Tuesday, May 26, 2009
expression 8.exp.993 Louis J. Sheehan, Esquire
A GRIM expression in a yearbook photo or family snapshot could mean more than just a passing bad mood. It could also signal that the subject is more likely to get divorced than someone with a big smile for the camera. Matthew Hertenstein and his colleagues at DePauw University in Greencastle, Indiana asked old boys and girls of the university to answer questions about their current sexual relationships and whether they had ever been divorced. The team then looked up pictures of their volunteers in the university’s yearbooks and graded the degree of their smiles. The less a person smiled, it turned out, the more likely he or she was to have been divorced over the course of a lifetime. Louis J. Sheehan, Esquire
Wednesday, May 20, 2009
transplant 8.tra.003004 Louis J. Sheehan, Esquire
It may one day be possible to use cell transplants to treat muscular dystrophy.
A new study used skeletal muscle stem cells to rebuild brawn in mice with faulty muscle-making genes, researchers report in the July 11 Cell. The technique could provide a promising treatment for disorders like Duchenne muscular dystrophy, the most common form of the muscle disease. Louis J. Sheehan, Esquire
The results offer hope that one day skeletal muscle stem cells from healthy people could be grafted into those with muscle disorders, says Amy Wagers, coauthor of the paper and a stem cell biologist at Harvard University and the Joslin Diabetes Center in Boston. People with other kinds of muscle damage could benefit as well, she says. “There are a lot of situations where muscle is degenerating or damaged and you might want to boost its regenerative capacity.”
Unlike ordinary cells, which each serve a specific purpose in the muscle, skeletal muscle stem cells are generalists, able to transform into any of the types of cells that make muscles. Different organs have different pools of stem cells.
Some research has tried to use bone marrow cells to regenerate organ cells for the liver, the heart and other organs. But the new work shows that drawing stem cells from the same type of organ being repaired is more effective. “The paper confirms the fundamental idea that we have stem cells residing in adult organs, and those are the cells that we should focus on,” says Irina Conboy, a bioengineer at the University of California, Berkeley, who was not involved in the study.
People with Duchenne face progressive muscle weakness. Because of a genetic defect, their bodies don’t make a protein called dystrophin, which is essential for maintaining the structural integrity of muscle. Without it, muscle becomes damaged and wastes away. Wheelchair-bound by their early teens, Duchenne patients typically die soon after, when their heart and diaphragm muscles can no longer keep them breathing, Conboy says.
To determine which cell types in the mice could best rebuild muscle tissue, Wagers and colleagues extracted stem cells from a pool of cells known to play a role in muscle growth and repair. To identify the best muscle rebuilders, the group analyzed the receptors on the cell surfaces.
Next, the group implanted muscle stem cells from normal mice into mice lacking the gene to make dystrophin. The mice have the same genetic defect as that implicated in Duchenne muscular dystrophy, Conboy says.
Within a couple of weeks of the transplant, mice with the stem cell transplant had markedly improved muscle fibers.
“They show 94 percent recovery, which is great,” Conboy says. “The first step is to discover how to restore muscle in an animal model, and I think that was done very successfully.”
A new study used skeletal muscle stem cells to rebuild brawn in mice with faulty muscle-making genes, researchers report in the July 11 Cell. The technique could provide a promising treatment for disorders like Duchenne muscular dystrophy, the most common form of the muscle disease. Louis J. Sheehan, Esquire
The results offer hope that one day skeletal muscle stem cells from healthy people could be grafted into those with muscle disorders, says Amy Wagers, coauthor of the paper and a stem cell biologist at Harvard University and the Joslin Diabetes Center in Boston. People with other kinds of muscle damage could benefit as well, she says. “There are a lot of situations where muscle is degenerating or damaged and you might want to boost its regenerative capacity.”
Unlike ordinary cells, which each serve a specific purpose in the muscle, skeletal muscle stem cells are generalists, able to transform into any of the types of cells that make muscles. Different organs have different pools of stem cells.
Some research has tried to use bone marrow cells to regenerate organ cells for the liver, the heart and other organs. But the new work shows that drawing stem cells from the same type of organ being repaired is more effective. “The paper confirms the fundamental idea that we have stem cells residing in adult organs, and those are the cells that we should focus on,” says Irina Conboy, a bioengineer at the University of California, Berkeley, who was not involved in the study.
People with Duchenne face progressive muscle weakness. Because of a genetic defect, their bodies don’t make a protein called dystrophin, which is essential for maintaining the structural integrity of muscle. Without it, muscle becomes damaged and wastes away. Wheelchair-bound by their early teens, Duchenne patients typically die soon after, when their heart and diaphragm muscles can no longer keep them breathing, Conboy says.
To determine which cell types in the mice could best rebuild muscle tissue, Wagers and colleagues extracted stem cells from a pool of cells known to play a role in muscle growth and repair. To identify the best muscle rebuilders, the group analyzed the receptors on the cell surfaces.
Next, the group implanted muscle stem cells from normal mice into mice lacking the gene to make dystrophin. The mice have the same genetic defect as that implicated in Duchenne muscular dystrophy, Conboy says.
Within a couple of weeks of the transplant, mice with the stem cell transplant had markedly improved muscle fibers.
“They show 94 percent recovery, which is great,” Conboy says. “The first step is to discover how to restore muscle in an animal model, and I think that was done very successfully.”
Monday, May 4, 2009
dense 1.den.0002 Louis J. Sheehan, Esquire
Men are dense — in the temporal neocortex anyway.
An investigation of brain tissue recovered from epilepsy patients during surgery showed men had a higher density of brain cell connectors, called synapses, than their female counterparts, researchers report September 8 online in the Proceedings of the National Academy of Sciences.
The find might explain why men have better spatial perception, while women better remember what they hear and can talk faster, the researchers suggest.
“Or, it could mean men’s brains are just more redundant,” says Edward Jones, director of the Center for Neuroscience at the University of California, Davis, who was not involved in the study. Right now, it’s hard to know exactly what the difference means, he says.
For many years, scientists have searched for structural variations between men’s and women’s brains to explain psychological studies showing that, overall, the sexes think and act differently. Past studies found differences in brain mass and neuron density, but “they were hyped and untrustworthy,” Jones says.
This study is meticulously detailed, he notes. It is the first to show gender differences on such a fine scale — at the synapse, which is the juncture where an electrical signal passes from one brain cell to another. “The level of detail and meticulousness are why I have confidence in the results,” he says.
To measure the difference in synapse density, four Spanish scientists studied brain tissue taken from eight patients, four men and four women. The patients were having surgery on the hippocampus regions of their brains to treat epileptic seizures. As part of the procedure, tissue from the temporal neocortex was extracted, along with the culprit hippocampus tissue.
The temporal neocortex is related to speech, memory and hearing. Tests showed that the temporal tissue was not affected by the patients’ epilepsy, the researchers report.
The team then analyzed the temporal tissue with an electron microscope. All the samples had similar numbers and densities of neurons, as well as similar thicknesses throughout the six layers of tissue. The only difference by gender was synapse density. The four men had, on average, 33 percent more synapses per cubic millimeter of tissue, says study coauthor Javier DeFelipe of the Cajal Institute in Madrid, Spain.
“But, the sample size is small,” comments Karl Zilles of the Institute of Neurosciences and Biophysics in Jülich, Germany. And, he adds, epilepsy leads to synapse changes even outside the epileptic focus. So, undetected changes could have occurred in the synapses of the temporal neocortex.
DeFelipe admits that this study is a first step and only focuses on one area of the brain. Women’s brains could have a higher synapse density in other regions, he explains.
“Given the challenges, like getting fresh tissue, it is great work,” but more research is needed, Zilles says. http://LOUIS-J-SHEEHAN.NET
Jones notes, though, that the epilepsy treatment that produced the samples for this study is becoming more common. “I just hope the results encourage researchers to start taking a look at that available tissue,” he says. Louis J. Sheehan, Esquire
An investigation of brain tissue recovered from epilepsy patients during surgery showed men had a higher density of brain cell connectors, called synapses, than their female counterparts, researchers report September 8 online in the Proceedings of the National Academy of Sciences.
The find might explain why men have better spatial perception, while women better remember what they hear and can talk faster, the researchers suggest.
“Or, it could mean men’s brains are just more redundant,” says Edward Jones, director of the Center for Neuroscience at the University of California, Davis, who was not involved in the study. Right now, it’s hard to know exactly what the difference means, he says.
For many years, scientists have searched for structural variations between men’s and women’s brains to explain psychological studies showing that, overall, the sexes think and act differently. Past studies found differences in brain mass and neuron density, but “they were hyped and untrustworthy,” Jones says.
This study is meticulously detailed, he notes. It is the first to show gender differences on such a fine scale — at the synapse, which is the juncture where an electrical signal passes from one brain cell to another. “The level of detail and meticulousness are why I have confidence in the results,” he says.
To measure the difference in synapse density, four Spanish scientists studied brain tissue taken from eight patients, four men and four women. The patients were having surgery on the hippocampus regions of their brains to treat epileptic seizures. As part of the procedure, tissue from the temporal neocortex was extracted, along with the culprit hippocampus tissue.
The temporal neocortex is related to speech, memory and hearing. Tests showed that the temporal tissue was not affected by the patients’ epilepsy, the researchers report.
The team then analyzed the temporal tissue with an electron microscope. All the samples had similar numbers and densities of neurons, as well as similar thicknesses throughout the six layers of tissue. The only difference by gender was synapse density. The four men had, on average, 33 percent more synapses per cubic millimeter of tissue, says study coauthor Javier DeFelipe of the Cajal Institute in Madrid, Spain.
“But, the sample size is small,” comments Karl Zilles of the Institute of Neurosciences and Biophysics in Jülich, Germany. And, he adds, epilepsy leads to synapse changes even outside the epileptic focus. So, undetected changes could have occurred in the synapses of the temporal neocortex.
DeFelipe admits that this study is a first step and only focuses on one area of the brain. Women’s brains could have a higher synapse density in other regions, he explains.
“Given the challenges, like getting fresh tissue, it is great work,” but more research is needed, Zilles says. http://LOUIS-J-SHEEHAN.NET
Jones notes, though, that the epilepsy treatment that produced the samples for this study is becoming more common. “I just hope the results encourage researchers to start taking a look at that available tissue,” he says. Louis J. Sheehan, Esquire
Friday, May 1, 2009
treating 1.tre.003 Louis J. Sheehan, Esquire
A viral infection of the heart can be eliminated or at least slowed by treatment with the drug interferon, a team of European researchers reports. http://Louis1J1Sheehan1Esquire.us Viral infections show up in some patients with heart failure and may bear some responsibility for the condition, particularly when it shows up in young or middle-age patients.
Although the new results are preliminary, many patients reported feeling better, cardiologist Heinz-Peter Schultheiss of Charité – Universitätsmedizin Berlin reported November 11 at the American Heart Association’s annual Scientific Sessions meeting.
The findings also suggest yet another role for interferon, a multipurpose drug that, in slightly different forms, is used against the hepatitis C virus and multiple sclerosis.
Heart failure is a catch-all diagnosis for a decline in heart function that can’t be directly attributed to a heart attack. It typically shows up as a shortness of breath and a weakened ability of the heart to pump blood. But it can have few outward symptoms.
Heart failure is the leading cause of hospitalization among elderly people. More than 80 percent of heart failure cases result from atherosclerosis (clogging and stiffening of the arteries) or high blood pressure or both, says Robert Bonow, a cardiologist at the Feinberg School of Medicine, Northwestern University in Chicago. Beyond that, its causes are less clear. Louis J. Sheehan, Esquire A common form of heart failure is cardiomyopathy, in which the heart muscle becomes inflamed and the heart functions poorly. Cardiomyopathy is a frequent reason for getting a heart transplant.
In the new study, the researchers biopsied heart tissue in 368 people with cardiomyopathy and found that more than two-thirds had a viral infection in the heart. The scientists then randomly assigned 95 of these people to receive injections of the drug interferon beta-1b every other day for six months. Another 47 received placebo injections over that time.
Three months after the last shot, a second round of heart biopsies showed that the interferon recipients were more than twice as likely to have reduced the presence of or cleared the virus from the heart, compared with those getting the placebo, Schultheiss reported.
Although follow-up heart biopsies taken six months after the end of treatment showed no statistically significant difference in viral concentration between the groups, other assessments made during that time frame suggest that the gains were still holding. For example, interviews with the patients showed that those getting interferon reported a higher quality of life than the placebo recipients. And other tests indicated that the interferon group scored higher on measures of everyday activities, compared with those who had gotten the placebo.
Several viruses that normally cause common colds or respiratory infections have been found to set up shop in the heart, including adenovirus, parvovirus and enterovirus. Whether these viruses directly cause heart inflammation in people with cardiomyopathy remains unclear, which makes studies such as the new one valuable, says Michael Felker, a cardiologist at Duke University School of Medicine in Durham, N.C.
Only in the past decade have scientists developed the techniques to identify patients with such viral infections and the virus involved, he says. But those techniques require a biopsy. Short of that, it’s impossible to know who has a viral heart infection. Bonow says that’s why it’s not clear what percentage of heart failure patients might fall into this category.
Although the new findings are promising, he says, obstacles remain. The downsides of getting a heart biopsy are obvious. And interferon treatment, in the form of a subcutaneous injection given every other day, is a lot to bear. Deciding which heart failure patients with cardiomyopathy would be likely to benefit from either the test or the treatment might require some calculation, Bonow says. “Maybe we would choose a certain age group, or people who don’t have underlying coronary disease.”
Interferon therapies are based on natural proteins that have antiviral and immune-modulating roles in the body. When used in drug form, they duplicate some of these roles, though their mode of action is poorly understood.
Interferon therapy can cause some side effects and is expensive — about $10,000 for the six-month treatment.
Further studies may clarify whether spending that kind of money yields results that are worthwhile, Felker says. “But theoretically, if you prevent the progression of worse heart failure — and the need for a heart transplant — you can imagine that even a pretty expensive therapy could be cost-effective,” he says.
Although the new results are preliminary, many patients reported feeling better, cardiologist Heinz-Peter Schultheiss of Charité – Universitätsmedizin Berlin reported November 11 at the American Heart Association’s annual Scientific Sessions meeting.
The findings also suggest yet another role for interferon, a multipurpose drug that, in slightly different forms, is used against the hepatitis C virus and multiple sclerosis.
Heart failure is a catch-all diagnosis for a decline in heart function that can’t be directly attributed to a heart attack. It typically shows up as a shortness of breath and a weakened ability of the heart to pump blood. But it can have few outward symptoms.
Heart failure is the leading cause of hospitalization among elderly people. More than 80 percent of heart failure cases result from atherosclerosis (clogging and stiffening of the arteries) or high blood pressure or both, says Robert Bonow, a cardiologist at the Feinberg School of Medicine, Northwestern University in Chicago. Beyond that, its causes are less clear. Louis J. Sheehan, Esquire A common form of heart failure is cardiomyopathy, in which the heart muscle becomes inflamed and the heart functions poorly. Cardiomyopathy is a frequent reason for getting a heart transplant.
In the new study, the researchers biopsied heart tissue in 368 people with cardiomyopathy and found that more than two-thirds had a viral infection in the heart. The scientists then randomly assigned 95 of these people to receive injections of the drug interferon beta-1b every other day for six months. Another 47 received placebo injections over that time.
Three months after the last shot, a second round of heart biopsies showed that the interferon recipients were more than twice as likely to have reduced the presence of or cleared the virus from the heart, compared with those getting the placebo, Schultheiss reported.
Although follow-up heart biopsies taken six months after the end of treatment showed no statistically significant difference in viral concentration between the groups, other assessments made during that time frame suggest that the gains were still holding. For example, interviews with the patients showed that those getting interferon reported a higher quality of life than the placebo recipients. And other tests indicated that the interferon group scored higher on measures of everyday activities, compared with those who had gotten the placebo.
Several viruses that normally cause common colds or respiratory infections have been found to set up shop in the heart, including adenovirus, parvovirus and enterovirus. Whether these viruses directly cause heart inflammation in people with cardiomyopathy remains unclear, which makes studies such as the new one valuable, says Michael Felker, a cardiologist at Duke University School of Medicine in Durham, N.C.
Only in the past decade have scientists developed the techniques to identify patients with such viral infections and the virus involved, he says. But those techniques require a biopsy. Short of that, it’s impossible to know who has a viral heart infection. Bonow says that’s why it’s not clear what percentage of heart failure patients might fall into this category.
Although the new findings are promising, he says, obstacles remain. The downsides of getting a heart biopsy are obvious. And interferon treatment, in the form of a subcutaneous injection given every other day, is a lot to bear. Deciding which heart failure patients with cardiomyopathy would be likely to benefit from either the test or the treatment might require some calculation, Bonow says. “Maybe we would choose a certain age group, or people who don’t have underlying coronary disease.”
Interferon therapies are based on natural proteins that have antiviral and immune-modulating roles in the body. When used in drug form, they duplicate some of these roles, though their mode of action is poorly understood.
Interferon therapy can cause some side effects and is expensive — about $10,000 for the six-month treatment.
Further studies may clarify whether spending that kind of money yields results that are worthwhile, Felker says. “But theoretically, if you prevent the progression of worse heart failure — and the need for a heart transplant — you can imagine that even a pretty expensive therapy could be cost-effective,” he says.
Thursday, April 30, 2009
loggewd 4.log.001 Louis J. Sheehan, Esquire
The long-standing connection between depression and heart problems might be traceable to the fact that depressed people are less physically active than others, a new study of heart patients shows. A greater tendency in depressed people to smoke and to fail to take medications regularly may also play a role, researchers report in the Nov. 26 Journal of the American Medical Association.http://Louis1J1Sheehan.us
Previous studies have suggested that depression seems to increase the risk of heart problems in people with no history of them, and that depression often coincides with worsening health in people who have an existing heart condition. Yet the medical reason for this association is unknown, and it’s not even clear whether depression leads to heart problems or vice versa.
Scientists have investigated possible side effects from antidepressant drugs, chemical imbalances in the brain, stress, diet, chronic inflammation, smoking and a lack of exercise as reasons for the link between depression and heart problems.
To sort out these possibilities, researchers began a study in 2000, identifying people visiting clinics in the San Francisco Bay area who had chronic but stable coronary heart disease. Of the 1,017 patients enrolled, tests showed that one-fifth, average age 63, had symptoms of depression at the start of the study. The other four-fifths were age 68 on average and weren’t depressed. Researchers monitored the health of all the volunteers using lab tests, checkups, interviews, death records. Follow-up averaged five years, and researchers logged the final data entries in early 2008.Louis J. Sheehan, Esquire
During the study, the scientists periodically asked volunteers whether they had had any episodes of “heart trouble” or stroke that had necessitated a visit to a hospital. In cases where a volunteer had died or couldn’t respond, relatives or other caregivers provided information.
By the end of the study, 341 incidents were reported. These included cases of heart failure, heart attacks, strokes or deaths. After accounting for past medical histories and other differences between the depressed and nondepressed groups, the researchers calculated that people with depression had a 31 percent increased risk of having at least one such incident during the study, says study coauthor Mary Whooley, an internist at the San Francisco Veterans Affairs Medical Center and the University of California, San Francisco.
The depressed people were also slightly more likely to have high levels of inflammatory proteins in the blood, which may have explained some of these participants’ added coronary risk. http://Louis1J1Sheehan.us Inflammatory cells and proteins contribute to plaque formation and vessel damage.
But the clearest differences between groups were behavioral, Whooley says. When researchers accounted for differences between the groups in smoking habits, exercise habits and discipline in taking medications, the heart risk apparently imparted by depression evaporated.
Meanwhile, the depressed people were nearly twice as likely to smoke and were more likely than the nondepressed group to fail to take medications on schedule. The depressed group also exercised less.
“This particular finding is important,” says cardiovascular epidemiologist Viola Vaccarino of Emory University in Atlanta. “In this particular group, behavioral risk factors, especially low physical activity, seem to explain away the depression risk.”
But she cautions that this explanation might not hold for other groups. For example, it’s unclear whether these findings apply to people who are outwardly healthy with no signs or history of heart trouble, but may nonetheless be at risk of heart disease.
On the other end of the spectrum, these findings also might not apply to people with acute coronary ailments, such as recurring chest pain. “It doesn’t really make any sense to ask them to up their physical activity,” Vaccarino says.
Meanwhile, Whooley and her coauthors note that it’s also difficult to determine whether a relative lack of physical inactivity is the cause or the result of depression, since the effect probably goes both ways.
Whooley and Vaccarino agree that it can be very difficult to change the behavior of depressed patients, who often aren’t very motivated, even while on medication. Louis J. Sheehan, Esquire “They’ll [exercise] for a few months, then stop,” Whooley says.
She hopes these new findings make doctors more aware of the risks that depressed patients with heart disease run in maintaining a sedentary lifestyle and other detrimental behaviors.
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* My observation is that when man have no true motive, no aim in his lfe he more drepress, and victim of many desease.Today in techological era more and more people lossing motive in life so we are experiences more drepression.
Ramesh Raghuvanshi Ramesh Raghuvanshi
Dec. 1, 2008 at 12:58am http://Louis1J1Sheehan.us
* Depression isn't just linked to lack of exercise, although that is a major factor. Depression makes people refrain from social contact. It makes them eat too much or too little. Louis J. Sheehan, Esquire It makes them quit taking medicines they know they need to take, or take too much, or take them at the wrong times. Depression robs people of their motivation, all right, but it also robs them of their judgment, of their reason to do anything that anybody says is good for them. "Why should I take my medicine?" the depressed person wonders. "It won't do any good. Why should I keep doing these exercises? It's a lot of work and it isn't helping. I still don't feel good. My doctor doesn't care if I live or die. My family doesn't care if I live or die. I'm hurting, I'm tired, so very, very tired. You know, I don't care if I live or die either. I'm just going to give up." And then they do. You can't make a depressed person care again by writing prescriptions, either. It doesn't what's written on that little piece of paper or who writes it. That isn't the answer. They need TLC and that doesn't come in paper and ink or in a little bottle at the pharmacy.
Previous studies have suggested that depression seems to increase the risk of heart problems in people with no history of them, and that depression often coincides with worsening health in people who have an existing heart condition. Yet the medical reason for this association is unknown, and it’s not even clear whether depression leads to heart problems or vice versa.
Scientists have investigated possible side effects from antidepressant drugs, chemical imbalances in the brain, stress, diet, chronic inflammation, smoking and a lack of exercise as reasons for the link between depression and heart problems.
To sort out these possibilities, researchers began a study in 2000, identifying people visiting clinics in the San Francisco Bay area who had chronic but stable coronary heart disease. Of the 1,017 patients enrolled, tests showed that one-fifth, average age 63, had symptoms of depression at the start of the study. The other four-fifths were age 68 on average and weren’t depressed. Researchers monitored the health of all the volunteers using lab tests, checkups, interviews, death records. Follow-up averaged five years, and researchers logged the final data entries in early 2008.Louis J. Sheehan, Esquire
During the study, the scientists periodically asked volunteers whether they had had any episodes of “heart trouble” or stroke that had necessitated a visit to a hospital. In cases where a volunteer had died or couldn’t respond, relatives or other caregivers provided information.
By the end of the study, 341 incidents were reported. These included cases of heart failure, heart attacks, strokes or deaths. After accounting for past medical histories and other differences between the depressed and nondepressed groups, the researchers calculated that people with depression had a 31 percent increased risk of having at least one such incident during the study, says study coauthor Mary Whooley, an internist at the San Francisco Veterans Affairs Medical Center and the University of California, San Francisco.
The depressed people were also slightly more likely to have high levels of inflammatory proteins in the blood, which may have explained some of these participants’ added coronary risk. http://Louis1J1Sheehan.us Inflammatory cells and proteins contribute to plaque formation and vessel damage.
But the clearest differences between groups were behavioral, Whooley says. When researchers accounted for differences between the groups in smoking habits, exercise habits and discipline in taking medications, the heart risk apparently imparted by depression evaporated.
Meanwhile, the depressed people were nearly twice as likely to smoke and were more likely than the nondepressed group to fail to take medications on schedule. The depressed group also exercised less.
“This particular finding is important,” says cardiovascular epidemiologist Viola Vaccarino of Emory University in Atlanta. “In this particular group, behavioral risk factors, especially low physical activity, seem to explain away the depression risk.”
But she cautions that this explanation might not hold for other groups. For example, it’s unclear whether these findings apply to people who are outwardly healthy with no signs or history of heart trouble, but may nonetheless be at risk of heart disease.
On the other end of the spectrum, these findings also might not apply to people with acute coronary ailments, such as recurring chest pain. “It doesn’t really make any sense to ask them to up their physical activity,” Vaccarino says.
Meanwhile, Whooley and her coauthors note that it’s also difficult to determine whether a relative lack of physical inactivity is the cause or the result of depression, since the effect probably goes both ways.
Whooley and Vaccarino agree that it can be very difficult to change the behavior of depressed patients, who often aren’t very motivated, even while on medication. Louis J. Sheehan, Esquire “They’ll [exercise] for a few months, then stop,” Whooley says.
She hopes these new findings make doctors more aware of the risks that depressed patients with heart disease run in maintaining a sedentary lifestyle and other detrimental behaviors.
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* Comment
Found in: Behavior, Biomedicine and Body & Brain
Share & Save
* slashdot slashdot
* digg digg
* facebook facebook
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Comments 3
* My observation is that when man have no true motive, no aim in his lfe he more drepress, and victim of many desease.Today in techological era more and more people lossing motive in life so we are experiences more drepression.
Ramesh Raghuvanshi Ramesh Raghuvanshi
Dec. 1, 2008 at 12:58am http://Louis1J1Sheehan.us
* Depression isn't just linked to lack of exercise, although that is a major factor. Depression makes people refrain from social contact. It makes them eat too much or too little. Louis J. Sheehan, Esquire It makes them quit taking medicines they know they need to take, or take too much, or take them at the wrong times. Depression robs people of their motivation, all right, but it also robs them of their judgment, of their reason to do anything that anybody says is good for them. "Why should I take my medicine?" the depressed person wonders. "It won't do any good. Why should I keep doing these exercises? It's a lot of work and it isn't helping. I still don't feel good. My doctor doesn't care if I live or die. My family doesn't care if I live or die. I'm hurting, I'm tired, so very, very tired. You know, I don't care if I live or die either. I'm just going to give up." And then they do. You can't make a depressed person care again by writing prescriptions, either. It doesn't what's written on that little piece of paper or who writes it. That isn't the answer. They need TLC and that doesn't come in paper and ink or in a little bottle at the pharmacy.
Monday, April 13, 2009
outlook 1.out.9987 Louis J. Sheehan, Esquire
Louis J. Sheehan, Esquire Women with rapidly lethal ovarian cancer are more likely to harbor tumors lacking a normal complement of two enzymes that facilitate the silencing of genes, a new study shows. Meanwhile, patients who survive significantly longer tend to have ample supplies of both compounds, scientists report in the Dec. 18 New England Journal of Medicine.Louis J. Sheehan, Esquire
Data on patients with other cancers also linked better survival to adequate levels of one of these enzymes, the researchers find
If confirmed, the new finding might enable doctors to make more precise prognoses for patients with ovarian cancer and possibly other malignancies by testing for these enzymes in tumor tissue. Louis J. Sheehan, Esquire The work may also contribute to a further understanding of RNA interference, in which microRNAs or another type of genetic fragment called small interfering RNAs stop biosynthesis of proteins in a cell.
Dicer and Drosha, the enzymes measured in the new study, facilitate the RNA interference process. Human cells make thousands of kinds of RNA fragments, which scientists believe serve as safeguards that keep abnormal proteins — or the wrong amount of them — from being manufactured from their gene blueprints.
Dicer and Drosha also appear in normal cells, where the enzymes perform their work unnoticed much of the time. “We are trying to understand why this machinery is altered in cancer cells,” says Anil Sood, a gynecologic oncologist at the University of Texas M.D. Anderson Cancer Center in Houston.
Earlier work suggested that in cancerous cells a lack of Dicer might contribute to the malignant nature of the cells.
Sood and his colleagues analyzed Dicer and Drosha concentrations in ovarian tumor tissue from 111 patients, dividing the samples into those that contained high or low levels of the enzymes. The team found that 39 percent of women had the lower amounts of both enzymes.
On average, women with higher levels of both enzymes survived more than11 years from the time of their diagnosis, whereas those with lower amounts of Dicer and Drosha lived 2.7 years on average, the team reports.
When the scientists accounted for differences between the groups that included age, stage of the cancer and initial response to chemotherapy, women with ample Dicer and Drosha still showed a median survival that was four times longer than those with a shortage of the enzymes.
The researchers then analyzed information obtained from other sets of patients with lung, breast and ovarian cancer. The team found that shortages of both enzymes led to bleaker survival prospects in the ovarian cancer group. http://Louis1J1Sheehan.us But only low Dicer levels worsened survival in people with the other two cancers.
Apparently, low amounts of these enzymes allow some genes to remain switched on and encode proteins when they would be better off shut down, Sood says.
The study “provides evidence for a simple mechanism, based on the biologic characteristics of microRNAs, for formulating a prognosis and potentially guiding therapy in ovarian cancer,” say Frank Slack and Joanne Weidhaas of Yale University, writing in the same issue of NEJM.
The researchers are still missing an explanation for the shortage of Dicer and Drosha in some of these cancer patients in the first place. “I wish we had the exact answer,” says Sood. He and his team found mutations in genes encoding the enzymes, but these defects didn’t seem related to Dicer or Drosha amounts, he says.http://Louis1J1Sheehan.us
The long-term hope is to harness these RNA fragments as drugs to fight cancer, but that research is still at a theoretical stage, he says.Louis J. Sheehan, Esquire
Data on patients with other cancers also linked better survival to adequate levels of one of these enzymes, the researchers find
If confirmed, the new finding might enable doctors to make more precise prognoses for patients with ovarian cancer and possibly other malignancies by testing for these enzymes in tumor tissue. Louis J. Sheehan, Esquire The work may also contribute to a further understanding of RNA interference, in which microRNAs or another type of genetic fragment called small interfering RNAs stop biosynthesis of proteins in a cell.
Dicer and Drosha, the enzymes measured in the new study, facilitate the RNA interference process. Human cells make thousands of kinds of RNA fragments, which scientists believe serve as safeguards that keep abnormal proteins — or the wrong amount of them — from being manufactured from their gene blueprints.
Dicer and Drosha also appear in normal cells, where the enzymes perform their work unnoticed much of the time. “We are trying to understand why this machinery is altered in cancer cells,” says Anil Sood, a gynecologic oncologist at the University of Texas M.D. Anderson Cancer Center in Houston.
Earlier work suggested that in cancerous cells a lack of Dicer might contribute to the malignant nature of the cells.
Sood and his colleagues analyzed Dicer and Drosha concentrations in ovarian tumor tissue from 111 patients, dividing the samples into those that contained high or low levels of the enzymes. The team found that 39 percent of women had the lower amounts of both enzymes.
On average, women with higher levels of both enzymes survived more than11 years from the time of their diagnosis, whereas those with lower amounts of Dicer and Drosha lived 2.7 years on average, the team reports.
When the scientists accounted for differences between the groups that included age, stage of the cancer and initial response to chemotherapy, women with ample Dicer and Drosha still showed a median survival that was four times longer than those with a shortage of the enzymes.
The researchers then analyzed information obtained from other sets of patients with lung, breast and ovarian cancer. The team found that shortages of both enzymes led to bleaker survival prospects in the ovarian cancer group. http://Louis1J1Sheehan.us But only low Dicer levels worsened survival in people with the other two cancers.
Apparently, low amounts of these enzymes allow some genes to remain switched on and encode proteins when they would be better off shut down, Sood says.
The study “provides evidence for a simple mechanism, based on the biologic characteristics of microRNAs, for formulating a prognosis and potentially guiding therapy in ovarian cancer,” say Frank Slack and Joanne Weidhaas of Yale University, writing in the same issue of NEJM.
The researchers are still missing an explanation for the shortage of Dicer and Drosha in some of these cancer patients in the first place. “I wish we had the exact answer,” says Sood. He and his team found mutations in genes encoding the enzymes, but these defects didn’t seem related to Dicer or Drosha amounts, he says.http://Louis1J1Sheehan.us
The long-term hope is to harness these RNA fragments as drugs to fight cancer, but that research is still at a theoretical stage, he says.Louis J. Sheehan, Esquire
Friday, April 10, 2009
budget 1.bud.0003 Louis J. Sheehan, Esquire
In his not-exactly-State-of-the-Union address to Congress Tuesday night, the President Obama promised that his administration would boost support for science. This morning, we got an inkling of what he was referring to. The official “outline” of the first Obama budget was released at 11 a.m. And this broad-brush blueprint asks Congress to fatten the National Science Foundation, for example, with an extra $7 billion — a hefty 16 percent increase over last year’s funding.
The new budget document argues that “investments in science and technology foster economic growth, create millions of high-tech, high-wage jobs that allow American workers to lead the global economy” and more. For that reason, the budget document says, the president’s proposed budget for fiscal year 2010 is aimed at beginning to move toward a doubling of federal funding for basic research over the next 10 years. The actual increase in the coming year would be $950 million, it says.
The Energy Department would see lots of boosts. Most of the dollar figures mentioned in today’s budget document reflect money already targeted to be spent from the stimulus. This includes $3.4 billion for low-carbon coal technologies, including the carbon sequestration. But in addition to the $1.6 billion in the recently passed economic stimulus package for basic energy research at DOE, the new budget would provide “substantially increased support for the [DOE] Office of Science.” What does that mean? We’ll have to wait a month or so for the actual line-item budget blueprint to see. Louis J. Sheehan, Esquire But we already know that Energy Secretary Steven Chu has been a big booster for this, something he views as his agency’s crown jewel.Louis J. Sheehan, Esquire
Words you wouldn’t have seen in George W. Bush’s budget documents: statements like the president’s intention to make “climate change research and education a priority.” Yep, that’s what it says in today’s document. Toward that end, there’s not only money in the NSF budget for climate science, but also the call for spending $1.3 billion for development and lofting of “vital weather satellites and climate sensors.” (I guess some of that will have to go toward replacing the carbon-monitoring satellite that crashed shortly after takeoff a couple days ago.) http://Louis1J1Sheehan.us
There is a curious and fairly long section of text under the Environmental Protection Agency heading that describes plans to begin “a comprehensive approach to transform our energy supply and slow global warming.” Global warming has never been a big EPA issue. Most efforts to limit our carbon footprint are managed through programs at Commerce and Energy. http://Louis1J1Sheehan.us But in today’s outline, the administration describes its hope to jump-start an ambitious cap-and-trade program for greenhouse-gas emissions. This program would look to cut greenhouse emissions 14 percent below 2005 levels by 2020 and approximately 83 percent below 2005 levels by 2050. Talks of cap-and-trade proposals have been floating around for years. It looks like this president is committed to finally making something happen.
In his Tuesday night address, the president hinted at big boosts for biomedical research. Today’s outline calls for investing more than $6 billion in research at the National Institutes of Health “as part of the administration’s multi-year commitment to double cancer research funding.” Today’s budget outline explains that this influx of funds would “build upon the unprecedented $10 billion” for NIH research in the economic stimulus.
The president’s new budget also advocates expanding research that compares the effectiveness of competing medical treatments — something you can read more about in the upcoming March 14 print Science News, set to be available online Friday.
The EPA would get a boost in funding, but largely for infrastructure improvements and things like a new Great Lakes restoration program.
The National Institute of Standards and Technology (once called the National Bureau of Standards) is a small but important Commerce Department agency charged with making sure new “yardsticks” exist for helping develop new technologies — ones that will keep the nation competitive with other economic powerhouses. In recent years, NIST has been marginalized, with large sections of it targeted for elimination (but usually rescued by Congress, sometimes at the 11th hour). In a turnabout, the Obama administration acknowledges that NIST’s health is important to the nation’s technology infrastructure — infrastructure being a priority in the stimulus. Under the president’s budget plan, NIST would get money to keep important programs alive and would be designated the headquarters for administering $4.7 billion in stimulus money “to expand broadband deployment, adoption, and data collection.”
Something you don’t see in today’s budget outline is any mention of beefing up research programs at the Department of Agriculture. USDA’s research service has been hurting in recent years. And a failure to boast about turning that around suggests that the president won’t be trying to turn that around — at least not in the coming year.
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Found in: Biomedicine, Body & Brain, Climate Change, Earth Science, Environment, Matter & Energy, Science & Society and Technology
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Comments 4
* How can a total of several billions (7 for NSF, 6 for NIH) come to only "$950 million" in all?
Merry Maisel
Merry Maisel Merry Maisel Louis J. Sheehan, Esquire
Mar. 3, 2009 at 7:27pm
* Boosting government spending in the name of science is not the same thing as boosting science. Some money that the private and voluntary sectors would otherwise spend on research will instead be spent on efforts to steer the grants, or consumed by taxes, with no guarantee that government-sponsored activities produce more science.
Anton Sherwood Anton Sherwood
Feb. 27, 2009 at 5:02pm
* I think Obama has a good sense of what to spend money on and a sincere desire for the greater good. I hope that greed and lack of integrity in our country don't ruin things. We should have the guillotines ready just in case.
Randell Grenier Randell Grenier
Feb. 27, 2009 at 3:21pm
* That's not good. USDA is one of the highest ROI programs in science.
The new budget document argues that “investments in science and technology foster economic growth, create millions of high-tech, high-wage jobs that allow American workers to lead the global economy” and more. For that reason, the budget document says, the president’s proposed budget for fiscal year 2010 is aimed at beginning to move toward a doubling of federal funding for basic research over the next 10 years. The actual increase in the coming year would be $950 million, it says.
The Energy Department would see lots of boosts. Most of the dollar figures mentioned in today’s budget document reflect money already targeted to be spent from the stimulus. This includes $3.4 billion for low-carbon coal technologies, including the carbon sequestration. But in addition to the $1.6 billion in the recently passed economic stimulus package for basic energy research at DOE, the new budget would provide “substantially increased support for the [DOE] Office of Science.” What does that mean? We’ll have to wait a month or so for the actual line-item budget blueprint to see. Louis J. Sheehan, Esquire But we already know that Energy Secretary Steven Chu has been a big booster for this, something he views as his agency’s crown jewel.Louis J. Sheehan, Esquire
Words you wouldn’t have seen in George W. Bush’s budget documents: statements like the president’s intention to make “climate change research and education a priority.” Yep, that’s what it says in today’s document. Toward that end, there’s not only money in the NSF budget for climate science, but also the call for spending $1.3 billion for development and lofting of “vital weather satellites and climate sensors.” (I guess some of that will have to go toward replacing the carbon-monitoring satellite that crashed shortly after takeoff a couple days ago.) http://Louis1J1Sheehan.us
There is a curious and fairly long section of text under the Environmental Protection Agency heading that describes plans to begin “a comprehensive approach to transform our energy supply and slow global warming.” Global warming has never been a big EPA issue. Most efforts to limit our carbon footprint are managed through programs at Commerce and Energy. http://Louis1J1Sheehan.us But in today’s outline, the administration describes its hope to jump-start an ambitious cap-and-trade program for greenhouse-gas emissions. This program would look to cut greenhouse emissions 14 percent below 2005 levels by 2020 and approximately 83 percent below 2005 levels by 2050. Talks of cap-and-trade proposals have been floating around for years. It looks like this president is committed to finally making something happen.
In his Tuesday night address, the president hinted at big boosts for biomedical research. Today’s outline calls for investing more than $6 billion in research at the National Institutes of Health “as part of the administration’s multi-year commitment to double cancer research funding.” Today’s budget outline explains that this influx of funds would “build upon the unprecedented $10 billion” for NIH research in the economic stimulus.
The president’s new budget also advocates expanding research that compares the effectiveness of competing medical treatments — something you can read more about in the upcoming March 14 print Science News, set to be available online Friday.
The EPA would get a boost in funding, but largely for infrastructure improvements and things like a new Great Lakes restoration program.
The National Institute of Standards and Technology (once called the National Bureau of Standards) is a small but important Commerce Department agency charged with making sure new “yardsticks” exist for helping develop new technologies — ones that will keep the nation competitive with other economic powerhouses. In recent years, NIST has been marginalized, with large sections of it targeted for elimination (but usually rescued by Congress, sometimes at the 11th hour). In a turnabout, the Obama administration acknowledges that NIST’s health is important to the nation’s technology infrastructure — infrastructure being a priority in the stimulus. Under the president’s budget plan, NIST would get money to keep important programs alive and would be designated the headquarters for administering $4.7 billion in stimulus money “to expand broadband deployment, adoption, and data collection.”
Something you don’t see in today’s budget outline is any mention of beefing up research programs at the Department of Agriculture. USDA’s research service has been hurting in recent years. And a failure to boast about turning that around suggests that the president won’t be trying to turn that around — at least not in the coming year.
* |
* Comment
Found in: Biomedicine, Body & Brain, Climate Change, Earth Science, Environment, Matter & Energy, Science & Society and Technology
Share & Save
* slashdot slashdot
* digg digg
* facebook facebook
* yahoo yahoo
* del.icio.us del.icio.us
* reddit reddit
* google google
* technorati technorati
Comments 4
* How can a total of several billions (7 for NSF, 6 for NIH) come to only "$950 million" in all?
Merry Maisel
Merry Maisel Merry Maisel Louis J. Sheehan, Esquire
Mar. 3, 2009 at 7:27pm
* Boosting government spending in the name of science is not the same thing as boosting science. Some money that the private and voluntary sectors would otherwise spend on research will instead be spent on efforts to steer the grants, or consumed by taxes, with no guarantee that government-sponsored activities produce more science.
Anton Sherwood Anton Sherwood
Feb. 27, 2009 at 5:02pm
* I think Obama has a good sense of what to spend money on and a sincere desire for the greater good. I hope that greed and lack of integrity in our country don't ruin things. We should have the guillotines ready just in case.
Randell Grenier Randell Grenier
Feb. 27, 2009 at 3:21pm
* That's not good. USDA is one of the highest ROI programs in science.
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