A new Facebook-like Web portal turns doctors and patients into research collaborators
Despite medical advances, the treatment of many chronic diseases remains haphazard and
inconsistent. Teenagers with Crohn’s disease, a painful digestive disorder often diagnosed in adolescence, for example, sometimes get conflicting information regarding medications, diet modifications and alternative therapies. To help improve the care these patients receive, a team of pediatricians and computer scientists is developing a new type of social network that turns doctors and patients into research collaborators.
Here is how it works: With each therapy or treatment modification, doctor and patient participate in a mini clinical trial. The patient records symptoms through daily reports, filed via text message or the Internet. The doctor uses that information to make immediate decisions. Should the dosage of medication be changed? Is the new diet helping to alleviate symptoms? And the data from those individual experiments are then deposited in a Web bank, where they can be aggregated with other patient data, from similar experiments, to further the understanding of the condition in question. In early tests of this process, doctors were able to increase the rate of remission from 55 to 78 percent without adding any new medications to their arsenal. “The idea is to make care continuous and to collect real-time data that will change our understanding and treatment of [Crohn’s],” says Peter Margolis of Cincinnati Children’s Hospital Medical Center, a co-founder of the new portal, the Collaborative Chronic Care Network.
The network, known as C3N, launched earlier this year at some 30 institutions around the country. For now it focuses on pediatric Crohn’s, but it could grow to include other conditions, such as diabetes, heart disease, psoriasis and some cancers. The site’s founders believe C3N will also provide a new platform for clinical research, one that is significantly less profit-driven. “Because largescale clinical trials are so expensive, we only ever really test the treatments that promise a big payoff,” says Ian Eslick, a Ph.D. candidate at the M.I.T. Media Lab and C3N’s chief Web architect. “With C3N, we can scientifically test all the other things—probiotics, gluten-free diets, changes in iron intake—that people are already trying at home and that seem promising, even if they aren’t profitable.”
Source of Information : Scientific American Magazine
Showing posts with label Health. Show all posts
Showing posts with label Health. Show all posts
Thursday, March 29, 2012
Thursday, December 23, 2010
Inflammation Brings on the Blues
Our immune system may mean well, but it might also cause depression
As if being stuck sick in bed wasn’t bad enough, several studies conducted during the past few years have found that the immune response to illness can cause depression. Recently scientists have pinpointed an enzyme that could be the culprit, as it is linked to both chronic inflammation— such as that found in patients with coronary heart disease, type 2 diabetes and rheumatoid arthritis—and depressive symptoms in mice.
In the new study, immunophysiologist Keith Kelley and his colleagues at the University of Illinois exposed mice to a tuberculosis vaccine that produces a low-grade, chronic inflammation. After inoculation, production in the mice brains of an enzyme called IDO, which breaks down tryptophan, spiked. The animals exhibited normal symptoms of illness such as moving around and eating less. Yet even after recovering from the physical illness induced by the vaccine, they showed signs of depression—for example, struggling less than control mice to escape from a bucket of water. Surprisingly, their listlessness was solved relatively simply. “If you block IDO, genetically or pharmaceutically, depression goes away” without interfering with the immune response, Kelley explains.
The research makes a solid case that the immune system communicates directly with the nervous system and affects important health-related behaviors such as depression. The findings could bring relief to patients afflicted with obesity, which leads to chronic inflammation, as well as to cancer patients treated with radiation and chemotherapy drugs that produce both inflammation and depression. “IDO is a new target for drug companies to aim for, to treat patients with both clinical depression and systemic inflammation,” Kelley says.
Source of Information : Scientific American Mind September-October 2009
As if being stuck sick in bed wasn’t bad enough, several studies conducted during the past few years have found that the immune response to illness can cause depression. Recently scientists have pinpointed an enzyme that could be the culprit, as it is linked to both chronic inflammation— such as that found in patients with coronary heart disease, type 2 diabetes and rheumatoid arthritis—and depressive symptoms in mice.
In the new study, immunophysiologist Keith Kelley and his colleagues at the University of Illinois exposed mice to a tuberculosis vaccine that produces a low-grade, chronic inflammation. After inoculation, production in the mice brains of an enzyme called IDO, which breaks down tryptophan, spiked. The animals exhibited normal symptoms of illness such as moving around and eating less. Yet even after recovering from the physical illness induced by the vaccine, they showed signs of depression—for example, struggling less than control mice to escape from a bucket of water. Surprisingly, their listlessness was solved relatively simply. “If you block IDO, genetically or pharmaceutically, depression goes away” without interfering with the immune response, Kelley explains.
The research makes a solid case that the immune system communicates directly with the nervous system and affects important health-related behaviors such as depression. The findings could bring relief to patients afflicted with obesity, which leads to chronic inflammation, as well as to cancer patients treated with radiation and chemotherapy drugs that produce both inflammation and depression. “IDO is a new target for drug companies to aim for, to treat patients with both clinical depression and systemic inflammation,” Kelley says.
Source of Information : Scientific American Mind September-October 2009
Wednesday, March 3, 2010
Horrors of the Kissing Bug
The U.S., too, suffers high rates of parasitic diseases. These so-called neglected infections of poverty closely resemble the neglected tropical diseases (NTDs) and are found pre-dominantly in areas of intense poverty. They disproportionately affect African-Americans and Hispanic-Americans, because a higher percentage of these populations live in poverty and under stressful conditions.
In the Mississippi Delta, post-Katrina Louisiana and other areas of the American South, as well as in inner cities, an estimated three million African-Americans are either currently infected or have been infected in the past with a helminth infection known as toxocariasis. The worm eggs are found in soil or sand laced with dog feces and can contaminate food. Once the worm eggs hatch in the digestive tract, the released larvae migrate through the lungs, liver and brain, leading to wheezing, seizures and developmental delays. Another infection is trichomoniasis, a sexually transmitted protozoan parasite that causes inflam-mation and hemorrhages in the cervix. It increases the risk of acquiring additional sexually transmitted diseases, possibly including HIV/AIDS.
Among Hispanic-Americans, two important infections of poverty are Chagas disease and cysticercosis. Chagas results from a trypanosome protozoan acquired when people are bitten by a kissing bug, a type of assassin bug—a cockroachlike insect often found in dilapidated housing where rats nest (photograph above). The parasites can produce a severe dilation of the heart and can prove fatal. An estimated 300,000 people in the U.S. have Chagas disease. Cysticercosis is a parasitic helminth infection that occurs in as many as 170,000 people and is the leading cause of seizures in cities near the Mexican border.
Most of these infections were not introduced into the U.S. as a result of immigration. Instead they most likely persist through transmission within U.S. borders. Despite their prevalence, research on these conditions has been fairly limited. Health officials do not know the precise numbers of people infected or why poverty is a risk factor. Diagnostic methods and treatments are also fairly rudimentary.
chagas disease afflicts an estimated 300,000 people in the U.S. Screening of donated blood, started in 2007, finds that cases are concentrated in areas with large numbers of immigrants from Latin America living in substandard housing.
Source of Information : Scientific American January 2010
In the Mississippi Delta, post-Katrina Louisiana and other areas of the American South, as well as in inner cities, an estimated three million African-Americans are either currently infected or have been infected in the past with a helminth infection known as toxocariasis. The worm eggs are found in soil or sand laced with dog feces and can contaminate food. Once the worm eggs hatch in the digestive tract, the released larvae migrate through the lungs, liver and brain, leading to wheezing, seizures and developmental delays. Another infection is trichomoniasis, a sexually transmitted protozoan parasite that causes inflam-mation and hemorrhages in the cervix. It increases the risk of acquiring additional sexually transmitted diseases, possibly including HIV/AIDS.
Among Hispanic-Americans, two important infections of poverty are Chagas disease and cysticercosis. Chagas results from a trypanosome protozoan acquired when people are bitten by a kissing bug, a type of assassin bug—a cockroachlike insect often found in dilapidated housing where rats nest (photograph above). The parasites can produce a severe dilation of the heart and can prove fatal. An estimated 300,000 people in the U.S. have Chagas disease. Cysticercosis is a parasitic helminth infection that occurs in as many as 170,000 people and is the leading cause of seizures in cities near the Mexican border.
Most of these infections were not introduced into the U.S. as a result of immigration. Instead they most likely persist through transmission within U.S. borders. Despite their prevalence, research on these conditions has been fairly limited. Health officials do not know the precise numbers of people infected or why poverty is a risk factor. Diagnostic methods and treatments are also fairly rudimentary.
chagas disease afflicts an estimated 300,000 people in the U.S. Screening of donated blood, started in 2007, finds that cases are concentrated in areas with large numbers of immigrants from Latin America living in substandard housing.Source of Information : Scientific American January 2010
Saturday, January 30, 2010
Does D Make a Difference?
New studies show low vitamin D levels may impair cognitive function
The push to prevent skin cancer may have come with unintended consequences—impaired brain function because of a deficiency of vitamin D. The “sunshine vitamin” is synthesized in our skin when we are exposed to direct sunlight, but sunblock impedes this process. And although vitamin D is well known for promoting bone health and regulating vital calcium levels—hence its addition to milk—it does more than that. Scientists have now linked this fat-soluble nutrient’s hormonelike activity to a number of functions throughout the body, including the workings of the brain. “We know there are receptors for vitamin D throughout the central nervous system and in the hippocampus,” said Robert J. Przybelski, a doctor and research scientist at the University of Wisconsin School of Medicine and Public Health. “We also know vitamin D activates and deactivates enzymes in the brain and the cerebrospinal fluid that are involved in neurotransmitter synthesis and nerve growth.” In addition, animal and laboratory studies suggest vitamin D protects neurons and reduces inflammation. Two new European studies looking at vitamin D and cognitive function have taken us one step further. The first study, led by neuroscientist David Llewellyn of the University of Cambridge, assessed vitamin D levels in more than 1,700 men and women from England, aged 65 or older. Subjects were divided into four groups based on vitamin D blood levels: severely deficient, deficient, insufficient (borderline) and optimum, then tested for cognitive function. The scientists found that the lower the subjects’ vitamin D levels, the more negatively impacted was their performance on a battery of mental tests. Compared with people with optimum vitamin D levels, those in the lowest quartile were more than twice as likely to be cognitively impaired.
A second study, led by scientists at the University of Manchester in England and published online this past May, looked at vitamin D levels and cognitive performance in more than 3,100 men aged 40 to 79 in eight different countries across Europe. The data show that those people with lower vitamin D levels exhibited slower information processing speed. This correlation was particularly strong among men older than 60 years. “The fact that this relationship was established in a largescale, clinical human study is very important,” Przybelski says, “but there’s still a lot we don’t know.” Although we now know that low levels of vitamin D are associated with cognitive impairment, we do not know if high or optimum levels will lessen cognitive losses. It is also unclear if giving vitamin D to those who lack it will help them regain some of these high-level functions. Because cognitive impairment is often a precursor for dementia and Alzheimer’s disease, vitamin D is a hot topic among Alzheimer’s scientists, who are racing to answer these questions. Przybelski, for example, is planning a study of vitamin D supplements in healthy, normal elderly adults living in an assisted-living community to see if it will affect their incidence of Alzheimer’s in the long term. So how much is enough vitamin D? Experts say 1,000 to 2,000 IU daily—about the amount your body will synthesize from 15 to 30 minutes of sun exposure two to three times a week—is the ideal range for almost all healthy adults. Keep in mind, however, that skin color, where you live and how much skin you have exposed all affect how much vitamin D you can produce. —Diane Welland
Source of Information : Scientific American Mind November-December 2009
The push to prevent skin cancer may have come with unintended consequences—impaired brain function because of a deficiency of vitamin D. The “sunshine vitamin” is synthesized in our skin when we are exposed to direct sunlight, but sunblock impedes this process. And although vitamin D is well known for promoting bone health and regulating vital calcium levels—hence its addition to milk—it does more than that. Scientists have now linked this fat-soluble nutrient’s hormonelike activity to a number of functions throughout the body, including the workings of the brain. “We know there are receptors for vitamin D throughout the central nervous system and in the hippocampus,” said Robert J. Przybelski, a doctor and research scientist at the University of Wisconsin School of Medicine and Public Health. “We also know vitamin D activates and deactivates enzymes in the brain and the cerebrospinal fluid that are involved in neurotransmitter synthesis and nerve growth.” In addition, animal and laboratory studies suggest vitamin D protects neurons and reduces inflammation. Two new European studies looking at vitamin D and cognitive function have taken us one step further. The first study, led by neuroscientist David Llewellyn of the University of Cambridge, assessed vitamin D levels in more than 1,700 men and women from England, aged 65 or older. Subjects were divided into four groups based on vitamin D blood levels: severely deficient, deficient, insufficient (borderline) and optimum, then tested for cognitive function. The scientists found that the lower the subjects’ vitamin D levels, the more negatively impacted was their performance on a battery of mental tests. Compared with people with optimum vitamin D levels, those in the lowest quartile were more than twice as likely to be cognitively impaired.
A second study, led by scientists at the University of Manchester in England and published online this past May, looked at vitamin D levels and cognitive performance in more than 3,100 men aged 40 to 79 in eight different countries across Europe. The data show that those people with lower vitamin D levels exhibited slower information processing speed. This correlation was particularly strong among men older than 60 years. “The fact that this relationship was established in a largescale, clinical human study is very important,” Przybelski says, “but there’s still a lot we don’t know.” Although we now know that low levels of vitamin D are associated with cognitive impairment, we do not know if high or optimum levels will lessen cognitive losses. It is also unclear if giving vitamin D to those who lack it will help them regain some of these high-level functions. Because cognitive impairment is often a precursor for dementia and Alzheimer’s disease, vitamin D is a hot topic among Alzheimer’s scientists, who are racing to answer these questions. Przybelski, for example, is planning a study of vitamin D supplements in healthy, normal elderly adults living in an assisted-living community to see if it will affect their incidence of Alzheimer’s in the long term. So how much is enough vitamin D? Experts say 1,000 to 2,000 IU daily—about the amount your body will synthesize from 15 to 30 minutes of sun exposure two to three times a week—is the ideal range for almost all healthy adults. Keep in mind, however, that skin color, where you live and how much skin you have exposed all affect how much vitamin D you can produce. —Diane Welland
Source of Information : Scientific American Mind November-December 2009
Friday, July 31, 2009
‘Trojan’ cells take on drug-resistant tumours
JUST one imitation horse was enough to conquer Troy, but it takes two waves of “Trojan” cell fragments to destroy drugresistant tumours in mice. The first wave releases RNA to disrupt drug resistance, making the tumours vulnerable, and the second delivers a fatal dose of chemotherapy. Himanshu Brahmbhatt and Jennifer MacDiarmid of the company Engeneic in Sydney, Australia, had already coaxed bacteria such as E. coli into dividing at their ends, rather than in the middle. This way they produce tiny buds of cytoplasm devoid of chromosomes and other organelles. After washing these “minicells” clear of bacterial toxins , the team loaded them up with chemotherapy drugs and tagged them with antibodies that bind only to tumours. When injected, the minicells destroyed tumours in animals .
However, because many tumours eventually become resistant to chemotherapy, the next step is to find ways to overcome drug resistance. One way cancer cells develop resistance is by overproducing a protein called MDR1, which helps pump the drugs out of the cell, reducing their toxicity. Brahmblatt’s team wondered if they could also use the minicells to block production of this protein. To find out, they created strands of small interfering RNA (siRNA) with a sequence designed to block the expression of the gene for MDR1, and loaded these into the minicells.
Next they injected these minicells into mice with a range of drug-resistant human cancers, including breast, colon and uterine tumours. The minicells were engulfed by the cancer cells, where they released the strands of siRNA (see diagram). The second wave of minicells containing high doses of the cancer drug doxorubicin was then injected, and the tumours shrank, indicating that the first batch had indeed blocked MDR1 (Nature Biotechnology, DOI: 10.1038/ nbt.1547). All of the treated mice were still alive 110 days after being implanted with the tumours, while a group of untreated mice had died by then. Brahmblatt says that the cancer cells engulf the minicells in their cell membranes – a process called endocytosis. Many different cells take in foreign cells or proteins this way, but it wasn’t clear that cancer cells would be capable of absorbing two rounds of minicells. “The first Trojan horse goes in and the cancer cell opens its door,” says Brahmbhatt. “The cell then regenerates its entire machinery for the next Trojan horse to come in and release a different payload.” Brahmbhatt adds that the minicells could be loaded with different drugs depending on the type of cancer and with different siRNAs to block the production of proteins responsible for other forms of drug resistance.
Double whammy to kill cancer cells
They could also be used to treat other diseases. siRNAs have been touted as a way to block a range of disease-causing genes but researchers have struggled to get them across cell membranes efficiently. “This is an exciting, novel technology with potential applicability to a number of different delivery problems,” agrees Daniel Anderson, who researches drugs delivery at the Massachusetts Institute of Technology. Linda Geddes
However, because many tumours eventually become resistant to chemotherapy, the next step is to find ways to overcome drug resistance. One way cancer cells develop resistance is by overproducing a protein called MDR1, which helps pump the drugs out of the cell, reducing their toxicity. Brahmblatt’s team wondered if they could also use the minicells to block production of this protein. To find out, they created strands of small interfering RNA (siRNA) with a sequence designed to block the expression of the gene for MDR1, and loaded these into the minicells.
Next they injected these minicells into mice with a range of drug-resistant human cancers, including breast, colon and uterine tumours. The minicells were engulfed by the cancer cells, where they released the strands of siRNA (see diagram). The second wave of minicells containing high doses of the cancer drug doxorubicin was then injected, and the tumours shrank, indicating that the first batch had indeed blocked MDR1 (Nature Biotechnology, DOI: 10.1038/ nbt.1547). All of the treated mice were still alive 110 days after being implanted with the tumours, while a group of untreated mice had died by then. Brahmblatt says that the cancer cells engulf the minicells in their cell membranes – a process called endocytosis. Many different cells take in foreign cells or proteins this way, but it wasn’t clear that cancer cells would be capable of absorbing two rounds of minicells. “The first Trojan horse goes in and the cancer cell opens its door,” says Brahmbhatt. “The cell then regenerates its entire machinery for the next Trojan horse to come in and release a different payload.” Brahmbhatt adds that the minicells could be loaded with different drugs depending on the type of cancer and with different siRNAs to block the production of proteins responsible for other forms of drug resistance.
Double whammy to kill cancer cellsThey could also be used to treat other diseases. siRNAs have been touted as a way to block a range of disease-causing genes but researchers have struggled to get them across cell membranes efficiently. “This is an exciting, novel technology with potential applicability to a number of different delivery problems,” agrees Daniel Anderson, who researches drugs delivery at the Massachusetts Institute of Technology. Linda Geddes
Saturday, May 3, 2008
Surrogate Goats
For mothers who have trouble breastfeeding or risk passing on HIV to their children, fortified goat milk could soon be the best alternative. Scientists at the Russian Academy of Sciences have genetically engineered goats that carry the human gene for the protein lactoferrin, normally found only in high concentrations in breast milk. The protein, which is absent in baby formula, is critical because it protects infants from bacteria and viruses while their immune systems are still maturing. In the next few years, scientists aim to stock a farm with engineered goats that would make fortified milk for rural villages, helping to lower infection babies.
*.* Source of Information : May 2008 Popular Science
*.* Source of Information : May 2008 Popular Science
Friday, May 2, 2008
Why do some people dream?
Why do some people dream more than others? Unless you’re a character in A Nightmare on Elm Street, you probably dream the same amount as everyone else: upward of two hours a night, according to the National Institutes of Health. The brain’s sleep cycle, however, makes it extremely difficult to remember dreams. “During sleep, our memory systems are completely shut down, and we’re basically living on a self-erasing tape,” explains neurologist Mark Mahowald, director of the Minnesota Regional Sleep Disorders Center. It’s like the “record” button in your brain has been switched off.
So why is it that some people regularly recall the intricate plots of their bizarre dreams? “The primary determinant of whether you’re going to remember a dream is if you awaken during it,” Mahowald says. Waking up snaps your memory into action, and it absorbs the bits of a dream that might otherwise fade into your subconscious. Frequent wakers are more likely to remember their dreams than deep sleepers, he adds. The content of your dreams might also play a role in retrieving your somnolent synapses. Bad dreams typically jolt you awake, so people who suffer from frequent nightmares may also be more likely to remember what they dream.
Research on dreaming has shown that it’s possible to train yourself to better recall whatever you were dreaming about just prior to waking up, says Alan Manevitz, a psychiatrist at Weill Cornell Medical Center in New York.
*.* Source of Information : May 2008 Popular Science
So why is it that some people regularly recall the intricate plots of their bizarre dreams? “The primary determinant of whether you’re going to remember a dream is if you awaken during it,” Mahowald says. Waking up snaps your memory into action, and it absorbs the bits of a dream that might otherwise fade into your subconscious. Frequent wakers are more likely to remember their dreams than deep sleepers, he adds. The content of your dreams might also play a role in retrieving your somnolent synapses. Bad dreams typically jolt you awake, so people who suffer from frequent nightmares may also be more likely to remember what they dream.
Research on dreaming has shown that it’s possible to train yourself to better recall whatever you were dreaming about just prior to waking up, says Alan Manevitz, a psychiatrist at Weill Cornell Medical Center in New York.
*.* Source of Information : May 2008 Popular Science
Thursday, May 1, 2008
WHY IS YAWNING CONTAGIOUS?
Go ahead; admit it—you’re yawning right now. That’s OK, we forgive you. We know it’s not because you’re bored. It’s just that seeing other people yawn, reading about yawning, or even just thinking about it can make you yawn. And it’s a good thing, too: Passing yawns around a campfi re might have kept our ancestors alive.
Picking up another person’s yawn may be an empathetic refl ex, says evolutionary psychologist Gordon Gallup of the State University of New York at Albany. When you see someone yawn, neurons in your brain fi re and cause you to “feel” what that person is experiencing, commanding you to perform the action even if you don’t actually feel the need.
Scientists have yet to figure out why we yawn at all, though. Some say it signals boredom, whereas others have suggested that it balances carbon dioxide and oxygen levels in the blood. Most recently, Gallup theorized in a study last year that yawns cool our brains so that they run effi ciently, similar to running a fan in a computer. He found that, contrary to common perception, cooling the brain with a yawn keeps people from nodding off.
Alternatively, E.O. Smith, an emeritus professor of anthropology at Emory University, contends that yawning may have encouraged our ancestors to go to bed early. “Contagious yawning didn’t arise in a vacuum on a Saturday afternoon,” Smith says. Spreading a case of the yawns around a bonfi re, he posits, may have prompted night owls to climb up into their comfy tree beds with their sleepier brethren, out of danger from stealthy predators.
*.* Source of Information : May 2008 Popular Science
Picking up another person’s yawn may be an empathetic refl ex, says evolutionary psychologist Gordon Gallup of the State University of New York at Albany. When you see someone yawn, neurons in your brain fi re and cause you to “feel” what that person is experiencing, commanding you to perform the action even if you don’t actually feel the need.
Scientists have yet to figure out why we yawn at all, though. Some say it signals boredom, whereas others have suggested that it balances carbon dioxide and oxygen levels in the blood. Most recently, Gallup theorized in a study last year that yawns cool our brains so that they run effi ciently, similar to running a fan in a computer. He found that, contrary to common perception, cooling the brain with a yawn keeps people from nodding off.
Alternatively, E.O. Smith, an emeritus professor of anthropology at Emory University, contends that yawning may have encouraged our ancestors to go to bed early. “Contagious yawning didn’t arise in a vacuum on a Saturday afternoon,” Smith says. Spreading a case of the yawns around a bonfi re, he posits, may have prompted night owls to climb up into their comfy tree beds with their sleepier brethren, out of danger from stealthy predators.
*.* Source of Information : May 2008 Popular Science
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