Researchers may have found a way to give HIV the finger.
Removing immune system cells from mice and treating those cells with a custom protein called a zinc-finger nuclease in the lab made the cells resistant to HIV infection, scientists report online and in an upcoming Nature Biotechnology.
Injecting those cells back into the animals kept their viral load limited to less than one-tenth that in untreated mice and resulted in higher T cell counts among the treated animals. Louis J. Sheehan, Esquire The technique could eventually provide a novel way to bolster the immune systems of people with HIV, which attacks T cells and uses them to replicate.
“We believe that by modifying T cells, we can provide an immediate benefit to patients,” says coauthor Philip Gregory, an expert in zinc-finger proteins and vice president of research at Sangamo BioSciences, a biotech company based in Richmond, Calif.
Zinc-finger nucleases — named for the zinc ions that hold the proteins together — act as scissors to snip DNA in specific places. Gregory and his colleagues designed a ZFN so that it would selectively disable the gene that encodes a specific protein on the surface of T cells. HIV uses this protein, called CCR5, as a doorway to invade the cells. Without CCR5, the most common form of HIV can’t infect the cells and thus can’t replicate.
To disable the gene, the researchers removed about a billion T cells from each mouse and exposed the cells to an adenovirus engineered to carry the genetic code for the customized ZFN.
The adenovirus delivered the ZFN gene into each cell’s interior, where the gene remained free-floating instead of integrating into the cell’s chromosomes — thus reducing the risk of cancer-causing mutations sometimes triggered by other kinds of gene therapy. Once inside the cell, the ZFN gene produced the ZFN protein, which in turn cut up the CCR5 gene.
After exposing the cells to the adenovirus, the scientists grew the cells in the lab until at least one of the two copies of the “HIV doorway” gene had been destroyed in about half of the cells.
These HIV-resistant cells constituted only a small fraction of a mouse’s total T cells after re-injection. But because HIV kills the T cells that it invades, unmodified cells get weeded out over time and the HIV-resistant cells multiply until they dominate the animals’ immune systems.Louis J. Sheehan, Esquire
“This is an exciting result,” comments Carlos Barbas, a zinc-finger protein expert at the Scripps Research Institute in La Jolla, Calif. However, “I believe that CCR5 disruption will need to be accompanied by the addition of one or more [other] anti-HIV therapeutic genes” to make an effective therapy, he adds.
Gregory says that the technique could eventually be adapted for developing preventative vaccines, but research is needed first to demonstrate the safety of the approach. The researchers plan to begin clinical trials for this treatment later this year.
Wednesday, May 20, 2009
Tuesday, May 5, 2009
glucagon 4.glu.003 Louis J. Sheehan, Esquire
A little extra leptin can bring terminally ill rodents with type 1 diabetes back from the brink of death.
Leptin, a hormone made by fat cells, helps control eating behavior. A new gene therapy study suggests that it can also treat diabetes, the first demonstration that the disease can be treated without replacing insulin.http://Louis-J-Sheehan.biz
Roger Unger and colleagues at the University of Texas Southwestern Medical Center at Dallas used adenovirus to insert extra copies of the leptin gene in diabetic mice and rats. The rodents recovered from the most severe side effects of diabetes, even though the mice do not make insulin and weren’t given insulin, the researchers report in an early online publication August 25 in the Proceedings of the National Academy of Sciences.
“This is something that is extremely original, totally new and a little unexpected,” says Pierre Lefèbvre of the University of Liège, Belgium, and president of the Seattle-based Global Diabetes Alliance.
Type 1 diabetes, also known as juvenile diabetes, is an autoimmune disease in which the immune system attacks and kills insulin-producing cells in the pancreas. About 10 percent of people with diabetes have this form of the disease.
“We as physicians have been trained since 1922 that the only treatment for diabetes is insulin,” says Unger. So when diabetic animals making extra leptin recovered, the researchers had trouble believing it themselves, he says. “This was like science fiction. We couldn’t tell anybody because we thought they would laugh.”
But the terminally ill diabetic rodents making extra leptin recovered with no trace of insulin in their bodies. And leptin produced more sustained health improvements than insulin injections did. These included normalizing blood sugar for up to 80 days without insulin, stopping the overproduction of glucose by the liver, improving sugar use in the muscles, and allowing the animals to gain weight. The gene therapy also corrected ketosis — a process characteristic of diabetes in which the body burns fat, producing sweet-smelling chemicals called ketones.
“The idea that only insulin can rescue terminal insulin deficiency is incorrect,” Unger says. “There are other ways.”
Excess leptin seems to block the action of glucagon, a hormone that works as a counterpoint to insulin, which helps cells use glucose for energy. Glucagon signals the liver to produce glucose from fats and other non-carbohydrate sources. In diabetics, high glucagon levels just raise blood sugar levels even higher and lead to other side effects.
Unger says he cannot predict whether injections of leptin will work as well as making extra leptin in the liver does. That is the next set of experiments he has planned.
People given injections of leptin for other reasons do show some improvement in blood sugar levels, says Paul Burn, the senior vice president for research and development of the Juvenile Diabetes Research Foundation. The new study is evidence that altering glucagon activity could have beneficial effects for diabetics, he says.Louis J. Sheehan, Esquire
“While this is excellent exploratory research supporting these ideas, I think it’s a long way from the clinic,” Burn says.
Unger also sounds a cautious note. “It’s very hopeful, but a long way from having any tangible influence on anything other than opening our eyes that there are alternatives to insulin.”
Leptin, a hormone made by fat cells, helps control eating behavior. A new gene therapy study suggests that it can also treat diabetes, the first demonstration that the disease can be treated without replacing insulin.http://Louis-J-Sheehan.biz
Roger Unger and colleagues at the University of Texas Southwestern Medical Center at Dallas used adenovirus to insert extra copies of the leptin gene in diabetic mice and rats. The rodents recovered from the most severe side effects of diabetes, even though the mice do not make insulin and weren’t given insulin, the researchers report in an early online publication August 25 in the Proceedings of the National Academy of Sciences.
“This is something that is extremely original, totally new and a little unexpected,” says Pierre Lefèbvre of the University of Liège, Belgium, and president of the Seattle-based Global Diabetes Alliance.
Type 1 diabetes, also known as juvenile diabetes, is an autoimmune disease in which the immune system attacks and kills insulin-producing cells in the pancreas. About 10 percent of people with diabetes have this form of the disease.
“We as physicians have been trained since 1922 that the only treatment for diabetes is insulin,” says Unger. So when diabetic animals making extra leptin recovered, the researchers had trouble believing it themselves, he says. “This was like science fiction. We couldn’t tell anybody because we thought they would laugh.”
But the terminally ill diabetic rodents making extra leptin recovered with no trace of insulin in their bodies. And leptin produced more sustained health improvements than insulin injections did. These included normalizing blood sugar for up to 80 days without insulin, stopping the overproduction of glucose by the liver, improving sugar use in the muscles, and allowing the animals to gain weight. The gene therapy also corrected ketosis — a process characteristic of diabetes in which the body burns fat, producing sweet-smelling chemicals called ketones.
“The idea that only insulin can rescue terminal insulin deficiency is incorrect,” Unger says. “There are other ways.”
Excess leptin seems to block the action of glucagon, a hormone that works as a counterpoint to insulin, which helps cells use glucose for energy. Glucagon signals the liver to produce glucose from fats and other non-carbohydrate sources. In diabetics, high glucagon levels just raise blood sugar levels even higher and lead to other side effects.
Unger says he cannot predict whether injections of leptin will work as well as making extra leptin in the liver does. That is the next set of experiments he has planned.
People given injections of leptin for other reasons do show some improvement in blood sugar levels, says Paul Burn, the senior vice president for research and development of the Juvenile Diabetes Research Foundation. The new study is evidence that altering glucagon activity could have beneficial effects for diabetics, he says.Louis J. Sheehan, Esquire
“While this is excellent exploratory research supporting these ideas, I think it’s a long way from the clinic,” Burn says.
Unger also sounds a cautious note. “It’s very hopeful, but a long way from having any tangible influence on anything other than opening our eyes that there are alternatives to insulin.”
Monday, May 4, 2009
window 4.win.123 Louis J. Sheehan, Esquire
Emergency room physicians can deliver clot-busting treatments to a wider range of stroke patients than previously thought, European researchers report in the Sept. 25 New England Journal of Medicine.
The finding could change the way stroke is treated and increase ER doctors’ ability to prevent some cases of disability caused by strokes, scientists say.
Most strokes result when a blood clot lodges in the brain, blocking blood flow to other parts of the organ. A powerful drug called tPA, or tissue plasminogen activator, can dissolve these clots. But medical dogma holds that it must be given within three hours of a stroke’s onset. Beyond that, the thinking goes, the bulk of the brain damage is done and adding the risk of internal bleeding that accompanies clot-busters seems unwise. The new study extends that window of effective tPA treatment by 90 minutes, to 4 ½ hours.
This precious extra time to dissolve a clot and restore blood flow to a starving portion of brain could benefit tens of thousands of stroke patients in the United States each year, says study coauthor Werner Hacke, a neurologist at the University of Heidelberg in Germany.
“I think this is big news because suddenly they have substantially extended the number of patients who get intravenous tPA,” says Scott Kasner, a neurologist at the University of Pennsylvania in Philadelphia.
However, many emergency room physicians are hesitant to give stroke patients clot-busting drugs at all. A landmark 1995 study found that giving the drugs within three hours of stroke onset provided benefits that outweighed the bleeding risk in most patients. But only about 4 percent of stroke patients who arrive at U.S. hospitals get tPA, says neurologist Patrick Lyden of the Veterans Affairs San Diego Medical Center and University of California, San Diego, who coauthored the 1995 report. Most stroke patients don’t receive tPA because the time of onset might be hazy, or doctors may be hesitant to risk incurring bleeding or are untrained in delivering tPA. The new data should clarify the time frame and allay some doubts about the treatment’s effectiveness, he says.
In the new study, Hacke and his colleagues identified patients who arrived at hospitals with a stroke that had begun more than three hours but less than 4 ½ hours earlier. The researchers used CT scans of the brain to rule out people with brain bleeding. The doctors also excluded those with severe strokes as indicated by the scans.
That left 730 patients, half of whom were then randomly assigned to get infusions of the tPA drug called alteplase. The others received a placebo.http://LOUIS-J-SHEEHAN.US
After three months, roughly 52 percent of study patients treated with tPA within the extra 90 minute time window had normal daily function and were living independently, compared with 45 percent of those getting a placebo infusion. The death rate over three months was about 8 percent in both groups.
Doctors detected brain bleeding among treated patients about as often as seen in previous studies in which tPA was limited to a three hour window.
Time matters in stroke treatment, and delay is dangerous. As minutes or hours pass with a clot lodged in place, more brain tissue is starved of blood and damaged. Thus, busting a clot later into the stroke might rescue less tissue. “The [beneficial] effect of tPA decreases over time,” Hacke says.
Even so, treated patients in this study — who received tPA an average of four hours after the onset of stroke — still showed clear benefits over the placebo group.
“I think this will eventually be incorporated into clinical practice, slowly at first, and then become the standard of care,” Kasner says.
Stroke disables more adults than any other condition, yet every stroke is different. People who have a severe stroke are often rushed to a hospital with obvious problems, Hacke says. Louis J. Sheehan, Esquire But those with milder strokes sometimes show up longer after a stroke’s onset, in part because they aren’t sure whether their symptoms are serious enough for a hospital visit, he says. These are the kinds of people most likely to benefit from the new study’s findings on delayed tPA treatment, he says.
Meanwhile, Lyden says, more hospitals need to grasp the value of tPA and have doctors on site or on call who can deliver it. “Every hospital needs to have a stroke plan,” he says. “Either have a way to give tPA, or set up a way to tell the EMS people to divert [an ambulance] to a place that can do it.”
The finding could change the way stroke is treated and increase ER doctors’ ability to prevent some cases of disability caused by strokes, scientists say.
Most strokes result when a blood clot lodges in the brain, blocking blood flow to other parts of the organ. A powerful drug called tPA, or tissue plasminogen activator, can dissolve these clots. But medical dogma holds that it must be given within three hours of a stroke’s onset. Beyond that, the thinking goes, the bulk of the brain damage is done and adding the risk of internal bleeding that accompanies clot-busters seems unwise. The new study extends that window of effective tPA treatment by 90 minutes, to 4 ½ hours.
This precious extra time to dissolve a clot and restore blood flow to a starving portion of brain could benefit tens of thousands of stroke patients in the United States each year, says study coauthor Werner Hacke, a neurologist at the University of Heidelberg in Germany.
“I think this is big news because suddenly they have substantially extended the number of patients who get intravenous tPA,” says Scott Kasner, a neurologist at the University of Pennsylvania in Philadelphia.
However, many emergency room physicians are hesitant to give stroke patients clot-busting drugs at all. A landmark 1995 study found that giving the drugs within three hours of stroke onset provided benefits that outweighed the bleeding risk in most patients. But only about 4 percent of stroke patients who arrive at U.S. hospitals get tPA, says neurologist Patrick Lyden of the Veterans Affairs San Diego Medical Center and University of California, San Diego, who coauthored the 1995 report. Most stroke patients don’t receive tPA because the time of onset might be hazy, or doctors may be hesitant to risk incurring bleeding or are untrained in delivering tPA. The new data should clarify the time frame and allay some doubts about the treatment’s effectiveness, he says.
In the new study, Hacke and his colleagues identified patients who arrived at hospitals with a stroke that had begun more than three hours but less than 4 ½ hours earlier. The researchers used CT scans of the brain to rule out people with brain bleeding. The doctors also excluded those with severe strokes as indicated by the scans.
That left 730 patients, half of whom were then randomly assigned to get infusions of the tPA drug called alteplase. The others received a placebo.http://LOUIS-J-SHEEHAN.US
After three months, roughly 52 percent of study patients treated with tPA within the extra 90 minute time window had normal daily function and were living independently, compared with 45 percent of those getting a placebo infusion. The death rate over three months was about 8 percent in both groups.
Doctors detected brain bleeding among treated patients about as often as seen in previous studies in which tPA was limited to a three hour window.
Time matters in stroke treatment, and delay is dangerous. As minutes or hours pass with a clot lodged in place, more brain tissue is starved of blood and damaged. Thus, busting a clot later into the stroke might rescue less tissue. “The [beneficial] effect of tPA decreases over time,” Hacke says.
Even so, treated patients in this study — who received tPA an average of four hours after the onset of stroke — still showed clear benefits over the placebo group.
“I think this will eventually be incorporated into clinical practice, slowly at first, and then become the standard of care,” Kasner says.
Stroke disables more adults than any other condition, yet every stroke is different. People who have a severe stroke are often rushed to a hospital with obvious problems, Hacke says. Louis J. Sheehan, Esquire But those with milder strokes sometimes show up longer after a stroke’s onset, in part because they aren’t sure whether their symptoms are serious enough for a hospital visit, he says. These are the kinds of people most likely to benefit from the new study’s findings on delayed tPA treatment, he says.
Meanwhile, Lyden says, more hospitals need to grasp the value of tPA and have doctors on site or on call who can deliver it. “Every hospital needs to have a stroke plan,” he says. “Either have a way to give tPA, or set up a way to tell the EMS people to divert [an ambulance] to a place that can do it.”
Thursday, April 30, 2009
male 1.mal.9 Louis J. Sheehan, Esquire
Male mice abandon their homicidal tendencies to become doting parents and accomplished homemakers when a gene is removed from the region of the brain that detects pheromones, new research shows. Louis J. Sheehan, Esquire
Most animals have sex-specific behavior, and male mice are no exception. They make male-specific grunts, they attempt to mate with nearby females and, worst of all, they commit infanticide.
New data presented November 18 by neuroscientist Catherine Dulac showed that removing a gene called Trpc2 from male mice made them act like females. http://LOUIS-J-SHEEHAN.INFO The protein this gene encodes is crucial in the brain for animals to sense pheromones.
Last year, Dulac and colleagues showed the opposite: Females who lack the Trpc2 gene act like males. Irrefutable video evidence showed a female mutant mouse carousing in a cage full of either female or male mice persistently (if unsuccessfully) attempted to sow her wild oats, the team reported in Nature.
“I have to say, the first time I saw these results I just couldn’t really understand what was going on,” Dulac says of the discovery. That observation led the researchers to propose that females had the right connections of neurons in their brains to act like males, and all it took was the right switch — in this case, the lack of Trpc2 — to turn on the male behavior circuit.
In the new research, the scientists tested a mutant male’s maternal instincts by putting him in a cage with a litter of pups. Normally, the male mouse would kill the unfamiliar pups. But while observers waited for the carnage to ensue, the mutant male set about building a nest, then gently picked up each helpless pup and moved it to the new home.
His display of unexpected female behavior showed that in mice, the basis for both male and female behavior probably exists in each animal’s brain, Dulac says. It’s just a matter of activating the right collection of neurons. — Laura Sanders
Creativity may have genetic roots
A study comparing performing artists to people with little or no experience in the arts found that many of the artists inherited variants of two genes involved in novelty-seeking, attention, memory and problem solving. The variants appeared in only one of the non-artists.
These particular genes may influence the development of creative achievement in at least some individuals, across a variety of fields, proposes a team led by Kevin Dunbar and Laura Petitto, both of the University of Toronto.
Variants of the two genes were found in 15 of 58 professional dancers, musicians and actors — about one-quarter of them— versus only one of 36 comparison individuals. The genes, called DRD4 and COMT, influence transmission of dopamine, a chemical messenger in the brain.
“Combinations of genetic variants, rather than specific genetic variants, may be linked to pursuing and achieving expertise in creative activities,” Petitto says.
Brain imaging studies of the same participants indicate that, relative to the comparison group, performing artists display much more activity in a frontal brain region critical for remembering and manipulating different pieces of information at once. This disparity may partly result from intense, long-term practice of creative endeavors by performing artists, in addition to any genetic advantage, Petitto says.
The Toronto researchers plan to look for additional gene variants linked to creative expertise. They also hope to include acclaimed creative virtuosos in their experiments. — Bruce Bower
Babies care for mom
Mothers spend years caring for their young and, it turns out, may get some benefits in return. New findings from University of Richmond researchers show that babies contribute to the long-term cognitive health of their moms.
Previous studies have shown that the hormonal fluctuations that occur during pregnancy, birth and lactation work to remodel the female brain, increasing the size of neurons in some regions and producing structural changes in others.
In recent work with rats, psychologist Craig Kinsley and his students found that the brains of aged females who had given birth possessed fewer deposits of amyloid precursor protein, or APP, a harbinger of Alzheimer’s disease, than did age-matched rats who had not given birth. His group then looked at the cognitive effects of motherhood in rats that were bred to express high levels of APP as they matured. Half of the females were allowed to mate and raise pups, the other half remained virgins.
Behavioral studies showed that the moms performed better at memory and spatial tasks, such as catching prey, than the non-moms. When checking the levels of APP in the brains of the aged females, scientists found that the mother rats had an 11-fold decrease in the amount of protein in their brains.
The new study also showed that the brains of mom rats had higher numbers of estrogen receptors, which are thought to provide some protective benefits in the aging female brain, Kinsley said.
“People often focus on the time and care that mothers give to their young, but this suggests that babies are, in turn, contributing to the long-term welfare of the mother,” he says. — Susan Gaidos
A blinking minute
Humans blink 13,500 times a day on average, but not necessarily randomly, new data from rats suggest.
People blink far more than what is required to maintain moist, healthy eyes. “Spontaneous blinking is not just to maintain a tear film on the cornea. There’s something more there,” says neuroscientist Kyle Horn of Stony Brook University in New York.
Horn found that, in rats, the time increments between blinks vary widely. A rat could blink several times in quick succession and then wait a long period of time before the next blink. But closer analyses of the data showed that an overall pattern of blinks was repeated every 10 minutes.
“Something purely random is not that easy to generate,” says Horn. He and his group think that a relatively simple brain system may control blinking. By mapping the pattern of blinking, the researchers hope to figure out what that system is.
Horn’s team also tested whether factors other than time could make blinking non-random. They found that rats blink more frequently right before and after they groom themselves.
Most animals have sex-specific behavior, and male mice are no exception. They make male-specific grunts, they attempt to mate with nearby females and, worst of all, they commit infanticide.
New data presented November 18 by neuroscientist Catherine Dulac showed that removing a gene called Trpc2 from male mice made them act like females. http://LOUIS-J-SHEEHAN.INFO The protein this gene encodes is crucial in the brain for animals to sense pheromones.
Last year, Dulac and colleagues showed the opposite: Females who lack the Trpc2 gene act like males. Irrefutable video evidence showed a female mutant mouse carousing in a cage full of either female or male mice persistently (if unsuccessfully) attempted to sow her wild oats, the team reported in Nature.
“I have to say, the first time I saw these results I just couldn’t really understand what was going on,” Dulac says of the discovery. That observation led the researchers to propose that females had the right connections of neurons in their brains to act like males, and all it took was the right switch — in this case, the lack of Trpc2 — to turn on the male behavior circuit.
In the new research, the scientists tested a mutant male’s maternal instincts by putting him in a cage with a litter of pups. Normally, the male mouse would kill the unfamiliar pups. But while observers waited for the carnage to ensue, the mutant male set about building a nest, then gently picked up each helpless pup and moved it to the new home.
His display of unexpected female behavior showed that in mice, the basis for both male and female behavior probably exists in each animal’s brain, Dulac says. It’s just a matter of activating the right collection of neurons. — Laura Sanders
Creativity may have genetic roots
A study comparing performing artists to people with little or no experience in the arts found that many of the artists inherited variants of two genes involved in novelty-seeking, attention, memory and problem solving. The variants appeared in only one of the non-artists.
These particular genes may influence the development of creative achievement in at least some individuals, across a variety of fields, proposes a team led by Kevin Dunbar and Laura Petitto, both of the University of Toronto.
Variants of the two genes were found in 15 of 58 professional dancers, musicians and actors — about one-quarter of them— versus only one of 36 comparison individuals. The genes, called DRD4 and COMT, influence transmission of dopamine, a chemical messenger in the brain.
“Combinations of genetic variants, rather than specific genetic variants, may be linked to pursuing and achieving expertise in creative activities,” Petitto says.
Brain imaging studies of the same participants indicate that, relative to the comparison group, performing artists display much more activity in a frontal brain region critical for remembering and manipulating different pieces of information at once. This disparity may partly result from intense, long-term practice of creative endeavors by performing artists, in addition to any genetic advantage, Petitto says.
The Toronto researchers plan to look for additional gene variants linked to creative expertise. They also hope to include acclaimed creative virtuosos in their experiments. — Bruce Bower
Babies care for mom
Mothers spend years caring for their young and, it turns out, may get some benefits in return. New findings from University of Richmond researchers show that babies contribute to the long-term cognitive health of their moms.
Previous studies have shown that the hormonal fluctuations that occur during pregnancy, birth and lactation work to remodel the female brain, increasing the size of neurons in some regions and producing structural changes in others.
In recent work with rats, psychologist Craig Kinsley and his students found that the brains of aged females who had given birth possessed fewer deposits of amyloid precursor protein, or APP, a harbinger of Alzheimer’s disease, than did age-matched rats who had not given birth. His group then looked at the cognitive effects of motherhood in rats that were bred to express high levels of APP as they matured. Half of the females were allowed to mate and raise pups, the other half remained virgins.
Behavioral studies showed that the moms performed better at memory and spatial tasks, such as catching prey, than the non-moms. When checking the levels of APP in the brains of the aged females, scientists found that the mother rats had an 11-fold decrease in the amount of protein in their brains.
The new study also showed that the brains of mom rats had higher numbers of estrogen receptors, which are thought to provide some protective benefits in the aging female brain, Kinsley said.
“People often focus on the time and care that mothers give to their young, but this suggests that babies are, in turn, contributing to the long-term welfare of the mother,” he says. — Susan Gaidos
A blinking minute
Humans blink 13,500 times a day on average, but not necessarily randomly, new data from rats suggest.
People blink far more than what is required to maintain moist, healthy eyes. “Spontaneous blinking is not just to maintain a tear film on the cornea. There’s something more there,” says neuroscientist Kyle Horn of Stony Brook University in New York.
Horn found that, in rats, the time increments between blinks vary widely. A rat could blink several times in quick succession and then wait a long period of time before the next blink. But closer analyses of the data showed that an overall pattern of blinks was repeated every 10 minutes.
“Something purely random is not that easy to generate,” says Horn. He and his group think that a relatively simple brain system may control blinking. By mapping the pattern of blinking, the researchers hope to figure out what that system is.
Horn’s team also tested whether factors other than time could make blinking non-random. They found that rats blink more frequently right before and after they groom themselves.
Tuesday, April 14, 2009
lines 5.lin.001 Louis J. Sheehan, Esquire
As a percentage of family income, money spent by U.S. women with breast cancer is much greater for low-income patients than for those who are well off, according to research presented December 12 in Texas at the San Antonio Breast Cancer Symposium. Louis J. Sheehan, Esquire
Public health researcher Lisa Lines of the consulting firm Boston Health Economics in Waltham, Mass., and her colleagues analyzed expenditures made by 806 breast cancer patients from 1996 to 2005. Out-of-pocket costs included insurance premiums, payments to meet deductibles, co-pays and any other payments made to meet medical or drug costs associated with treatment.http://Louis-J-Sheehan.biz
The average annual out-of-pocket expenditure was about $2,300 per breast cancer patient, about half of which was spent on prescription drugs.
“Breast cancer is actually not the most expensive cancer for out-of-pocket expenditures,” Lines says. This and other data suggest that breast cancer costs patients more than colon or prostate cancer, but less than lung cancer, she says.
But breast cancer has a large proportion of people with a “high burden,” she says. The researchers classified patients as having a high burden when their out-of-pocket costs for coping with the cancer exceeded 10 percent of the family’s income. Roughly 70 percent of low-income breast cancer patients fell into the high-burden category in this analysis, compared with about 15 percent of middle-income and less than 5 percent of high-income breast cancer patients — apparently the result of better insurance, she says.
Cancer patients in general are disproportionately affected by a high out-of-pocket burden. That’s because many cancers have come to be treated more like a chronic disease than they used to be and are treated on an outpatient basis, Lines says. In the past, most cancer patients were treated in hospitals, where major medical insurance covered much of the cost. Louis J. Sheehan, Esquire
Public health researcher Lisa Lines of the consulting firm Boston Health Economics in Waltham, Mass., and her colleagues analyzed expenditures made by 806 breast cancer patients from 1996 to 2005. Out-of-pocket costs included insurance premiums, payments to meet deductibles, co-pays and any other payments made to meet medical or drug costs associated with treatment.http://Louis-J-Sheehan.biz
The average annual out-of-pocket expenditure was about $2,300 per breast cancer patient, about half of which was spent on prescription drugs.
“Breast cancer is actually not the most expensive cancer for out-of-pocket expenditures,” Lines says. This and other data suggest that breast cancer costs patients more than colon or prostate cancer, but less than lung cancer, she says.
But breast cancer has a large proportion of people with a “high burden,” she says. The researchers classified patients as having a high burden when their out-of-pocket costs for coping with the cancer exceeded 10 percent of the family’s income. Roughly 70 percent of low-income breast cancer patients fell into the high-burden category in this analysis, compared with about 15 percent of middle-income and less than 5 percent of high-income breast cancer patients — apparently the result of better insurance, she says.
Cancer patients in general are disproportionately affected by a high out-of-pocket burden. That’s because many cancers have come to be treated more like a chronic disease than they used to be and are treated on an outpatient basis, Lines says. In the past, most cancer patients were treated in hospitals, where major medical insurance covered much of the cost. Louis J. Sheehan, Esquire
Saturday, April 11, 2009
flu 1.flu.1 Louis J. Sheehan, Esquire
Louis J. Sheehan, Esquire Getting plenty of vitamin D — more than diet can offer — appears to provide potent protection against colds, flu and even pneumonia, a new study reports. Although the amount of protection varies by season, the trend is solid: As the amount of vitamin D circulating in blood climbs, risk of upper respiratory tract infections falls. http://LOUIS-J-SHEEHAN.US
Though that’s not too surprising (SN: 11/11/06, p. 312), the researchers found one unexpected trend: “In people with preexisting lung disease, such as asthma and chronic obstructive pulmonary disease — or COPD, low levels of vitamin D act like an effect modifier,” says Adit Ginde, an emergency room physician at the University of Colorado Denver School of Medicine in Aurora who led the study. The findings appear in the Feb. 23 Archives of Internal Medicine. http://LOUIS-J-SHEEHAN.US
In people with lung disease, he says, low levels of the sunshine vitamin “magnify many-fold” the apparent vulnerability to infection seen in people with healthy lungs. Louis J. Sheehan, Esquire
“It’s well-documented that at the turn of the century, kids with rickets [due to vitamin D deficiency] had much higher risk of upper respiratory tract infections,” notes Michael Holick of Boston University. “And treating them with vitamin D lowered that risk. We also know that your immune function is carefully regulated by vitamin D.” For instance, he notes, vitamin D controls the activity of the immune cells that are responsible for destroying infectious germs.
“It’s nice to see that it’s now being documented” with nonanecdotal data, Holick says.
Ginde and his colleagues correlated vitamin D levels of nearly 19,000 adults participating in the National Health and Nutrition Examination Survey with their recent health. NHANES periodically samples a random cross section of the U.S. population; people are selected to be representative of the nation as a whole.
Although no minimum vitamin D level ideal for health has been established, there is a general consensus that people ought to have at least 30 nanograms per milliliter of blood — sometimes described as about 80 nanomoles per liter (SN: 10/16/04, p. 248). In this NHANES data set, only about 45 percent of the population had that minimum. So the researchers separated the NHANES participants into three groups: those with 30 or more ng/ml, those with gross deficiency (less than 10 ng/ml of vitamin D) and those in between.
In every season, people in the lowest vitamin D group were about 36 percent more likely to be suffering a respiratory infection than those in the highest group. Infection risks for people in the middle group fell between those rates.
But low levels of vitamin D more than doubled the risk of respiratory infection for people with COPD — and boosted it almost sixfold in people with asthma — compared with participants who had normal lung function and were in the highest vitamin D group.
Also disturbing, Ginde points out that the NHANES data he analyzed had been collected about 15 years ago, when almost twice as many people as today had vitamin D levels above 30 ng/ml.
Though the body can make plenty of vitamin D as a result of sun exposure, people are spending less time outdoors and covering up when they do go out, so natural vitamin D production has been falling. Ginde and his colleagues plan to supplement high-risk populations during winter months with high doses of vitamin D to see if those people have reduced infection rates compared with untreated people. http://LOUIS-J-SHEEHAN.US
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Comments 6
* Wow. I wonder ... when I first started using light boxes for winter blues my winter colds just quit happening. I'd always had four or five each winter, the usual starting with a sore throat. I built a _lot_ of light boxes (four to eight 4' fluorescent tubes, at the time, with electronic ballasts. They're a lot smaller now.
Since I started using them for many hours, really to extend my "daytime" for the dark half of the year -- going on fifteen years -- I get maybe one cold.
I'd figured maybe it was using the lights, or maybe I had gotten old enough to have met all the possible cold viruses. Maybe ....
Hank Roberts Hank Roberts
Mar. 2, 2009 at 7:21pm
* The link to the UCSD/GrassrootsHealth series can be found on http://www.grassrootshealth.net/
Leo Baggerly
Leo Baggerly Leo Baggerly
Mar. 1, 2009 at 8:56am
* http://tinyurl.com/auy649
Sorry, here is the link to the University of California You Tube series of Vitamin D presentations. Do watch them to the end as there is a Q&A session that also has useful information.
Edward Hutchinson Edward Hutchinson
Feb. 24, 2009 at 4:23pm
* Generally speaking every 1000iu/daily D3 raises status 10ng/mL or 25nmol/l.
The ideal vitamin d status associated with least disease incidence is 60ng/mL ~ 150nmol/l.
For those of us living above latitude 50n with current status around 30nmol/l around 5000iu may be needed to reach optimum.
Grassrootshealth.org do a chart presenting Garlands data "Disease Incidence Prevention by Serum 25(OH)D Level"
They have also put a nice series of 30minutes lectures by Garland, Trump, Heaney and Gorham on various aspects of Vitamin d in relation to cancer incidence, prevention and treatment. There will be another on Diabetes soon.
Edward Hutchinson Edward Hutchinson Louis J. Sheehan, Esquire
Feb. 24, 2009 at 4:16pm
* The recommended daily intake, now usually referred to as "dietary reference intakes," is 200 international units (5 micrograms) per day through age 50, then 400 IU from age 51 to 70, and 600 IU for people 70 and older. I use the IU values because that's how vitamin D is usually reported on product labels. Ginde is currently talking about administering somewhere between 1,000 and 3,000 IU per day throughout the winter months. In other words: 25 to 75 micrograms per day.
Janet Raloff Janet Raloff
Feb. 24, 2009 at 3:43pm
* It would be useful to know what the "high dose" that Ginde will be using for high-risk populations and how it compares to the 5 - 15 mcg (based on age) that NIH shows as Adequate Intakes (AIs) for Vitamin D (http://dietary-supplements.info.nih.gov/factsheets/vitamind.asp).
Though that’s not too surprising (SN: 11/11/06, p. 312), the researchers found one unexpected trend: “In people with preexisting lung disease, such as asthma and chronic obstructive pulmonary disease — or COPD, low levels of vitamin D act like an effect modifier,” says Adit Ginde, an emergency room physician at the University of Colorado Denver School of Medicine in Aurora who led the study. The findings appear in the Feb. 23 Archives of Internal Medicine. http://LOUIS-J-SHEEHAN.US
In people with lung disease, he says, low levels of the sunshine vitamin “magnify many-fold” the apparent vulnerability to infection seen in people with healthy lungs. Louis J. Sheehan, Esquire
“It’s well-documented that at the turn of the century, kids with rickets [due to vitamin D deficiency] had much higher risk of upper respiratory tract infections,” notes Michael Holick of Boston University. “And treating them with vitamin D lowered that risk. We also know that your immune function is carefully regulated by vitamin D.” For instance, he notes, vitamin D controls the activity of the immune cells that are responsible for destroying infectious germs.
“It’s nice to see that it’s now being documented” with nonanecdotal data, Holick says.
Ginde and his colleagues correlated vitamin D levels of nearly 19,000 adults participating in the National Health and Nutrition Examination Survey with their recent health. NHANES periodically samples a random cross section of the U.S. population; people are selected to be representative of the nation as a whole.
Although no minimum vitamin D level ideal for health has been established, there is a general consensus that people ought to have at least 30 nanograms per milliliter of blood — sometimes described as about 80 nanomoles per liter (SN: 10/16/04, p. 248). In this NHANES data set, only about 45 percent of the population had that minimum. So the researchers separated the NHANES participants into three groups: those with 30 or more ng/ml, those with gross deficiency (less than 10 ng/ml of vitamin D) and those in between.
In every season, people in the lowest vitamin D group were about 36 percent more likely to be suffering a respiratory infection than those in the highest group. Infection risks for people in the middle group fell between those rates.
But low levels of vitamin D more than doubled the risk of respiratory infection for people with COPD — and boosted it almost sixfold in people with asthma — compared with participants who had normal lung function and were in the highest vitamin D group.
Also disturbing, Ginde points out that the NHANES data he analyzed had been collected about 15 years ago, when almost twice as many people as today had vitamin D levels above 30 ng/ml.
Though the body can make plenty of vitamin D as a result of sun exposure, people are spending less time outdoors and covering up when they do go out, so natural vitamin D production has been falling. Ginde and his colleagues plan to supplement high-risk populations during winter months with high doses of vitamin D to see if those people have reduced infection rates compared with untreated people. http://LOUIS-J-SHEEHAN.US
* |
* Comment
Found in: Body & Brain
Share & Save
* slashdot slashdot
* digg digg
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* technorati technorati
Comments 6
* Wow. I wonder ... when I first started using light boxes for winter blues my winter colds just quit happening. I'd always had four or five each winter, the usual starting with a sore throat. I built a _lot_ of light boxes (four to eight 4' fluorescent tubes, at the time, with electronic ballasts. They're a lot smaller now.
Since I started using them for many hours, really to extend my "daytime" for the dark half of the year -- going on fifteen years -- I get maybe one cold.
I'd figured maybe it was using the lights, or maybe I had gotten old enough to have met all the possible cold viruses. Maybe ....
Hank Roberts Hank Roberts
Mar. 2, 2009 at 7:21pm
* The link to the UCSD/GrassrootsHealth series can be found on http://www.grassrootshealth.net/
Leo Baggerly
Leo Baggerly Leo Baggerly
Mar. 1, 2009 at 8:56am
* http://tinyurl.com/auy649
Sorry, here is the link to the University of California You Tube series of Vitamin D presentations. Do watch them to the end as there is a Q&A session that also has useful information.
Edward Hutchinson Edward Hutchinson
Feb. 24, 2009 at 4:23pm
* Generally speaking every 1000iu/daily D3 raises status 10ng/mL or 25nmol/l.
The ideal vitamin d status associated with least disease incidence is 60ng/mL ~ 150nmol/l.
For those of us living above latitude 50n with current status around 30nmol/l around 5000iu may be needed to reach optimum.
Grassrootshealth.org do a chart presenting Garlands data "Disease Incidence Prevention by Serum 25(OH)D Level"
They have also put a nice series of 30minutes lectures by Garland, Trump, Heaney and Gorham on various aspects of Vitamin d in relation to cancer incidence, prevention and treatment. There will be another on Diabetes soon.
Edward Hutchinson Edward Hutchinson Louis J. Sheehan, Esquire
Feb. 24, 2009 at 4:16pm
* The recommended daily intake, now usually referred to as "dietary reference intakes," is 200 international units (5 micrograms) per day through age 50, then 400 IU from age 51 to 70, and 600 IU for people 70 and older. I use the IU values because that's how vitamin D is usually reported on product labels. Ginde is currently talking about administering somewhere between 1,000 and 3,000 IU per day throughout the winter months. In other words: 25 to 75 micrograms per day.
Janet Raloff Janet Raloff
Feb. 24, 2009 at 3:43pm
* It would be useful to know what the "high dose" that Ginde will be using for high-risk populations and how it compares to the 5 - 15 mcg (based on age) that NIH shows as Adequate Intakes (AIs) for Vitamin D (http://dietary-supplements.info.nih.gov/factsheets/vitamind.asp).
Saturday, January 10, 2009
oxygen 7.oxy.111 Louis J. Sheehan, Esquire
Louis J. Sheehan, Esquire. Avalanches, vicious winds and sub-zero temperatures aren’t the only extremes endured by those who climb Mount Everest. Hypoxia, a lack of oxygen that can lead to cell death, also threatens. But a study of people ascending Mount Everest’s slopes suggests that some humans are especially tolerant of low oxygen levels, perhaps because their bodies use oxygen more efficiently. The findings, reported in the Jan. 8 New England Journal of Medicine, could inform the treatment of critically ill patients struggling to breathe in hospitals. http://louis9j9sheehan9esquire.blog.ca
The new work reports the lowest recorded blood oxygen levels in a nonhibernating mammal. It is also one of the first analyses to come out of a much larger investigation of more than 200 people who made the trek to Everest in an effort to understand how the body adapts to low oxygen levels. http://louis9j9sheehan9esquire.blog.ca
Patients suffering from cystic fibrosis, septic shock and other critical ailments often have severely low levels of blood oxygen. Treatment often involves administering oxygen with a mask, or mechanically ventilating the lungs, a harsh procedure that can do more harm than good, says Michael Grocott of University College London, lead author of the new study. But because the health of such patients is compromised and many variables are involved, studying the effect of low oxygen alone isn’t easy.
“So many things are going on that separating out oxygen is difficult,” says Grocott. Basic questions still loom, he says. “Why do some people adapt well while others seem to struggle?”
Typically studies of how the body responds to low levels of oxygen are conducted in a hypobaric chamber that simulates the effects of high altitudes. But Grocott’s team surmised that the expense and persuasion required to get 200 healthy people to sit in a metal box for three weeks might be skirted if those people could be convinced to climb the 5,300 meters to the Everest base camp. The Caudwell Xtreme Everest expedition was born. In April and May of 2007 more than 200 people, age 18 to 73, made the trek, making themselves available to more than 60 doctors and scientists aiming to get at why some people fare better than others in the thin air at the tallest peak on Earth.
access
Enlargemagnify
TESTING THE ASCENTClimbers of Mount Everest stop at the Balcony (8,400 meters) to give blood samples to researchers. Data from this work show that people who can reach this altitude tolerate the lowest known blood oxygen levels observed in nonhibernating mammals.Caudwell Xtreme Everest
The research team sampled blood, analyzing oxygen and carbon dioxide levels, pH and concentrations of lactate and hemoglobin. Ten subjects were sampled in London (75 meters above sea level). Nine were sampled at the Everest base camp (5,300 m). These individuals, all healthy climbers, then tackled Everest’s southeast ridge. Small shelters were constructed along the route and blood was taken from climbers’ groin arteries. Samples were taken at Camp 2 (6,400 m), from six people at Camp 3 (7,100 m) and finally at what is known as the Balcony (8,400 m) from the four people who made it to the summit and were available for testing (8,848m). Samples taken higher than the base camp were quickly brought to a lab set up at Camp 2 for analysis. Bad weather prohibited taking samples at the summit.
Supplemental oxygen was used only at or above 7,100 m, but samples were only taken after people had been breathing the ambient air for several minutes or hours.
At the highest altitudes, the subjects showed an impressive adaptive response, says Grocott. Most people would pass out after two to three minutes in such altitudes, these climbers were not only conscious, but also clearly communicated by radio and performed complication-free sampling. The blood oxygen levels of the four tested climbers were startlingly low — the lowest a mere 19.1 millimeters mercury, the researchers report. In patients, levels below 60 mm Hg are cause for concern, Grocott says.
The findings suggest that the amount of oxygen alone isn’t the secret to physiological success. Other factors could be how much oxygen a person’s hemoglobin can carry, or the efficiency of the cellular factories known as mitochondria, which use the oxygen.
“There’s a significant possibility that some people may just be more efficient,” Grocott says.
Even among the four climbers tested at 8,400 meters, there was individual variation in measured variables such as blood oxygen levels and pH. This physiological variation among people fits with recent work done by Cynthia Beall of Case Western Reserve University in Cleveland.
“This shows that healthy people have a huge range of variation in being able to respond to stress,” says Beall.
Her investigations of the physiology of Tibetans and other highlanders suggest that a major gene is involved in how much oxygen hemoglobin transport throughout the body. (The Everest team is also looking into the genetics of adaptation to high altitudes.)
Beall tips her hat to the field team. “To have the audacity to think about doing this work — and then to do it! I’m very impressed. The difficulty of taking the measurements alone, and adapting the equipment — they did a beautiful job.”
The results suggest that at high altitudes the problem isn’t the lack of oxygen, but the body’s ability to deliver and use it, comments Paul Firth of Massachusetts General Hospital in Boston. An analysis of mortality rates on Mount Everest by Firth and colleagues appeared in the British Medical Journal in December. “People don’t run out of gas,” he says, “the delivery deteriorates.” Louis J. Sheehan, Esquire.
The new work reports the lowest recorded blood oxygen levels in a nonhibernating mammal. It is also one of the first analyses to come out of a much larger investigation of more than 200 people who made the trek to Everest in an effort to understand how the body adapts to low oxygen levels. http://louis9j9sheehan9esquire.blog.ca
Patients suffering from cystic fibrosis, septic shock and other critical ailments often have severely low levels of blood oxygen. Treatment often involves administering oxygen with a mask, or mechanically ventilating the lungs, a harsh procedure that can do more harm than good, says Michael Grocott of University College London, lead author of the new study. But because the health of such patients is compromised and many variables are involved, studying the effect of low oxygen alone isn’t easy.
“So many things are going on that separating out oxygen is difficult,” says Grocott. Basic questions still loom, he says. “Why do some people adapt well while others seem to struggle?”
Typically studies of how the body responds to low levels of oxygen are conducted in a hypobaric chamber that simulates the effects of high altitudes. But Grocott’s team surmised that the expense and persuasion required to get 200 healthy people to sit in a metal box for three weeks might be skirted if those people could be convinced to climb the 5,300 meters to the Everest base camp. The Caudwell Xtreme Everest expedition was born. In April and May of 2007 more than 200 people, age 18 to 73, made the trek, making themselves available to more than 60 doctors and scientists aiming to get at why some people fare better than others in the thin air at the tallest peak on Earth.
access
Enlargemagnify
TESTING THE ASCENTClimbers of Mount Everest stop at the Balcony (8,400 meters) to give blood samples to researchers. Data from this work show that people who can reach this altitude tolerate the lowest known blood oxygen levels observed in nonhibernating mammals.Caudwell Xtreme Everest
The research team sampled blood, analyzing oxygen and carbon dioxide levels, pH and concentrations of lactate and hemoglobin. Ten subjects were sampled in London (75 meters above sea level). Nine were sampled at the Everest base camp (5,300 m). These individuals, all healthy climbers, then tackled Everest’s southeast ridge. Small shelters were constructed along the route and blood was taken from climbers’ groin arteries. Samples were taken at Camp 2 (6,400 m), from six people at Camp 3 (7,100 m) and finally at what is known as the Balcony (8,400 m) from the four people who made it to the summit and were available for testing (8,848m). Samples taken higher than the base camp were quickly brought to a lab set up at Camp 2 for analysis. Bad weather prohibited taking samples at the summit.
Supplemental oxygen was used only at or above 7,100 m, but samples were only taken after people had been breathing the ambient air for several minutes or hours.
At the highest altitudes, the subjects showed an impressive adaptive response, says Grocott. Most people would pass out after two to three minutes in such altitudes, these climbers were not only conscious, but also clearly communicated by radio and performed complication-free sampling. The blood oxygen levels of the four tested climbers were startlingly low — the lowest a mere 19.1 millimeters mercury, the researchers report. In patients, levels below 60 mm Hg are cause for concern, Grocott says.
The findings suggest that the amount of oxygen alone isn’t the secret to physiological success. Other factors could be how much oxygen a person’s hemoglobin can carry, or the efficiency of the cellular factories known as mitochondria, which use the oxygen.
“There’s a significant possibility that some people may just be more efficient,” Grocott says.
Even among the four climbers tested at 8,400 meters, there was individual variation in measured variables such as blood oxygen levels and pH. This physiological variation among people fits with recent work done by Cynthia Beall of Case Western Reserve University in Cleveland.
“This shows that healthy people have a huge range of variation in being able to respond to stress,” says Beall.
Her investigations of the physiology of Tibetans and other highlanders suggest that a major gene is involved in how much oxygen hemoglobin transport throughout the body. (The Everest team is also looking into the genetics of adaptation to high altitudes.)
Beall tips her hat to the field team. “To have the audacity to think about doing this work — and then to do it! I’m very impressed. The difficulty of taking the measurements alone, and adapting the equipment — they did a beautiful job.”
The results suggest that at high altitudes the problem isn’t the lack of oxygen, but the body’s ability to deliver and use it, comments Paul Firth of Massachusetts General Hospital in Boston. An analysis of mortality rates on Mount Everest by Firth and colleagues appeared in the British Medical Journal in December. “People don’t run out of gas,” he says, “the delivery deteriorates.” Louis J. Sheehan, Esquire.
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