Boost for Health? Researchers Isolate Protein Linking Exercise to Health Benefits

A team led by researchers at Dana-Farber Cancer Institute has isolated a natural hormone from muscle cells that triggers some of the key health benefits of exercise. (Credit: © Imre Forgo / Fotolia

Science Daily — A team led by researchers at Dana-Farber Cancer Institute has isolated a natural hormone from muscle cells that triggers some of the key health benefits of exercise. They say the protein, which serves as a chemical messenger, is a highly promising candidate for development as a novel treatment for diabetes, obesity and perhaps other disorders, including cancer.

"It's exciting to find a natural substance connected to exercise that has such clear therapeutic potential," said Bostroöm.Bruce Spiegelman, PhD, a cell biologist at Dana-Farber, is senior author of the report, posted as an advanced online publication by the journal Nature. The first author is Pontus Bostroöm, MD, PhD, a postdoctoral fellow in the Spiegelman lab.

Spiegelman dubbed the hormone "irisin," after Iris, a Greek messenger goddess. He said the discovery is an important first step in understanding the biological mechanisms that translate physical exercise into beneficial changes throughout the body, both in healthy people and in preventing or treating disease.

"There has been a feeling in the field that exercise 'talks to' various tissues in the body," said Spiegelman, a professor of cell biology at Harvard Medical School. "But the question has been, how?"

According to the report, the irisin hormone has direct and "powerful effects" on adipose, or fatty, tissue -- subcutaneous deposits of white fat that store excess calories and which contribute to obesity.

When irisin levels rise through exercise -- or, in this study, when irisin was injected into mice -- the hormone switches on genes that convert white fat into "good" brown fat. This is beneficial because brown fat burns off more excess calories than does exercise alone.

Only a small amount of brown fat is found in adults, but infants have more -- an evolutionary echo of how mammals keep themselves warm while hibernating. In the wake of findings by Spiegelman and others, there has been a surge of interest in the therapeutic possibilities of increasing brown fat in adults.

Along with stimulating brown fat development, irisin was shown to improve glucose tolerance, a key measure of metabolic health, in mice fed a high-fat diet.

The discovery won't allow people will be able to skip the gym and build muscles by taking irisin supplements, Spiegelman cautioned, because the hormone doesn't appear to make muscles stronger. Experiments showed that irisin levels increase as a result of repeated bouts of prolonged exercise, but not during short-term muscle activity.

The Dana-Farber team identified irisin in a search for genes and proteins regulated by a master metabolic regulator, called PGC1-alpha, that is turned on by exercise. Spiegelman's group had discovered PGC1-alpha in previous research.

Bostroöm said the hunt for molecular targets of increased PGC1-alpha activity ultimately pinpointed irisin, which turned out to be located within the outer membrane of muscle cells. This discovery ran counter to other scientists' contentions that such a protein would reside in the cell's nucleus.

To test whether increasing irisin alone could mimic exercise benefits, the scientists injected modest amounts into sedentary mice that were obese and pre-diabetic.

With 10 days of treatment, the mice had better control of blood sugar and insulin levels -- in effect, preventing the onset of diabetes -- and lost a small amount of weight. Although the weight loss was small, Spiegelman said that the hormone may have a greater effect when given for longer periods.

There were no signs of toxicity or side effects, which was predicted since the researchers limited the increase of irisin to levels typically caused by exercise.

In part because it is a natural substance and because the mouse and human forms of the protein are identical, Spiegelman said it should be possible to move an irisin-based drug rapidly into clinical testing -- perhaps within two years.

The irisin discovery has been licensed by Dana-Farber exclusively to Ember Therapeutics for drug development. Ember is a Boston-based startup co-founded by Spiegelman and scientists at the Joslin Diabetes Center and the Scripps Research Institute in Florida.

The scientists said their findings merely scratch the surface of irisin's multiple effects. They are continuing to explore the hormone's possible benefits in metabolic diseases like diabetes, insulin resistance, and obesity, which constitute a growing epidemic around the world, as well as neurodegenerative illnesses like Parkinson's disease.

Spiegelman added that as growing evidence implicates obesity and physical inactivity in cancer development, it's conceivable irisin-based drugs may have value in prevention and treatment of the disease.

Other authors, in addition to Spiegelman and Boström, are from Dana-Farber; Harvard Medical School; Brigham and Women's Hospital; University of California at San Francisco; Universita Politecnica delle Marche, Ancona, Italy; Odense University Hospital, Denmark; and LakePharma, Belmont, Calif.

Master Controller of Memory Identified

Yingxi Lin, a member of the McGovern Institute for Brain Research and the the Frederick and Carole Middleton Career Development Assistant Professor of Brain and Cognitive Sciences. (Credit: Photo courtesy Kent Dayton)                  Science Daily  — When you experience a new event, your brain encodes a memory of it by altering the connections between neurons. This requires turning on many genes in those neurons. Now, MIT neuroscientists have identified what may be a master gene that controls this complex process.

The research team, led by Yingxi Lin, a member of the McGovern Institute for Brain Research at MIT, focused on the Npas4 gene, which previous studies have shown is turned on immediately following new experiences. The gene is particularly active in the hippocampus, a brain structure known to be critical in forming long-term memories.The findings, described in the Dec. 23 issue of Science, not only reveal some of the molecular underpinnings of memory formation -- they may also help neuroscientists pinpoint the exact locations of memories in the brain.

Lin and her colleagues found that Npas4 turns on a series of other genes that modify the brain's internal wiring by adjusting the strength of synapses, or connections between neurons. "This is a gene that can connect from experience to the eventual changing of the circuit," says Lin, the Frederick and Carole Middleton Career Development Assistant Professor of Brain and Cognitive Sciences.

To investigate the genetic mechanisms of memory formation, the researchers studied a type of learning known as contextual fear conditioning: Mice receive a mild electric shock when they enter a specific chamber. Within minutes, the mice learn to fear the chamber, and the next time they enter it, they freeze.

The researchers showed that Npas4 is turned on very early during this conditioning. "This sets Npas4 apart from many other activity-regulated genes," Lin says. "A lot of them are ubiquitously induced by all these different kinds of stimulations; they are not really learning-specific."

Furthermore, Npas4 activation occurs primarily in the CA3 region of the hippocampus, which is already known to be required for fast learning.

"We think of Npas4 as the initial trigger that comes on, and then in turn, in the right spot in the brain, it activates all these other downstream targets. Eventually they're going to modify synapses in a way that's likely changing synaptic inhibition or some other process that we're trying to figure out," says Kartik Ramamoorthi, a graduate student in Lin's lab and lead author of the paper.

Genetic regulation

So far, the researchers have identified only a few of the genes regulated by Npas4, but they suspect there could be hundreds more. Npas4 is a transcription factor, meaning it controls the copying of other genes into messenger RNA -- the genetic material that carries protein-building instructions from the nucleus to the rest of the cell. The MIT experiments showed that Npas4 binds to the activation sites of specific genes and directs an enzyme called RNA polymerase II to start copying them.

"Npas4 is providing this instructive signal," Ramamoorthi says. "It's telling the polymerase to land at certain genes, and without it, the polymerase doesn't know where to go. It's just floating around in the nucleus."

When the researchers knocked out the gene for Npas4, they found that mice could not remember their fearful conditioning. They also found that this effect could be produced by knocking out the gene just in the CA3 region of the hippocampus. Knocking it out in other parts of the hippocampus, however, had no effect. Though they focused on contextual fear conditioning, the researchers believe that Npas4 will also prove critical for other types of learning.

Gleb Shumyatsky, an assistant professor of genetics at Rutgers University, says that an important next step is to identify more of the genes controlled by Npas4, which should reveal more of its role in memory formation. "It's definitely one of the major players," says Shumyatsky, who was not involved in this research. "Future experiments will show how major a player it is."

The MIT team also plans to investigate whether the same neurons that turn on Npas4 when memories are formed also turn it on when memories are retrieved. This could help them pinpoint the exact neurons that are storing particular memories.

"We're hunting for the memory, and we think we can use Npas4 to mark where it is," Ramamoorthi says. "That's because it's turned on specifically and now we can label the cells and maybe fish out where in the brain the memory is sitting."

Study links posture with back pain

CHRIS THOMAS, SCIENCENETWORK WA

According to new research from a Murdoch University PhD student, back pain has a direct linear link with a person’s balance. While chiropractor Alex Ruhe said there had always been a known relationship, this was the first time a linear connection had been established. “Possibly [the] relationship was deemed of low relevance because few direct clinical applications arise from it,” he says. Using 210 patients with low-back, mid-back and neck pain, Mr Ruhe asked them to rate their pain on a scale from zero (no pain) to 10 (the worst possible pain). Body sway was measured on a solid fore plate after patients closed their eyes and changes in weight shifts were recorded by pressure sensors in each corner of the plate. The recordings of pain sufferers were compared to sway data from healthy individuals of a similar age. “We discovered body sway increased with higher pain intensities and this increase followed a linear fashion,” Mr Ruhe said. “Similar results were observed for the three painful regions. “In follow-up studies, we observed changes in body sway as pain decreased after a course of three manual therapeutic interventions at three to four day intervals. “The results showed that sway was lowered as pain levels decreased, maintaining the linear relationship previously observed. “Long-term damage or changes to the nervous system due to the pain appears unlikely because reduced sway in association with pain reduction was observed after just a few days.” As a result of his research, Mr Ruhe said the focus should be on pain control when treating people with back pain in the future, particularly the elderly. “The age-related decrease in neurological function renders them prone to falls and sustaining injuries as a consequence,” he said. “Previous theories regarding damage to and adaptations of the nervous system because of chronic painful stimulation appear less likely. “Instead, pain interference appears more to cause increased postural sway in patients.” Mr Ruhe said, in simple terms, this referred to decreased muscular control due to a painful stimulus inhibiting normal automatic body sway corrections. “A return-to-normal body sway occurred directly following a pain decrease—a longer recovery period would have been expected in the case of neurological damage,” he said.   “This research marks an important finding for clinicians. It is an objective monitoring tool for patients suffering from back pain under treatment and rehabilitation.” Editor's Note: Original news release can be found here.

நுரையீரலைப் பற்றி தெரிந்து கொள்வோம்

ஒரு நிமிடத்திற்கு சராசரியாக 18 முதல் 20 சுவாசம் என சீராக வைப்பது மூளையில் உள்ள முகுளத்தின் வேலை. மொத்த நுரையீரலின் கொள்ளளவு சராசரியாக 6 லிட்டர் தான். மிகவும் இழுத்து மூச்சுவிடும் போது காற்றின் அளவு 5 லிட்டர்தான். எப்போதும் நுரையீரலுக்குள்ளே இருந்துகெண்டிருக்கும் காற்றின் அளவு 1 லிட்டர்.  பொதுவாக நுரையீரலில் சுரக்கும் சளி போன்ற நீர்மம் சில தூசிகளை அகற்றி வெளியேற்றும். இதுபோல் மூச்சுக் குழாய்களில் மேல் சிலியா என்ற பொருள் இருக்கும். இதுவும் மிக நுண்ணிய தூசியைக் கூட அகற்றிவிடும்.  இது மூச்சுக் குழாய்களில் வரும் தூசியை மேல்நோக்கி திருப்பி அனுப்பிவிடும். நாம் அறியாமலே சில சமயங்களினித உடலின் செயல்பாடுகளுக்கு ஒவ்வொரு உறுப்பும் இன்றியமையாததாகும். இதில் உடலுக்கு மெயின் சுவிட்சு போல் செயல்பட்டு, காற்றை உள்வாங்கி, வெளிவிட்டு உடலுக்கு உயிர் சக்தியைத் தரும் மோட்டார்தான் நுரையீரல். வாயுப் பரிமாற்றம் (Exchange of gas) நுரையீரலின் முக்கிய பணியாகும். மேலும் சில முக்கிய வேதிப் பொருட்களை உருவாக்குவதற்கும், வேறு சில வேதிப் பொருட்களை செயலிழக்கச் செய்வதும் இதன் மற்ற பணிகளாகும். நுரையீரலானது உடலியக்கத்திற்கு ஆற்றல் தரும் ஆக்ஸிஜனை உள் எடுத்துக் கொள்வதற்கும் கார்பன்-டை- ஆக்ஸைடை வெளியேற்றுவதற்கும் முக்கிய உறுப்பாக செயல்படுகிறது. ஒரு நாளைக்கு சராசரியாக ஒரு மனிதன் 22,000 முறை மூச்சு விடுகிறான். கிட்டத்தட்ட 255 கன மீட்டர் (9000 கன அடி) காற்றை உள்ளிழுத்து வெளிவிடுகிறான்.  நுரையீரலின் செயல்பாடு. நுரையீரல் எவ்வாறு தன்னுடைய பணியை திறம்பட செய்கிறது என்பதைப் பார்ப்போம்.  மூக்கின் வழியாக நாம் உள்ளிழுக்கும் காற்று மூச்சுக் குழாய் (Trachea) வழியாக நுரையீரலுக்கு செல்கிறது. மூச்சுக் குழாய் மார்புப் பகுதியில் இரண்டாக பிரிந்து வலது, இடது நுரையீரலுக்குச் செல்கிறது. நுரையிரலுக்குள் நுழைந்தவுடன் மூச்சுக்குழல் ஒவ்வொன்றிலிருந்தும் கிளைகள் பிரியும். பின்னர் அவற்றிலிருந்து இன்னும் சிறு கிளைகள் என நிறைய பிரிவுகள் ஒரு மரத்தின் பெரிய கிளையிலிருந்து பரந்து பிரிந்து சின்னச்சின்ன தளிர்கள் வருவதுபோல் பிரிகின்றன. அதனாலேயே இதனை மூச்சுமரம் (Respiratory tree) என்று அழைக்கின்றோம். முதல் நிலை மூச்சுக் குழல் (Primary bronchi), இரண்டாம் நிலை மூச்சுக் குழல், மூன்றாம் நிலை மூச்சுக்குழல், மூச்சுக் குறுங்குழல் (bronchiole) என்று படிப்படியாகப் பிரிந்து கடைசியாக சின்னச் சின்ன பலூன்கள் மாதிரி தோன்றும் குட்டிக்குட்டி அறைகளுக்குள் இந்த குழல்கள் நீட்டிக் கொண்டிருக்கும். இவற்றை காற்று நுண்ணறைகள் (Alveoli) என்று அழைக்கிறோம். நாம் இழுக்கும் மூச்சுக்காற்று மூச்சு மரம் வழியாக காற்று நுண்ணறைகளுக்குள் வந்துவிடும்.  உடலில் பல பாகங்களிலும் இருந்து பயன்படுத்தப்பட்ட ரத்தம் இதயத்தின் வலது வெண்டிரிக்கலை அடையும். அங்கிருந்து நுரையீரல், தமணி மூலம் நுரையீரலுக்கு கொண்டுசெல்லப்படுகிறது. நுரையீரல் தமணியும், வலது கிளை, இடது கிளை, என்று இரண்டாகப் பிரிந்து இரண்டு நுரையீரலுக்கும் செல்கிறது. இதுவும் பலமுறை கிளைகளாகப் பிரியும். இப்படிப் பிரியும்போது காற்று நுண்ணறைகளின் பக்கத்தில் தமணிகளின் மிக மிகச் சிறிய கிளைகள் அமைந்திருக்கும். இந்தச் சின்ன தமணிக் கிளைகள்தான் தந்துகிகள் (Capillaries) எனப்படுகிறது. காற்று நுண்ணறை பக்கத்திலேயே தந்துகிகள் இரண்டின் சுவர்களும் மிக மிக நுண்ணியவையாக இருக்கும். அடுத்தடுத்து நுண்ணறைக்குள் காற்று நிறைந்திருக்கும் தந்துகிக்குள் ரத்தம் நிறைந்திருக்கும்.  வெளியிலிருந்து மூச்சுக்குழல் மூலம் உள்ளிழுக்கப்பட்ட காற்றில் நிறைய ஆக்ஸிஜன் இருக்கும். எனவே, நுண்ணறைக்குள்ளும் அதே அளவு ஆக்ஸிஜன் இருக்கும். தந்துகியில் உள்ள ரத்தத்தின் ஆக்ஸிஜன் அளவு குறைவு. கார்பன்டை ஆக்ஸைடின் அளவு அதிகம். உடலுக்கு வேண்டாத உடலிலிருந்து வெளியேற்றப்பட வேண்டிய மற்ற சில பொருட்களும் தந்துகியில் உண்டு. இந்த நிலையில் நுண்ணறை – தந்துகி சுவர்களின் வழியாக ஒரு பரிமாற்றம் நடக்கிறது. நுண்ணறையில் அடர்த்தியாக இருக்கும் ஆக்ஸிஜன் தந்துகிக்குள் பாயும். தந்துகியில் அடர்த்தியாக இருக்கும் கார்பன்டை ஆக்ø-ஸடு நுண்ணறைக்குள் பாயும். இதுதான் வாயுப் பரிமாற்றம் (Exchange & gases). இதைத்தான் ரத்த சுத்திகரிப்பு என்று அழைக்கிறோம்.  ஆக்ஸிஜன் ஊட்டப்பட்ட ரத்தம் நுரையீரலிலிருந்து சிரைகள் மூலமாக இதயத்தின் இடது வெண்டிரிக்கிளுக்குள் எடுத்துச் செல்லப் படுகிறது. அங்கிருந்து மீண்டும் உடலின் பல பாகங்களுக்கு தமனிகள் மூலம் இந்த சுத்த ரத்தம் எடுத்துச் செல்லப்படுகிறது. நுரையீரலைச் சுற்றி இரண்டு உறைகள் உள்ளன.  1. வெளிப்படலம் (Outer pleura) 2. உள்படலம் (Inner pleura)  இந்த இரண்டு படலங்களுக்கும் இடையே ஒரு இடம் உண்டு. அதற்கு ஃப்ளூரல் இடம் என்று பெயர். இதனுள் மிகச் சிறிய அளவு ஃப்ளூரல் திரவம் இருக்கும். இந்தத் திரவம்தான் சுவாசத்தின் போது நுரையீரல்களின் அசைவினால் உராய்வு ஏற்படாமல் தடுக்கிறது. சுவாசத்தைக் கட்டுப்படுத்தி சீராக வைப்பதே முகுளப்பகுதி. அதால் அதை விழுங்கிவிடுவோம். உடல் நலம் சரியில்லாமல் போனால் மட்டுமே அவை சளியாக மூக்கின் வழியாக வெளியேறும். இதையும் தாண்டி ஏதேனும் தூசு உள்ளே நுழைந்தால் இருமல், தும்மல் முதலியவற்றால் வெளியேற்றப் பட்டுவிடும்.  நுரையீரலின் பணிகள் காற்றில் உள்ள ஆக்ஸிஜனை (ஆக்ஸிஜன்= உயிர்வளி, பிராணவாயு) இரத்தத்தில் சேர்ப்பதும், இரத்ததில் உள்ள கார்பன்-டை ஆக்ஸைடை (கரியமில வாயு) பிரித்து உடலிலிருந்து வெளியேற்றுவதும் நுரையீரலின் முக்கிய பணியாகும். இதயத்திற்கு இரு புறமும் பாதுகாப் பாக இருந்து இதயத்தை அதிர்வுகளிலிருந்து காப்பாற்றுகிறது.  சில முக்கிய வேதிப் பொருட்களை உற்பத்தி செய்வது, வேறு சில வேதிப் பொருட்களை செயலிழக்கச் செய்வது போன்ற உடலுக்கு உயிர்தரும் வேலைகளை நுரையீரல் செய்து வருகிறது.  நுரையீரல் பாதிப்பு  உலகில் இலச்சக்கணக்கான மக்கள் ஒவ்வொரு வருடமும் நுரையீரல் சம்பந்தப்பட்ட நோயின் தாக்குதலுக்கு ஆளாகின்றனர்.  காற்று மாசுபாடு  காற்று மாசுபாடு அதாவது சிலிகா, ஆஸ்பெட்டாஸ், கந்தகம், போன்றவற்றைப் பயன்படுத்தும் தொழிற் சாலைகளில் பணி புரிபவர்களின் நுரையீரல்கள் அதிகம் பாதிக்கப்படுவதாக தகவல்கள் தெரிவிக்கின்றன. புகை பிடிப்பது உடல் நலத்துக்கு கேடு என்ற செய்தி அனைவரும் அறிந்ததே புகைபிடிப்பது:  புகை பிடிக்கும்போது நிறைய கரித் துகள்கள் (Carbon particles) நுரையீரலுக்குள் சென்று அங்கேயே படிந்து விடுகின்றன. இதனால் ஆக்ஸிஜன்- கார்பன்டை ஆக்ஸைடு பரிமாற்றம் தடைபடுகிறது. மற்றும் சிகரெட், சுருட்டு, இவற்றிலுள்ள நிகோடின் என்ற வேதிப்பொருள் ரத்தத்தில் உள்ள ஆக்ஸிஜன் அளவைக் குறைத்து கனிமப் பொருள்களின் அளவுகளில் மாற்றத்தை ஏற்படுத்தி, ரத்தக் குழாய்களின் அடைப்பை உண்டாக்குகிறது. புகைப் பழக்கத்தால் மூச்சுக்குழல் அலர்ஜி, காற்றறைகளின் சுவர்கள் சிதைந்துபோதல், எம்ஃபசிமா, நுரையீரல் புற்றுநோய் ஆகியவை உண்டாகின்றன. புகைப் பிடிப்பவர்களுக்கு மட்டுமல்ல, பக்கத்தில் இருப்பவர்களுக்கும் (Passive smoking) இதே தீங்குகள் நேரிடும். நுரையீரல் பாதிப்பின் அறிகுறிகள் இருமல் மூச்சு வாங்குதல் மூச்சு இழுப்பு நெஞ்சுவலிஹீமாப்டிஸிஸ் (இருமும்போது ரத்தம் வெளியேறுதல்)  நுரையீரலைத் தாக்கும் சில முக்கிய நோய்கள் மூச்சுக்குழாய் அலர்ஜி(Bronchitis), நுரையீரல் அலர்ஜி (Pneumonia), காற்றறைகள் சிதைந்து போதல்(Emphysema), மூச்சுக்குழல்கள் சுருங்கிக் கொள்ளுதல் (Asthma). நுரையீரலை பாதுகாக்க சில எளிய வழிகள் தூசு நிறைந்த பகுதிகளுக்கு செல்லும் போது மூக்கில் துணியைக் கட்டிக்கொள்வது (Mask) நல்லது.   பிராணயாமம், நாடி சுத்தி, ஆழ்ந்த மூச்சுப் பயிற்சி போன்றவற்றை தினமும் கடைப்பிடிப்பது.   புகைப் பிடிப்பதை தவிர்ப்பது உடலில் நோய் எதிர்ப்பு சக்தியை அதிகரிக்கும் உணவு வகைகளை சாப்பிடுவது இன்றைய சூழ்நிலையில் மாசடைந்த காற்று அதிகம் இருப்பதால் நுரையீரல் சம்பந்தப்பட்ட நோய்களின் தாக்குதலும் அதிகம் இருக்கிறது. இதனால் எதிர்காலத்தில் மினரல் வாட்டர் பாட்டிலைப் போல் ஆக்ஸிஜனை பாக்கெட்டுகளில் வாங்க வேண்டிய நிலை ஏற்படலாம். இந்நிலை மாற சுற்றுப்புறத்தை தூய்மையாகவும், பசுமை நிறைந்த பகுதிகளாகவும் மாற்றினாலே போதும்.. ஆரோக்கிய வாழ்வைப் பெற்றிட முடியும்.   Engr. சுல்தான்

The illusion of courage: Why people mispredict their behavior in embarrassing situations

Whether it's investing in stocks, bungee jumping or public speaking, why do we often plan to take risks but then "chicken out" when the moment of truth arrives?

In a new paper in the Journal of Behavioral Decision Making, scientists from the University of Colorado Boulder and Carnegie Mellon University argue that this "illusion of courage" is one example of an "empathy gap"— that is, our inability to imagine how we will behave in future emotional situations. According to the empathy gap theory, when the moment of truth is far off you aren't feeling, and therefore are out of touch with, the fear you are likely to experience when push comes to shove. The research team also included Cornell University's David Dunning and former CMU graduate student Ned Welch, currently a consultant for McKinsey.

In a series of three experiments, the researchers found that people overestimate their willingness to engage in psychologically distant embarrassing public performances, and also found that they could reduce this illusion of courage by inducing immediate emotions that effectively put them in touch with the fear they would experience.

In the first two experiments, college students were asked if they would be willing to engage in a future embarrassing situation — telling a funny story to their class in one study, and dancing to James Brown's "Sex Machine" in front of the class in the other — in exchange for a few dollars. Students were either asked outright or after being exposed to short films that aroused mild experiences of fear and anger. Students who did not view movie clips significantly overestimated their willingness to sing or dance. When they experienced negative emotions — fear and anger — as a result of watching the movie clips, students were much more accurate in predicting their own future lack of interest in performing.

"Because social anxiety associated with the prospect of facing an embarrassing situation is such a common and powerful emotion in everyday life, we might think that we know ourselves well enough to predict our own behavior in such situations," said Leaf Van Boven, associate professor of psychology and neuroscience at the University of Colorado Boulder. "But the ample experience most of us should have gained with predicting our own future behavior isn't sufficient to overcome the empathy gap — our inability to anticipate the impact of emotional states we aren't currently experiencing."

The illusion of courage has practical consequences. "People frequently face potential embarrassing situations in everyday life, and the illusion of courage is likely to cause us to expose ourselves to risks that, when the moment of truth arrives, we wish we hadn't taken," said George Loewenstein, the Herbert A. Simon University Professor of Economics and Psychology within CMU's Dietrich College of Humanities and Social Sciences. "Knowing that, we might choose to be more cautious, or we might use the illusion of courage to help us take risks we think are worth it, knowing full well that we are likely to regret the decision when the moment of truth arrives."

Provided by Carnegie Mellon University

"The illusion of courage: Why people mispredict their behavior in embarrassing situations." January 17th, 2012.http://medicalxpress.com/news/2012-01-illusion-courage-people-mispredict-behavior.html

 

Posted by
Robert Karl Stonjek

A first: Brain support cells from umbilical cord stem cells

For the first time ever, stem cells from umbilical cords have been converted into other types of cells, which may eventually lead to new treatment options for spinal cord injuries and multiple sclerosis, among other nervous system diseases.

"This is the first time this has been done with non-embryonic stem cells," says James Hickman, a University of Central Florida bioengineer and leader of the research group, whose accomplishment is described in the Jan. 18 issue of the journal ACS Chemical Neuroscience.

"We're very excited about where this could lead because it overcomes many of the obstacles present with embryonic stem cells."

Stem cells from umbilical cords do not pose an ethical dilemma because the cells come from a source that would otherwise be discarded. Another major benefit is that umbilical cells generally have not been found to cause immune reactions, which would simplify their potential use in medical treatments.

The pharmaceutical company Geron, based in Menlo Park, Calif., developed a treatment for spinal cord repair based on embryonic stem cells, but it took the company 18 months to get approval from the FDA for human trials due in large part to the ethical and public concerns tied to human embryonic stem cell research. This and other problems recently led to the company shutting down its embryonic stem cell division, highlighting the need for other alternatives.

Sensitive Cells

The main challenge in working with stem cells is figuring out the chemical or other triggers that will convince them to convert into a desired cell type. When the new paper's lead author, Hedvika Davis, a postdoctoral researcher in Hickman's lab, set out to transform umbilical stem cells into oligodendrocytes--critical structural cells that insulate nerves in the brain and spinal cord--she looked for clues from past research.

Davis learned that other research groups had found components on oligodendrocytes that bind with the hormone norepinephrine, suggesting the cells normally interact with this chemical and that it might be one of the factors that stimulates their production. So, she decided this would be a good starting point.

In early tests, she found that norepinephrine, along with other stem cell growth promoters, caused the umbilical stem cells to convert, or differentiate, into oligodendrocytes. However, that conversion only went so far. The cells grew but then stopped short of reaching a level similar to what's found in the human nervous system.

Davis decided that, in addition to chemistry, the physical environment might be critical.

To more closely approximate the physical restrictions cells face in the body, Davis set up a more confined, three-dimensional environment, growing cells on top of a microscope slide, but with a glass slide above them. Only after making this change, and while still providing the norepinephrine and other chemicals, would the cells fully mature into oligodendrocytes.

"We realized that the stem cells are very sensitive to environmental conditions," Davis said.

Medical Potential

This growth of oligodendrocytes, while crucial, is only a first step to potential medical treatments. There are two main options the group hopes to pursue through further research. The first is that the cells could be injected into the body at the point of a spinal cord injury to promote repair.

Another intriguing possibility for the Hickman team's work relates to multiple sclerosis and similar conditions. "Multiple sclerosis is one of the holy grails for this kind of research," said Hickman, whose group is collaborating with Stephen Lambert at UCF's medical school, another of the paper's authors, to explore biomedical possibilities.

Oligodendrocytes produce myelin, which insulates nerve cells, making it possible for them to conduct the electrical signals that guide movement and other functions. Loss of myelin leads to multiple sclerosis and other related conditions such as diabetic neuropathy.

The injection of new, healthy oligodendrocytes might improve the condition of patients suffering from such diseases. The teams are also hoping to develop the techniques needed to grow oligodendrocytes in the lab to use as a model system both for better understanding the loss and restoration of myelin and for testing potential new treatments.

"We want to do both," Hickman said. "We want to use a model system to understand what's going on and also to look for possible therapies to repair some of the damage, and we think there is great potential in both directions."

More information: Paper online: http://pubs.acs.org/doi/abs/10.1021/cn200082q

 

Provided by University of Central Florida

"A first: Brain support cells from umbilical cord stem cells." January 17th, 2012. http://medicalxpress.com/news/2012-01-brain-cells-umbilical-cord-stem.html

 

Posted by
Robert Karl Stonjek

Gossip can have social and psychological benefits

For centuries, gossip has been dismissed as salacious, idle chatter that can damage reputations and erode trust. But a new study from the University of California, Berkeley, suggests rumor-mongering can have positive outcomes such as helping us police bad behavior, prevent exploitation and lower stress.

"Gossip gets a bad rap, but we're finding evidence that it plays a critical role in the maintenance of social order," said UC Berkeley social psychologist Robb Willer, a coauthor of the study published in this month's online issue of the Journal of Personality and Social Psychology.

The study also found that gossip can be therapeutic. Volunteers' heart rates increased when they witnessed someone behaving badly, but this increase was tempered when they were able to pass on the information to alert others.

"Spreading information about the person whom they had seen behave badly tended to make people feel better, quieting the frustration that drove their gossip," Willer said.

So strong is the urge to warn others about unsavory characters that participants in the UC Berkeley study sacrificed money to send a "gossip note" to warn those about to play against cheaters in economic trust games. Overall, the findings indicate that people need not feel bad about revealing the vices of others, especially if it helps save someone from exploitation, the researchers said.

"We shouldn't feel guilty for gossiping if the gossip helps prevent others from being taken advantage of," said Matthew Feinberg, a UC Berkeley social psychologist and lead author of the paper.

The study focused on "prosocial" gossip that "has the function of warning others about untrustworthy or dishonest people," said Willer, as opposed to the voyeuristic rumor-mongering about the ups and downs of such tabloid celebrities as Kim Kardashian and Charlie Sheen.

In a series of four experiments, researchers used games in which the players' generosity toward each other was measured by how many dollars or points they shared. In the first experiment, 51 volunteers were hooked up to heart rate monitors as they observed the scores of two people playing the game. After a couple of rounds, the observers could see that one player was not playing by the rules and was hoarding all the points.

Observers' heart rates increased as they witnessed the cheating, and most seized the opportunity to slip a "gossip note" to warn a new player that his or her contender was unlikely to play fair. The experience of passing on the information calmed this rise in heart rate.

"Passing on the gossip note ameliorated their negative feelings and tempered their frustration," Willer said. "Gossiping made them feel better."

In the second experiment, 111 participants filled out questionnaires about their level of altruism and cooperativeness. They then observed monitors showing the scores from three rounds of the economic trust game, and saw that one player was cheating.

The more prosocial observers reported feeling frustrated by the betrayal and then relieved to be given a chance to pass a gossip note to the next player to prevent exploitation.

"A central reason for engaging in gossip was to help others out – more so than just to talk trash about the selfish individual," Feinberg said. "Also, the higher participants scored on being altruistic, the more likely they were to experience negative emotions after witnessing the selfish behavior and the more likely they were to engage in the gossip."

To raise the stakes, participants in the third experiment were asked to go so far as to sacrifice the pay they received to be in the study if they wanted to send a gossip note. Moreover, their sacrifice would not negatively impact the selfish player's score. Still, a large majority of observers agreed to take the financial hit just to send the gossip note.

"People paid money to gossip even when they couldn't affect the selfish person's outcome," Feinberg said.

In the final study, 300 participants from around the country were recruited via Craigslist to play several rounds of the economic trust game online. They played using raffle tickets that would be entered in a drawing for a $50 cash prize –-an extra incentive to hold on to as many raffle tickets as possible.

Some players were told that the observers during a break could pass a gossip note to players in the next round to alert them to individuals not playing fairly. The threat of being the subject of negative gossip spurred virtually all the players to act more generously, especially those who had scored low on an altruism questionnaire taken prior to the game.

Together, the results from all four experiments show that "when we observe someone behave in an immoral way, we get frustrated," Willer said. "But being able to communicate this information to others who could be helped makes us feel better."

Provided by University of California - Berkeley

"Gossip can have social and psychological benefits." January 17th, 2012. http://medicalxpress.com/news/2012-01-gossip-social-psychological-benefits.html

 

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Robert Karl Stonjek

Mental illness protects some inmates from returning to jail

People with mental illness have gotten a bad rap in past research studies, being labeled the group of people with the highest return rates to prison. But a researcher from the Mandel School of Applied Social Sciences at Case Western Reserve University counters those findings in a new study—demonstrating that inmates with severe mental illnesses alone actually have lower rates of recidivism than those with substance abuse issues or no mental or substance abuse issues.

Past studies compared inmates with severe mental illnesses, like schizophrenia and severe affective disorders, with a general population of released inmates and found that those with mental illnesses had higher recidivism rates.

The study's principal investigator Amy B. Wilson, assistant professor of social work at Case Western Reserve, said the researchers took a novel approach to studying recidivism among released inmates from one of the country's largest jail systems (Philadelphia) and separated inmates into four categories: those with severe mental illnesses, those with a substance abuse problem, those with dual problems of mental illness and substance abuse, and those with neither problem.

When looking at individual groups, those with mental illnesses alone fared better—even compared against those with no mental or substance abuse issues.

The findings from the study, "Examining the impact of mental illness and substance use on recidivism in a county jail," were reported in theInternational Journal of Law and Psychiatry.

The researchers looked at recidivism rates for 20,112 inmates admitted to the Philadelphia jail system in 2003 and then tracked their return rates over the next four years. Using data from Philadelphia's behavioral health system on Medicaid records and from the Philadelphia Country's jail system on admission, release and demographic information, the researchers were able to categorize the individuals into the four groups and follow their readmissions.

Of those readmitted to jail, 32 percent took place in the first year, increased to 45 percent by year two, 54 percent by year three, and 60 percent by year four.

At the end of four years, 54 percent of those with severe mental illness returned to jail, while 66 percent of those with substance abuse problems did, 68 percent of those with co-occurring issues, and 60 percent of those with no diagnosis did.

Each year of the study, those with severe mental illnesses had lower return rates than those in the other three groups.

Wilson says further study is needed, but she speculates that the services offered to those with mental illness alone upon release are more readily available than social services for individuals with dual problems or substance abuse. But much is yet to be learned about how mental illness can protect the inmates from further recidivism, Wilson said.

"These findings point to a possible need for more integrated services for mental and substance abuse, and more attention being paid generally to the ways that substance abuse involvement among people with serious mental illness complicates these individuals involvement with the criminal justice system" Wilson explains.

Provided by Case Western Reserve University

"Mental illness protects some inmates from returning to jail." January 17th, 2012. http://medicalxpress.com/news/2012-01-mental-illness-inmates.html

 

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Robert Karl Stonjek

Cell's 'battery' found to play central role in neurodegenerative disease

 

A devastating neurodegenerative disease that first appears in toddlers just as they are beginning to walk has been traced to defects in mitochondria, the 'batteries' or energy-producing power plants of cells.

This finding by researchers at Queen Mary, University of London and Montreal Neurological Institute and Hospital - The Neuro - at McGill University, is published in this week's issue of the Proceedings of the National Academy of Sciences.

The disorder, Autosomal Recessive Spastic Ataxia of Charlevoix-Saguenay (ARSACS), primarily affects the cerebellum, a center for movement coordination in the brain. It was first identified in the late 1970s in a large group of patients from Quebec in Canada.

ARSACS strikes at an early age. Symptoms, which worsen over time, include poor motor coordination, spastic stiffness, distal muscle wasting, uncoordinated eye movements and slurred speech. Most patients with the disease are wheelchair-bound by their early 40s and have a reduced life expectancy. ARSACS is not unique to French-Canada as scientists have now found over 100 separate mutations in people worldwide including, including patients in the UK.

The research significantly increases understanding of the disease and reveals an important common link with other neurodegenerative diseases, providing renewed hope and potential new therapeutic strategies for those affected around the world.

"This finding is the most important discovery about ARSACS since the identification of the mutated gene because it gives an indication of the underlying cellular mechanism of the disease," says Dr Paul Chapple, cell biologist at Queen Mary. He adds: "This work is an essential first step towards developing therapeutic strategies for ARSACS".

In 2000, scientists identified the gene associated with the disease, which produces a massive 4,579 amino acid protein called sacsin, but until now the role of the sacsin protein has been unknown.

The multi-institutional collaborative research led jointly by Dr Paul Chapple at Queen Mary and Dr Bernard Brais and Dr Peter McPherson in Montreal indicates that that the sacsin protein has a mitochondrial function, and that mutations causing the this ataxia are linked to a dysfunction of mitochondria in neurons.

By studying neurons in culture as well as in knockout mice (which do not produce sacsin), the team found that loss of the sacsin protein results in abnormally shaped and poorly functioning mitochondria. In cells mitochondria are constantly fusing together and dividing, with loss of sacsin causing this network to become more interconnected. This disruption led to defective changes in and eventual death of the neurons. In the knockout mice, these disruptions led to neuron death specifically in the cerebellum, suggesting that this is the basis for the neurodegenerative impairments suffered by ARSACS patients.

"Mitochondrial dysfunction has also been identified in major neurodegenerative diseases such as Parkinson, Alzheimer, and Huntington diseases," says Dr McPherson. "This common link means that research being done on a large-scale on these other diseases may prove critically informative to rarer neurological diseases such as ARSACS, and the inverse may be true, our findings may be fundamental to the study and treatment of other neurodegenerative diseases."

Dr Chapple adds: "These links between ARSACS and more common neurodegenerations underline the value of studying rare diseases".

Provided by Queen Mary, University of London

"Cell's 'battery' found to play central role in neurodegenerative disease." January 17th, 2012. http://medicalxpress.com/news/2012-01-cell-battery-central-role-neurodegenerative.html

 

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Robert Karl Stonjek

Planet of the Apes: Survival of the self-promoters

We humans can be a cocky species - so much so that a realistic self-image can be seen as a symptom of trouble.

Take the reaction to a recent survey in which about 52 percent of college students rated their emotional health as below average. About half of them are, after all, going to be below average. But the UCLA researchers who did the survey say it indicates a deeper problem. In past surveys, at least 64 percent of the respondents said they were above average.

What's going on here? Are we truly living in Lake Wobegon, where all the children are above average?

Several scientists blame evolution for our ego-inflating tendencies - call it survival of the self-promoters.

We naturally tend to puff ourselves up and kid ourselves, says Rutgers University evolutionary biologist Robert Trivers. That's because evolution has shaped many organisms into natural-born liars. In his new book, "The Folly of Fools, Trivers lays out a case that we humans are such good liars we even lie to ourselves.

People tend to overrate themselves on looks, smarts, and leadership ability, he says. Academics, he notes, are particularly deluded - in one survey, 94 percent thought they were in the top half of their profession.

Wouldn't a clear-eyed view of reality give us all the best chance for survival? Not necessarily, says Trivers, since much of our success in life and mating hinges on deception. And what better way to improve our powers of deception than to believe our own lies? It's survival of the deluded.

Trivers achieved scientific prominence in the 1970s, when he revolutionized the scientific understanding of altruistic behavior, showing how it can pay off as long as good deeds are reciprocated. He also pioneered the idea that evolution works at the level of individual genes - a concept Richard Dawkins popularized in his breakout best seller "The Selfish Gene."

Trivers starts his book with a discussion about ordinary deception, which happens throughout the natural world. Male sunfish fight over territory to get a mate, but small male sunfish can avoid all that by imitating females. That way, the little male gets to share the favors of a female with a clueless dominant male. Butterflies take on the appearance of toxic species to avoid being eaten without expending the energy of making toxins.

Among primates, the bigger the brain, the greater the tendency to deceive, says Trivers. We're the dishonest apes. Over the eons, it has been to our ancestors' advantage to convince the world they were nicer, prettier, and smarter than they really were.

Believing your own lies makes you more convincing, as long as you don't go overboard to the point that people laugh at you behind your back. Among children, he says, those who score highest on intelligence tests are most likely to lie to themselves and others.

Humans can also work together to magnify self-deception. In his chapter on religion, he notes the obvious problem with all religions that claim to be the one true system of belief about the one true God. They can't all be right.

From his part-time home in Jamaica, Trivers said he sees a blizzard of deception and self-deception in America today. One antidote, he said, is humor, of the type doled out by his favorite television personalities - Jon Stewart and Stephen Colbert.

University of Pennsylvania evolutionary psychologist Rob Kurzban agrees there can be an advantage to self-inflation. He lays out more examples in his book, "Why Everyone Else Is a Hypocrite."

People who have had more than 100 sex partners say they are less likely than the average person to get a sexually transmitted disease, for example, and those who have been hospitalized following serious car crashes rate themselves as good or excellent drivers.

It's ironic, says Kurzban, but we expect people to be systematically wrong when it comes to evaluating themselves.

He, too, blames evolution for clouding our vision. "The social world is competitive," he said. "I want people to think I'm good."

But Kurzban offers a very different explanation. For him, there's no such thing as self-deception because there is no true single self to deceive.

He lays out a picture of the human mind as a collection of different parts, or modules, all working partially independently. Two of those parts can disagree, but neither part is the true self - both are simply components of a whole. Some modules of our brains act as press secretaries, and they tend to believe we're a little better than we really are.

The modules are like apps on an iPhone, he says. They don't necessarily share information, and that can lead to hypocrisy.

The module that judges other people might not be in complete agreement with the part that controls our behavior. So a person might make a snide remark about a friend's weight gain, attributing it to lack of willpower, and the next night eat a pint of ice cream and not notice the inconsistency.

The idea that we're not aware of most of the workings of our own minds goes back at least to Freud, with his emphasis on the drives that are unconscious or subconscious. Kurzban says the idea of a subconscious mind has given way to the more contemporary modular view.

He adds that it may be hard to distinguish self-deception from being wrong. Some people don't hide the truth from themselves - they just don't know it, and they don't know they don't know it.

Trivers says the idea of the mind as a collection of modules has some use, but it has been taken beyond the realm of reason when people start saying there is no self.

Neither Kurzban nor Trivers could explain integrity or how it fits into their different frameworks for understanding the mind. Too bad. That should be the subject of another book.

In "The Folly of Fools," Trivers applies the science of self-deception to science itself, and finds plenty of examples in which people or whole fields were led astray temporarily.

However fallible individual scientists may be, he says, science is a self-correcting process. "Over the long haul ... falsehood has no chance, which is why over time science tends to outstrip competing enterprises."

(c)2012 The Philadelphia Inquirer 
Distributed by MCT Information Services

"Planet of the Apes: Survival of the self-promoters." January 17th, 2012. http://www.physorg.com/news/2012-01-planet-apes-survival-self-promoters.html

 

Posted by
Robert Karl Stonjek