Friday, April 30, 2010
Brain Tumor Awareness Month Fundraiser
May is Brain Tumor Awareness Month, and Channing Hall Charter School is fundraising for the cause.
Tomas Hollenbach, an 8-year-old student at the school, was diagnosed in February with an inoperable tumor on his brain stem. After going through 6 weeks of treatment, his tumor has shrunk but Hollenbach and his family are burdened with many medical expenses that Channing Hall is working to help with, using funds donated from those who appreciate the Hollenbach and his parents' strength throughout the ordeal.
There are a few of things the school is doing to raise money for the family:
Inspire Hope, Take Action: Support Brain Tumor Awareness Month. T-shirts emblazoned with this phrase will be sold at Channing Hall beginning May 5.
Tomas Hollenbach Charitable Account at America First Bank. Anyone can make a donation to Account #9040718.
Finally, Channing Hall is holding a raffle and yard sale at the school on May 22nd. They're still looking for raffle items from local businesses, so if you or anyone you know would be willing to make a donation during National Brain Tumor Awareness Month, don't hesitate.
Most of us are lucky enough not to be affected by brain tumors. We don't even think about something like this happening until it does- which is exemplified by FUTURE Brain Cancer Institute closing its doors in 2008 because of lack of funding. It seems that Utahns may be especially oblivious to this issue affecting over 600,000 people in the U.S., as we currently have no fundraising efforts for Brain Tumor Awareness, while there are annual walks in places like New York, San Francisco, even Delaware.
Appreciate how lucky you are to be unaffected by brain tumors- support Tomas Hollenbach and his family, or even go big for the cause as a whole and organize a walk by visiting the National Brain Tumor Society.
Brain Research to Ameliorate Impaired Neurodevelopment: Home-based Intervention Trial (BRAIN-HIT)
This randomized controlled trial aims to evaluate the effects of an early developmental intervention program on the development of young children in low- and low-middle-income countries who are at risk for neurodevelopmental disability because of birth asphyxia. A group of children without perinatal complications are evaluated in the same protocol to compare the effects of early developmental intervention in healthy infants in the same communities.
Birth asphyxia is the leading specific cause of neonatal mortality in low- and low-middle-income countries and is also the main cause of neonatal and long-term morbidity including mental retardation, cerebral palsy, and other neurodevelopmental disorders. Mortality and morbidity from birth asphyxia disproportionately affect more infants in low- and low-middle-income countries, particularly those from the lowest socioeconomic groups.
There is evidence that relatively inexpensive programs of early developmental intervention, delivered during home visit by parent trainers, are capable of improving neurodevelopment in infants following brain insult due to birth asphyxia.
Methods: This trial is a block-randomized controlled trial that has enrolled 174 children with birth asphyxia and 257 without perinatal complications, comparing early developmental intervention plus health and safety counseling to the control intervention receiving health and safety counseling only, in sites in India, Pakistan, and Zambia. The interventions are delivered in home visits every two weeks by parent trainers from 2 weeks after birth until age 36 months.
The primary outcome of the trial is cognitive development, and secondary outcomes include social-emotional and motor development. Child, parent, and family characteristics and number of home visits completed are evaluated as moderating factors.DiscussionThe trial is supervised by a trial steering committee, and an independent data monitoring committee monitors the trial.
Findings from this trial have the potential to inform about strategies for reducing neurodevelopmental disabilities in at-risk young children in low and middle income countries.Trial Registration: Clinicaltrials.gov NCT00639184
Author: Jan WallanderElizabeth McClureFred BiasiniShivaprasad GoudarOmrana PashaElwyn ChombaDarlene ShearerLinda WrightVanessa ThorstenHrishikesh ChakrabortySangappa DhadedNiranjana MahantshettiRoopa BelladZahid AbbasiWaldemar CarloBRAIN-HIT Investigators
Birth asphyxia is the leading specific cause of neonatal mortality in low- and low-middle-income countries and is also the main cause of neonatal and long-term morbidity including mental retardation, cerebral palsy, and other neurodevelopmental disorders. Mortality and morbidity from birth asphyxia disproportionately affect more infants in low- and low-middle-income countries, particularly those from the lowest socioeconomic groups.
There is evidence that relatively inexpensive programs of early developmental intervention, delivered during home visit by parent trainers, are capable of improving neurodevelopment in infants following brain insult due to birth asphyxia.
Methods: This trial is a block-randomized controlled trial that has enrolled 174 children with birth asphyxia and 257 without perinatal complications, comparing early developmental intervention plus health and safety counseling to the control intervention receiving health and safety counseling only, in sites in India, Pakistan, and Zambia. The interventions are delivered in home visits every two weeks by parent trainers from 2 weeks after birth until age 36 months.
The primary outcome of the trial is cognitive development, and secondary outcomes include social-emotional and motor development. Child, parent, and family characteristics and number of home visits completed are evaluated as moderating factors.DiscussionThe trial is supervised by a trial steering committee, and an independent data monitoring committee monitors the trial.
Findings from this trial have the potential to inform about strategies for reducing neurodevelopmental disabilities in at-risk young children in low and middle income countries.Trial Registration: Clinicaltrials.gov NCT00639184
Author: Jan WallanderElizabeth McClureFred BiasiniShivaprasad GoudarOmrana PashaElwyn ChombaDarlene ShearerLinda WrightVanessa ThorstenHrishikesh ChakrabortySangappa DhadedNiranjana MahantshettiRoopa BelladZahid AbbasiWaldemar CarloBRAIN-HIT Investigators
If this is your brain on drugs, we want no part of drugs
Anyway, it's a disturbing picture of what "Illegal Drugs" might be like. If we were shown this as part of our DARE propaganda, we can't help but think we would have steered far clear of drugs -- not just illegal, but legal as well. Can't be too careful after seeing something like this.
Scientists race to create cat-level artificial brain
Complex task akin to reverse-engineering biological design of the brainPentagon-backed scientists aim to create a human-like machine, at some point. But they are starting out with the goal of crafting artificial intelligence on the level of a cat's brain. Still there are vast challenges.
If they get far enough, however, one scientist says that they could theoretically achieve feline intelligence with a mouse-sized artificial brain and an even smaller body.
That's because bigger brains by themselves don't necessarily mean greater intelligence or more complex behavior — for instance, cats show more smarts than cows despite having a feline brain 10 times smaller than a bovine brain. What might really matter is that humans and some other species have bigger brains for their body size.
"If they're trying to get cat-level behavior, there's no necessary reason to go for a cat-level brain unless they need a cat-level body of some kind," said Mark Changizi, a neurobiologist at Rensselaer Polytechnic Institute in Troy, N.Y. Changizi discussed his idea with an IBM researcher working on the SyNAPSE project run by the U.S. Defense Advanced Research Projects Agency (DARPA). The Pentagon agency has recruited the help of IBM, HP and leading research institutes to try to develop an artificial brain that is approximately cat-like in terms of size, number of brain cells and synapses, anatomical structure and even behavioral complexity.
Such a massive and complicated undertaking could easily falter short of the goal, even if various researchers have begun working on electronic devices that can mimic cat brain cells. Changizi compared the task at hand with trying to reverse-engineer the biological design of the brain and trace its evolution backwards over hundreds or thousands of years.
A mystery of bigger brains
But reservations aside, Changizi does see the small ray of hope for the DARPA project regarding the brain size required to achieve feline intelligence. His observation goes to the heart of what he calls the "big embarrassment of neurobiology," or the scientific uncertainty about why brain sizes scale up
But reservations aside, Changizi does see the small ray of hope for the DARPA project regarding the brain size required to achieve feline intelligence. His observation goes to the heart of what he calls the "big embarrassment of neurobiology," or the scientific uncertainty about why brain sizes scale up
so much in bigger bodies.
"Animals which are a thousand times bigger are just as dumb as the ones that are small," Changizi told LiveScience.
Bigger brains do allow for quantitative rather than qualitative improvements, such as finer resolution, higher sensitivity or greater precision in certain senses. They pack in more neurons, and add even more synapses (connections with other neurons) per neuron to keep all of the brain cells interconnected so that they can send signals to one another.
Bigger brains also tend to have more compartments, where well-connected regions of the brain are located physically close together as a way of minimizing wire costs and neural delay between neurons. But greater intelligence does not seem to depend on having more compartments, more complex wiring or more neurons. To better appreciate the puzzlement among neuroscientists, consider that a large mammal's brain is about a million times bigger than an insect's brain. Yet a survey of behavioral studies showed that mammals only have about two or three times as many behavioral functions compared with insects. Complex social behaviors among ants, bees and other insects also suggest their tiny brains can still pack a lot of behavioral complexity.
Artificial neural networks have even demonstrated that a relatively few neurons can carry out fairly complex cognitive tasks. Insects would likely have evolved over millions of generations to maximize their tiny brains' computing power — something that human scientists have only recently begun trying to recreate.
Boost the brain, shrink the body
Size only matters when an organism has a high brain-body size ratio. In other words, certain species such as humans have relatively big brains for their body size, as compared with the brain-body size ratios of other species. Mammals in particular show a higher number of behaviors when they have bigger brains relative to their body sizes.
Size only matters when an organism has a high brain-body size ratio. In other words, certain species such as humans have relatively big brains for their body size, as compared with the brain-body size ratios of other species. Mammals in particular show a higher number of behaviors when they have bigger brains relative to their body sizes.
Even if neuroscientists don't currently understand the connection with brain-body size ratio, Changizi says that solving the mystery might make the DARPA effort a bit easier. Rather than painstakingly recreating an artificial cat brain, researchers could make smaller artificial brains with even smaller bodies that are still capable of carrying out complex behaviors or tasks.
Changizi speculated that smarter brains might depend upon the diversity of neuron types, or a more efficient division of labor within the mind. But he readily acknowledged that most of the brain remains a mysterious "black box" for scientists.
"Lay people tend to think that we neuroscientists know what we're doing and that we're on the cusp of understanding it all, but that's so far from the truth," Changizi said.
The Talents of a Middle-Aged Brain
After we hit 40, many of us begin to worry about our aging brains. Will we spend our middle years searching for car keys and forgetting names?
The new book “The Secret Life of the Grown-Up Brain: The Surprising Talents of the Middle-Aged Mind,” by Barbara Strauch, has the answers, and the news is surprisingly upbeat. Sure, brains can get forgetful as they get old, but they can also get better with age, reports Ms. Strauch, who is also the health editor at The New York Times. Ms. Strauch, who previously tackled teenage brains in her book “The Primal Teen,” spoke with me this week about aging brains and the people who have them. Here’s our conversation:
The new book “The Secret Life of the Grown-Up Brain: The Surprising Talents of the Middle-Aged Mind,” by Barbara Strauch, has the answers, and the news is surprisingly upbeat. Sure, brains can get forgetful as they get old, but they can also get better with age, reports Ms. Strauch, who is also the health editor at The New York Times. Ms. Strauch, who previously tackled teenage brains in her book “The Primal Teen,” spoke with me this week about aging brains and the people who have them. Here’s our conversation:
Q. After exploring the teenage brain, why did you decide to write a book about grown-ups?
A. Well, I have a middle-aged brain, for one thing. When I would go give talks about “The Primal Teen,” I’d be driven to the airport or back by a middle-aged person, and they’d turn to me and say: “You should do something about my brain. My brain is suddenly horrible. I can’t remember names.” That’s why I started looking into it. I had my own middle-aged issues like going into an elevator and seeing somebody and thinking, “Who are you?”
Q. So what’s the bad news about the middle-aged brain?
A. Obviously, there are issues with short-term memory. There are declines in processing speed and in neurotransmitters, the chemicals in our brain. But as it turns out, modern middle age is from 40 to 65. During this long time in the middle, if we’re relatively healthy our brains may have a few issues, but on balance they’re better than ever during that period.
Q. Do teenage brains and middle-aged brains have much in common?
A. The thing the middle-aged brain shares with the teenage brain is that it’s still developing. It’s not some static blob that is going inextricably downhill. Scientists found that when they watched the brains of teenagers, the brains were expanding and growing and cutting back and shaping themselves, even when the kids are 25 years old. I think for many years scientists just left it at that. They thought that from 25 on, we just get “stupider.” But that’s not true. They’ve found that during this period, the new modern middle age, we’re better at all sorts of things than we were at 20.
Q. So what kinds of things does a middle-aged brain do better than a younger brain?
A. Inductive reasoning and problem solving — the logical use of your brain and actually getting to solutions. We get the gist of an argument better. We’re better at sizing up a situation and reaching a creative solution. They found social expertise peaks in middle age. That’s basically sorting out the world: are you a good guy or a bad guy? Harvard has studied how people make financial judgments. It peaks, and we get the best at it in middle age.
Q. Doesn’t that make sense, since our young adult lives are often marked by bad decisions?
A. I think most of us think that while we make bad decisions in our 20s, we also have the idea that we were the sharpest we ever were when we were in college or graduate school. People think if I tried to go to engineering school or medical school now, I couldn’t do it. Because of these memory problems that happen in middle age, we tend to think of our brains as, on the whole, worse than in our 20s. But on the whole, they’re better.
Q. So what’s happening in middle age that leads to these improvements?
A. What we have by middle age is all sorts of connections and pathways that have been built up in our brain that help us. They know from studies that humans and animals do better if they have a little information about a situation before they encounter it. By middle age we’ve seen a lot. We’ve been there, done that. Our brains are primed to navigate the world better because they’ve been navigating the world better for longer.
There also are some other physical changes that they can see. We used to think we lost 30 percent of our brain cells as we age. But that’s not true. We keep them. That’s probably the most encouraging finding about the physical nature of our brain cells.Q. Is there anything you can do to keep your brain healthy and improve the deficits, like memory problems?
A. There’s a lot of hype in this field in terms of brain improvement. I did set out to find out what actually works and what we know. What we do with our bodies has a huge impact on our brains. Our brains are more like our hearts in that everything you do for your heart is thought to be equally as good or better for your brain. Exercise is the best studied thing you can do to your brain. It increases brain volume, produces new baby brain cells in grownup brains. Even when our muscles contract, it produces growth chemicals. Using your body can help your brain.
Q. What about activities like learning to play an instrument or learning a foreign language?
A. The studies on this are slim. We’ve all been told to do crossword puzzles. Learning a foreign language, walking a different way to work, all that is an effort to make the brain work hard. And it’s true we need to make our brains work hard. One of the most intriguing findings is that if you talk to people who disagree with you, that helps your brain wake up and refine your arguments and shake up the cognitive egg, which is what you want to do.
Q. Do social connections and relationships make a difference in how the brain ages?
A. There is a whole bunch of science about being social and how cognitive function seems to be better if you are social. There is a fascinating study in Miami where they studied people who lived in apartments. Those who had balconies where they could see their neighbors actually aged better cognitively than others. There are a whole bunch of studies like that. People who volunteer and help kids seem to age better and help their brains. We forget how difficult it is to meet, greet and deal with another human being. It’s hard on our brains and good for them.
Q. What was the most surprising thing you learned about the middle-aged brain?
A. The hope I saw from real scientists was surprising. A lot of the myths we think of in terms of middle age, myths that I grew up with, turn out to be based on almost nothing. Things like the midlife crisis or the empty nest syndrome. We’re brought up to think we’ll enter middle age and it will be kind of gloomy. But as scientists look at real people, they find out the contrary. One study of men found that well-being peaked at age 65. Over and over they find that middle age, instead of being a time of depression and decline, is actually a time of being more optimistic overall.
Bret Michaels returns to hospital due to complications from his brain hemorrhage
"Health is a state of complete physical, mental and social well-being, and not merely the absence of disease or infirmity." ~World Health Organization, 1948
What does it take to be hospitalized for massive brain hemorrhaging and seizures one night and then be planning to tour only a little over a month later barring unforeseen complications? A complete devotion and passion for what you love. And that is what Bret Michael's, 47, showed us, until a complication arose, which led him back to the hospital. The mind/body connection, including attitude, desire, devotion, and passion are extremely powerful forces which are believed to aid in more speedy recoveries from physical ailments.
Bret Michael's was the lead singer for the '80s glam-metal "hair band" Poison, a judge on Nashville Star, a reality star headlining the VH1 show "Rock of Love with Bret Michaels", and just recently appeared on "Celebrity Apprentice" working hard to raise money for his charity, the non-profit organization, The American Diabetes Association.
Michael's suffered from a subarachnoid hemorrhage which is a type of bleeding stroke that occurs between the tissues around the brain and the brain itself. Sometimes there is simply no answer to what causes such strokes. Prognoses of this kind of complication depend on amount of bleeding, age, and symptom severity. About 35% of people die when they have a subarachnoid hemorrhage due to an aneurysm because it results in extensive brain damage. Another 15% die within a few weeks because of bleeding from a second rupture. People who survive for 6 months but who do not have surgery for the aneurysm have a 3% chance of another rupture each year.
Michael's responded well to his initial treatment; however, had another rupture and now remains in critical condition in ICU under 24 hour supervision by doctors and medical staff. Sources say that the next 7-10 days will be the most critical as an additional rupture or other complications may arise. We hope for Bret's strong mental attitude to continue to help with a speedy recovery.
Bret had to cancel some shows due to his hospitalization, but still plans to continue his tour on May 26, 2010.
What does it take to be hospitalized for massive brain hemorrhaging and seizures one night and then be planning to tour only a little over a month later barring unforeseen complications? A complete devotion and passion for what you love. And that is what Bret Michael's, 47, showed us, until a complication arose, which led him back to the hospital. The mind/body connection, including attitude, desire, devotion, and passion are extremely powerful forces which are believed to aid in more speedy recoveries from physical ailments.
Bret Michael's was the lead singer for the '80s glam-metal "hair band" Poison, a judge on Nashville Star, a reality star headlining the VH1 show "Rock of Love with Bret Michaels", and just recently appeared on "Celebrity Apprentice" working hard to raise money for his charity, the non-profit organization, The American Diabetes Association.
Michael's suffered from a subarachnoid hemorrhage which is a type of bleeding stroke that occurs between the tissues around the brain and the brain itself. Sometimes there is simply no answer to what causes such strokes. Prognoses of this kind of complication depend on amount of bleeding, age, and symptom severity. About 35% of people die when they have a subarachnoid hemorrhage due to an aneurysm because it results in extensive brain damage. Another 15% die within a few weeks because of bleeding from a second rupture. People who survive for 6 months but who do not have surgery for the aneurysm have a 3% chance of another rupture each year.
Michael's responded well to his initial treatment; however, had another rupture and now remains in critical condition in ICU under 24 hour supervision by doctors and medical staff. Sources say that the next 7-10 days will be the most critical as an additional rupture or other complications may arise. We hope for Bret's strong mental attitude to continue to help with a speedy recovery.
Bret had to cancel some shows due to his hospitalization, but still plans to continue his tour on May 26, 2010.
Bret Michaels’ Doctors Hopeful for a ‘Full Recovery’
The rocker is in “good spirits” after the brain hemorrhage he suffered last week, but doctors say his recovery may take weeks or even months.
bret_michaels.pngBret Michaels’ family, friends and fans breathed a much-awaited sigh of relief when they learned that his condition is slowly improving after undergoing major brain surgery last week.
Doctors for the 47-year-old former Poison front man and top Celebrity Apprentice 3 contender said his recovery will be slow, but that he “is very lucky, as his condition could have been fatal,” his tour manager, Janna Elias told fans on his website, BretMichaels.com on April 27. Due to the severity of the hemorrhage, Michaels continues to remain hospitalized in an intensive care unit in critical but stable condition at an undisclosed hospital, she said.
Despite his ordeal, Michaels is conscious, talking slowly and in good spirits, his rep told People April 28.
Ten days after the Rock of Love star underwent an emergency appendectomy, he was rushed to the hospital again on April 22 with a headache he said felt like getting “hit with a baseball bat again and again,” a source told People earlier this week.
His massive headache came from a subarachnoid hemorrhage, a type of stroke that causes bleeding in the fluid-filled spaces around the base of the brain, wrote Elias. “It presents itself suddenly as the sound of a loud gunshot or thunderclap at the back of the head causing severe cranial pain and muscle spasms,” she said.
With further testing and rehabilitation, she said, doctors “are hopeful that Bret will gradually improve as the blood surrounding the brain dissolves and is reabsorbed into his system, which can be a very painful recovery and take several weeks to months.”
Michaels remains under 24-hour observation in the ICU, but “is in positive spirits,” she wrote. “He is responding well to tests and treatments.”
An Unsettling Complication
Even though Michaels’ condition has stabilized, he faces a new medical setback — seizures caused by a lack of sodium in the body, which is a common side effect from a brain hemorrhage, Elias wrote.
Still, she remains optimistic. “Even though today was a minor setback doctors remain hopeful for a full recovery and plan to release more specific information next Monday,” she said.
While some people are speculating that the stroke may have come after he was struck in the head by a falling piece of the set at the Tony awards last June, he will undergo further tests throughout the week to try to detect the exact cause of the rupture, said Elias. “Coupled with the fact that Michaels is a lifelong Type 1 diabetic and has recently undergone emergency appendectomy surgery while on tour in San Antonio, he will remain monitored closely by his medical team to make sure no complications occur from the diabetes.”
Friends Rally for Their Beloved Pal
Friends of Michaels from around the world have come forth to wish him well. Sharon Osbourne, who has been a friend of the singer’s for 30 years and stars with him on Apprentice, told US Magazine, “It’s devastating, and it makes you feel all these different things. Your heart goes out to his family, your heart goes out to him. He’s the nicest guy in the world. And then you start thinking about your own mortality. You start thinking, ‘Oh my God.’ It just makes you appreciate how lucky we all are.”
Apprentice honcho Donald Trump said on Today that Michaels “would work so hard, maybe harder than anybody else. And he’s doing well.”
Michaels’ longtime friend and guitar player in the Bret Michaels Band, Pete Evick, thanked fans on Michaels website for their outpouring of support, saying “we who are closest to Bret are overwhelmed with the amount of love and well wishes he is receiving. I know that everyone is waiting for some official news, however we just can’t give any right now. This is a time for family, a time for healing and a time for love.”
He praised Michaels for his work ethic, saying “I thought I was a hard worker. I didn’t understand that a man ten years older than me, battling a lifelong war with juvenile diabetes, more fame than most, and more money than he knows what to do with, could possibly get up every day with more drive and passion than myself. I was wrong! I didn’t understand what it meant to be a loyal friend. The kind that would do anything you ever needed without even asking why, what, who or where.
“Bret is the kind of guy that wakes up every day and treats it like it is his first, and may be his last,” he wrote. “He is full of passion, energy and love. But most of all, he is a survivor. Against the odds of a critical music industry, or battling a crippling disease, over and over again Bret has come out on top and ahead of the game. I personally expect nothing less from him in this situation.”
A New Michaels’ Song Released
To thank fans for their support, Evick released a “teaser” from Michael’s upcoming album, Custom Built, on the Web Page Audio portion of Michaels website. Evick released part of a song called “Wasted Time,” which he writes is “full of Bret Michaels’ emotion and heart. While not the final mix, I took some of the vocal we have laid down on the bus during the tour and comped together a piece of NEW MUSIC for you all. I believe all the fans will agree with me that this teaser is an amazing song. I hope you all use it, like I have this week, to remind you how amazing my great friend Bret is.”
bret_michaels.pngBret Michaels’ family, friends and fans breathed a much-awaited sigh of relief when they learned that his condition is slowly improving after undergoing major brain surgery last week.
Doctors for the 47-year-old former Poison front man and top Celebrity Apprentice 3 contender said his recovery will be slow, but that he “is very lucky, as his condition could have been fatal,” his tour manager, Janna Elias told fans on his website, BretMichaels.com on April 27. Due to the severity of the hemorrhage, Michaels continues to remain hospitalized in an intensive care unit in critical but stable condition at an undisclosed hospital, she said.
Despite his ordeal, Michaels is conscious, talking slowly and in good spirits, his rep told People April 28.
Ten days after the Rock of Love star underwent an emergency appendectomy, he was rushed to the hospital again on April 22 with a headache he said felt like getting “hit with a baseball bat again and again,” a source told People earlier this week.
His massive headache came from a subarachnoid hemorrhage, a type of stroke that causes bleeding in the fluid-filled spaces around the base of the brain, wrote Elias. “It presents itself suddenly as the sound of a loud gunshot or thunderclap at the back of the head causing severe cranial pain and muscle spasms,” she said.
With further testing and rehabilitation, she said, doctors “are hopeful that Bret will gradually improve as the blood surrounding the brain dissolves and is reabsorbed into his system, which can be a very painful recovery and take several weeks to months.”
Michaels remains under 24-hour observation in the ICU, but “is in positive spirits,” she wrote. “He is responding well to tests and treatments.”
An Unsettling Complication
Even though Michaels’ condition has stabilized, he faces a new medical setback — seizures caused by a lack of sodium in the body, which is a common side effect from a brain hemorrhage, Elias wrote.
Still, she remains optimistic. “Even though today was a minor setback doctors remain hopeful for a full recovery and plan to release more specific information next Monday,” she said.
While some people are speculating that the stroke may have come after he was struck in the head by a falling piece of the set at the Tony awards last June, he will undergo further tests throughout the week to try to detect the exact cause of the rupture, said Elias. “Coupled with the fact that Michaels is a lifelong Type 1 diabetic and has recently undergone emergency appendectomy surgery while on tour in San Antonio, he will remain monitored closely by his medical team to make sure no complications occur from the diabetes.”
Friends Rally for Their Beloved Pal
Friends of Michaels from around the world have come forth to wish him well. Sharon Osbourne, who has been a friend of the singer’s for 30 years and stars with him on Apprentice, told US Magazine, “It’s devastating, and it makes you feel all these different things. Your heart goes out to his family, your heart goes out to him. He’s the nicest guy in the world. And then you start thinking about your own mortality. You start thinking, ‘Oh my God.’ It just makes you appreciate how lucky we all are.”
Apprentice honcho Donald Trump said on Today that Michaels “would work so hard, maybe harder than anybody else. And he’s doing well.”
Michaels’ longtime friend and guitar player in the Bret Michaels Band, Pete Evick, thanked fans on Michaels website for their outpouring of support, saying “we who are closest to Bret are overwhelmed with the amount of love and well wishes he is receiving. I know that everyone is waiting for some official news, however we just can’t give any right now. This is a time for family, a time for healing and a time for love.”
He praised Michaels for his work ethic, saying “I thought I was a hard worker. I didn’t understand that a man ten years older than me, battling a lifelong war with juvenile diabetes, more fame than most, and more money than he knows what to do with, could possibly get up every day with more drive and passion than myself. I was wrong! I didn’t understand what it meant to be a loyal friend. The kind that would do anything you ever needed without even asking why, what, who or where.
“Bret is the kind of guy that wakes up every day and treats it like it is his first, and may be his last,” he wrote. “He is full of passion, energy and love. But most of all, he is a survivor. Against the odds of a critical music industry, or battling a crippling disease, over and over again Bret has come out on top and ahead of the game. I personally expect nothing less from him in this situation.”
A New Michaels’ Song Released
To thank fans for their support, Evick released a “teaser” from Michael’s upcoming album, Custom Built, on the Web Page Audio portion of Michaels website. Evick released part of a song called “Wasted Time,” which he writes is “full of Bret Michaels’ emotion and heart. While not the final mix, I took some of the vocal we have laid down on the bus during the tour and comped together a piece of NEW MUSIC for you all. I believe all the fans will agree with me that this teaser is an amazing song. I hope you all use it, like I have this week, to remind you how amazing my great friend Bret is.”
Q: Is pregnancy brain a myth?
A: Probably. Research suggests pregnant women are no more forgetful than other women.
It's always been considered part and parcel of pregnancy, along with a swollen belly, varicose veins and food cravings. It' s so-called 'pregnancy brain' (sometimes called 'placenta brain' or 'mumnesia'); a pattern of woolly thinking and the forgetfulness that seems to accompany pregnancy.
Many pregnant women believe they experience it, which is not surprising given that most pregnancy books and manuals warn them to expect it.
Some people say 'pregnancy brain' is caused by high levels of oestrogen and other sex hormones during pregnancy – one theory even suggests it's an evolutionary development that allows a pregnant woman to become oblivious of outside distractions, so she can focus on the all-important task of preparing for the birth.
But is there any evidence for pregnancy brain?
Often women think they have poor memory, yet objective tests show their memory is perfectly normal, she says.
Christensen and other Australian researchers concluded this after studying 1,241 women over an eight-year period. The researchers took a random sample of women from the electoral roll, aged 20 to 24 at the beginning of the study, and followed them up over time, watching to see who got pregnant. (Of the 1,241 women, 76 were pregnant when they had their first interview, 188 became mothers during the study – but were not pregnant during the first interview – and another 542 didn't get pregnant. The rest were dropped from the study for a variety of reasons).
All the women were given standard tests of mental ability to see how well they could recall and repeat words and numbers. The pregnant women were given tests before, during and after their pregnancies; and their results were compared to the test results of the women who didn't become pregnant.
The researchers found no essential differences between pregnant versus non-pregnant women. Some women in late pregnancy appeared to take longer to do a speed task, but the researchers say this effect might not be real and it needs to be further investigated before it can be confirmed.
Their overall conclusion was that 'pregnancy brain' has no basis in fact.
Christensen thinks it may be that these women, especially in the later stages of pregnancy and after childbirth, simply have a lot on their mind. So what appears to be poor memory could be just a proneness to distraction, as the women ponder the tasks that lie ahead. (However, the study didn't actually test this hypothesis).
Also, some pregnant women are prone to anxiety and depression. Both these conditions can affect memory regardless of whether you are pregnant or not, Christensen says.
Another possible explanation is sleep deprivation – a common complaint throughout pregnancy and the early years of motherhood. Sleep deprivation is known to contribute to forgetfulness, in men as well as women.
And for some women, the expectation of poor memory may become self-fulfilling, says Christensen. These women believe pregnancy brain is a normal part of pregnancy, so they look for signs that they are experiencing it.
So women don't need to plan their nine-month odyssey on the expectation of a foggy mental state. That's the good news.
The bad news: pregnant women who don't want to be pestered may no longer have the excuse of pregnancy brain. Although they still have plenty of other excuses – fatigue, swollen feet, indigestion…
Dr Helen Christensen is the director of the Centre for Mental Health Research, at the Australian National University in Canberra. She spoke to Peter Lavelle.
Have your say
What's been your experience of 'pregnancy brain'? Did you, or someone you know, have problems remembering things? Have your say on the messageboard below.
Conditions of Use
Conditions of Use
Many pregnant women believe they experience it, which is not surprising given that most pregnancy books and manuals warn them to expect it.
Some people say 'pregnancy brain' is caused by high levels of oestrogen and other sex hormones during pregnancy – one theory even suggests it's an evolutionary development that allows a pregnant woman to become oblivious of outside distractions, so she can focus on the all-important task of preparing for the birth.
But is there any evidence for pregnancy brain?
No basis in fact
New research suggests not, says Professor Helen Christensen, director of the Centre for Mental Health Research at the Australian National University.Often women think they have poor memory, yet objective tests show their memory is perfectly normal, she says.
Christensen and other Australian researchers concluded this after studying 1,241 women over an eight-year period. The researchers took a random sample of women from the electoral roll, aged 20 to 24 at the beginning of the study, and followed them up over time, watching to see who got pregnant. (Of the 1,241 women, 76 were pregnant when they had their first interview, 188 became mothers during the study – but were not pregnant during the first interview – and another 542 didn't get pregnant. The rest were dropped from the study for a variety of reasons).
All the women were given standard tests of mental ability to see how well they could recall and repeat words and numbers. The pregnant women were given tests before, during and after their pregnancies; and their results were compared to the test results of the women who didn't become pregnant.
The researchers found no essential differences between pregnant versus non-pregnant women. Some women in late pregnancy appeared to take longer to do a speed task, but the researchers say this effect might not be real and it needs to be further investigated before it can be confirmed.
Their overall conclusion was that 'pregnancy brain' has no basis in fact.
A myth explained
So why then do so many pregnant women believe they are foggy-brained?Christensen thinks it may be that these women, especially in the later stages of pregnancy and after childbirth, simply have a lot on their mind. So what appears to be poor memory could be just a proneness to distraction, as the women ponder the tasks that lie ahead. (However, the study didn't actually test this hypothesis).
Also, some pregnant women are prone to anxiety and depression. Both these conditions can affect memory regardless of whether you are pregnant or not, Christensen says.
Another possible explanation is sleep deprivation – a common complaint throughout pregnancy and the early years of motherhood. Sleep deprivation is known to contribute to forgetfulness, in men as well as women.
And for some women, the expectation of poor memory may become self-fulfilling, says Christensen. These women believe pregnancy brain is a normal part of pregnancy, so they look for signs that they are experiencing it.
So women don't need to plan their nine-month odyssey on the expectation of a foggy mental state. That's the good news.
The bad news: pregnant women who don't want to be pestered may no longer have the excuse of pregnancy brain. Although they still have plenty of other excuses – fatigue, swollen feet, indigestion…
Dr Helen Christensen is the director of the Centre for Mental Health Research, at the Australian National University in Canberra. She spoke to Peter Lavelle.
'Cyborg brain op gives Barry new lease of life
A PARKINSON’S sufferer has told how a miracle operation has transformed his life – allowing him to ditch his wheelchair and become a healthy sportsman.
Grandfather Barry Salter, 61, was struck down with neurological disorder Parkinson’s at the age of 48 and could not wash, dress or feed himself.
He was confined to a wheelchair and had to down a cocktail of 20 different pills a day to combat crippling aches and pains and symptoms including hallucinations and anxiety.
But thanks to a revolutionary “brain pacemaker” fitted by surgeons in an eight-hour operation, Barry’s life has been turned around.
He now goes to the gym twice a week, practises martial arts, swims and plays table tennis regularly.
Barry has even been able to make two trips across the globe to visit friends in Australia, whom he thought he would never see again.
Delighted Barry compared himself to Star Trek creatures “the Borg” and said the Deep Brain Stimulator operation could transform the lives of thousands of fellow sufferers in the UK.
The former health service manager from Newmarket said: “Parkinson’s is like an insidious disease, it creeps up on you and gets worse.
“My movement deteriorated, I wasn’t sleeping, I was anxious, suffering aches and pains and hallucinations and had to give up work.
“It had a devastating effect. It got so bad I had a wheelchair. I was only in my 50s.”
But neurologist Dr Graham Lennox, of Newmarket Hospital, provided a lifeline by recommending the Deep Brain Stimulator (DBS) operation.
During specialist surgery at the National Hospital for Neurology and Neurosurgery in London, four electrodes, in the form of 5in-long titanium rods, were placed inside his brain.
The brain pacemaker sends electrical impulses into the titanium electrodes and alleviates symptoms of Parkinson’s.
Now Barry carries a remote control to regulate how much voltage the pacemaker administers to his brain.
He said: “I feel like the Borg from Star Trek. Now I work out in the gym twice a week and do tai chi as well.”
The rods and wires mean Barry cannot walk through airport security scanners and was once quizzed by staff at Next, in Cambridge, after setting off the door alarms.
Barry said the operation in 2005 meant he could look forward to enjoying life again with his wife Sheila, 60.
Dr Keiran Breen, director of research and development at Parkinson’s UK, said the operation was clearly a success and should be made available to more sufferers.
Creativity, the Brain, and Evolution
Creativity: Adaptation or a byproduct of increased intelligence?
We humans are a creative species. When we compare what we do and make with what other species do and make, it is self-evident that we are the most creative species. But what has the role of creativity been over the course of our evolution? Is it just a by-product, an emergent property, of more fundamental cognitive processes, such as those involving problem-solving ability, memory, language, attention, and so on? Or is creativity a distinct and identifiable cognitive process of its own, which varies from individual-to-individual? Heritable genetic variation is the raw material on which natural selection works, so assessing the plausibility of creativity as an important human adaptation depends on understanding variation at both the genetic and neuroanatomical levels.
Psychologists have studied creativity for decades, developing a variety of tests to assess creativity and creative potential in individuals. Using these tests to guide them, cognitive neuroscientists are now using sophisticated neuroimaging tools to assess the neuroanatomical differences between more-creative and less-creative individuals, with the hopes of developing an understanding of creativity from the bottom-up, so to speak. If we are ever to understand creativity in an evolutionary perspective, then we must be able to link the extraordinary painting or inspired insight to the brain structures from which they sprang. This may sound unduly reductionist and coldly scientific to some (you know who you are), but understanding creativity should not make us appreciate it any less. I think it's safe to say that scientists who devote their time and energy to studying creativity probably have as deep an appreciation for the creative process and its results as anyone.
In the 1970s, based on studies of split-brain patients, the idea that the right hemisphere "controlled" creativity became very popular, especially in the public's imagination. This model is now considered overly simplistic; Alice Flaherty (2005, Journal of Comparative Neurology 493:147-153) has provided us with an updated model for the neurological control of creativity, based on research from neuroimaging, lesion analysis, and the effects of drugs. She begins with a definition (p. 147): "A creative idea will be defined simply as one that is both novel and useful (or influential) in a particular social setting." She is concerned that any neurological model of creativity should focus not just on artistic outlets (such as painting and music) but encompass other domains, such as language and mathematics. Such a model is necessarily going to have to involve a network of brain regions, rather than be localized to one part of the brain or one hemisphere. Flaherty proposes first that cortical interactions between the temporal and frontal lobes are critical for regulating creative expression. Temporal lobe deficits can increase the generation of creative ideas, sometimes at the expense of quality, as in various manic states. In contrast, frontal lobe deficits can inhibit creative thinking. Thus via mutually inhibitory pathways, the frontal and temporal lobes work together to not simply generate ideas but those that are "novel and useful"--creative ideas.
In addition to the fronto-temporal network, another brain system is also critical for creative expression: the dopamine pathways of the subcortical limbic system (which also have strong connections to parts of the frontal lobe). Being creative is not a passive process, and creative people are more responsive to sensory stimulation, have higher baseline levels of arousal, and increased goal-directed behavior. In Flaherty's model, people vary in terms of their level of creative drive according to the activity of the dopamine pathways of the limbic system. Dopamine mediates reward-seeking behavior and appreciation for music and beautiful faces--Flaherty suggests that creative motivation also originates in these dopaminergic pathways. The evidence for the involvement in dopamine in creativity comes primarily from drug studies: dopamine agonists (such as cocaine and levodopa) heighten arousal and goal-seeking behaviors while dopamine antagonists (such as antipsychotics) can shut down the free associations that may be necessary for creativity.
Flaherty's model is presented quite clearly and succinctly, and I recommend her paper to anyone as a starting point in exploring the brain and creativity. A couple of papers have been published recently that are clearly relevant to the model. First, Rex Jung and his colleagues (2010, Human Brain Mapping 31:398-409) looked at the correlation between creativity and regional cortical thickness in a group of 61 young adult men and women. They assessed creativity using an instrument called the Creative Achievement Questionnaire, which assesses creativity in ten different domains (e.g., visual arts, music, etc.); in addition, divergent thinking was tested using a variety of design tasks, with the results consensually assessed by raters into a "composite creativity index." Magnetic resonance images of the subjects' brains were compared to one another, and an automated program was used to look at the correlation between the various creative measures and the cortical thickness (the surface gray matter) of the subjects' brains.
Jung and colleagues found several brain regions in which cortical thickness showed statistically significant correlations with performance on these tests of creativity and divergent thinking. These regions were in both hemispheres and included parts of the frontal lobe, and regions on the border between the temporal and occipital/parietal lobes. Without worrying too much about the specific regions here, these results strongly suggest that creativity in the brain does not depend on a specific region or hemisphere but on a dispersed network of brain regions. This is consistent with Flaherty's model, although the regions involved were not all predicted by that model. Furthermore, not all of the statistical associations identified by Jung and colleagues were positive. Composite creative index (CCI) scores were positively correlated with increased thickness in the right posterior cingulate cortex (this is the cortex that surrounds the corpus callosum on the medial surface of the hemisphere, near the medial portion of the frontal lobe); however, CCI scores were negatively correlated with cortical thickness in the left lingual gyrus (another medial surface structure located close to the boundary between the occipital and temporal lobes). Obviously, these results do not support a simple more-is-better model; however, they are consistent with aspects of the Flaherty model, which posits that creativity results in part from mutually inhibitory interactions between parts of the frontal and temporal lobes.
Another paper using a similar methodology sheds some light on the association between the size of dopamine-rich regions of the brain and creativity. In this study by Hikaru Takeuchi and colleagues (2010, NeuroImage 51:575-585), regional brain volume (assessed from MRIs using an automated program) was correlated with performance on a test of creativity and divergent thinking (the S-A creativity test). They found strong associations between performance on this test and larger gray matter volume in dopamine-rich subcortical regions such as the substantia nigra and other fronto-striatal regions; in addition, a portion of the right dorsolateral prefrontal cortex was also correlated with higher creative test performance. Takeuchi and colleagues see their results as supporting the important role of dopamine in creative thinking, but they also stress that this is in the context of a more expansive brain network.
From an evolutionary perspective, these studies provide a couple of potential insights. First, there is clearly quantitative individual variation in creativity that is associated with neuroanatomical variation. Of course, we do not know if this is due to genetics or the environment, but it gets us a step closer to understanding the material basis of creativity, which is an important first step. Second, both studies show that performance on these tests of creativity were largely independent of performance on basic intelligence tests (with the caveat that the subjects were mostly college students with above average in intelligence). Both intelligence (in the IQ test sense) and creativity appear to be the products of widely distributed functional networks in the brain, which are at least partly independent of one another. This leaves open the possibility that creativity, in evolutionary terms, is not simply an emergent property of increased intelligence.
We humans are a creative species. When we compare what we do and make with what other species do and make, it is self-evident that we are the most creative species. But what has the role of creativity been over the course of our evolution? Is it just a by-product, an emergent property, of more fundamental cognitive processes, such as those involving problem-solving ability, memory, language, attention, and so on? Or is creativity a distinct and identifiable cognitive process of its own, which varies from individual-to-individual? Heritable genetic variation is the raw material on which natural selection works, so assessing the plausibility of creativity as an important human adaptation depends on understanding variation at both the genetic and neuroanatomical levels.
Psychologists have studied creativity for decades, developing a variety of tests to assess creativity and creative potential in individuals. Using these tests to guide them, cognitive neuroscientists are now using sophisticated neuroimaging tools to assess the neuroanatomical differences between more-creative and less-creative individuals, with the hopes of developing an understanding of creativity from the bottom-up, so to speak. If we are ever to understand creativity in an evolutionary perspective, then we must be able to link the extraordinary painting or inspired insight to the brain structures from which they sprang. This may sound unduly reductionist and coldly scientific to some (you know who you are), but understanding creativity should not make us appreciate it any less. I think it's safe to say that scientists who devote their time and energy to studying creativity probably have as deep an appreciation for the creative process and its results as anyone.
In the 1970s, based on studies of split-brain patients, the idea that the right hemisphere "controlled" creativity became very popular, especially in the public's imagination. This model is now considered overly simplistic; Alice Flaherty (2005, Journal of Comparative Neurology 493:147-153) has provided us with an updated model for the neurological control of creativity, based on research from neuroimaging, lesion analysis, and the effects of drugs. She begins with a definition (p. 147): "A creative idea will be defined simply as one that is both novel and useful (or influential) in a particular social setting." She is concerned that any neurological model of creativity should focus not just on artistic outlets (such as painting and music) but encompass other domains, such as language and mathematics. Such a model is necessarily going to have to involve a network of brain regions, rather than be localized to one part of the brain or one hemisphere. Flaherty proposes first that cortical interactions between the temporal and frontal lobes are critical for regulating creative expression. Temporal lobe deficits can increase the generation of creative ideas, sometimes at the expense of quality, as in various manic states. In contrast, frontal lobe deficits can inhibit creative thinking. Thus via mutually inhibitory pathways, the frontal and temporal lobes work together to not simply generate ideas but those that are "novel and useful"--creative ideas.
In addition to the fronto-temporal network, another brain system is also critical for creative expression: the dopamine pathways of the subcortical limbic system (which also have strong connections to parts of the frontal lobe). Being creative is not a passive process, and creative people are more responsive to sensory stimulation, have higher baseline levels of arousal, and increased goal-directed behavior. In Flaherty's model, people vary in terms of their level of creative drive according to the activity of the dopamine pathways of the limbic system. Dopamine mediates reward-seeking behavior and appreciation for music and beautiful faces--Flaherty suggests that creative motivation also originates in these dopaminergic pathways. The evidence for the involvement in dopamine in creativity comes primarily from drug studies: dopamine agonists (such as cocaine and levodopa) heighten arousal and goal-seeking behaviors while dopamine antagonists (such as antipsychotics) can shut down the free associations that may be necessary for creativity.
Flaherty's model is presented quite clearly and succinctly, and I recommend her paper to anyone as a starting point in exploring the brain and creativity. A couple of papers have been published recently that are clearly relevant to the model. First, Rex Jung and his colleagues (2010, Human Brain Mapping 31:398-409) looked at the correlation between creativity and regional cortical thickness in a group of 61 young adult men and women. They assessed creativity using an instrument called the Creative Achievement Questionnaire, which assesses creativity in ten different domains (e.g., visual arts, music, etc.); in addition, divergent thinking was tested using a variety of design tasks, with the results consensually assessed by raters into a "composite creativity index." Magnetic resonance images of the subjects' brains were compared to one another, and an automated program was used to look at the correlation between the various creative measures and the cortical thickness (the surface gray matter) of the subjects' brains.
Jung and colleagues found several brain regions in which cortical thickness showed statistically significant correlations with performance on these tests of creativity and divergent thinking. These regions were in both hemispheres and included parts of the frontal lobe, and regions on the border between the temporal and occipital/parietal lobes. Without worrying too much about the specific regions here, these results strongly suggest that creativity in the brain does not depend on a specific region or hemisphere but on a dispersed network of brain regions. This is consistent with Flaherty's model, although the regions involved were not all predicted by that model. Furthermore, not all of the statistical associations identified by Jung and colleagues were positive. Composite creative index (CCI) scores were positively correlated with increased thickness in the right posterior cingulate cortex (this is the cortex that surrounds the corpus callosum on the medial surface of the hemisphere, near the medial portion of the frontal lobe); however, CCI scores were negatively correlated with cortical thickness in the left lingual gyrus (another medial surface structure located close to the boundary between the occipital and temporal lobes). Obviously, these results do not support a simple more-is-better model; however, they are consistent with aspects of the Flaherty model, which posits that creativity results in part from mutually inhibitory interactions between parts of the frontal and temporal lobes.
Another paper using a similar methodology sheds some light on the association between the size of dopamine-rich regions of the brain and creativity. In this study by Hikaru Takeuchi and colleagues (2010, NeuroImage 51:575-585), regional brain volume (assessed from MRIs using an automated program) was correlated with performance on a test of creativity and divergent thinking (the S-A creativity test). They found strong associations between performance on this test and larger gray matter volume in dopamine-rich subcortical regions such as the substantia nigra and other fronto-striatal regions; in addition, a portion of the right dorsolateral prefrontal cortex was also correlated with higher creative test performance. Takeuchi and colleagues see their results as supporting the important role of dopamine in creative thinking, but they also stress that this is in the context of a more expansive brain network.
From an evolutionary perspective, these studies provide a couple of potential insights. First, there is clearly quantitative individual variation in creativity that is associated with neuroanatomical variation. Of course, we do not know if this is due to genetics or the environment, but it gets us a step closer to understanding the material basis of creativity, which is an important first step. Second, both studies show that performance on these tests of creativity were largely independent of performance on basic intelligence tests (with the caveat that the subjects were mostly college students with above average in intelligence). Both intelligence (in the IQ test sense) and creativity appear to be the products of widely distributed functional networks in the brain, which are at least partly independent of one another. This leaves open the possibility that creativity, in evolutionary terms, is not simply an emergent property of increased intelligence.
A computer isn’t a replacement for your brain
As part of one of our research projects, one of my students has just acquired a set of tiny electrodes, set into plastic in a grid-like pattern. We’ll use this array to measure the electrical conductivity of various fluids. We don’t need 60 electrodes, about 4 would do nicely, but the particular company concerned makes the electrode arrays like this, so that’s what we’ve got. My student asked the reasonable question of whether the presence of the unused electrodes would significantly change the electric fields set up by the 4 that we would be using – i.e. would it significantly affect our measurements of conductivity.
Well, a metal electrode, even one not connected to anything, isn’t fluid, so yes, there would be some effect, but how big? Is it one we need to worry about? I suggested he use a piece of computer software we have to ‘model’ this situation – let the computer find what the electric fields look like with all the redundant electrodes present and see.
Easier said than done. Poor student devoted last Saturday to the task, which was unsuccessful. The software seems to be playing up. So I said that I’d have a good look at his work and see if I could work out what was going on. So yesterday morning, I basically pulled apart the computer model he had made and reconstructed it again, making sure everything was correct. And, bingo, the software ran, solved the problem, and gave me some lovely pictorial representations of the electric fields around these tiny electrodes.
Problem solved? Well, no. Because at this point I start applying my brain to the problem, and ask whether the solution (as pretty as it is) looks physically reasonable. What do I mean by that? Well, I know that electric field lines travel from high potential to low potential. They hit good conductors at normal incidence to the conductor. Where there is a field in a conductor, currents are going to flow. And so on. And looking carefully at the solution the computer gave me, I could see that in one aspect it didn’t look right. All my extra electrodes seemed to have magically earthed themselves. Why? I have no idea. I’ve trawled through the model and can’t find anywhere where I’ve told the computer that these things are earthed. I just don’t know at the moment what’s going on.
But, here is my point (at last, I hear you say). If I just assumed the output from the computer programme was ‘right’, I’d have been making a big mistake. A computer programme, no matter how much it costs, always has to be run in parallel with your brain. You’ve got to ask yourself whether the output looks physically reasonable before you go and do anything with it, especially things that could prove expensive if you get it wrong. I’m glad I took the time to do this, before giving my already overworked student duff results.
Well, a metal electrode, even one not connected to anything, isn’t fluid, so yes, there would be some effect, but how big? Is it one we need to worry about? I suggested he use a piece of computer software we have to ‘model’ this situation – let the computer find what the electric fields look like with all the redundant electrodes present and see.
Easier said than done. Poor student devoted last Saturday to the task, which was unsuccessful. The software seems to be playing up. So I said that I’d have a good look at his work and see if I could work out what was going on. So yesterday morning, I basically pulled apart the computer model he had made and reconstructed it again, making sure everything was correct. And, bingo, the software ran, solved the problem, and gave me some lovely pictorial representations of the electric fields around these tiny electrodes.
Problem solved? Well, no. Because at this point I start applying my brain to the problem, and ask whether the solution (as pretty as it is) looks physically reasonable. What do I mean by that? Well, I know that electric field lines travel from high potential to low potential. They hit good conductors at normal incidence to the conductor. Where there is a field in a conductor, currents are going to flow. And so on. And looking carefully at the solution the computer gave me, I could see that in one aspect it didn’t look right. All my extra electrodes seemed to have magically earthed themselves. Why? I have no idea. I’ve trawled through the model and can’t find anywhere where I’ve told the computer that these things are earthed. I just don’t know at the moment what’s going on.
But, here is my point (at last, I hear you say). If I just assumed the output from the computer programme was ‘right’, I’d have been making a big mistake. A computer programme, no matter how much it costs, always has to be run in parallel with your brain. You’ve got to ask yourself whether the output looks physically reasonable before you go and do anything with it, especially things that could prove expensive if you get it wrong. I’m glad I took the time to do this, before giving my already overworked student duff results.
Sex hormones control masculinization
A new study has uncovered some information about how sex hormones control masculinization of the brain during development and drive gender related behaviors in adult males.
Published by Cell Press in the April 29 issue of the journal Neuron , the study demonstrates that direct action of testosterone, the prototypical male hormone, is unnecessary for masculinizing the brain and behavior.
Testosterone and estrogen are thought to play an essential role in organizing and activating gender-specific patterns of behavior in sexually reproducing animals.
Testosterone is produced by the testes and directly activates the androgen receptor (AR) in target tissues such as muscle. Estrogen is produced by the ovaries and is nearly undetectable in the circulation of males of most species. However, circulating testosterone in males can be converted into estrogen in the brain, and this testosterone-derived estrogen has been shown to control many male behaviors.
"It was known that testosterone and estrogen are essential for typical male behaviors in many vertebrate species," explains the study's senior author, Dr. Nirao M. Shah from the Department of Anatomy at the University of California, San Francisco. "However, how these two hormones interact to control masculinization of the brain and behavior remained to be established."
Dr. Shah and colleagues found that during the neonatal testosterone surge there is very little AR expressed in the developing brain, making it unlikely that testosterone signaling via AR plays a major role in masculinizing neural pathways. Importantly, they went on to show that the male pattern of AR expression in the brain was dependent on testosterone-derived estrogen signaling.
The researchers then used a genetic approach to knock out the AR in the mouse nervous system and observed that these mutants still exhibited male type mating, fighting, and territorial marking behaviours.
However, these mutant males had striking reductions in specific components of these masculine behaviors.
These results show that testosterone signaling via AR does not control masculine differentiation of the brain and behavior but regulates the frequency and extent of male typical behaviors.
"Our findings in conjunction with previous work suggest a model for the control of male pattern behaviors in which estrogen masculinizes the neural circuits for mating, fighting, and territory marking, and testosterone and estrogen signaling generate the male typical levels of these behaviors," concludes Dr. Shah. "It will be interesting in future studies to identify the molecular and circuit level mechanisms that are controlled by these hormones."
Published by Cell Press in the April 29 issue of the journal Neuron , the study demonstrates that direct action of testosterone, the prototypical male hormone, is unnecessary for masculinizing the brain and behavior.
Testosterone and estrogen are thought to play an essential role in organizing and activating gender-specific patterns of behavior in sexually reproducing animals.
Testosterone is produced by the testes and directly activates the androgen receptor (AR) in target tissues such as muscle. Estrogen is produced by the ovaries and is nearly undetectable in the circulation of males of most species. However, circulating testosterone in males can be converted into estrogen in the brain, and this testosterone-derived estrogen has been shown to control many male behaviors.
"It was known that testosterone and estrogen are essential for typical male behaviors in many vertebrate species," explains the study's senior author, Dr. Nirao M. Shah from the Department of Anatomy at the University of California, San Francisco. "However, how these two hormones interact to control masculinization of the brain and behavior remained to be established."
Dr. Shah and colleagues found that during the neonatal testosterone surge there is very little AR expressed in the developing brain, making it unlikely that testosterone signaling via AR plays a major role in masculinizing neural pathways. Importantly, they went on to show that the male pattern of AR expression in the brain was dependent on testosterone-derived estrogen signaling.
The researchers then used a genetic approach to knock out the AR in the mouse nervous system and observed that these mutants still exhibited male type mating, fighting, and territorial marking behaviours.
However, these mutant males had striking reductions in specific components of these masculine behaviors.
These results show that testosterone signaling via AR does not control masculine differentiation of the brain and behavior but regulates the frequency and extent of male typical behaviors.
"Our findings in conjunction with previous work suggest a model for the control of male pattern behaviors in which estrogen masculinizes the neural circuits for mating, fighting, and territory marking, and testosterone and estrogen signaling generate the male typical levels of these behaviors," concludes Dr. Shah. "It will be interesting in future studies to identify the molecular and circuit level mechanisms that are controlled by these hormones."
Energy drinks start their kick as soon as they touch your tongue
London, Apr 30 (ANI): Energy drinks starting their “kick work” as soon as they touch your tongue, concludes a new study.
In the study, Nicholas Gant at the University of Auckland in New Zealand and team had 16 participants tire out their biceps by flexing them for 11 minutes before rinsing their mouths with either a carbohydrate drink or a non-calorific, taste-matched one.
“One second after rinsing, the team applied transcranial magnetic stimulation to the participants’ scalps, which aided the detection of activity in the motor cortex, a brain area known to send signals to biceps.
“The team found that the volunteers who swilled with carbohydrates were able to flex with more force immediately afterwards, and had a 30 per cent stronger neural response compared with those given placebo,” reports New Scientist.
The study has been published in Brain Research.
In the study, Nicholas Gant at the University of Auckland in New Zealand and team had 16 participants tire out their biceps by flexing them for 11 minutes before rinsing their mouths with either a carbohydrate drink or a non-calorific, taste-matched one.
“One second after rinsing, the team applied transcranial magnetic stimulation to the participants’ scalps, which aided the detection of activity in the motor cortex, a brain area known to send signals to biceps.
“The team found that the volunteers who swilled with carbohydrates were able to flex with more force immediately afterwards, and had a 30 per cent stronger neural response compared with those given placebo,” reports New Scientist.
The study has been published in Brain Research.
Use the arts to fight early Alzheimer's
For 5.3 million Americans and their families and friends, Alzheimer’s disease is life-altering.
Although the duration of early Alzheimer’s varies, whatever time one has left still can be enjoyed, says Deborah Mitchell, author of How to Live Well With Early Alzheimer’s. A few examples:
View art. Researchers say art has a positive effect on emotions and can reduce aggression, agitation, apathy and anxiety. At galleries, let paintings “evoke whatever memories come up.” Doing art projects at home can improve hand-eye coordination and stimulate neuron activity in the brain.
Play music. Music can relax patients. Songs they enjoyed in the past can foster conversation.
Dance. Lessons can “provide physical exercise, increase the level of brain chemicals that stimulate nerve cells to grow and help some people recall forgotten memories when they dance to music they used to know.”
Although the duration of early Alzheimer’s varies, whatever time one has left still can be enjoyed, says Deborah Mitchell, author of How to Live Well With Early Alzheimer’s. A few examples:
View art. Researchers say art has a positive effect on emotions and can reduce aggression, agitation, apathy and anxiety. At galleries, let paintings “evoke whatever memories come up.” Doing art projects at home can improve hand-eye coordination and stimulate neuron activity in the brain.
Play music. Music can relax patients. Songs they enjoyed in the past can foster conversation.
Dance. Lessons can “provide physical exercise, increase the level of brain chemicals that stimulate nerve cells to grow and help some people recall forgotten memories when they dance to music they used to know.”
Coming soon: treatments for ‘winter blues’
Washington, April 30 (ANI): Researchers at the Universities of Edinburgh and Manchester are hopeful they have made a key step towards creating new treatments for Seasonal Affective Disorder (SAD), also known as winter depression or winter blues.
The researchers have discovered two ‘body clock’ genes that reveal how seasonal changes in hormones are controlled. Eventually, it is hoped that the findings could help lead to new ways to tackle SAD – a form of depression suffered during the winter months.
The researchers have been investigating how genes affect changes in the body caused by the seasons. They found that one of these genes (EYA3) has a similar role in both birds and mammals, showing a common link that has been conserved for more than 300 million years.
Scientists studied thousands of genes in Soay sheep. This breed, which dates back to the Bronze Age, is considered to be one of the most primitive with seasonal body clocks unaffected by cross breeding throughout the centuries.
For a long time, scientists had speculated that a key molecule – termed tuberalin – was produced in the pituitary gland at the base of the brain and sent signals to release hormones involved in driving seasonal changes.
However, until now scientists have had no idea about the nature of this molecule, how it works or how it is controlled.
The team focussed on a part of the brain that responds to melatonin – a hormone known to be involved in seasonal timing in mammals.
The study revealed a candidate molecule for the elusive tuberalin, which communicates within the pituitary gland to signal the release of another hormone – prolactin – when days start getting longer. This helps animals adapt to seasonal changes in the environment.
The researchers subsequently identified two genes – TAC1 and EYA3 – that were both activated early when natural hormone levels rise due to longer days.
Professor Dave Burt, of The Roslin Institute at the University of Edinburgh, said: ‘For more than a decade scientists have known about the presence of this mysterious molecule tuberalin, but until now nobody has known quite how it worked. Identifying these genes not only sheds light on how our internal annual body clocks function but also shows a key link between birds and mammals that has been conserved over 300 million years.’
The study suggests that the first gene TAC1 could only work when the second gene EYA3 – which is also found in birds – was present. The second gene may act to regulate TAC 1 so that it could be switched on in response to increasing day length.
Professor Andrew Loudon, of the University of Manchester’s Faculty of Life Sciences, said: ‘A lot of our behaviour is controlled by seasons. This research sheds new light on how animals adapt to seasonal change, which impacts on factors including hibernation, fat deposition and reproduction as well as the ability to fight off diseases.’
The findings have been published in the journal Current Biology.
The researchers have discovered two ‘body clock’ genes that reveal how seasonal changes in hormones are controlled. Eventually, it is hoped that the findings could help lead to new ways to tackle SAD – a form of depression suffered during the winter months.
The researchers have been investigating how genes affect changes in the body caused by the seasons. They found that one of these genes (EYA3) has a similar role in both birds and mammals, showing a common link that has been conserved for more than 300 million years.
Scientists studied thousands of genes in Soay sheep. This breed, which dates back to the Bronze Age, is considered to be one of the most primitive with seasonal body clocks unaffected by cross breeding throughout the centuries.
For a long time, scientists had speculated that a key molecule – termed tuberalin – was produced in the pituitary gland at the base of the brain and sent signals to release hormones involved in driving seasonal changes.
However, until now scientists have had no idea about the nature of this molecule, how it works or how it is controlled.
The team focussed on a part of the brain that responds to melatonin – a hormone known to be involved in seasonal timing in mammals.
The study revealed a candidate molecule for the elusive tuberalin, which communicates within the pituitary gland to signal the release of another hormone – prolactin – when days start getting longer. This helps animals adapt to seasonal changes in the environment.
The researchers subsequently identified two genes – TAC1 and EYA3 – that were both activated early when natural hormone levels rise due to longer days.
Professor Dave Burt, of The Roslin Institute at the University of Edinburgh, said: ‘For more than a decade scientists have known about the presence of this mysterious molecule tuberalin, but until now nobody has known quite how it worked. Identifying these genes not only sheds light on how our internal annual body clocks function but also shows a key link between birds and mammals that has been conserved over 300 million years.’
The study suggests that the first gene TAC1 could only work when the second gene EYA3 – which is also found in birds – was present. The second gene may act to regulate TAC 1 so that it could be switched on in response to increasing day length.
Professor Andrew Loudon, of the University of Manchester’s Faculty of Life Sciences, said: ‘A lot of our behaviour is controlled by seasons. This research sheds new light on how animals adapt to seasonal change, which impacts on factors including hibernation, fat deposition and reproduction as well as the ability to fight off diseases.’
The findings have been published in the journal Current Biology.
Inside the human brain
Controversial Body Worlds exhibit coming to Calgary
Calgarians have an opportunity to discover what’s happening in their brain when they learn something new, listen to music and even when they’re in love.
“Body Worlds & The Brain” opens today at the Telus World of Science. The exhibit showcases bodies and parts from approximately 200 people preserved through Plastination, a process invented by Dr. Gunther von Hagens.
“Three pounds of grey and white matter shape our ‘reality,” a sign reads behind a preserved human brain. As visitors tour the exhibit they will discover that everything they know, everything they’ve experienced and everything they feel boils down to the creation and location of neurons.
“The brain is the most powerful and important organ. It is of utmost importance,” said Dr. Angelina Whalley, Managing Director for Body Worlds. Through the exhibit, she says, “people get a complete understanding of themselves.”
In a survey six months after viewing Body Worlds, 10 per cent of respondents had stopped smoking, 30 per cent were eating healthier and 50 per cent said they exercised more, according to Whalley.
One Calgarian, Adrian Koegler, is looking forward to seeing the exhibit.
“It’s one thing to read about it in a book, but totally different to see it on actual human bodies.”
There has been some controversy surrounding Body Worlds, but, Whalley said it “has mostly been brought up by people who haven’t seen it, they have a different understanding of what the exhibit is.”
Calgarians have an opportunity to discover what’s happening in their brain when they learn something new, listen to music and even when they’re in love.
“Body Worlds & The Brain” opens today at the Telus World of Science. The exhibit showcases bodies and parts from approximately 200 people preserved through Plastination, a process invented by Dr. Gunther von Hagens.
“Three pounds of grey and white matter shape our ‘reality,” a sign reads behind a preserved human brain. As visitors tour the exhibit they will discover that everything they know, everything they’ve experienced and everything they feel boils down to the creation and location of neurons.
“The brain is the most powerful and important organ. It is of utmost importance,” said Dr. Angelina Whalley, Managing Director for Body Worlds. Through the exhibit, she says, “people get a complete understanding of themselves.”
In a survey six months after viewing Body Worlds, 10 per cent of respondents had stopped smoking, 30 per cent were eating healthier and 50 per cent said they exercised more, according to Whalley.
One Calgarian, Adrian Koegler, is looking forward to seeing the exhibit.
“It’s one thing to read about it in a book, but totally different to see it on actual human bodies.”
There has been some controversy surrounding Body Worlds, but, Whalley said it “has mostly been brought up by people who haven’t seen it, they have a different understanding of what the exhibit is.”
Low vitamin D levels linked to multiple sclerosis brain atrophy
Washington, DC: In a new study, neurologists at the University at Buffalo have shown that low vitamin D levels may be associated with more advanced physical disability and cognitive impairment in persons with multiple sclerosis.
The study results, reported at the American Academy of Neurology meeting, held earlier this month, indicated that: The majority of MS patients and healthy controls had insufficient vitamin D levels.
Clinical evaluation and magnetic resonance imaging (MRI) images show low blood levels of total vitamin D and certain active vitamin D byproducts are associated with increased disability, brain atrophy and brain lesion load in MS patients.
A potential association exists between cognitive impairment in MS patients and low vitamin D levels.
The MRI study involved 236 MS patients -- 208 diagnosed with the relapsing-remitting type and 28 with secondary progressive, a more destructive form of MS -- and 22 persons without MS.
All participants provided blood serum samples, which were analyzed for total vitamin D (D2 and D3) levels as well as levels of active vitamin D byproducts. MRI scans performed within three months of blood sampling were available for 163 of the MS patients.
Results showed that only 7%of persons with secondary-progressive MS showed sufficient vitamin D, compared to 18.3% of patients with the less severe relapsing-remitting type.
Higher levels of vitamin D3 and vitamin D3 metabolism byproducts (analyzed as a ratio) also were associated with better scores on disability tests, results showed, and with less brain atrophy and fewer lesions on MRI scans.
Bianca Weinstock-Guttman, MD, UB associate professor of neurology/Jacobs Neurological Institute and director of the Baird Multiple Sclerosis Center, is first author on the study. Commenting on these results, Weinstock-Guttman said: "Clinical studies are necessary to assess vitamin D supplementation and the underlying mechanism that contributes to MS disease progression."
The study results, reported at the American Academy of Neurology meeting, held earlier this month, indicated that: The majority of MS patients and healthy controls had insufficient vitamin D levels.
Clinical evaluation and magnetic resonance imaging (MRI) images show low blood levels of total vitamin D and certain active vitamin D byproducts are associated with increased disability, brain atrophy and brain lesion load in MS patients.
A potential association exists between cognitive impairment in MS patients and low vitamin D levels.
The MRI study involved 236 MS patients -- 208 diagnosed with the relapsing-remitting type and 28 with secondary progressive, a more destructive form of MS -- and 22 persons without MS.
All participants provided blood serum samples, which were analyzed for total vitamin D (D2 and D3) levels as well as levels of active vitamin D byproducts. MRI scans performed within three months of blood sampling were available for 163 of the MS patients.
Results showed that only 7%of persons with secondary-progressive MS showed sufficient vitamin D, compared to 18.3% of patients with the less severe relapsing-remitting type.
Higher levels of vitamin D3 and vitamin D3 metabolism byproducts (analyzed as a ratio) also were associated with better scores on disability tests, results showed, and with less brain atrophy and fewer lesions on MRI scans.
Bianca Weinstock-Guttman, MD, UB associate professor of neurology/Jacobs Neurological Institute and director of the Baird Multiple Sclerosis Center, is first author on the study. Commenting on these results, Weinstock-Guttman said: "Clinical studies are necessary to assess vitamin D supplementation and the underlying mechanism that contributes to MS disease progression."
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