Cell molecule identified as central player in the formation of new blood vessels

 by Biomechanism                                                                                                                           Scientists at the University of North Carolina at Chapel Hill School of Medicine have identified a cellular protein that plays a central role in the formation of new blood vessels. The molecule is the protein Shc (pronounced SHIK), and new blood vessel formation, or angiogenesis, is seriously impaired without it.

The study, which appeared online November 16, 2011 in the journal Blood, was led by associate professor of cell and molecular physiology at UNC, Ellie Tzima, PhD, who is also a member of the university’s Lineberger Comprehensive Cancer Center and the McAllister Heart Institute.

Control endothelial cells embedded in fibrin gel sprout and form new capillary-like tubes whereas Shc knockout endothelial cells fail to form new vessels. This experiment models angiogenesis in vivo where endothelial cells must sprout off of a parent vessel in order to make a new blood vessel during development, wound healing and tumor growth. Credit: Tzima Lab, UNC-Chapel Hill

“Angiogenesis is the formation of new blood vessels from existing blood vessels and it’s a process that’s important during embryonic development and in the development of diseases such as cancer,” Tzima said. “So understanding the molecular mechanisms of how blood vessels form is important from the basic science perspective and for understanding and treating disease.”

Vascular networks form and expand by sprouting, similar to the way trees grow new branches. The process allows fresh oxygen and nutrients to be delivered to tissues, whether in a developing embryo or a cancerous tumor. Blood vessel formation is spurred by a variety of chemical signals that zoom along complex pathways. Some are cues that come from growth factors, others from the tissue matrix that the cells sit on. This extracellular matrix (ECM) serves the cell in a number of ways, such as supporting the cell’s structure, helping to regulate cell-to-cell communication.

The protein Shc, is known to regulate a number of important molecular signaling pathways, but its role in angiogenesis has remained unknown until now, Tzima says. She also points out that Shc is evolutionarily conserved, which indicates its essential importance across species.

“We hypothesized that Shc would be the central player that accepts signals from all of the stimuli that have been previously shown to be important for regulating blood vessel formation and would process them and regulate the cell’s response,” Tzima said. “And that is what we found – that Shc coordinates signals, those coming from growth factors as well as from the extracellular matrix.”

Tzima suggests that we imagine the cell as a complex highway network with electronic toll plazas through which cars with a transponder can whiz at highway speeds without slowing down. The system works because the transponder’s personalized signal is relayed to a computer system that calculates the toll and charges the car’s account in a flash. “Shc is the toll plaza, the checkpoint through which signals crucial to blood vessel formation must pass and get coordinated for proper angiogenesis to occur.”

In the study, Tzima and her team found that Shc is required for angiogenesis in zebrafish, mouse and human endothelial cell culture models of blood vessel formation.

“The animal studies gave us the broad perspective that Shc may be important to this process,” said graduate student and study first-author Daniel T. Sweet. “Zebrafish and mice have previously been used to explore blood vessel formation in vivo. We found that without Shc, blood vessel formation is impaired.”

“Then for a closer look we used a cell culture model to determine which endothelial cell processes require Shc for angiogenesis. We found it mediates signals from growth factor receptors and extracellular matrix receptors,” Sweet said. “Shc is important for the crosstalk between these processes, meaning that they need to “talk” to each other in order to properly form a tube or to sprout and migrate. That’s the exciting thing about this paper.”

Tzima notes that elegant genetic models of mice have been used to understand important cellular processes, including angiogenesis. “But if you want to think about designing therapeutics it becomes much more important to understand the molecular mechanism. And this was the strength of the study. We went all the way down to molecular interactions that allowed us to figure out this new angiogenesis pathway.”

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UNC co-authors with Tzima and Sweet are Zhongming Chen, David M. Wiley, and Victoria L. Bautch. The research was supported by grants from the National Heart, Lung and Blood Institute, American Heart Association and Ellison Medical Foundation.

Androgen-related disorder in women

 by Biomechanism 

Androgens may be called “male hormones,” but don’t let the name fool you. Both men’s and women’s bodies produce androgens, just in differing amounts. In fact, androgens have more than 200 actions in women.

The principal androgens are testosterone and androstenedione. They are, of course, present in much higher levels in men and play an important role in male traits and reproductive activity. Other androgens include dihydrotestosterone (DHT), dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEA-S).

In a woman’s body, one of the main purposes of androgens is to be converted into the female hormones called estrogens.

Androgens in Women

In women, androgens are produced in the ovaries, adrenal glands and fat cells. In fact, women may produce too much or too little of these hormones––disorders of androgen excess and deficiency are among the more common hormonal disorders in women.

In women, androgens play a key role in the hormonal cascade that kick-starts puberty, stimulating hair growth in the pubic and underarm areas. Additionally, these hormones are believed to regulate the function of many organs, including the reproductive tract, bone, kidneys, liver and muscle. In adult women, androgens are necessary for estrogen synthesis and have been shown to play a key role in the prevention of bone loss, as well as sexual desire and satisfaction. They also regulate body function before, during and after menopause.

Androgen-Related Disorders

High Androgen Levels

Excess amounts of androgens can pose a problem, resulting in such “virilizing effects” as acne, hirsutism (excess hair growth in “inappropriate” places, like the chin or upper lip) and thinning hair.

Many women with high levels of a form of testosterone called “free” testosterone havepolycystic ovary syndrome (PCOS), characterized by irregular or absent menstrual periods, infertility, blood sugar disorders, and, in some cases, symptoms like acne and excess hair growth. Left untreated, high levels of androgens, regardless of whether a woman has PCOS or not, are associated with serious health consequences, such as insulin resistance and diabetes, high cholesterol, high blood pressure and heart disease.

In addition to PCOS, other causes of high androgen levels (called hyperandrogenism) include congenital adrenal hyperplasia (a genetic disorder affecting the adrenal glands that afflicts about one in 14,000 women) and other adrenal abnormalities, and ovarian or adrenal tumors. Medications such as anabolic steroids can also cause hyperandrogenic symptoms.

Low Androgen Levels

Low androgen levels can be a problem as well, producing effects such as low libido(interest or desire in sex), fatigue, decreased sense of well-being and increased susceptibility to bone disease. Because symptoms like flagging desire and general malaise have a variety of causes, androgen deficiency, like hyperandrogenism, often goes undiagnosed.

Low androgen levels may affect women at any age but most commonly occur during the transition to menopause, or “perimenopause,” a term used to describe the time before menopause (usually two to eight years). Androgen levels begin dropping in a woman’s 20s, and by the time she reaches menopause, they have declined 50 percent or more from their peak as androgen production declines in the adrenal glands and the midcycle ovarian boost evaporates.

Further declines in the decade following menopause indicate ever-decreasing ovarian function. For many women, the effects of this further decline include hot flashes and accelerated bone loss. These effects may not become apparent until the women are in their late 50s or early 60s.

Treatment for Low Androgen Levels

Combination estrogen/testosterone medications are available for women in both oral and injected formulations. Small studies find they are effective in boosting libido, energy and well-being in women with androgen deficiencies, as well as providing added protection against bone loss. However, the risks from the combination of estrogen and testosterone include increased risk of breast and endometrial cancer, adverse effects on blood cholesterol and liver toxicity.

Testosterone is also an effective treatment for AIDS-related wasting and is undergoing studies for treating premenstrual syndrome (PMS) and autoimmune diseases. Women with PMS may have below-normal levels of testosterone throughout the menstrual cycle, suggesting a supplement may help.

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References

• LaCroix AZ, Chlebowski RT, Manson JE, et al. “Health outcomes after stopping conjugated equine estrogens among postmenopausal women with prior hysterectomy: A randomized clinical trial.” JAMA. 2011;305(13):1305-14.
• Tamimi RM, Hankinson SE, Chen WY, Rosner B, Colditz GA. “Combined estrogen and testosterone use and risk of breast cancer in postmenopausal women. Arch Intern Med. 2006;166(14):1483-1489.
• Jakiel G, Baran A. “Androgen deficiency in women.” Endokrynol Pol. 2005 Nov-Dec;56(6):1016-20.
• Davis SR, Panjari M, Stanczyk FZ. “DHEA Replacement for postmenopausal women.” J Clin Endocrinol Metab. March 16, 2011 (e-pub ahead of print).
• “Dehydroepiandrosterone and its sulfate.” Uptodate.com. Last reviewed October 2008. Subscription necessary to view text. www.uptodate.com. Accessed February 2009.
• “Use of combination estrogen-progestin contraceptives in the treatment of hyperandrogenism and hirsutism.” Uptodate.com. Last reviewed October 2008. Subscription necessary to view text. www.uptodate.com. Accessed February 2009.
• “Testosterone for low libido in postmenopausal women not taking estrogen.” N Engl J Med. 2008 Nov 6;359(19):2005-17. http://www.ncbi.nlm.nih.gov. Accessed February 2009.
• “Androgens and estrogens: systemic.” Information for professionals. Drugs.com. Updated January 2009. http://www.drugs.com. Accessed February 2009.
• “Estrogen Plus Progestin Study Stopped Due to Increased Breast Cancer Risk, Lack of Overall Benefit.” National Heart, Lung and Blood Institute. http://www.nhlbi.nih.gov. Updated July 9, 2002; accessed September 2003.
• “Androgen Replacement No Panacea for Women’s Libido.” The American College of Obstetricians and Gynecologists. News Release. October 2000. http://www.acog.org
• Miller K. “Androgen Deficiency in Women.” J Clin Endocrinol Metab. 2001;86(6).
• Estratest Fact Sheet. Solvay Pharmaceuticals. August 2001.http://www.solvaypharmaceuticals-us.com
• Estratest information from Solvay Pharmaceuticals. November 2005. Available at:http://www.solvaypharmaceuticals-us.com. Accessed November 2005.
• Buster JE, Kingsberg SA, Aguirre O, Brown C, Breaux JG, Buch A, et al. Testosterone patch for low sexual desire in surgically menopausal women: a randomized trial. Obstet Gynecol. 2005;105:944-52.

Caltech biologists deliver neutralizing antibodies that protect against HIV infection in mice

Over the past year, researchers at the California Institute of Technology (Caltech), and around the world, have been studying a group of potent antibodies that have the ability to neutralize HIV in the lab; their hope is that they may learn how to create a vaccine that makes antibodies with similar properties. Now, biologists at Caltech led by Nobel Laureate David Baltimore, president emeritus and Robert Andrews Millikan Professor of Biology, have taken one step closer to that goal: they have developed a way to deliver these antibodies to mice and, in so doing, have effectively protected them from HIV infection.

Caption: An illustration shows the crystal structure of the adeno-associated virus used to deliver broadly neutralizing antibodies as Vectored ImmunoProphylaxis against HIV. Credit: Alejandro Balazs / California Institute of Technology

This new approach to HIV prevention — called Vectored ImmunoProphylaxis, or VIP — is outlined in the November 30 advance online publication of the journalNature.

Traditional efforts to develop a vaccine against HIV have been centered on designing substances that provoke an effective immune response — either in the form of antibodies to block infection or T cells that attack infected cells. With VIP, protective antibodies are being provided up front.

“VIP has a similar effect to a vaccine, but without ever calling on the immune system to do any of the work,” says Alejandro Balazs, lead author of the study and a postdoctoral scholar in Baltimore’s lab. “Normally, you put an antigen or killed bacteria or something into the body, and the immune system figures out how to make an antibody against it. We’ve taken that whole part out of the equation.”

Because mice are not sensitive to HIV, the researchers used specialized mice carrying human immune cells that are able to grow HIV. They utilized an adeno-associated virus (AAV) — a small, harmless virus that has been useful in gene-therapy trials — as a carrier to deliver genes that are able to specify antibody production.

The AAV was injected into the leg muscle of mice, and the muscle cells then put broadly neutralizing antibodies into the animals’ circulatory systems. After just a single AAV injection, the mice produced high concentrations of these antibodies for the rest of their lives, as shown by intermittent sampling of their blood. Remarkably, these antibodies protected the mice from infection when the researchers exposed them to HIV intravenously.

The team points out that the leap from mice to humans is large — the fact that the approach works in mice does not necessarily mean it will be successful in humans. Still, the researchers believe that the large amounts of antibodies that the mice were able to produce — coupled with the finding that a relatively small amount of antibody has proved protective in the mice — may translate into human protection against HIV infection.

“We’re not promising that we’ve actually solved the human problem,” says Baltimore. “But the evidence for prevention in these mice is very clear.”

The paper also notes that in the mouse model, VIP worked even in the face of increased exposure to HIV. To test the efficacy of the antibody, the researchers started with a virus dose of one nanogram, which was enough to infect the majority of the mice who received it. When they saw that the mice given VIP could withstand that dose, they continued to bump it up until they were challenging them with 125 nanograms of virus.

“We expected that at some dose, the antibodies would fail to protect the mice, but it never did — even when we gave mice 100 times more HIV than would be needed to infect 7 out of 8 mice,” says Balazs. “All of the exposures in this work were significantly larger than a human being would be likely to encounter.”

He points out that this outcome likely had more to do with the properties of the antibody that was tested than the method, but adds that VIP is what enabled the large amount of this powerful antibody to circulate through the mice and fight the virus. Furthermore, VIP is a platform technique, meaning that as more potent neutralizing antibodies are isolated or developed for HIV or other infectious organisms, they can also be delivered using this method.

“If humans are like mice, then we have devised a way to protect against the transmission of HIV from person to person,” says Baltimore. “But that is a huge if, and so the next step is to try to find out whether humans behave like mice.”

He says the team is currently in the process of developing a plan to test their method in human clinical trials. The initial tests will ask whether the AAV vector can program the muscle of humans to make levels of antibody that would be expected to be protective against HIV.

“In typical vaccine studies, those inoculated usually mount an immune response — you just don’t know if it’s going to work to fight the virus,” explains Balazs. “In this case, because we already know that the antibodies work, my opinion is that if we can induce production of sufficient antibody in people, then the odds that VIP will be successful are actually pretty high.”

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The study, “Antibody-based Protection Against HIV Infection by Vectored ImmunoProphylaxis,” was funded by the Bill and Melinda Gates Foundation, the National Institutes of Health, and the Caltech-UCLA Joint Center for Translational Medicine. Caltech biology researchers Joyce Chen, Christin M. Hong, and Lili Yang also contributed to the paper, as well as Dinesh Rao, a hematologist from the University of California, Los Angeles.

Medical researchers discover hidden side of prion diseases

Medical researchers in Canada and the United States recently published their joint findings that fatal prion diseases, which include BSE or “mad cow disease,” have a hidden signature.

Findings published this month in the peer-reviewed journal, Public Library of Science (PLoS) Pathogens, demonstrate that up to seven months before an animal shows physical signs of having a prion infection, a particular prion protein in the brain was being eradicated. This member of the prion family is known as shadoo protein.

“What we discovered is that as the early prion disease process unfolds in an infected brain, that the shadoo protein is simultaneously disappearing,” said lead author and co-principal investigator, David Westaway, a researcher in the Faculty of Medicine & Dentistry at the University of Alberta.

“This is telling us there is a process within the disease that we were previously unaware of, a process that is happening before the infected animals are getting sick. It’s telling us that the brain cells are more active in defending themselves than what we thought they were. The brain cells are in fact trying to get rid of the prion protein and as a consequence, this bystander shadoo protein is being destroyed unintentionally.

“This finding suggests that prion diseases are dynamic and not necessarily unstoppable, that there could be a cellular process trying to destroy the infectious prions as they appear. And if we could help that process a little bit more, that might be an avenue to attenuate the disease.”

Westaway, who works in both the Division of Neurology of the Faculty of Medicine & Dentistry, and the Centre for Prions and Protein Folding Diseases at the U of A, collaborated with a team of researchers from Ontario, the University of California, the Institute for Systems Biology in Washington, the McLaughlin Research Institute in Montana and a researcher in Germany, on this discovery.

The same day this paper was published, very similar findings were published by a team of researchers from the University of California, which demonstrates “these new chemical changes are a concrete and reproducible hallmark of prion disease,” says Westaway.

Co-principal investigator George Carlson, from the McLaughlin Research Institute, added: “Given that shadoo may be destroyed by a process that actually targets infectious prions, it was surprising that when we increased the amount of shadoo in laboratory models that the course of disease was not changed. We need to understand why.”

The next step for Westaway’s research team is to determine why this shadoo protein is disappearing.

The finding opens up a new window of research opportunities.

“We need to better understand this. We want to solve this mystery,” he says.

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The research was funded by the Canadian Institutes of Health Research, Alberta Innovates – Health Solutions, the Alberta Prion Research Institute, the National Institutes of Health and the United States Public Health Service.

No cure for pain: study links excess paracetamol use to fatal liver damage

PAUL ROLAN, THE UNIVERSITY OF ADELAIDE

"Life-threatening liver damage can occur without the intention of self harm in desperate patients trying to get some relief for pain."

Medicines need not only to be effective but also safe. Now a Scottish study has shown that paracetamol, perhaps the most commonly consumed painkiller in the country, could lead to death if taken in large doses over a period of time. In the last couple of days, we’ve also heard other adverse information about widely used painkillers, which raises concerns about the dwindling pool of available medicines for pain. And now it seems patients being led to apparently safer alternatives may be risking their lives. Although the number of individual pain relieving medications on the market is very large, they all come from only a very small number of drug classes. We have the familiar paracetamol and aspirin, another group called the non-steroidal anti-inflammatory drugs (NSAIDS), opioids and adjuvant drugs, which include antidepressants and anti-epileptics. Earlier this week, the Australian drug regulator, the Therapeutic Goods Administration(TGA), announced it would be removing four products containing dextropropoxyphene – Capadex, Di-Gesic, Doloxene and Paradex – from the market by March 1. The withdrawal follows adverse assessments from US and European regulators because of concerns about causing ECG changes, which could lead to cardiac arrest. However, some years ago, when the availability of such drugs was severely restricted in the United Kingdom, patients flooded back to their doctors because they weren’t able to get comparable relief from other products. Painkiller safety issues There’s increasing concern over the long-term safety of the opioids. The adverse effects of NSAIDS on the gastrointestinal and cardiovascular systems has been widely reported in the mainstream press. These effects have been the reason for high profile withdrawals, such as that of Merck’s Vioxx. Aspirin is not used for pain very much given its well-recognised potential to cause ulcers and bleeding the gastrointestinal tract. So doctors like myself frequently advise patients to return to the ubiquitous and everyday paracetamol. At recommended doses paracetamol is remarkably safe although it’s known that even moderate excess can cause fatal hepatotoxicity or overdose death. As many of these overdoses have traditionally been impulsive, major reductions in mortality in the United Kingdom were brought about by the simple step of reducing pack size. So doctors are familiar with advising patients not to exceed the recommended dose of 8 tablets a day. But an article published yesterday in the British Journal of Clinical Pharmacologyhas shown that inadvertent “overdoses” from consuming large quantities over a period of time in an attempt to control pain cause also cause life-threatening liver damage. Paracetamol study The authors of the paper looked at data from a large university-linked referral unit where patients showing probable or suspected paracetamol hepatotoxicity were treated. They compared patients with a typical “single overdose”, with patients who’d taken large doses of paracetamol over a period of a few days and suffered a “staggered overdose”. The major reason for the single overdose was attempted suicide. But this was only the motive in one-third of the patients who had a staggered overdose. The majority of these people had simply been seeking pain relief. Somewhat surprisingly, the average total dose in the staggered group (24 grams) was less than that in the single overdose (27 grams). And of greatest concern is that the minimum dose in the staggered group was 10 grams, which is only 20 tablets. Clearly, the key message here is that life-threatening liver damage can occur without the intention of self harm in desperate patients trying to get some relief for pain. Taking care Although people recognise that the number of pills they can take at any given time may not be safely increased, they may take the drug at more frequent intervals than recommended, losing track of cumulative dose and unintentionally putting themselves at risk. Unfortunately, it seems therapeutic options are being reduced by safety concerns – perhaps appropriately – but even the drugs thought to be relatively safe may unintentionally be posing a risk. The key to preventing the problem of staggered paracetamol overdose is education and we are fortunate in Australia to have an organisation such as National Prescribing Service (NPS), which is best placed to do this. We also need education about how medicines may not produce adequate analgesia and that other approaches are needed. Ideally, a mixed approach will enable doctors to help patients manage their pain in the face of the shrinking number of safe therapeutic options. Editor's Note: This article was originally published by The Conversation, here, and is licenced as Public Domain under Creative Commons. See Creative Commons - Attribution Licence.

Online therapy beats the blues

THE AUSTRALIAN NATIONAL UNIVERSITY

People who used the online programs their depressive symptoms stayed reduced for at least six months after the intervention was finished. Image: ahlobystov/iStockphoto A new study from The Australian National University shows that online therapy programs can play a major and long-lasting role in treating depression. Dr Lou Farrer, from the ANU Centre for Mental Health Research (CMHR), trialled the effectiveness of online programs MoodGYM and BluePages when used in conjunction with telephone counselling services provided by Lifeline. Dr Farrer said there was an immediate drop in symptoms of depression among callers to Lifeline who used the two programs. “We worked with Lifeline centres in Melbourne, Sydney, Brisbane and the Sunshine Coast. Lifeline counsellors in these centres identified callers who seemed to be experiencing symptoms of depression or anxiety,” said Dr Farrer. “We then split these callers up into groups. Some were asked to complete MoodGYM and BluePages on their own; others were given these programs as well as weekly phone calls to see how they were progressing. Another group received weekly phone calls without using the online programs and the final group received the usual Lifeline service. “What we found was that the groups who had used MoodGYM and BluePages had a significant, immediate drop in symptoms of depression. Surprisingly the difference between the groups who completed the programs with and without the weekly phone calls was minor. This was surprising as we expected that the programs might be more effective for those who received the weekly phone calls,” she said. Dr Farrer also said that the online therapy programs had a long-lasting impact on depression symptoms. “What is really exciting is that we found that for people who used the online programs their depressive symptoms stayed reduced for at least six months after the intervention was finished. So, the online programs not only had short term effects, but the effects lasted. “The study further supports the usefulness of these programs. Online treatment programs are not only inexpensive and readily accessible; they are also effective.  Hopefully, they will continue to have a bigger role in the future. “Lifeline already refers people to MoodGYM, but whether it becomes a more formalised part of their service may be something to look toward in the future. I am hopeful that the positive results of the study will translate to more people with depression and anxiety accessing interventions in the future,” she said. MoodGYM and BluePages are free online depression treatment programs developed and managed by ANU. Editor's Note: Original news release can be found here.

How phantom limbs form

NEUROSCIENCE RESEARCH AUSTRALIA

The state of nerves in the limb during the formation of the phantom is crucial in determining how it develops.  Image: kyoshino/iStockphoto New studies on how phantom limbs form show there is no default position that the phantom moves into after it forms. "Our research suggests that the state of nerves in the limb at the time the phantom is forming is very important in determining how the phantom develops," says Prof Simon Gandevia from Neuroscience Research Australia (NeuRA). Because distortions of body image, such as phantom limbs, are difficult to treat, a better understanding of the mechanisms behind their formation will help developing more effective treatments. What is a phantom limb? A person has a 'phantom limb' when they continue to perceive sensations in their limb even when the body part is no longer there, such as after amputation. A phantom limb can also develop when the sensory system no longer functions properly, such as in a complete spinal cord injury or after administration of an anaesthetic. People usually perceive their phantom limbs to be in distinct positions, and often experience pain in the limb – however, the cause of this is not well understood. Prof Gandevia and colleague Dr Lee Walsh conducted a study in which they temporarily anaesthetised participants' hands to induce a phantom limb. The team found that the state of the nerves – i.e. how much they were being stimulated – over the period when participants were losing sensation in their hand was key in determining the final perceived position of the phantom hand. "This might also be true for phantom pain," says Prof Gandevia. "In other words, the amount and type of nerve stimulation around the time of amputation or injury could also be important in determining the type and degree of pain perceived in the phantom limb." 'Dynamic changes in the perceived posture of the hand during ischaemic anaesthesia of the arm' was published (1 Dec 2011) in The Journal of Physiology. Editor's Note: Original news release can be found here.

Hindu Devotional - Geethai Sonna Kannan

Why do some people never forget a face?

(Medical Xpress) -- “Face recognition is an important social skill, but not all of us are equally good at it,” says Beijing Normal University cognitive psychologist Jia Liu. But what accounts for the difference? A new study by Liu and colleagues Ruosi Wang, Jingguang Li, Huizhen Fang, and Moqian Tian provides the first experimental evidence that the inequality of abilities is rooted in the unique way in which the mind perceives faces. “Individuals who process faces more holistically” -- that is, as an integrated whole -- “are better at face recognition,” says Liu. The findings will appear in an upcoming issue of Psychological Science, a journal published by the Association for Psychological Science.

In daily life, we recognize faces both holistically and also “analytically”—that is, picking out individual parts, such as eyes or nose. But while the brain uses analytical processing for all kinds of objects—cars, houses, animals—“holistic processing is thought to be especially critical to face recognition,” says Liu.

To isolate holistic processing as the key to face recognition, the researchers first measured the ability of study participants—337 male and female students—to remember whole faces, using a task in which they had to select studied faces and flowers from among unfamiliar ones.

The next two tasks measured performance in tasks that mark holistic processing. The composite-face effect (CFE) shows up when two faces are split horizontally and stuck together. It’s easier to identify the top half-face when it’s misaligned with the bottom one than when the two halves are fitted smoothly together. “That’s because our brain automatically combines them to form a new”—and unfamiliar—“face,” says Liu: evidence of holistic processing. The other marker of holistic processing is the whole-part effect (WPE). In this one, people are shown a face, then asked to recognize a part of it—say, the nose. They do better when the feature is presented within the whole face than when it stands on its own among other noses: again, we remember the nose integrated into the whole face. The researchers also assessed participants’ general intelligence.

The results: Those participants who scored higher on CFE and WPE—that is, who did well in holistic processing—also performed better at the first task of recognizing faces. But there was no link between facial recognition and general intelligence, which is made up of various cognitive processes—a suggestion that face processing is unique.

“Our findings partly explains why some never forget faces, while others misrecognize their friends and relatives frequently,” says Liu. That’s why the research holds promise for therapies for that second category of people, who may suffer disorders such as prosopagnosia (face blindness) and autism. Knowing that the mind receives a face as one whole thing and not as a collection of individual parts, “we may train people on holistic processing to improve their ability in recognizing faces,” Liu says.

Provided by Association for Psychological Science

"Why do some people never forget a face?." December 1st, 2011. http://medicalxpress.com/news/2011-12-people.html

 

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