinks the parts of the brain involved in learning, memory, and mood. (It also delays wound healing, promotes atherosclerosis, and increases blood pressure.)

It should go without saying that short-term cognitive and physical performance is not boosted by fasting, due to metabolic changes including decrease in body temperature, decreased heart rate and blood pressure and decreased glucose and insulin levels, so you’re better off not planning a marathon or a demanding work session during a fasting period.

As part of a healthy lifestyle the prescription of moderating food intake, exercising, and eating anti-oxidant rich foods is what we’ve long known will boost longevity, but it’s good to know that we can bring our brains along with us as we make it into those golden years without being the 1 in 7 who suffers from dementia. Keep your fingers crossed and eat some rosemary chicken.

by Rebecca Sato @ The Daily Galaxy
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Brain Images

2008-10-08T12:19:00.000-07:00

People are more likely to believe findings from a neuroscience study when the report is paired with a coloured image of a brain as opposed to other representational images of data such as bar graphs, according to a new Colorado State University study.

Image - Aaron Kondziela

Persuasive influence on public perception

Scientists and journalists have recently suggested that brain images have a persuasive influence on the public perception of research on cognition. This idea was tested directly in a series of experiments reported by David McCabe, an assistant professor in the Department of Psychology at Colorado State, and his colleague Alan Castel, an assistant professor at University of California, Los Angeles. The forthcoming paper, to be published in the journal Cognition, was recently published online.

"We found the use of brain images to represent the level of brain activity associated with cognitive processes clearly influenced ratings of scientific merit," McCabe said. "This sort of visual evidence of physical systems at work is typical in areas of science like chemistry and physics, but has not traditionally been associated with research on cognition.

"We think this is the reason people find brain images compelling. The images provide a physical basis for thinking."

In a series of three experiments, undergraduate students were either asked to read brief articles that made fictitious and unsubstantiated claims such as "watching television increases math skills," or they read a real article describing research showing that brain imaging can be used as a lie detector.

When the research participants were asked to rate their agreement with the conclusions reached in the article, ratings were higher when a brain image had accompanied the article, compared to when it did not use a brain image or included a bar graph representing the data.

This effect occurred regardless of whether the article described a fictitious, implausible finding or realistic research.

"Cognitive neuroscience studies which appear in mainstream media are often oversimplified and conclusions can be misrepresented," McCabe said. "We hope that our findings get people thinking more before making sensational claims based on brain imaging data, such as when they claim there is a 'God spot' in the brain."
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Like Goldilocks, the brain seeks proportions that are "just right."
Brain needs perfection in synapse number from Baylor College of Medicine
What Emotional Memories are made of from John Hopkins Medicine
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Cambridge Neuroscience

2008-09-18T08:30:00.000-07:00

Cambridge University launch a new initiative to raise the profile of neuroscience at Cambridge by enhancing multi-disciplinary research and teaching across the University and affiliated Institutes.

See cutting-edge collaborative research happening in Cambridge.
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Ghosts in The Machine by Steven Pinker @ Cosmos Magazine
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Natural Antioxidants

2008-09-13T12:13:00.000-07:00

Antioxidants such as vitamins C and E, carotene, lycopene, lutein and many other substances may play a role in helping to prevent diseases such as cancer, cardiovascular disease, Alzheimer’s disease and macular degeneration.

Antioxidants are thought to help because they can neutralize free radicals, which are toxic byproducts of natural cell metabolism. The human body naturally produces antioxidants but the process isn’t 100 percent effective and that effectiveness declines with age.

Research at the Mayo Clinic is increasingly showing that those who eat antioxidant-rich foods reap health benefits. Foods, rather than supplements, may boost antioxidant levels because foods contain an unmatchable array of antioxidant substances. A supplement may contain a single type of antioxidant or even several. However, foods contain thousands of types of antioxidants, and it’s not known which of these substances confer the benefits.

Some of the better food sources of antioxidants are:

Berries: Blueberries, blackberries, raspberries, strawberries and cranberries
Beans: Small red beans and kidney, pinto and black beans
Fruits: Many apple varieties (with peels), avocados, cherries, green and red pears, fresh or dried plums, pineapple, oranges, and kiwi
Vegetables: Artichokes, spinach, red cabbage, red and white potatoes (with peels), sweet potatoes and broccoli
Beverages: Green tea, coffee, red wine and many fruit juices
Nuts: Walnuts, pistachios, pecans, hazelnuts and almonds
Herbs: Ground cloves, cinnamon or ginger, dried oregano leaf and turmeric powder
Grains: Oat-based products
Dessert: Dark chocolate
Though supplements containing antioxidants are generally considered safe, two recent studies have suggested that taking higher than recommended doses of supplements such as vitamin E over time may actually be harmful and possibly toxic.

In contrast, many foods higher in antioxidants offer an array of health benefits, such as being high in fiber, protein and other vitamins and minerals and low in saturated fat and cholesterol.
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Eye of the Beholder

2008-07-07T10:50:00.000-07:00

Colour is in the Eye of the Beholder
Pumpkin seed oil and water. Credit: iStockphoto/Glenn Bristol

The unique makeup of the cells in our retina, as well as the specific physical properties of substances themselves, explain why we occasionally see things change colour before our very eyes! Samo and Marko Kreft from the University of Ljubljana in Slovenia investigated this phenomenon using pumpkin seed oil as an example. They have just published their research online in Springer’s journal Naturwissenschaften.

In some regions of Central Europe, salad dressing is made preferably with pumpkin seed oil, which has a strong characteristic nutty flavor and striking colour properties. Indeed, in a bottle it appears red, but it looks green in a salad dressing or mixed with yoghurt.

Samo and Marko Kreft’s paper examines the remarkable two-tone (or dichromatic) colour of pumpkin seed oil, by the use of a combination of imaging and CIE (International Commission on Illumination) chromaticity coordinates. The paper also explains why human vision perceives substances like pumpkin seed oil as dichromatic or polychromatic (exhibiting a variety of colours).

Two phenomena explain the perceived shift in colour of pumpkin seed oil from red to green:

Firstly, the distinctive change in colour shade of the oil is due to a change in oil layer thickness. As the oil layer thickens, the oil changes its appearance from bright green to bright red. The observed colour is neither dependent on the angle of observation nor on the direction or type of light.

Secondly, the shift in colour is due to the unique characteristics of the cells in the human retina. Our eyes have two types of photoreceptor cells: rods and cones. Rod photoreceptor cells are very sensitive and operate in dim illumination conditions. Cone photoreceptor cells function well in bright light conditions. They are also the basis of colour perception in our visual image. It is the presence of multiple classes of cone cells, each with a different spectral sensitivity, that gives us the ability to discriminate colours.
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Taxol Bristle Ball

2007-09-19T01:00:00.000-07:00

Cancer-clogging drugs loaded onto nanospheres from Rice University

Rice chemists have discovered a way to load dozens of molecules of the anticancer drug paclitaxel onto tiny gold spheres. The result is a ball many times smaller than a living cell that literally bristles with the drug.

Paclitaxel, which is sold under the brand name Taxol®, prevents cancer cells from dividing by jamming their inner works.

First isolated from the bark of the yew tree in 1967, paclitaxel is one of the most widely prescribed chemotherapy drugs in use today. The drug is used to treat breast, ovarian and other cancers. Paclitaxel works by attaching itself to structural supports called microtubules, which form the framework inside living cells. To divide, cells must break down their internal framework, and paclitaxel stops this process by locking the support into place.

Since cancer cells divide more rapidly than healthy cells, paclitaxel is very effective at slowing the growth of tumors in some patients. However, one problem with using paclitaxel as a general inhibitor of cell division is that it works on all cells, including healthy cells that tend to divide rapidly. This is why patients undergoing chemotherapy sometimes suffer side effects like hair loss and suppressed immune function.

"Ideally, we'd like to deliver more of the drug directly to the cancer cells and reduce the side effects of chemotherapy," Zubarev said. "In addition, we'd like to improve the effectiveness of the drug, perhaps by increasing its ability to stay bound to microtubules within the cell."

The new delivery system centers on a tiny ball of gold that's barely wider than a strand of DNA. Finding a chemical process to attach a uniform number of paclitaxel molecules to the ball - without chemically altering the drug - was not easy. Only a specific region of the drug binds with microtubules. This region of the drug fits neatly into the cell's support structure, like a chemical "key" fitting into a lock. Zubarev and Gibson knew they had to find a way to make sure the drug's key was located on the face of each bristle.

Zubarev and Gibson first designed a chemical "wrapper" to shroud the key, protecting it from the chemical reactions they needed to perform to create the ball. Using the wrapped version of the drug, they undertook a series of reactions to attach the drug to linker molecules that were, in turn, attached to the ball. In the final step of the reaction, they dissolved the wrapper, restoring the key."We are already working on follow-up studies to determine the potency of the paclitaxel-loaded nanoparticles," Zubarev said. "Since each ball is loaded with a uniform number of drug molecules, we expect it will be relatively easy to compare the effectiveness of the nanoparticles with the effectiveness of generally administered paclitaxel."
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New Cancer Weapon

2007-09-01T00:02:00.000-07:00

Nuclear Nanocapsules

Rice University chemists have found a way to package some of nature's most powerful radioactive particles inside DNA-sized tubes of pure carbon - a method they hope to use to target tiny tumors and even lone leukemia cells.

"There are no FDA-approved cancer therapies that employ alpha-particle radiation," said lead researcher Lon Wilson, professor of chemistry. "Approved therapies that use beta particles are not well-suited for treating cancer at the single-cell level because it takes thousands of beta particles to kill a lone cell.

By contrast, cancer cells can be destroyed with just one direct hit from an alpha particle on a cell nucleus."

In the study, Wilson, Rice graduate student Keith Hartman, University of Washington (UW) radiation oncologist Scott Wilbur and UW research scientist Donald Hamlin, developed and tested a process to load astatine atoms inside short sections of carbon nanotubes.

Because astatine is the rarest naturally occurring element on Earth - with less than a teaspoon estimated to exist in the Earth's crust at any given time - the research was conducted using astatine created in a UW cyclotron.

Astatine, like radium and uranium, emits alpha particles via radioactive decay. Alpha particles, which contain two protons and two neutrons, are the most massive particles emitted as radiation. About 4,000 times more massive than the electrons emitted by beta decay - the type of radiation most commonly used to treat cancer.

"It's something like the difference between a cannon shell and a BB," Wilson said. "The extra mass increases the amount of damage alpha particles can inflict on cancer cells."

The speed of radioactive particles is also an important factor in medical use. Beta particles travel very fast. This, combined with their small size, gives them significant penetrating power.

In cancer treatment, for example, beams of beta particles can be created outside the patient's body and directed at tumors. Alpha particles move much more slowly, and because they are also massive, they have very little penetrating power. They can be stopped by something as flimsy as tissue paper.

"The unique combination of low penetrating power and large particle mass make alpha particle ideal for targeting cancer at the single-cell level," Wilson said. "The difficulty in developing ways to use them to treat cancer has come in finding ways to deliver them quickly and directly to the cancer site."

In prior work, Wilson and colleagues developed techniques to attach antibodies to carbon fullerenes like nanotubes. Antibodies are proteins produced by white blood cells. Each antibody is designed to recognize and bind only with a specific antigen, and doctors have identified a host of cancer-specific antibodies that can be used to kill cancer cells.

In follow-up research, Wilson hopes to test the single-celled cancer targeting approach by attaching cancer-specific antibodies to astatine-loaded nanotubes.

One complicating factor in any astatine-based cancer therapy will be the element's short, 7.5-hour half-life. In radioactive decay, the term half-life refers to the time required for any quantity of a substance to decay by half its initial mass.

Due to astatine's brief half-life, any treatment must be delivered in a timely way, before the particles lose their potency.
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Area responsible for Self Control

2007-08-24T09:06:00.000-07:00

The area of the brain responsible for self-control is separate from the area associated with taking action.

Image Above: Brain area in the fronto-median cortex that was activated when participants intentionally withhold a planned action in the last moment

The results illuminate a very important aspect of the brain's control of behavior, the ability to hold off doing something after you've developed the intention to do it-one might call it 'free won't' as opposed to free will," says Martha Farah, PhD, of the University of Pennsylvania. "It is very important to identify the circuits that enable 'free won't' because of the many psychiatric disorders for which self-control problems figure prominently-from attention deficit disorder to substance dependence and various personality disorders." Farah was not involved in the experiment.

The findings broaden understanding of the neural basis for decision making, or free will, and may help explain why some individuals are impulsive while others are reluctant to act, says lead author Marcel Brass, PhD, of the Max Planck Institute for Human Cognitive and Brain Sciences and Ghent University. Brass and Patrick Haggard, PhD, of University College London, used functional magnetic resonance imaging (fMRI) to study the brain activity of participants pressing a button at times they chose themselves. They compared data from these trials to results when the participants prepared to hit the button, then decided to hold back or veto the action.

Fifteen right-handed participants were asked to press a button on a keyboard. They were asked to choose some cases in which they stopped just before pressing the button. Participants also indicated on a clock the time at which they intended to press the button or decided to hold back. When Brass and Haggard compared fMRI images of the two scenarios, they found that pulling back yielded activity in the dorsal fronto-median cortex (dFMC), an area on the midline of the brain directly above the eyes, which did not show up when participants followed through and made the action. In addition, those who chose to stop the intended action most often showed greatest contrast in dFMC activity.

"The capacity to withhold an action that we have prepared but reconsidered is an important distinction between intelligent and impulsive behavior," says Brass, "and also between humans and other animals."

Future study will involve methods with a better time resolution such as EEG to determine whether the inhibitory process could operate in the brief time period between the time of conscious intention and the point of no return for motor output.

Image: Max Planck Institute for Human Cognitive and Brain Sciences
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Milestone In The Regeneration Of Brain Cells
Brain Cells Work Differently Than Previously Thought
One Step Closer To Transplanting Stem Cells In The Brain
Researchers Identify Brain Network That May Help Prevent Or Slow Alzheimer's
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Ancestors help Bird Memory

2007-08-21T07:10:00.001-07:00

Birds learn to fly with a little help from their Ancestors

A University of Sheffield researcher has discovered that the reason birds learn to fly so easily is because latent memories may have been left behind by their ancestors.

It is widely known that birds learn to fly through practice, gradually refining their innate ability into a finely tuned skill, and these skills may be easy to refine because of a genetically specified latent memory for flying.

Dr Dr Jim Stone from the University of Sheffield´s Department of Psychology, used simple models of brains called artificial neural networks and computer simulations to test his theory.

He discovered that learning in previous generations indirectly induces the formation of a latent memory in the current generation and therefore decreases the amount of learning required. These effects are especially pronounced if there is a large biological 'fitness cost' to learning, where biological fitness is measured in terms of the number of offspring each individual has.

The beneficial effects of learning also depend on the unusual form of information storage in neural networks. Unlike computers, which store each item of information in a specific location in the computer's memory chip, neural networks store each item distributed over many neuronal connections. If information is stored in this way then evolution is accelerated, explaining how complex motor skills, such as nest building and hunting skills, are acquired by a combination of innate ability and learning over many generations.

However not every bird automatically knows how to fly.
A crowling which has been blown from its nest, had a great fall and hurt its legs, may never fly - though there be nothing wrong with its wings at all. Birds learn fear, pain and doubt too. - Q9
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New Caledonian Crows Find Two Tools Better Than One
Uncertainties Of Savanna Habitat Drive Birds To Cooperative Breeding
Birds With Child-care Assistance Invest Less In Eggs @ Science Daily
Are Artist's Born or Taught from Hank @ Scientific Blogging
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Functioning Neuron Produced

2007-08-10T08:28:00.000-07:00

Scientists with the Institute of Stem Cell Biology and Medicine at UCLA were able to produce from human embryonic stem cells a highly pure, large quantity of functioning neurons that will allow them to create models of and study diseases such as Alzheimer's, Parkinson's, prefrontal dementia and schizophrenia.

Researchers previously had been able to produce neurons - the impulse-conducting cells in the brain and spinal cord - from human embryonic stem cells. However, the percentage of neurons in the cell culture was not high and the neurons were difficult to isolate from the other cells.

UCLA's Yi Sun, an associate professor of biobehavioural sciences, and Howard Hughes Medical Institute investigator Thomas Südhof at the University of Texas Southwestern Medical Center were able to produce 70 to 80 percent of neurons in cell culture. Sun and Südhof also were able to isolate the neurons and determine that they had a functional synaptic network, which the neurons use to communicate. Because they were functional, the neurons can be used to create a variety of human neurological disease models.

"Previously, the system to grow and isolate neurons was very messy and it was unknown whether those neurons were functioning," Sun said. "We're excited because we have been able to purify so many more neurons out of the cell culture and they were, surprisingly, healthy enough to form synapses. These cells will be excellent for doing gene expression studies and biochemical and protein analyses."

Sun's method prodded human embryonic stem cells to differentiate into neural stem cells, the cells that give rise to neurons. When the time was right, Sun's team added protein growth factors into the cell culture that stopped the neural stem cells from self-renewing and prodded them into differentiating into neurons.

To isolate the cells, Sun and her team added an enzyme that digests a sort of protein matrix that holds cells in culture together. The neurons could then be separated from the neural stem cells that had not yet differentiated, a sort of chemical round-up that isolated the neurons. The cells were then put into a cell strainer that allowed passage through of the isolated neurons.

The large number of pure neurons produced will allow Sun and her team to study their biological form and structure, the genes they express, the development of synapses and the electric and chemical communication activities within the synapse network.

"We will be able to study the cellular properties of neurons in a very defined way that will maybe tell us what goes wrong in diseases such as Alzheimer's and Parkinson's," Sun said. "We're currently creating many models of human neurological diseases that may provide the answers we're looking for. We don't know what causes prefrontal dementia, Huntington's disease or schizophrenia. The key is likely in the quality of neuronal communications. By studying the chemical and electrical transmissions, we may be able to determine what goes wrong that leads to these debilitating diseases and find a way to stop or treat it."

Sun will be among the first researchers to be able to study true neuron function.

A second important discovery in Sun's study showed that two embryonic stem cells lines derived in similar manners, and therefore expected to behave similarly when differentiating, did not. Using the same techniques to prod the two embryonic stem cells lines to differentiate, Sun found that one line had a bias to become neurons that are found in the forebrain. The other line differentiated into neurons found in rear portions of the brain and spinal cord. The finding was surprising, and significant, Sun said.

"The realization that not all human embryonic stem cell lines are born equal is critical," Sun said. "If you're studying a disease found in a certain part of the brain, you should use a human embryonic stem cell line that produces the neurons from that region of the brain to get the most accurate results from your study.

Huntington's disease, for example, is a forebrain disease, so the neurons should be differentiated from a cell line that is biased to produce neurons from the forebrain."Sun said there are ways to prod an embryonic stem cell line biased to become neurons found in the rear brain to become neurons found in the forebrain. However, there are limits to how much prodding can be done.

Sun and her team confirmed that the two embryonic stem cell lines were different through gene expression analysis - neurons that perform different functions in different parts of the brain express different genes.

The cell line prone to becoming neurons found in the forebrain expressed genes typically found in those neurons, while the other line expressed genes found in the rear brain and spinal cord.

The team now are studying why the two human embryonic stem cell lines have biases to become different types of neurons. "If we knew that, we might be able to tweak or alter whatever is driving the bias so that limitation in the stem cell line could be bypassed," Sun said.

Study results were recently published in an early online edition of the journal Proceedings of the National Academy of Sciences.

Functioning Neurons From Human Embryonic Stem Cells Produced
UCLA Institute of Stem Cell Biology
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Pain Perception

2007-08-08T03:11:00.000-07:00

Treatment of pain-related suffering requires knowledge of how pain signals are initially interpreted and subsequently transmitted and perpetuated.

Clinical pain is a serious public health issue.
Our understanding of the neural correlates of pain perception in humans has improved with the advent of neuroimaging. Relating neural activity changes to the varied pain experiences has led to an increased awareness of how factors (e.g., cognition, emotion, context, injury) can separately influence pain perception.

It has been suggested that the brainstem plays a pivotal role in gating the degree of nociceptive transmission so that the resultant pain experienced is appropriate for the particular situation of the individual.

Pain that persists for more than three months is defined as chronic and as such is one of largest medical health problems in the developed world. While the management and treatment of acute pain is reasonably good, the needs of chronic pain sufferers are largely unmet, creating an enormous emotional and financial burden to sufferers, carers, and society.

The mechanisms that contribute to the generation and maintenance of a chronic pain state are increasingly investigated and better understood. A consequent shift in mindset that treats chronic pain as a disease rather than a symptom is accelerating advances in this field considerably.

Pain is a conscious experience, an interpretation of the nociceptive input influenced by memories, emotional, pathological, genetic, and cognitive factors. Resultant pain is not necessarily related linearly to the nociceptive drive or input; neither is it solely for vital protective functions. This is especially true in the chronic pain state. Furthermore, the behavioral response by a subject to a painful event is modified according to what is appropriate or possible in any particular situation. Pain is, therefore, a highly subjective experience “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.”

By its very nature, pain is therefore difficult to assess, investigate, manage, and treat. Figure 1 (above) illustrates the mixture of factors that we know influence nociceptive inputs to amplify, attenuate, and color the pain experience.

Because pain is a complex, multifactorial subjective experience, a large distributed brain network is subsequently accessed during nociceptive processingm and was first described this as the pain “neuromatrix,” but it's now more commonly referred to as the “pain matrix”; simplistically it can be thought of as having lateral (sensory-discriminatory) and medial (affective-cognitive-evaluative) neuroanatomical components. However, because different brain regions play a more or less active role depending upon the precise interplay of the factors involved in influencing pain perception (e.g., cognition, mood, injury, and so forth), what comprises the pain matrix is not unequivocally defined.

For both chronic and acute pain sufferers, mood and emotional state has a significant impact on the resultant pain perception and ability to cope. For example, it is a common clinical and experimental observation that anticipating and being anxious about pain can exacerbate the pain experienced. Anticipating pain is highly adaptive; we all learn in early life to avoid hot pans on stoves and not to put your finger into a candle flame. However, for the chronic pain patient it becomes maladaptive and can lead to fear of movement, avoidance, anxiety, and so forth.

Another negative cognitive and mood affect that impacts pain is catastrophizing. This construct incorporates magnification of pain-related symptoms, rumination about pain, feelings of helplessness, and pessimism about pain-related outcomes, and it is defined as a set of negative emotional and cognitive processes. A study on fibromyalgia patients found that pain catastrophizing, independent of the influence of depression, was significantly associated with increased activity in brain areas related to anticipation of pain (medial frontal cortex, cerebellum), attention to pain (dorsal ACC, dorsolateral prefrontal cortex), emotional aspects of pain (claustrum, closely connected to amygdala), and motor control.

Clearly, these results support the notion that catastrophizing influences pain perception through altering attention and anticipation, as well as heightening emotional responses to pain.

It is interesting to speculate whether activity in such “emotional” brain regions due to chronic pain impacts performance in tasks requiring emotional decision making. A card game developed to study emotional decision making, chronic pain patients displayed a specific cognitive deficit compared to controls, suggesting such an impact might exist in everyday life.

Such experiments are hard to reproduce in animal studies.

As the problem of pain and the key role of the brain becomes increasingly well recognized, more research is being directed toward a better understanding of the underlying mechanisms. Some of the newest and more novel areas of investigation are briefly summarized here.

The recent finding that significant atrophy exists in the brains of chronic pain patients highlights the need to perform more advanced structural imaging measures and image analyses to quantify fully these effects.

Determining what the possible causal factors are that produce such neurodegeneration is difficult. Candidates include the chronic pain condition itself (i.e., excitotoxic events due to barrage of nociceptive inputs), the pharmacological agents prescribed, or perhaps the physical lifestyle change subsequent to becoming a chronic pain patient.
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Backache Sufferers Who Fear Pain Change Movements from Science Daily
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Music on the Brain

2007-08-06T06:14:00.000-07:00

Music moves brain to pay attention

Using brain images of people listening to short symphonies by an obscure 18th-century composer, a research team from the Stanford University School of Medicine has gained valuable insight into how the brain sorts out the chaotic world around it.

The research team showed that music engages the areas of the brain involved with paying attention, making predictions and updating the event in memory. Peak brain activity occurred during a short period of silence between musical movements—when seemingly nothing was happening.

Beyond understanding the process of listening to music, their work has far-reaching implications for how human brains sort out events in general. The findings are published in the Aug. 2 issue of Neuron.

The researchers caught glimpses of the brain in action using functional magnetic resonance imaging, or fMRI, which gives a dynamic image showing which parts of the brain are working during a given activity. The goal of the study was to look at how the brain sorts out events, but the research also revealed that musical techniques used by composers 200 years ago help the brain organize incoming information.

The team used music to help study the brain’s attempt to make sense of the continual flow of information the real world generates, a process called event segmentation. The brain partitions information into meaningful chunks by extracting information about beginnings, endings and the boundaries between events.

See Video & Read more @ Stanford University School Of Medicine news release
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Neuro Genesis in Korea?

2007-08-02T23:03:00.001-07:00

Toward An Alternative To Stem Cells For Treating Chronic Brain Diseases
Image Courtesy of Injae Shin, Yonsei University, Korea.

Scientists in Korea are reporting the first successful use of a drug-like molecule to transform human muscle cells into nerve cells. This advance could lead to new treatments for stroke, Alzheimer's disease, Parkinson's disease and other neurological disorders.

The researchers exposed immature mouse muscle cells myoblasts (image left) growing in laboratory cell cultures to neurodazine, a synthetic small molecule. After one week, 40-50 percent of the myoblasts were transformed into cells that resembled both the structure and function of nerve cells (image right), including expression of neuron-specific proteins. Additional studies showed a similar transformation in a group of human skeletal muscle cells that were exposed to the same chemical for several days, they add.

"In conclusion, we have developed the first small molecule that can induce neurogenesis of non-pluripotent myoblasts and the cells derived from mature, human skeletal muscle," the report states. "These studies build upon recent research illustrating the value of chemical approaches for providing tools that differentiate lineage-committed cells into other cell types."
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How Real is Synesthesia?

2007-07-27T03:03:00.000-07:00

Hearing Colours And Seeing Sounds:
How Real Is Synesthesia?

In the psychological phenomenon known as "synesthesia," individuals' sensory systems are a bit more intertwined than usual. Some people, for example, report seeing colours when musical notes are played.

One of the most common forms is grapheme-colour synesthesia, in which letters or numbers (collectively called "graphemes") are highlighted with particular colours. Although synesthesia has been well documented, it is unknown whether these experiences, reported as vivid and realistic, are actually being perceived or if they are a byproduct of some other psychological mechanism such as memory.

New research published in the June issue of Psychological Science, a journal of the Association for Psychological Science, sheds some light on the veracity of these perceptions.

When anyone views a particular colour, specific neurons in the visual cortex area of our brain are activated. These specific neurons will deactivate, however, if a colour from the opposite end of the spectrum is presented.

Any neuron activated when the colour blue is present will deactivate when it's exact opposite, yellow, comes into the visual field.

Read more from Science Daily
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UC Irvine scientists unveil the 'face' of a new memory Breakthrough study also links learning to a specific chemical process in brain cells
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Protein's Internal Motion

2007-07-19T23:15:00.000-07:00

Researchers at the University of Pennsylvania School of Medicine are the first to observe and measure the internal motion inside proteins, or its “dark energy.” This research, appearing in the current issue of Nature, has revealed how the internal motion of proteins affects their function and overturns the standard view of protein structure-function relationships, suggesting why rational drug design has been so difficult.

“The situation is akin to the discussion in astrophysics in which theoreticians predict that there is dark matter, or energy, that no one has yet seen,” says senior author A. Joshua Wand, PhD, Benjamin Rush Professor of Biochemistry. “Biological theoreticians have been kicking around the idea that proteins have energy represented by internal motion, but no one can see it. We figured out how to see it and have begun to quantify the so-called ‘dark energy’ of proteins.”

Proteins are malleable in shape and internal structure, which enables them to twist and turn to bind with other proteins. “The motions that we are looking at are very small, but very fast, on the time scale of billions of movements per second,” explains Wand. “Proteins just twitch and shake.” The internal motion represents a type of energy called entropy.

Current models of protein structure and function used in research and drug design often do not account for their non-static nature. “The traditional model is almost a composite of all the different conformations a protein could take,” says Wand.

The researchers measured a protein called calmodulin and its interactions with six other proteins when bound to a protein partner one at a time. These binding partners included proteins important in smooth muscle contraction and a variety of brain functions.

Using nuclear magnetic resonance spectroscopy, the investigators were able to look at the changes in the internal motion of calmodulin itself in each of the six different protein binding situations. They found a direct correlation between a change in calmodulin’s entropy – a component of its stored energy – and the total entropy change leading to the formation of the calmodulin-protein complex.

Finding out the contribution from individual proteins versus the entropy, or movement, of the entire protein complex has been more difficult and has been overcome in this study. From this individual contribution they deduced that changes in the entropy of the protein are indeed important to the process of calmodulin binding its partners.

“Before these unexpected results, most researchers in our field would have predicted that entropy’s contribution to protein-protein interactions would be zero or negligible,” says Wand. “But now it’s clearly an important component of the total energy in protein binding.”

Because of this new information, the researchers suggest that the entropy component may explain why drug design fails more often than it works. Currently, drugs are designed generally based on the precise structures of their biological targets, active regions on proteins that are intended to inhibit key molecules. However, the number of designed molecules actually binding to their targets is low for many engineered molecules. “We think that this is because the design is based on a model of a static protein, not the moving, hyper protein that is constantly changing shape,” say Wand. “We need to figure out how this new information fits in and perhaps drug design could be significantly improved.”

Future directions include understanding whether the principles revealed by this study are universal and impact the thousands of protein-protein interactions that underlie biology and disease. As Wand explains, “Protein-protein interactions are central to ‘signalling’, which is often the molecular origin of diseases. Cancer, diabetes, and asthma are three important examples. We are currently looking at the role of protein entropy in the control of critical signaling events in all three.”

Artist rendering of calmodulin molecule depicting protein "dark energy."
Image Credit: Mary Leonard and Michael Marlow, UP School of Medicine.

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Unravelling the Physics of DNA

2007-07-17T12:02:00.001-07:00

Researchers at Duke University's School of Engineering have uncovered a missing link in scientists' understanding of the physical forces that give DNA its famous double helix shape.

The stability of DNA is fundamental to life. To create accurate models of DNA to study its interaction with proteins or drugs, you need to understand the basic physics of the molecule. For that, you need solid measurements of the forces that stabilize DNA.

Each DNA strand includes a sugar and phosphate "backbone" attached to one of four bases, which encode genetic sequences. The strength of the interactions within individual strands comes largely from the chemical attraction between the stacked bases. But the integrity of double-stranded DNA depends on both the stacking forces between base units along the length of the double helix and on the pairing forces between complementary bases, which form the rungs of the twisted ladder.

Earlier studies have focused more attention on the chemical bonds between opposing bases, measuring their strength by "unzipping" the molecules' two strands. Studies of intact DNA make it difficult for researchers to separate the stacking from the pairing forces.

To get around that problem in the new study, the Duke team used an atomic force microscope (AFM) to capture the "mechanical fingerprint" of the attraction between bases within DNA strands. The bonds within the molecules' sugar and phosphate backbones remained intact and therefore had only a minor influence on the force measurements.

Researchers tugged on individual strands that were tethered at one end to gold and measured the changes in force as they pulled. The AFM technique allows precise measurements of forces within individual molecules down to one pico-Newton--a trillionth of a Newton. For a sense of scale, the force of gravity on a two-liter bottle of soda is about 20 Newtons.

They captured the range of stacking forces by measuring two types of synthetic DNA strands: some made up only of the base thymine, which is known to have the weakest attraction between stacked units, and some made up only of the base adenine, known to have the strongest stacking forces. Because of those differences in chemical forces, the two types of single-stranded DNA take on different structures. Single strands of adenine coil in a fairly regular fashion to form a helix of their own, while thymine chains take on a more random shape.

The pure adenine strands exhibited an even more complex form of elasticity than had been anticipated, the researchers reported. As they stretched the adenine chains with increasing force, the researchers noted two places--at 23 and 113 pico-Newtons--where their measurements leveled off.

"Those plateaus reflect the breaking and unfolding of the helix," professor of mechanical engineering and materials sciences at Duke, Marszalek explained. With no bonds between bases to break, the thymine chains' showed little resistance to extension and no plateau.

Based on the known structure of the single stranded DNA molecules, they had expected to see only one such plateau as the stacking forces severed. Exactly what happens at the molecular level at each of the two plateaus will be the subject of continued investigation.
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White Blood Cells Are Picky About Sugar

2007-07-13T07:29:00.000-07:00

Biology textbooks are blunt--neutrophils are mindless killers. These white blood cells patrol the body and guard against infection by bacteria and fungi, identifying and destroying any invaders that cross their path.

But new evidence, which may lead to better drugs to fight deadly pathogens, indicates that neutrophils might actually distinguish among their targets.

A scientist in the lab of Whitehead Member Gerald Fink has discovered that neutrophils recognize and respond to a specific form of sugar called beta-1,6-glucan on the surface of fungi. This sugar comprises just a small fraction of the fungal cell wall, much less than another sugar with a slightly different chemical conformation called beta-1,3-glucan. Because the scarce form of the sugar elicits a much stronger reaction from immune cells than the abundant one, it appears that neutrophils can distinguish between two nearly identical chemicals.

"These results show that engulfment and killing by neutrophils varies, depending on cell wall properties of the microbe," explains Whitehead postdoctoral researcher Ifat Rubin-Bejerano, first author on the paper, which appears July 11 in the journal Cell Host & Microbe. "We showed that neutrophils respond in a completely different way to slight changes in sugar composition. If we are able to use this unique sugar to excite the immune system, it may help the human body fight infection."

"Previously, everyone thought that these key cells of the immune system weren't picky and would eat anything that looked foreign," adds Fink, who is also an MIT professor of biology. "Ifat's work has shown that the cells aren't little Pac-Men, but can discriminate one pathogen from another."

Rubin-Bejerano had evidence that neutrophils respond to beta-glucan. After coating tiny beads with a variety of substances (including beta-1,3-glucan and beta-1,6-glucan), she exposed them to the neutrophils and was surprised to see a striking difference in their response to the two sugars. The neutrophils quickly engulfed many of the beads coated with beta-1,6-glucan, but only a few of those covered in beta-1,3-glucan.

Previous studies indicated that blood serum (basically blood minus cells) helps neutrophils recognize their enemies, so Rubin-Bejerano decided to look for clues to their response in this mixture. She identified several proteins in serum that bind to beta-1,6-glucan, but not beta-1,3-glucan, and then pinpointed a molecule on the surface of the neutrophil that recognizes these proteins.

To link her experiments back to real fungi, Rubin-Bejerano worked with the pathogen Candida albicans, which is the most common fungus in blood stream infections. She used an enzyme to digest beta-1,6-glucan from the fungal cell wall, leaving the beta-1,3-glucan intact. She then unleashed the neutrophils on these altered cells and observed a 50 percent reduction in the immune response.

Our bodies maintain a fine balance between the immune system and microbes. Antibiotics and antifungals tilt the balance in favor of the immune system by targeting the microbes directly. A substance like beta-1,6-glucan could help tilt this balance further by stimulating immune cells.

Rubin-Bejerano's work offers hope for combating the growing problem of microbial infections, which can seriously threaten human health--particularly in patients with compromised immune systems. In fact, Rubin-Bejerano co-founded a company called ImmuneXcite to explore this possibility.

Source: Whitehead Institute for Biomedical Research
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How DNA strands separate

2007-07-09T03:00:00.000-07:00

Cornell researchers have answered a fundamental question about how two strands of DNA, known as a double helix, separate to start a process called replication, in which genes copy themselves.

Credit: Chris Pelkie and Daniel Ripoll/Cornell Theory Center

This image shows a DNA double helix (green and purple strands) being separated by a helicase enzyme (green globule) at the junction where the two strands fork. To show that helicases actively separate the two strands of DNA, the researchers attached one end of a DNA strand to a microscope cover slip and attached the end of the other DNA strand to a micron-sized plastic bead. The bead was then trapped in a tightly focused laser beam (red), which allowed the researchers to measure the motion of the helicase as it unwound the DNA.

The research, published in the current issue of the journal Cell, examined the role of an enzyme called a helicase, which plays a major role in separating DNA strands so that replication of a single strand can occur.

Scientists have known that helicases bind to the area of a double helix where the two strands fork away from each other, like the free ends of two pieces of thread wound around each other. The forked area opens and closes very rapidly. But scientists have debated whether helicases actively separate the two strands at the fork or if they passively wait for the fork to widen on its own.

The research found that the helicase appears to actively exert a force onto the fork and separate the two strands.

"A simple passive unwinding mechanism does not explain our data," said Michelle Wang, associate professor of physics and the paper's senior author.

"Defects in helicases are associated with many human diseases, ranging from predisposition to cancer to premature aging," said co-author Smita Patel, a biochemistry professor at the Robert Wood Johnson Medical School in Piscataway, N.J. "Helicases are involved in practically all DNA and RNA metabolic processes."

The researchers made their discovery by anchoring one end of one of the strands in a double helix to the surface of a microscope cover slip. The end of the other strand was attached to a micron-sized plastic bead. They then focused a laser beam on the tiny bead and trapped the bead in place within the beam of light. This setup allowed the researchers to measure the position and force on the bead, creating a very precise sensor of the helicase motion. As the helicase moved toward the fork and the double helix unwound, the tension on the two strands lessened. Using statistical mechanics models, the researchers could then compare actual measurements of movement with predictions based on both active and passive scenarios.

"The unwinding has to have some active component to it, and based on our data, we can tell you exactly how active it is," said Wang. "Basically, it is an active unwinding motor."

While helicases unwind very rapidly in cells, in test tube experiments the unwinding is much slower. The researchers believe that helicases work with other enzymes, where "accessory proteins are helping the helicase out by destabilizing the fork junction," said Wang.

Original Source: Cornell University
Cornell researchers determine how an enzyme plays a key role in gene copying
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Prions key in Alzheimer's disease

2007-07-01T00:49:00.000-07:00

Proteins which cause mad cow disease may also protect against Alzheimer's disease, UK researchers say. Prions naturally present in the brain appear to prevent the build up of a key protein associated with the condition.

In laboratory tests, beta amyloid, the building block of Alzheimer's "plaques", did not accumulate if high levels of the prions were present. The findings could lead to new treatments, the Proceedings of the National Academy of Sciences reported.

In variant Creutzfeldt-Jakob disease (vCJD), the human version of mad cow disease, the normal version of the prion protein present in brain cells is corrupted by infectious prions causing it to change shape, resulting in brain damage and death. But little is known about purpose of the normal prion proteins.

Due to the similarities between Alzheimer's and diseases such as variant CJD, researchers at the University of Leeds, looked for a link.

Plaque formation

They found that in cells in the laboratory, high levels of the prions reduced the build-up of beta-amyloid protein, which is found in the brains of people with Alzheimer's disease. In comparison, when the level of the prions was low or absent, beta amyloid formation was found to go back up again, suggesting they have a preventive effect on the development of the condition.

The researchers also looked at mice who had been genetically engineered to lack the prion proteins and again found that the harmful beta-amyloid proteins were able to form.

Study leader Professor Nigel Hooper said they now needed to look at whether ageing had an affect on the ability of the prion proteins to protect against Alzheimer's.

"Until now, the normal function of prion proteins has remained unclear, but our findings clearly identify a role for normal prion proteins in regulating the production of beta-amyloid and in doing so preventing formation of Alzheimer's plaques.

"Whether this function is lost as a result of the normal ageing process, or if some people are more susceptible to it than others we don't know yet."

He said although they needed to learn more, theoretically if a treatment could be designed to mimic the effect of the prions it could halt the progression of the disease.

Professor Clive Ballard, director of research at the Alzheimer's Society said this was the first time a link had been made between prions and Alzheimer's. "These are early findings, which suggest prion proteins may have a regulatory effect on the development of beta amyloid." He added: "This provides the foundations for a novel approach to finding new therapeutic targets in Alzheimer's disease."

Original Source BBC health news 19 June 2007
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Cancer inhibitor

2007-06-25T03:50:00.000-07:00

A TopoisomeraseIB protein (green) is hindered in unwinding DNA loops by the cancer inhibitor topotecan (red). The DNA polymerase protein (grey), a protein which duplicates DNA, is hindered by the DNA loops.

Credit: Delft University of Technology / Tremani

Researchers in Delft University of Technology's Kavli Institute of Nanoscience in The Netherlands have cast new light on the workings of the important cancer inhibitor topotecan. Little had been known about the underlying molecular mechanism, but the Delft scientists can now view the effects of the medicine live at the levelin of a single DNA molecule.

The medicine investigated, topotecan, interacts with an important protein (TopoIB), causing a (cancer) cell to malfunction. The TopoIB protein is responsible for the removal of loops from DNA, which arise amongst other things during cell division. The TopoIB protein binds to the DNA molecule, clamps around it and cuts one of the two DNA strands, after which it allows it to unwind and finally joins the broken ends together.

Until now it has been supposed that topotecan only causes the TopoIB protein to reside longer than normal on the DNA molecule, disturbing the cell division and damaging the (cancer) cell. But the Delft researchers have now discovered to their surprise that adding topotecan also dramatically impedes the unwinding and that DNA loops accumulate as a result. The accumulation of these DNA loops forms the basis for an alternative mechanism, and could help in the development of better cancer medicine.

PhD candidate Daniel Koster, Master's student Elisa Bot and researcher Nynke Dekker of the Molecular Biophysics group of the Kavli Institute of Nanoscience Delft have managed to unravel this mechanism in an extremely direct manner. In the laboratory they fixed a single DNA molecule between a glass plate and a magnetic sphere. With the help of two magnets they could both pull and twist the DNA molecule.

When they added TopoIB to a twisted piece of DNA, they saw that the loops were slowly removed. What is exceptional is that the action of one TopoIB enzyme on one DNA molecule could be observed live. In collaboration with St. Jude Children's Research Hospital Memphis (USA) the mechanism could also be observed in living yeast cells.

The research was published in the journal Nature (June 24). The lead author of the article, Daniel Koster, will receive his PhD at TU Delft partly on the results described in the article. The research is supported by the Foundation for Fundamental Research on Matter and the Netherlands Organisation for Scientific Research.

TU DElft - Delft Research Centres
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Toward a cure for inherited eye disease

2007-06-20T21:54:00.000-07:00

Isolated mouse photoreceptor sensory cilium. Red is the rootlet, which helps connect the cilium to the cell. Green is the axoneme, the central part of the cilium. Scale bar 5 microns.
Credit: Qin Liu, MD, PhD and Eric A. Pierce, MD, PhD, University of Pennsylvania School of Medicine.

Researchers at the University of Pennsylvania School of Medicine have identified proteins in the rod and cones of the eye that could lead to the discovery of the genetic causes of a host of inherited eye diseases. The investigators hope to gain a clearer understanding of what goes wrong at the most basic level in these diseases that cause blindness and other disorders.

Specifically, they have identified and measured the types and amounts of proteins in the light-sensing parts of the eye’s retina. These light-sensitive structures, called photoreceptor sensory cilia, enable the rod and cone cells of the retina to detect light. While the proteins of cilia in single-celled organisms have been studied, this is the first time that a comprehensive description of the proteins of a mammalian cilium – used for movement and sensing – has been determined.

“We want to understand how cilia work normally and how their function is disrupted in disease, because their dysfunction is such an important cause of disease,” says senior author Eric A. Pierce, MD, PhD, Associate Professor of Ophthalmology at the F.M. Kirby Center for Molecular Ophthalmology at Penn. “One of the first steps to achieve this is to put together a complete parts list. Now that we have that, we can figure out how all 2000 proteins we’ve identified fit together correctly.”

Cilia, specialized structures that extend from cells, have recently taken the spotlight in studying genetic diseases. They are commonly used by cells for movement or sensory purposes, and, in many cases with mammals, have been thought to be remnants of evolution without much purpose. But new research has shown that mutations in genes that encode the proteins of cilia are common causes of a host of genetic diseases, including inherited retinal diseases and polycystic kidney disease.

Cilia diseases can also affect multiple organ systems in such disorders as Bardet-Biedl Syndrome, which causes kidney disease, obesity, polydactyly, diabetes, and retinal degeneration; Senior-Loken Syndrome, which causes kidney disease and retinal degeneration; Joubert Syndrome, which causes neurological disease, kidney disease, and retinal degeneration; Usher Syndrome, which causes deafness and blindness; and Meckel Syndrome, which causes kidney disease and neural tube defects.

Lead author Qin Liu, MD, PhD, Research Assistant Professor, and Pierce collaborated with a team at The Wistar Institute led by David Speicher to perform the analyses for this study. The researchers used mass spectrometry to identify and measure the amounts of proteins in mouse photoreceptor sensory cilia. They found many proteins in the cilia that had not been identified in photoreceptors before. This includes proteins involved in intraflagellar transport, which is a process that moves materials from the cell body into the cilia. Mutations in proteins associated with this transport system lead to a number of cilia-related diseases.

The investigators also found 60 proteins encoded by genes on chromosomes implicated in 23 inherited cilia-related disorders. Armed with this knowledge, researchers hope to be able to more quickly find the exact genetic mutations that cause these 23 cilia diseases, which include eye and kidney diseases, among others.

Pierce is a pediatric ophthalmologist who specializes in caring for children with inherited retinal degenerations. He says that about half of his patients with degenerative eye diseases have a type of disease that can be identified according to its genetic mutation. He believes that this research will help identify the genetic causes behind the other half of his patients’ conditions.
“We’re narrowing the field,” says Pierce. “This research in and of itself can’t find a cure, but it’s a great start because it tells you what proteins to study.”

University of Pennsylvania - School of Medicine
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Have I Been Here Before?

2007-06-08T03:01:00.000-07:00

New research could lead to treatments for memory-related disorders.

Dentate Gyrus NMDA Receptors Mediate Rapid Pattern Separation in the Hippocampal Network.
Dentate gyrus pattern.
(Credit: Matt Jones)

In today's fast-moving world of look-alike hotel rooms and comparable corridors, it can take a bit of thinking to answer this simple question. University of Bristol neuroscientists working with colleagues at the Massachusetts Institute of Technology (MIT) report in the June 7 early online edition of Science that they have identified a neuronal mechanism that our brains may use to rapidly distinguish similar, yet distinct places.

The work could lead to treatments for memory-related disorders, as well as for the confusion and disorientation that plague elderly individuals who have trouble distinguishing between separate but similar places and experiences.

Forming memories of places and contexts in which episodes occur engages a part of the brain called the hippocampus. The laboratory of Nobel Laureate, Susumu Tonegawa, Picower Professor of Biology and Neuroscience at MIT, has been exploring how each of the three hippocampal subregions-the dentate gyrus, CA1 and CA3-contribute uniquely to different aspects of learning and memory.

In the current study, co-authors Matthew Jones, Research Councils UK (RCUK) Academic Fellow in the Department of Physiology at the University of Bristol and Dr Thomas McHugh, a Picower Institute research scientist, have revealed that the learning in the dentate gyrus is crucial in rapidly recognizing and amplifying the small differences that make each place unique.

"We constantly make split-second decisions about how best to behave at a given place and time. To achieve this, our nervous system must employ highly efficient ways of rapidly recognising and learning important changes in our environment" said Dr Jones.

"This paper demonstrates that a particular protein signalling molecule (the NMDA receptor) in a particular network of brain neurons (the dentate granule cells of the hippocampus) is essential for these rapid discrimination processes, hopefully paving the way for therapies targeting learning and behavioural disorders."

Researchers believe that a set of neurons called 'place cells' fire to provide a sort of blueprint for any new space we encounter. The next time we see the space, those same neurons fire. Thus we know when we've been somewhere before and don't have to relearn our way around familiar turf. But similar spaces may activate overlapping neuronal blueprints, leaving room for confusion if the neurons are not fine-tuned.

In this study, the researchers used a line of genetically altered mice to pinpoint how the dentate gyrus contributes to the kind of pattern separation involved in identifying new and old spaces. Whilst the mice behaved normally in most situations, they became confused when required to discriminate between different spaces. This may model the difficulties in forming distinct memories for similar but distinct places and experiences that afflicts some elderly individuals.

Have I Been Hear Before?
Neuronal Mechanism Could Help Explain Déjà-vu
Bristol University Press release issued 7 June 2007
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Latent Cell Memory

2007-05-27T23:30:00.000-07:00

Artistic impression of nucleosomes interaction.
Credit: Mette Høst, CMOL, Niels Bohr Institute, University of Copenhagen

New Danish research has examined the mechanisms behind latent cell memory, which can come to life and cause previously non-existent capacities suddenly to appear. Special yeast cells for example, can abruptly change from being of a single sex to hermaphrodite.

Researchers from the Niels Bohr Institute at the University of Copenhagen have used mathematical models and computer simulations to examine fundamental mechanisms of cell memory. The research is an interdisciplinary cooperation between molecular biologists and physicists and has just been published in the journal CELL (article by Dodd et al., 18 May issue).

Dormant capacities

Our genetic material - DNA -- is a blueprint for how we look and are. This genetic material is very stable and it is faithfully transmitted to our descendants. Once in a while though, a change occurs to the DNA, either large or small. Such changes are at the origin of the immense and varied animal and plant life on earth. Constructive changes in the DNA, that is, changes creating new functions, normally arise by a slow and gradual process that involves natural selection operating over many generations.

Sometimes however, dramatic and very sudden changes are observed in one individual in the absence of any kind of change to the DNA. This happens in fact in all of us as our body develops: cells with identical genetic information adopt very different fates, forming tissues that have apparently very little in common with each other, such as skin, brain, or bones. Mechanisms at the origin of this so-called cellular differentiation are those for which researchers at the University of Copenhagen have a possible clarification.

"The explanation for the sudden changes is that it is not the DNA itself that is altered - it is its immediate surroundings that change and thereby cause a cell to activate some of its dormant capacities" says Kim Sneppen, professor in Biophysics at the Niels Bohr Institute, University of Copenhagen .

The environment controls the DNA

The DNA coils itself around protein complexes called nucleosomes. Importantly, nucleosomes can carry various chemical modifications that either allow, or prevent, the expression of the DNA wrapped around them. Every time a cell divides into new cells, its double-stranded DNA splits into two single strands, which then each produce a new double-strand.

Nucleosomes though are not duplicated like the DNA-strands. Rather, they are distributed between the two new DNA double strands and the empty spaces are filled by new nucleosomes. Cell division is therefore an opportunity for changes in the nucleosomal composition of a specific DNA region. Changes can also happen during the lifetime of a cell due to chemical reactions allowing interconversions between the different nucleosome types. The effect of these changes can be that a latent capacity that was dormant comes to life, or, conversely, that a previously active capacity shuts down.

Same inheritance -- different traits

In the practical experiment molecular biologists used a mutant of a yeast cell which was bi-stable, in that it could become either of a single sex or hermaphrodite. The experiment showed that a spontaneous change occurred in the yeast cells about every 2000 cell-generations. By building a mathematical model based on positive feedback from the microscopic state of the nucleosomes, the research group could simulate the experimental results and in this way gained insight into the mechanisms by which living cells with identical DNA can achieve extreme differentiation.

The research at the 'Models of Life' Basic Research Center at the Niels Bohr Institute has shown that communication between nucleosomes and positive feedback are likely to constitute fundamental memory mechanisms in individual cells. The mechanism gives both stability and openness to new influences which the cell could need to change state. Nature has a partner which controls the cells latent memory.

Latent Memory Of Cells Comes To Life
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Mother Birds 'Engineer' Their Offspring from Science Daily
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Nanomedicine & Nerve Cells

2007-05-21T22:18:00.000-07:00

Nanomedicine Opens The Way For Nerve Cell Regeneration

Credit: Stockphoto - Sebastian Kaulitzki

The ability to regenerate nerve cells in the body could reduce the effects of trauma and disease in a dramatic way. In two presentations at the NSTI Nanotech 2007 Conference, researchers describe the use of nanotechnology to enhance the regeneration of nerve cells.

In the first method, developed at the University of Miami, researchers show how magnetic nanoparticles (MNPs) may be used to create mechanical tension that stimulates the growth and elongation of axons of the central nervous system neurons. The second method from the University of California, Berkeley uses aligned nanofibers containing one or more growth factors to provide a bioactive matrix where nerve cells can regrow.

It is known that injured neurons in the central nervous system (CNS) do not regenerate, but it is not clear why. Adult CNS neurons may lack an intrinsic capacity for rapid regeneration, and CNS glia create an inhibitory environment for growth after injury. Can these challenges be overcome even before we fully understand them at a molecular level?

Dr. Mauris N. De Silva describes the novel nanotechnology based approach designed that includes the use of magnetic nanoparticles and magnetic fields for addressing the challenges associated with regeneration of central nervous system after injury. "By providing mechanical tension to the regrowing axon, we may be able to enhance the regenerative axon growth in vivo." This mechanically induced neurite outgrowth may provide a possible method for bypassing the inhibitory interface and the tissue beyond a CNS related injury.

Using optic nerve and spinal cord tissues as in vivo models and dissociated retinal ganglion neurons as an in vitro model, De Silva and his colleagues are currently investigating how these magnetic nanoparticles can be incorporated into neurons and axons at the site of injury. Although, this study is at a very preliminary stage to explore the possibility of using magnetic nanoparticles for enhancing in vivo axon regeneration, this work may have significant implications for the treatment of spinal cord injuries, and is a vital "next step" in bringing this new technology to clinical use.

The second presentation focuses on peripheral nerve injury, which affects 2.8% of all trauma patients and quite often results in lifelong disability. Since peripheral nerves relay signals between the brain and the rest of the body, injury to these nerves results in loss of sensory and motor function. Upper extremity paralysis alone affects more than 300,000 individuals annually in the US. The most serious form of peripheral nerve injury is complete severance of the nerve.

The severed nerve can regenerate; the nerve fibers from the nerve end closest to the spinal cord have to grow across the injury gap, enter the other nerve segment and then work their way through to their end targets (skin, muscle, etc). Usually, when the gap between the severed nerve endings is larger than a few millimeters, the nerve does not regenerate on its own. If left untreated, the end result is permanent sensory and motor paralysis. A few hundred thousand people suffer from this debilitating condition annually in the US.

Currently, the most successful form of treatment is to take a section of healthy nerve (autograft) from another part of the patient's body to bridge the damaged one. This autograft then serves as a guide for nerve fibers to cross the injury gap. Although successful, this autograft procedure has major drawbacks including loss of function at the donor site, multiple surgeries and, quite often, it's just not possible to find a suitable nerve to use as a graft. Various synthetic nerve grafts are currently available but none work better than the autograft and can't bridge gaps larger than 4 centimeters.

Researchers at the University of California, Berkeley have developed a technology that has the potential to serve as a better alternative than currently available synthetic nerve grafts. The graft material is composed entirely of aligned nanoscale polymer fibers. These polymer fibers act as physical guides for regenerating nerve fibers. They have also developed a way to make these aligned nanofibers bioactive by attaching various biochemicals directly onto the surfaces of the nanofibers. Thus, the bioactive aligned nanofiber technology mimics the nerve autograft by providing both physical and biochemical cues to enhance and direct nerve growth.

This technology has been tested by culturing rat nerve tissue ex vivo on our bioactive aligned nanofiber scaffolds. When the nerve tissue was cultured on unaligned nanofibers there was no nerve fiber growth onto the scaffolds. However, on aligned nanofiber scaffolds, they not only observed nerve fibers growing from the tissue but the nerve fibers were aligned in the same orientation as the nanofibers. Furthermore, when there were biochemicals present on the nanofibers, the nerve fiber growth was enhanced 5 fold. In a matter of just 5 days, nerve fibers had extended 4 millimeters from the nerve tissue in a bipolar fashion on the bioactive aligned nanofiber scaffolds. Thus, this technology can induce, enhance and direct nerve fiber regeneration in a straight and organized manner.

In order to make the technology clinically viable, they have also developed a novel graft fabrication technology in their laboratory. The most common method for fabricating polymer nanofibers is to use an electrical field to "spin" very thin fibers. This technique is called electrospinning and can be used to make nanofiber scaffolds in various shapes such as sheets and tubes. They have made a key innovation to this technology that enables us to fabricate tubular nerve grafts composed entirely of polymer nanofibers aligned along the length of tubes. This technology also allows customization of the length, diameter and thickness of the aligned tubular nanofiber grafts. The group will evaluate the performance of these aligned nanofiber nerve grafts in small animal pre-clinical studies starting in mid-May.

The technology presented herein is being patented by the University of California, Berkeley and has been licensed to NanoNerve, Inc.

According to Principal Investigator, Shyam Patel, "Speed is the key to successful nerve regeneration. Our aligned nanofiber technology takes full advantage of the fact that the shortest distance between damaged nerve endings is a straight line. It directs straightforward nerve growth and never lets them stray from the fast lane."

The presentation on magnetic nanoparticles is "Developing Super-Paramagnetic Nanoparticles for Central Nervous System Axon Regeneration" by M.N. De Silva, M.V. Almeida and J.L. Goldberg, from the University of Miami. The talk on aligned nanofibers is "Bioactive Aligned Nanofibers for Nerve Regeneration" by S. Patel and S. Li, from the University of California, Berkeley, CA.

Story adapted from a news release by Elsevier Health Sciences.
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Circadian Clocks

2007-05-20T09:19:00.000-07:00

Graphic of the ribbon structure of the vivid protein with a rising sun signifies the circadian clock (24-hour cycle). (Credit: Image courtesy of Cornell University)

Circadian clocks regulate the timing of biological functions in almost all higher organisms. Anyone who has flown through several time zones knows the jet lag that can result when this timing is disrupted.

Now, new research by Cornell and Dartmouth scientists explains the biological mechanism behind how circadian clocks sense light through a process that transfers energy from light to chemical reactions in cells. Circadian clocks in cells respond to differences in light between night and day and thereby allow organisms to anticipate changes in the environment by pacing their metabolism to this daily cycle.

The clocks play a role in many processes: timing when blooming plants open their petals in the morning and close them at night; or setting when fungi release spores to maximize their reproductive success. In humans, the clocks are responsible for why we get sleepy at night and wake in the morning, and they control many major regulatory functions.

Disruptions of circadian rhythms can cause jet lag, mental illness and even some forms of cancer.
"These clocks are highly conserved in all organisms, and in organisms separated by hundreds of millions of years of evolution," said Brian Crane, the paper's senior author and an associate professor in Cornell's Department of Chemistry and Chemical Biology.

The study revealed how a fungus (Neurospora crassa) uses circadian clock light sensors to control production of carotenoids, which protect against damage from the sun's ultraviolet radiation just after sunrise. The researchers studied a protein called vivid, which contains a chromophore or "light-absorbing molecule".

The chromophore captures a photon or particle of light, and the captured energy from the light triggers a series of interactions that ultimately lead to conformational changes on the surface of the vivid protein. These structural changes on the protein's surface kick off a cascade of events that affect the expression of genes, such as those that turn carotenoid production on and off.

By substituting a single atom (sulphur for oxygen) on the surface of the vivid protein, the researchers were able to shut down the chain of events and prevent the structural changes on the protein's surface, thereby disrupting the regulation of carotenoid production.

"We can now show that this conformational change in the protein is directly related to its function in the organism," said Brian Zoltowski, the paper's lead author and a graduate student at Cornell in chemical biology.

The circadian clock allows the fungus to regulate and produce carotenoids only when they are needed for protection against the sun's rays. A similar "switch" may be responsible for timing the sleep cycle in humans.

"We were interested in trying to understand behavior at the molecular level," said Crane. "This a great example of chemical biology, in that we can perturb the chemistry of a single molecule in a particular way and actually change the behavior of a complex organism."

The study was supported by grants from the National Institutes of Health.
The research is published in the May 18 issue of the journal Science.
Story adapted from a news release issued by Cornell University
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Event Structure Perception

2007-05-07T02:06:00.000-07:00

Thinking Thing by Thinkingthing

In order to comprehend the continuous stream of cacophonies and visual stimulation that battle for our attention, humans will breakdown activities into smaller, more digestible chunks, a phenomenon that psychologists describe as "event structure perception."

Event structure perception was originally believed to be confined to our visual system, but new research shows that a similar process occurs when reading about everyday events as well.

Nicole Speer and her colleagues at Washington University examined event structure perception by having subjects read narratives about everyday activities while undergoing functional Magnetic Resonance Imaging (fMRI) to measure neural activity. The subjects were then invited back a few days later to reread these same narratives, this time without the fMRI scan. Instead, they were asked to divide the narrative where they believed one segment of narrative activity ended and another segment began.

Speer, surmised that if changes in neural activity occurred at the same points that the subjects divided the stories, then it could be safe to suggest that humans are physiologically disposed to break down activities into narratives (remember that the same subjects had no idea during the first part of the experiment that they would later be asked to segment the story).

As expected, activity in certain areas of the brain increased at the points that subjects had identified as the beginning or end of a segment, otherwise known as an "event boundary." Consistent with previous research, such boundaries tended to occur during transitions in the narrative such as changes of location or a shift in the character's goals. Researchers have hypothesized that readers break down narrated activities into smaller chunks when they are reading stories. However, this is the first study to demonstrate that this process occurs naturally during reading, and to identify some of the brain regions that are involved in this process.

The fact that these results occurred with narratives that described mundane events is particularly important to our understanding of how humans comprehend everyday activity. Speer writes that the findings "provide evidence not only that readers are able to identify the structure of narrated activities, but also that this process of segmenting continuous text into discrete events occurs during normal reading."

In addition, a subset of the network of brain regions that also responds to event boundaries while subjects view movies of everyday events was activated. Speer believes that "this similarity between processing of visual and narrated activities may be more than mere coincidence, and may reflect the existence of a general network for understanding event structure." Future research will ultimately address the relationship between the two perception systems, and whether a global mechanism underlies event structure perception.

Article: "Human Brain Activity Time-Locked to Narrative Event Boundaries " May issue of Psychological Science, a journal of the Association for Psychological Science.
Association for Psychological Science aps
Human Brain Breaks Down Events Into Smaller Units From Science Daily
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Multitasking Is Hardest In The Early Morning
Mirror Neurons: How We Reflect On Behaviour
How The Brain's Backup System Compensates For Stroke
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Green Tea

2007-05-02T08:00:00.000-07:00

A new study from the University of Michigan Health System suggests that a compound in green tea may provide therapeutic benefits to people with rheumatoid arthritis. Credit: Stockphoto Science Daily

The compound from green tea was found to suppress the inflammatory products in the connective tissue of people with rheumatoid arthritis.

The study, presented April 29 at the Experimental Biology 2007 in Washington, D.C., looks at a potent anti-inflammatory compound derived from green tea. Researchers found that the compound – called epigallocatechin-3-gallate (EGCG) – inhibited the production of several molecules in the immune system that contribute to inflammation and joint damage in people with rheumatoid arthritis.

To conduct the research, the scientists isolated cells called synovial fibroblasts from the joints of patients with rheumatoid arthritis. These fibroblasts – cells that form a lining of the tissue surrounding the capsule of the joints – then were cultured in a growth medium and incubated with the green tea compound.

The fibroblasts were then stimulated with pro-inflammatory cytokine IL-1b, a protein of the immune system known to play an important role in causing joint destruction in people with rheumatoid arthritis. The researchers looked at whether the green tea compound has the capability to block the activity of two potent molecules, IL-6 and cyclooxygenase-2 (COX-2), which also are actively involved in causing boneerosion in the joints of people with rheumatoid arthritis.

When untreated cells were stimulated with IL-1b, a sequence of molecular events occurred that resulted in production of the bone-destructive molecules. But the scientists found that pre-incubation with EGCG was capable of inhibiting the production of these molecules. EGCG also inhibited the production of prostaglandin E2, a hormone-like substance that causes inflammation in the joints.

The cell signaling pathways that regulate levels of these immune system molecules under both normal and rheumatoid arthritis situations are well studied, and the researchers were able to trace the effects of the green tea compound infusion to see that it worked by inhibiting these pathways.

Green Tea Compound, May Be A Therapy For Rheumatoid Arthritis
Rheumatoid Arthritis And The Impact Of Genetic Factors On Mortality
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Weighing living cells

2007-05-01T08:00:00.000-07:00

New MIT technique weighs single living cells.
For the first time, MIT researchers have found a way to measure the mass of single cells with high accuracy.

The new technique, which is based on a micromechanical detector, could allow researchers to develop inexpensive, portable diagnostic devices and might also offer a unique glimpse into how cells change as they undergo cell division.

Unlike conventional methods, the MIT technique allows cells to remain in fluid while they are being measured, opening up a new realm of possible applications, says Scott Manalis, senior author of a paper on the work that will appear in the April 26 issue of Nature.

In addition to weighing cells, the technology can be used to "weigh nanoparticles or sub-monolayers of biomolecules with a resolution in solution that is six orders of magnitude more sensitive than commercial mass sensor methods. One direction we're pursuing is mass-based flow cytometry, a way to weigh and count specific cells," said Manalis, an associate professor in MIT's Departments of Biological Engineering and Mechanical Engineering.

Current mass-measurement methods achieve a resolution down to a zeptogram (10 to the minus 21 grams) but only work with non-living things because the procedure must be performed inside a vacuum. So, the MIT researchers decided to turn the conventional system inside out.

In the traditional method, the molecules to be weighed are placed on top of a tiny slab, or cantilever, made of silicon. The slab vibrates at its resonant frequency (the frequency at which the material naturally tends to vibrate) inside a vacuum. When a molecule sits on the slab, the frequency changes slightly, and the mass of the molecule can be calculated by measuring that change.

This measurement must be performed in a vacuum to prevent air (or fluid) from interfering with the frequency of oscillation. However, cells cannot survive in a vacuum, so they must be measured in fluid, which diminishes the accuracy of the measurement.

The researchers solved this dilemma by placing the fluid containing the sample inside the silicon slab, which still oscillates within a vacuum surrounding it. The biological sample is pumped through a microchannel that runs across the slab, without impairing its ability to vibrate.

"The resonator is sealed in a tiny vacuum cavity inside the chip, so there is virtually no resistance to the vibration," said co-lead author Thomas Burg, a research associate in biological engineering. "This lets us measure a mass change, say 10 parts in a billion, of the already very light microcantilever."

So far, the researchers have weighed particles with a resolution down to slightly below a femtogram (10 to the minus 15 grams), but Manalis believes that with refinements, the sensitivity could potentially be lowered by several orders of magnitude within a few years. "Every step along the way will open up new possibilities."

The researchers can also measure the mass density of particles or cells "by varying the density of the surrounding solution," said Michel Godin, co-lead author.

The research team is already looking into several applications for the new technique. One area of great promise is creating a device that would mimic the cell-counting capabilities of flow cytometers. However, flow cytometry devices, which work by bouncing light off a flowing stream of cells, are too large and expensive to be useful in developing countries.

A tiny chip that could count cells using the new MIT weighing method would be a "cheap and robust" alternative to commercially available flow cytometers, which typically cost more than $20,000, Manalis said. "Since the device is batch-fabricated by conventional semiconductor processing techniques, it could potentially be used in a disposable format."

"Simply put, a cheap, simple CD4 counting device that can be used by a community health worker … would be a breakthrough advance in global health," according to Rodriguez.

Manalis is also planning a collaboration with MIT associate professor of biology Angelika Amon, who is interested in studying how the mass density of a single cell changes as it goes through cell division. Using the new method, scientists can ultimately trap a single cell and observe it over a long period of time. Changes in mass could correlate to production of proteins, offering a new way to study what the cell does during division, Manalis said.

Another application of the new technology is to measure small particles, or beads. It's important to know the size of particles used in paint, drug-delivery devices, coatings and nanocomposite materials, said Manalis, who added that the new technology could become the "gold standard" way to measure these particles one by one.

This illustration shows an artistic depiction of the concept that enables measuring the mass of a single bacterium and single nanoparticles in fluid with a very high resolution. A hollow resonator, represented by a hollow, fluid-filled guitar, vibrates while small particles, represented here by a bacterium, flow through it. As the particles flow through the resonator, they change the frequency (tone) of the vibration. (Credit: Image courtesy Thomas Burg)

Other authors on the Nature paper are Scott Knudsen, MIT postdoctoral associate in biological engineering; Wenjiang Shen, Greg Carlson and John S. Foster of Innovative Micro Technology in Santa Barbara, Calif.; and Ken Babcock of Innovative Micro Technology and Affinity Biosensors in Santa Barbara.

The research was funded by the National Institutes of Health Cell Decision Process Center, the Institute for Collaborative Biotechnologies from the U.S. Army Research Office, the Air Force Office of Sponsored Research, the National Science Foundation and the Natural Sciences and Engineering Research Council of Canada.
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The Max Planck Society Press Releases
Everything starts with Recognition 23rd April 2007
Asymmetry due to Perfect Balance 25th April 2007
Electrons Caught in the Act of Tunnelling 12th April 2007
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Mind, Body & Quantumness

2007-04-27T08:00:00.000-07:00

Increasingly we are made aware that humans are composed of more parts than we can see or measure.

We have Stephen Hawking whose body suffers from a degenerative disorder yet is able to maintain a lucid (and brilliant) Mind. Of course we are aware that it is other parts of his body and not the brain, which are degenerating rapidly. The same with other degenerative conditions such as MS, where the 'person' is losing 'control' of the body, but retains an otherwise alert mind - unless of course they are struck by epilepsy or some other electrical imapct or damage to the neural system in the brain.

On the other hand we are becoming increasingly aware that in a 'modern' society like the US with over 5 million Alzheimer's sufferers, people with otherwise healthy or quasi-healthy bodies, and no discernible physical deterioration of the brain, are losing access to memory and memories.

Maybe there is information loss in black-holes. Of course it all depends what kind of information we are referring to, and which type of blackhole.

Though we may be able to look at the distant past and reconstruct a cosmological or geological picture of what might have been - we have absolutely no knowledge of peoples' thoughts (dreams, emotions, beliefs and memories) other than those carefully preserved in ancient scrolls, papirii or texts, and nowdays on 'record' (vynil) or tape (magnetic tape) or video tape, or more modern CDs, DVDs and the latest memory sticks.

Of course these are only but a fraction of any thoughts, or memories, or theories, which people have chosen to record or debate publicly whether thru course work or the internet.

We may even have some recorded mobile phone messages from 9/11 or those passengers on a flight before a crash, but in general most mobile phone conversations, like face to face conversations are discarded (or evaporate) into thin air as soon as they leave the speakers mouth.

But there is something more - we are increasingly becoming aware that man (or woman) is more than just their DNA. How the brain formed from that DNA, and is then educated or interacts with its environment - is what is commonly termed nurture (versus nature).

It has always been possible for a brilliant mind to be born into a severely disabled body, and equally it has always been accepted that a healthy body does not necessarily come accompanied by a smart brain, nor a healthy & lucid mind.

Furthermore it is increasingly becoming clear that is is not DNA or memory defines who we are. We cannot be selective with our DNA (yet) - we are born into it. But we are clearly selective with our memory, we can choose to keep (or romanticise) one memory whilst discarding another, and sometimes we cannot shake off a memory (pleasant or unpleasant) no matter how much we try. Though by enlarge few of us try to discard pleasant memories, since it seems we are seeking to create (or store) a selection & collection of pleasant memories and experiences. Bar in the few exceptions - which are not uncommon - where people strive for unpleasant, or painful and maccabre memories and experiences.

People often choose to remember or believe what they will.

Experimentalists probe the structure of the proton by scattering electrons (white line) off quarks which interact by exchanging a quantum of light (wavy line) known as a photon.
Visual QCD

So where am I leading with all this. It is to address the duality whereby some would like to believe that the DNA could carry not only our genes (always mutated) but some of our memory and the so called inherent abilities or skills (always truncated) - whilst others can more clearly see that one is independent of another. A king can be born the son of a carpenter, a musician can be born the son of a nuclear physicist, a painter can be born the son of a cleaner, and a Caesar can be born the son of a slave. All human hierarchies are purely artificial, imposed by the surrounding environment or society - and have nothing to do with Natural Law.

One still cannot give any verifiable testimony to the quantum leap 'life' makes from one lifeform (or lifetime) to the next. But this is only a mathematical equation. After all even the body you are in has already changed dramatically several times from the one you were in yesterday or yesteryear or ten and four score years ago.

The only thing that is clear upon death, is that there is something visible missing from the lifeless bofy or form. The lifeforce which gave it life.

And whilst all other information like memory, thoughts, feelings. emotions, may or not disappear down a blackhole (and reach a point of no return) it is clear that the lifeforce stripped of these continues thru Space and spacetime - to take up another form.

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Memory Restored In Mice Through Enriched Environment
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Mice whose brains had lost a large number of neurons due to neurodegeneration regained long-term memories and the ability to learn after their surroundings were enriched with toys and other sensory stimuli, according to new studies by Howard Hughes Medical Institute researchers. The scientists were able to achieve the same results when they treated the mice with a specific type of drug that encourages neuronal growth.

The results of the experiments suggest that the term "memory loss" may be an inaccurate description of the kinds of mental deficits associated with neurodegenerative diseases. "The memories are still there, but they are rendered inaccessible by neural degeneration," said the senior author Li-Huei Tsai, a Howard Hughes Medical Institute researcher at the Massachusetts Institute of Technology.

"I believe that these findings could have particular significance for treatment of people who already have advanced neurodegenerative disease," said Tsai. "Most current treatments seem to be aimed at affecting the early stages of the disease. But our mouse model shows that even when there has been a significant loss of neurons, it is still possible to improve learning and memory."

Memory Restored In Mice Through Enriched Environment
So doctor Tsai, can the mouse recognise its grandaughter?
Can the mouse memorise or remember how to play chess?
Can the mouse remember which bank it has an account with?
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Reversing Cancer Cells To Normal Cells
Multiple Sclerosis Is Increasingly Becoming A Woman's Disease
Brain Processes Sense Of Smell Better Than Previously Thought
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Chiral Recognition

2007-04-24T14:00:00.000-07:00

A human body has more than 10 to the power of 27 molecules with about one hundred thousand different shapes and functions. Interactions between molecules determine our structure and keep us alive.

Researchers at the Max Planck Institute for Solid State Research in Stuttgart in collaboration with scientists from the Fraunhofer Institute in Freiburg and King’s College London have followed the interaction of only two individual molecules to show the basic mechanism underlying recognition of dipeptides.

By means of scanning tunnelling microscopy movies and theoretical simulations they have shown how dynamic interactions induce the molecular fit needed for the transfer of structural information to higher levels of complexity. This dynamic picture illustrates how recognition works at the very first steps, tracking back the path in the evolution of complex matter.

If one thinks that there are possibly thousands of times more molecules forming our body than stars in the universe it is astonishing how all these molecules can work together in such an organised and efficient way. How can our muscles contract to make us walk? How can food be metabolised every day? How can we use specific drugs to relieve pain?

To work as a perfect machine, our body ultimately relies on the capability of each little part (molecule) to know a specific function and location out of countless possibilities. To do this, molecules carry information in different ways. An international team at the Max Planck Institute for Solid State Research in Stuttgart, in collaboration with scientists from the Fraunhofer Institute in Freiburg and King's College London are seeking to find out how the information can be passed on at the very first steps: from the single molecule level to structures of increasing complexity and functionality.

The key to understanding all biological processes is recognition. Each molecule has a unique composition and shape that allows it to interact with other molecules. The interactions between molecules let us - as well as bacteria, animals, plants and other living systems - move, sense, reproduce and accomplish the processes that keep all living creatures alive.

A very common example of recognition can be experienced in daily life whenever one meets someone and shakes right hands. In principle, one can also shake left hands; the fact that we do it with the right has historically been a sign of peace, used to show that both people hold no weapon. But, have you ever attempt to shake the right hand of a person using your left hand? No matter how the two hands are oriented, you will never fit your left hand with the right hand of your friend.

Many molecules can recognise each other and transfer information exactly in the same way, they can either be "right handed" (D) or "left handed" (L). This property called "chirality" is a spectacular way to store information: a chiral molecule can recognise molecules that have the same chirality (same "handedness", L to L or D to D) and discriminate the ones of different chirality (L to D and D to L).

Probably one of the most exciting mysteries of Nature is why the building blocks of life, i.e. amino acids (the building blocks of proteins) are exclusively present in the chiral L form and sugars (which constitute DNA) are all in the D form. Once more, the reason for this preference is "historical", but this time goes back millions of years till the origins of the biological world. Scientists believe that current life forms could not exist without the uniform chirality ("homochirality") of these blocks, because biological processes need the efficiency in recognition achieved with homochiral substances. In other words, the separation of molecules by chirality was the crucial process during the Archean Era when life first emerged.

Researchers of the Max Planck Institute for Solid State Research have now used the "nanoscopic eye" of a scanning tunnelling microscope to make movies following how two adsorbed molecules (diphenylalanine, the core recognition motif of Alzheimer amyloid polypeptide) of the same chirality can form structures (pairs, chains) while molecules of different chirality discriminate and cannot form stable structures.

As it occurs when you shake the hand of your friend, the fact that the two homochiral hands are complementary by shape is not enough, you both have to dynamically adapt and adjust your hands to reach a better fit, a comfortable situation. By a combination with theoretical simulations done at Kings College London, the researchers have shown for the first time this dynamic mechanism of how two molecules "shake hands" and recognise each other by mutually induced conformational changes at the single molecule level.

We live in houses, wear clothes and read books made of chiral cellulose. Most of the molecules that mediate the processes of life like hormones, antibodies and receptors are chiral. Fifty of the top hundred best-selling drugs worldwide are chiral. With this contribution to the basic mechanism of chiral recognition, the researchers have not only tracked back to the very first steps in the evolution of living matter but have also shed light on our understanding and control of synthetic (man-made) materials of increasing complexity.

Reference: Magalí Lingenfelder, Giulia Tomba, Giovanni Costantini, Lucio Colombi Ciacchi, Alessandro De Vita, Klaus Kern, "Tracking the Chiral Recognition of Absorbed Dipeptides at the Single-Molecule Level," Angewandte Chemie Int. Ed. (2007)

Max Planck Society press release 23rd April 2007
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Neural Paths

2007-04-20T08:00:00.000-07:00

THE CHOSEN: A new study finds that neurons compete to be in the lucky 20 percent that make a memory during learning or training activities.
Image: © ISTOCKPHOTO/SEBASTIAN KAULITZKI

The Brain May Use Only 20 Percent of Its Memory-Forming NeuronsStudy shows that that pace at which a brain cell activates a key protein may influence its role in memory formation—a finding that could lead to new Alzheimer therapies
By Nikhil Swaminathan @ Scientific American

Remember the old myth that people only use 10 percent of their brains? Although a new study confirmed that bromide to be apocryphal, it did find that we may only use 20 percent of the nerve cells in our midbrain to form memories.

Researchers at the University of California, Los Angeles, and The Hospital for Sick Children in Toronto monitored neurons in the lateral amygdalae (two almond-shaped regions on either side of the midbrain associated with learning and memory) of mice to see whether the presence of the CREB (cAMP response element binding) protein plays a key role in signaling brain cells to make memories.

CREB, a transcription factor that typically increases the production of other proteins in cells, is believed to be involved in memory formation in organisms from sea slugs to humans. Scientists hope that their findings, reported in the current issue of Science, may help pave the way to new treatments for Alzheimer's Disease.

In the future, Josselyn says, this mechanism could be harnessed to produce a new treatment for Alzheimer's disease. "In time, we're going to have some sort of neuron-replacement therapy for Alzheimer's," she says, conceding, "It's a little sci-fi right now." But, if new neurons are inserted into a damaged brain, modulating CREB function could help bias the healing brain to use the functioning neurons and not its injured population.
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Alzheimer's Roots

2007-04-12T08:00:00.000-07:00

New study zeroes in on the genetic roots of Alzheimer's

Scientists have known for more than a decade that individuals with a certain gene are at higher risk for developing Alzheimer’s disease.

Now research, led by scientists at the Oklahoma Medical Research Foundation (OMRF), has uncovered a molecular mechanism that links the susceptibility gene to the process of Alzheimer’s disease onset. The findings appear in the April 11 issue of The Journal of Neuroscience and may lead to new pathways for development of Alzheimer’s therapeutics.

Approximately 15 percent of the population carries a gene that causes their bodies to produce a lipoprotein—a combination of fat and protein that transports lipids (fats) in the blood—known as apolipoprotein (Apo) E4. Studies have found that those who inherit the E4 gene from one parent are three times more likely than average to develop Alzheimer’s, while those who get the gene from both parents have a tenfold risk of developing the disease.

The new study discovered that ApoE4 (along with other apolipoproteins) attaches itself to a particular receptor on the surface of brain cells. That receptor, in turn, adheres to a protein known as amyloid precursor protein. The brain cells then transport the entire protein mass inside.

Once inside, cutting enzymes—called proteases—attack the amyloid precursor protein. These cuts create protein fragments that, when present in the brain for long periods of time, are believed to cause the cell death, memory loss and neurological dysfunction characteristic of Alzheimer’s.

Although researchers have known for more than a decade that ApoE4 was involved—somehow—in development of Alzheimer’s, Tang’s new study is the first to connect the process of protein fragment formation to ApoE4.

Alzheimer’s disease is a neurological disorder characterized by slow, progressive memory loss due to the gradual death of brain cells. According to the Alzheimer’s Association, the disease affects more than 5 million Americans, including nearly half the population over the age of 85.
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Quantum Sys-stems

2007-04-06T12:00:00.000-07:00

Science Tunnel - Max Planck Society

Nothing in the physical sciences predicts the phenomenon of consciousness. Yet its reality is apparent to each and every one of us

Consciousness is as fundamental as matter - in some ways, more fundamental. Advances in physics, psychology, and philosophy have shown that reality is not what it seems.

Take vision, for example. When we look at a tree, light reflected from its leafs is focused onto cells in the retina of the eye, where it triggers a cascading chemical reaction releasing a flow of electrons.

Neurons connected to the cells convey these electrical impulses to the brain’s visual cortex, where raw data is processed and integrated. Then — in ways that are still a complete mystery — an image of the tree appears in our consciousness.

It may seem that we are directly perceiving the tree in the physical world, but what we are actually experiencing is an image generated in our mind.

The same is true of every other experience. All that we see, hear, taste, touch, smell and feel has been created from the data received by our sensory organs. All we ever know of the world around are the mental images constructed from that data. However real and external they may seem, they are all phenomena within our mind.

Peter Russell
The Universe as a hologram by Michael Talbot
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The human brain stores and processes its information at the level of single organic molecules and is a single macroscopic quantum system. Acts of consciousness may be viewed as incorporating quantum events.
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Gateway to Gene Control

2007-03-29T08:00:00.000-07:00

Artist's illustration showing a portion of the genome. A long DNA molecule (red cord) is wrapped up into nucleosome structures with a histone-protein core (white spheres). The gateway to gene transcription spans the control switch (coils) on the left nucleosome to the beginning of the gene (green arrow) on the right nucleosome. Credit: Christina Ullman.

Penn State scientists reveal structure of gateways to gene control
The map pinpoints the locations of certain key gene-controlling nucleosomes -- spool-like structures that wrap short regions of DNA around a protein core. The research suggests how these nucleosomes, positioned at important transcription-promoter sites throughout the cell's DNA, control whether or not a gene's function can be turned on in a particular cell.

The study's many surprising findings together reveal an intimate relationship between the architecture of nucleosome structures and the underlying DNA sequences they regulate. "We now know exactly where these nucleosomes are positioned on the DNA molecule and which DNA building blocks they have wrapped up under their tight control," B. Franklin Pugh, professor of biochemistry and molecular biology at Penn State said. Among those building blocks, Pugh and his colleagues revealed the architecture of a critical gateway, controlled by the nucleosome, which must be unlocked before a gene can be transcribed.

The study revealed that almost all genes have the same kind of structure where transcription begins, that this beginning contains a critical gateway for transcription, and that the transcription gateway of each gene almost always is located at the same place on a nucleosome. The researchers also discovered some genes whose pattern is somewhat different from this norm, and these unusual sequences also are reported in the Nature paper. "We previously had a low-resolution idea that these structures all could be roughly in the same position, but now this high-resolution map makes it very clear that they really are in exactly the same position. It's a remarkably consistent arrangement," Pugh said.

The study also revealed that the nucleosomes at the transcription-promoter control centers occupy several overlapping positions on the DNA molecule, typically 10 base pairs apart, which exactly matches the periodic rotation of the DNA double helix." It is striking how well these positions match with the architecture of the DNA as it wraps around the nucleosome's protein core," Pugh said.

This result powerfully simplifies previous theories about the possible architecture of gene packaging. "There is a certain DNA sequence that shapes the gene's architecture in the same way, producing the same structure in every gene," Pugh said. The overall sequence of DNA building blocks is different in each gene, but the underlying architecture is the same."

Another discovery is that transcription-control centers tend to be located on the outside edge of the nucleosome and tend to face outward on the DNA helix, allowing the cell's transcription proteins to find them more easily. "This arrangement makes sense, because when signaling proteins arrive at a control center they are well situated to help push the nucleosome out of the way so the reading of the gene can begin," Pugh said.

"Previous research had indicated that DNA sequences located upstream of a gene might be a region that controls whether that gene is read or not, but we did not know the architecture of those sequences -- whether they were exposed and therefore ready for work. Now we know that the gateway to transcription is a part of this control region and that the nucleosome keeps it locked so the gene cannot be turned on until it is needed," Pugh said. When the gene is needed, the cell's molecular machinery loosens the DNA wrapping around the nucleosome, unlocking the transcription gateway to give access to the cell's molecular transcription machinery. "We think that the function of the nucleosome is to control the gateway to transcription," Pugh said.

The research reveals how the pieces of DNA that regulate genes at the transcription-promoter sites are packaged on nucleosomes. The knowledge that these sites are located on the outside edge of the nucleosome spool will help to focus research designed to manipulate gene expression. "Our study has provided a much clearer picture of the architecture of the DNA in the control regions, allowing us to understand much better how genes are regulated, which is important because gene regulation is a critical process for the survival of living things," Pugh explained.
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Beta-peptides

2007-02-05T08:00:00.000-08:00

Ribbon diagram representations of a beta-peptide bundle illustrating packing between helices and within the hydrophobic (green) core.
(Credit: Schepartz/Yale)

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Chemists at Yale have done what Mother Nature chose not to -- make a protein-like molecule out of non-natural building blocks, according to a report featured early online in the Journal of the American Chemical Society.

Nature uses alpha-amino acid building blocks to assemble the proteins that make life as we know it possible. Chemists at Yale now report evidence that nature could have used a different building block -- beta-amino acids -- and show that peptides assembled from beta-amino acids can fold into structures much like natural protein.

The ability to mimic natural proteins makes beta-peptides powerful new tools for basic research and drug discovery. Like a taped recording, their greatest value may be in their difference from a live performance.

Natural proteins are composed of linear chains of alpha-amino acids. Beta-peptides are composed of beta-amino acids, which have an extra carbon in their backbone. Like alpha-amino acids, beta-amino acids are generated under simulated pre-biotic conditions, are isolated from meteorites, and are byproducts of metabolism, but they are not genetically encoded like natural proteins, nor are they built into chains by cells.

Citation: J. American Chemical Society, ASAP Article DOI:10.1021/ja068678n 19/01/07
More From: Science Daily releases 6/02/07
Nature Could Have Used Different Protein Building Blocks, Chemists Show
Man-made Proteins from the Howard Hughes Medical Institute
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Electrons Travel Through Proteins Like Urban Commuters
Electron movements through certain "electron-transfer" proteins that lie at the heart of many processes essential for life. Such processes include harvesting light in photosynthesis in plant cells and generating energy in animal cells.

"I think we have discovered the physical framework for thinking about all such protein electron-transfer chemistry," said David Beratan of Duke University. "Having this rule book in place will let scientists pose some hard but interesting questions about evolutionary pressures on protein structures.

"Another payoff may be new insight for designing biologically based artificial systems that, for instance, can capture solar energy or make fertilizer from air," he added.

For more than 50 years, theoreticians have been pondering the most likely itineraries that electrons follow through electron-transfer proteins. These proteins are believed to shuttle electrons around, one at a time, but not to do any chemistry that involves the forming or breaking of chemical bonds.

Earlier theoretical work from Beratan's group indicated that electrons can take short cuts through the proteins by following the spooky guidelines of quantum mechanics.

That means the electrons may sometimes leak from one chemical bond to a neighboring bond, he said. They also can take forbidden walks on the wild side by tunneling through open space.

Those findings prompted scientists to conjecture that electron-transfer proteins actually evolved their shapes to allow electrons the option of using quantum rules in negotiating molecular folds and crevices. The possibilities of such quirky routing options have vastly increased the challenge for theoreticians such as Beratan.

Using ever larger networks of computers to calculate the most favorable routes of electron travel, Beratan and his colleagues analyze these proteins in much the same way that commuters pore over transportation maps to plot the fastest destination routes.

Read more from Science Daily release 05/02/07
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Famous Quotes
The body is an instrument, the mind its function,
the witness and reward of its operation. George Santayana
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Microwave thermotherapy

2007-01-31T08:00:00.000-08:00

Image at left shows process of detecting and destroying an enemy missile using MIT targeted radar. Microwave energy is fixed on a missile while simultaneously nullifying enemy jammers. On right, microwave energy is aimed at a cancerous tumor with a deep focused beam while simultaneously nullifying any energy that would overheat surrounding healthy tissue.
Image courtesy of Lincoln Laboratory

Treating cancer with heat is not a new idea, but researchers were having trouble using it to treat tumors deep within the body.

The microwaves in the new technique heat--and kill--cells containing high amounts of water and ions, or electrically charged atoms. Cancer cells typically have a high content of both, while healthy breast tissue contains much less. The outpatient procedure uses a single tiny needle probe to sense and measure parameters during treatment. Side effects appear to be minimal.

In this study tumors shrunk by approximately 50 percent more in women treated with both the MIT technique and chemotherapy, versus women treated with chemotherapy alone.

The results of both clinical studies will be presented at the 17th Annual National Interdisciplinary Breast Center Conference in Las Vegas, from Feb. 25-28.

Another, larger clinical study for patients with large breast cancer tumors is expected to begin later this year at six institutions in the United States and Canada.

Other potential clinical studies for treating recurrent breast cancer, ductal carcinoma in situ and benign breast lesions with the MIT thermotherapy treatment, as well as its use to enhance anti-estrogen therapy for breast cancer prevention, are also described in the book.

Read More: Breast Cancer Treatment by Focused Microwave Thermotherapy
(Jones and Bartlett Publishers, 2007)
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Probing Proteins Can Lead To Better Understanding Of Anti-Tumor Agents
Predicting The Risk Of RA For Early Arthritis Patients from Science Daily
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Foxp3

2007-01-23T08:00:00.000-08:00

This schematic represents the researchers' strategy to identify where Foxp3 physically interacts with the genome in T cells. The background is a microarray where the red probes reveal regions of DNA where Foxp3 is bound.
(Image: Tom DiCesare)
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The immune system is a defense network that guards the body from invaders.
Autoimmune diseases such as type 1 diabetes, lupus and rheumatoid arthritis occur when the immune system fails to regulate itself. But researchers have not known precisely where the molecular breakdowns responsible for such failures occur.

Now, a team of scientists from the Whitehead Institute and the Dana-Farber Cancer Institute have identified a key set of genes that lie at the core of autoimmune disease, findings that may help scientists develop new methods for manipulating immune system activity.

A group of white blood cells called T cells are the frontline soldiers of immune defense, engaging invading pathogens head on. These T cells are commanded by a second group of cells called regulatory T cells. Regulatory T cells prevent biological "friendly fire" by ensuring that the T cells do not attack the body's own tissues. Failure of the regulatory T cells to control the frontline fighters leads to autoimmune disease.

Regulatory T cells are themselves controlled by a master gene regulator called Foxp3. Master gene regulators bind to specific genes and control their level of activity, which in turn affects the behavior of cells.

In fact, when Foxp3 stops functioning, the body can no longer produce working regulatory T cells. When this happens, the frontline T cells damage multiple organs and cause symptoms of type 1 diabetes and Crohn's disease. However, until now, scientists have barely understood how Foxp3 controls regulatory T cells because they knew almost nothing about the actual genes under Foxp3's purview.

More from Science Daily
Cracking Open The Black Box Of Autoimmune Disease
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