Synopsis
Kyle falls into an ice hole and when Stan comes to rescue him, they find a frozen man embedded in the ice. The boys pull the ice man out, Mephesto takes the ice man back to his laboratory to thaw him out. He discovers that the ice man has been frozen since 1996. The government wants to get him for their own experiments, but Stan and Kyle free him, so the government hires Steve Irwin (from "Crocodile Hunter") to track him down.
Full Recap
After watching The Crocodile Hunter the boys decide to go searching for crocodiles. Kyle trips on a stone and slides down a hill and falls into a hole. At the bottom of the hole, Kyle finds he is in a cave. When Stan comes down to rescue him he discovers a prehistoric iceman. Kyle and Stan speculate on what kind of reward they might get for finding the icemen. Somehow, the 4 boys manage to get a man encased in a block of ice out of the hole. Stan decides that iceman's name should be “Gorak” and Kyle thinks it should be “Steve.” And so Stan and Kyle begin their fight over who should get the credit for finding the iceman. The town is debating capital punishment, when the boys arrive with the icemen. Dr. Mephisto arrives on the scene and agrees to thaw the iceman. He can't reward the boys, but lets them give the iceman a name. Kyle quickly yells out “Steve.” Dr. Mephisto starts thawing the iceman and determines that given his clothing, he must be from 1996. Reporters arrive on the scene and Kyle has been given credit for the discovery, much to the chagrin of Stan. Dr. Mephisto is ready to do the autopsy when they realize that the iceman is still alive. Dr. Mephisto (oblivious to the fact that “Steve” is speaking perfectly good English) seeks out a way to communicate with the thawed iceman. He decides the simple mind of a child will do the trick, so he requests that Officer Barbrady bring one of boys to help. All the boys arrive at the lab, where Stan easily communicates with “Steve.” Then “Steve” freaks out when he finds out that he has been frozen for 32 months. Dr. Mephisto gives him a sedative. Kyle blames Stan for causing the freak out and they begin to fight, each claiming to the other that Cartman is now his best friend.
Some men arrive and offer to help Dr. Mephisto with his experiments with the iceman. Dr. Mephisto shows them the habit that he and Kevin have setup for the iceman, which duplicates the environment of 1996. The men help Dr. Mephisto raise funds for his experiments by putting the iceman on display. The boys object to the iceman being put on display. Later that night, Stan comes to bust "Gorak" out and Kyle also arrives on the scene with plans to rescue "Steve." Stan and Kyle begin fighting over who is going to do the rescuing; when Stan opens for the door for the iceman whose real name is Larry. Larry leaves the lab while the boys are in the midst of their fight, which ends with them planning to fight at the bus stop the following afternoon. Meanwhile, Larry is out wandering the streets of South Park. Dr. Mephisto and the men discover the iceman's escape and wonder where he might have gone off to. The men realize they will need "special assistance" to find the iceman. Larry arrives at the door of his home and when his wife answers, she doesn't recognize him. She introduces him to current lover and tells him the story of their attempt to rescue him. Larry is dejected and decides that he might as well refreeze himself. Stan is talking to him as he is doing this, when Kyle arrives on the scene, with some information for "Steve." Kyle shows him a brochure for Des Moines, a place that is two years behind the time, just like Larry. Both Kyle and Stan plan to get the iceman to Des Moines and escape just as Dr. Mephisto and the men arrive on the scene. They've brought their specialist with them, The "Crocodile Hunter," who claims he can track anything.
Stan and Kyle try to buy Larry a one-way train ticket to Des Moines. The boys pause for a moment to start their fight. The “Crocodile Hunter” is one the trail of iceman, when he gets distracted by the Rocky Mountain rattler. Larry gets his train ticket and thanks Stan and Kyle for their help, telling them what he's learned about friendship, as Stan and Kyle continue to beat the crap out of each other. The train leaves the station as Dr. Mephisto, the men and the Crocodile Hunter arrives at the scene. They all go in pursuit of the train and catch up to it. The Crocodile Hunter manages to corner Larry and gets his thumb in Larry's butt hole. The men, with aid of a helicopter manage to stop the train. The blades from the helicopter manage to dice and slice the Crocodile Hunter quite nicely. Dr. Mephisto and the men search for Larry, who manages to steal the helicopter and escape to Des Moines. The men, who it turns out, were from the government; have to give up on their plans to use the iceman in their plot against Sweden. Kyle and Stan agree to become best friends again as "Crocodile Hunter" Cartman attempts to stick his thumb in the butt hole of a cow.
Kenny dies when he pulled underneath the conveyor used for the tourists in the iceman display. As they are in the midst of their fight when this happens, when Stan says his catchphrase "Oh my God, they killed Kenny…," he waits for Kyle's standard response, which doesn't come. Kyle looks at him and says "What? I'm not talking to you."
Tuesday, June 30, 2009
Saturday, May 23, 2009
results are still hazy 2.rah.000746 Louis J. Sheehan, Esquire
Louis J. Sheehan, Esquire While research is being published at a rapid rate (more than 50 breath-related papers so far in 2008), scientists are still figuring out which breath-bound molecules are most meaningful and what collection methods work best.
“It’s unclear what we should be looking for in there—there’s stuff from A to Z,” says Rohit Katial, director of the allergy and immunology program at the National Jewish Medical and Research Center in Denver. Breath is “an intriguing source of a bodily sample,” he says. “But it is still in its infancy—the detection techniques just aren’t there yet.”
Although the results are still hazy in some areas of research, breath analysis is a reliable non-invasive means of detecting certain ills, such as lung inflammation, says John Hunt, a respiratory medicine specialist at the University of Virginia Children’s Hospital in Charlottesville. Breath from a normal airway is mildly alkaline, about pH 8, but someone with acute respiratory disease might have a breath pH of 3. “Kind of like putting lemonade in your eye,” says Hunt.
An airway making this much acid can be an early sign of pulmonary disease or lung transplant rejection, says Hunt, who cofounded a company that makes equipment for collecting breath condensate. And severe asthma—a suite of symptoms, not a disease—may be triggered by a number of cellular irritants, from viral infections to exposure to diesel emissions. Analyzing breath condensate can help discern whether acid reflux is causing irritation or contributing to it, helping doctors target drugs more effectively, says Hunt.
“It’s unclear what we should be looking for in there—there’s stuff from A to Z,” says Rohit Katial, director of the allergy and immunology program at the National Jewish Medical and Research Center in Denver. Breath is “an intriguing source of a bodily sample,” he says. “But it is still in its infancy—the detection techniques just aren’t there yet.”
Although the results are still hazy in some areas of research, breath analysis is a reliable non-invasive means of detecting certain ills, such as lung inflammation, says John Hunt, a respiratory medicine specialist at the University of Virginia Children’s Hospital in Charlottesville. Breath from a normal airway is mildly alkaline, about pH 8, but someone with acute respiratory disease might have a breath pH of 3. “Kind of like putting lemonade in your eye,” says Hunt.
An airway making this much acid can be an early sign of pulmonary disease or lung transplant rejection, says Hunt, who cofounded a company that makes equipment for collecting breath condensate. And severe asthma—a suite of symptoms, not a disease—may be triggered by a number of cellular irritants, from viral infections to exposure to diesel emissions. Analyzing breath condensate can help discern whether acid reflux is causing irritation or contributing to it, helping doctors target drugs more effectively, says Hunt.
Wednesday, May 13, 2009
inhibitor 5.inh.0098 Louis J. Sheehan, Esquire
A new HIV drug can, when combined with other therapies, suppress even the most drug-resistant strains of the virus that causes AIDS, Louis J. Sheehan, Esquire scientists report in two papers in the July 24 New England Journal of Medicine.
The study looks at one group of HIV patients for whom the standard, clinically approved HIV medications are not working.
“These people are very sick, and they have few if any other treatment options because they have a form of HIV that is resistant to just about any clinically approved medication,” says study coauthor Jeffrey L. Lennox, who directs the HIV/AIDS care clinic at Grady Memorial Hospital in Atlanta. “Without this new drug, some of the patients might not be with us today.”
When combined with other anti-HIV medications, the drug, raltegravir, was an effective treatment for patients in the study, Lennox says.
The MERCK drug is the first in a novel class of antiretroviral drugs called integrase inhibitors, which disrupt the virus’s ability to integrate its DNA into uninfected cells. If the virus cannot infect healthy cells with its genetic material, the virus cannot replicate and continue to spread throughout the body.
“I was impressed with how potent raltegravir proved to be for a group of patients that are hardest to treat,” says Steven Johnson, chief of the University of Colorado Denver’s HIV clinic in Aurora, who was not involved in the new studies.
The study led to FDA approval of raltegravir last year, Lennox notes. As with many clinical trials, the FDA reviewed the studies’ unpublished data after patients had been taking raltegravir in combination with other drugs for 24 weeks. Researchers measured patients’ levels of HIV in the blood, and patients taking raltegravir showed a significant reduction in their virus levels compared with those taking a placebo in combination with other antiretroviral drugs. Because of the promise raltegravir showed, early in the studies, the administration fast-tracked the HIV-suppressor for clinical use in October of 2007, Lennox says.
“These newly reported data out to week 48 confirm the 24-week results that led to regulatory approval for clinical use,” says MERCK scientist Bach-Yen Nguyen.
In order to participate, patients needed to have more than 1,000 copies of HIV-1 RNA per milliliter of blood while receiving antiretroviral therapy. After 48 weeks, 62.1 percent of raltegravir recipients had HIV-1 RNA levels below 50 copies per milliliter of blood compared with 32.9 percent in the placebo group.
While the first paper reports on the efficacy and safety of raltegravir, the second looks at the virus’s ability to grow resistant to the new drug.Louis J. Sheehan, Esquire
Some study patients became resistant even to the new drug, especially when it was used without other anti-HIV medications. Johnson says the finding reinforces the practice of treating HIV with a combination of medications.
The researchers also report that the group taking the new drug had slightly higher rates of cancer than the control group. Cancers were detected in 3.5 percent of patients taking raltegravir, while 1.7 percent of placebo-taking participants showed cancer growths. Longer term studies are needed to watch for these problems, Johnson says, but “the benefits likely outweigh the risks.”
The study looks at one group of HIV patients for whom the standard, clinically approved HIV medications are not working.
“These people are very sick, and they have few if any other treatment options because they have a form of HIV that is resistant to just about any clinically approved medication,” says study coauthor Jeffrey L. Lennox, who directs the HIV/AIDS care clinic at Grady Memorial Hospital in Atlanta. “Without this new drug, some of the patients might not be with us today.”
When combined with other anti-HIV medications, the drug, raltegravir, was an effective treatment for patients in the study, Lennox says.
The MERCK drug is the first in a novel class of antiretroviral drugs called integrase inhibitors, which disrupt the virus’s ability to integrate its DNA into uninfected cells. If the virus cannot infect healthy cells with its genetic material, the virus cannot replicate and continue to spread throughout the body.
“I was impressed with how potent raltegravir proved to be for a group of patients that are hardest to treat,” says Steven Johnson, chief of the University of Colorado Denver’s HIV clinic in Aurora, who was not involved in the new studies.
The study led to FDA approval of raltegravir last year, Lennox notes. As with many clinical trials, the FDA reviewed the studies’ unpublished data after patients had been taking raltegravir in combination with other drugs for 24 weeks. Researchers measured patients’ levels of HIV in the blood, and patients taking raltegravir showed a significant reduction in their virus levels compared with those taking a placebo in combination with other antiretroviral drugs. Because of the promise raltegravir showed, early in the studies, the administration fast-tracked the HIV-suppressor for clinical use in October of 2007, Lennox says.
“These newly reported data out to week 48 confirm the 24-week results that led to regulatory approval for clinical use,” says MERCK scientist Bach-Yen Nguyen.
In order to participate, patients needed to have more than 1,000 copies of HIV-1 RNA per milliliter of blood while receiving antiretroviral therapy. After 48 weeks, 62.1 percent of raltegravir recipients had HIV-1 RNA levels below 50 copies per milliliter of blood compared with 32.9 percent in the placebo group.
While the first paper reports on the efficacy and safety of raltegravir, the second looks at the virus’s ability to grow resistant to the new drug.Louis J. Sheehan, Esquire
Some study patients became resistant even to the new drug, especially when it was used without other anti-HIV medications. Johnson says the finding reinforces the practice of treating HIV with a combination of medications.
The researchers also report that the group taking the new drug had slightly higher rates of cancer than the control group. Cancers were detected in 3.5 percent of patients taking raltegravir, while 1.7 percent of placebo-taking participants showed cancer growths. Longer term studies are needed to watch for these problems, Johnson says, but “the benefits likely outweigh the risks.”
Saturday, May 2, 2009
vaccine 1.vac.003 Louis J. Sheehan, Esquire
A simplified vaccine for poliomyelitis might be just what the doctor ordered. Louis J. Sheehan, Esquire
A pared-down vaccine that was introduced in 2005 is knocking back the poliovirus better than the long-standing vaccine, two studies published in the Oct. 16 New England Journal of Medicine show. The newer vaccine overcomes a curious weakness that has developed in the older version.
The new findings might put the campaign against polio back on a beeline toward eradication after being sidetracked in recent years. That setback arose from a combination of limited effectiveness of the old vaccine and a disastrous immunization stoppage in Nigeria in 2003 that allowed the virus to regain momentum there and spread to 20 other countries in short order. http://LOUIS-J-SHEEHAN.INFO
The newer vaccine and a revised vaccination strategy helped to reverse the Nigerian outbreak by 2007 and may form the basis of a public health model that could lead to eradication, says Nicholas Grassly, a mathematical epidemiologist at Imperial College London who coauthored one of the studies, an analysis of the Nigerian campaign. “It is certainly achievable,” he says.
Polio exists only in humans, having no other animal host. And although there is no cure for polio, effective vaccines make it vulnerable to elimination, just as smallpox was wiped out in the 1970s.
The poliovirus comes in three types — dubbed 1, 2 and 3. All three cause infection, which results in mild and even unnoticed disease in nearly all patients. But about 1 percent of people who are infected suffer paralysis.
Researcher Albert Sabin devised and licensed a trivalent, or triple-acting, oral polio vaccine a half century ago that engenders at least some immunity against all three types. This inexpensive vaccine, delivered in oral drops, uses a weakened live virus and remains the standard throughout most of the world, although industrialized countries have reverted to the original, injectable form, which uses a killed virus. The typical polio vaccine regimen, be it oral or injected, is three to four doses.
The broad effects of the oral vaccination have been potent enough to knock out polio in most of the world. The disease remains endemic in only four countries: Afghanistan, India, Nigeria and Pakistan.
Research in the past decade, however, suggests that the vaccine induces an imbalanced immunity, leaving gaps in its coverage that no one could have foreseen.
It turns out that not all three types are created equal. Over the years, the type 2 component of the vaccine has been more aggressive than the others and has out-competed them in the intestines, where the bulk of poliovirus — and the vaccine — gets absorbed into cells. That means people immunized against polio develop a potent antibody corps against type 2 but much less protection against the other types of polio.
As a result, naturally occurring type 2 polio has disappeared.
While that would seem like a success story, it actually has made the final coup de grace against polio more difficult to deliver because now the trivalent vaccine is dominated by the wrong component. “It’s really good against type 2, which is gone,” says Grassly.
That in part explains why, just when it seemed that polio was on its last legs, the virus has hung on doggedly in Asia and Africa, he says.
In one of the new studies, Grassly and his colleagues analyzed the effect of two orally administered vaccines — the standard trivalent vaccine and a monovalent, or single-acting, vaccine against type 1, one of the two remaining dangerous types. The team found that in the Nigerian epidemic the monovalent vaccine was four times as effective against type 1 as the trivalent vaccine. The trivalent vaccine did confer some protection against type 3 polio.
While the trivalent vaccine still offers some broad coverage, the findings suggest that monovalent vaccines against type 1 or type 3 can have dramatic effects in stopping outbreaks, Grassly says.
Polio is highly contagious, spreading through contaminated water or by person-to-person contact. “In an epidemic, you want to quickly raise the immunity levels in the population to stop transmission,” says Mohamed Wahdan, an infectious disease physician with the World Health Organization’s Cairo, Egypt office. “You can push immunity higher more quickly with a monovalent dose than with the trivalent.”
For example, public health officials in Yemen recently quelled an outbreak there by using a combination of monovalent vaccine aimed at type 1 and routine trivalent vaccination, says Wahdan.
In the other new study, Wahdan worked with an international team of scientists in Egypt who randomly assigned 421 newborns to get an oral dose of polio vaccine at birth and again at one month. Of these, 231 got a monovalent vaccine aimed at type 1 and 190 received the trivalent vaccine.
The researchers assessed the infants at age 2 months and found that more than half of those getting the monovalent vaccine had generated antibodies against type 1 polio, which was nearly twice as many as those receiving the trivalent vaccine. While the type 1 monovalent vaccine didn’t protect against the type 3 virus, the trivalent vaccine wasn’t much better — protecting only about 17 percent of newborns from type 3.
When a new outbreak of polio occurs, mainly from travelers exiting polio-endemic countries, “you want to hit it hard with the best thing we’ve got, and that thing is probably the monovalent vaccines,” says virologist Ellie Ehrenfeld of the National Institute of Allergy and Infectious Diseases in Bethesda, Md. “Both of these papers report data that document that.”
Type 1 poliovirus seems more prevalent than type 3. But, even though scientists have devised live attenuated monovalent vaccines against both, these probably won’t eradicate polio, she says. Like other live-virus vaccines, these leave open a glaring risk — that the virus built into the vaccines will swap genes with other viruses and become rogue but real polio viruses, she says. This has happened with the trivalent vaccine, albeit rarely, and has caused paralysis in about one person per 2.5 million vaccinated, by some estimates.
Therefore, Ehrenfeld says, the endgame for polio may rest not on using these live-but-weakened viruses developed by Sabin, but rather with the original — the injectable polio vaccine devised by Jonas Salk. While more expensive, Ehrenfeld says, that vaccine is ultimately safer because it uses a killed virus that can’t recombine with anything.
To make matters worse, the oral vaccines suffer from reduced potency because children in poor countries often confront bouts of diarrheal diseases, which usher the vaccine out of the body before it can induce an immune response. The injectable vaccine isn’t compromised by diarrhea.
A pared-down vaccine that was introduced in 2005 is knocking back the poliovirus better than the long-standing vaccine, two studies published in the Oct. 16 New England Journal of Medicine show. The newer vaccine overcomes a curious weakness that has developed in the older version.
The new findings might put the campaign against polio back on a beeline toward eradication after being sidetracked in recent years. That setback arose from a combination of limited effectiveness of the old vaccine and a disastrous immunization stoppage in Nigeria in 2003 that allowed the virus to regain momentum there and spread to 20 other countries in short order. http://LOUIS-J-SHEEHAN.INFO
The newer vaccine and a revised vaccination strategy helped to reverse the Nigerian outbreak by 2007 and may form the basis of a public health model that could lead to eradication, says Nicholas Grassly, a mathematical epidemiologist at Imperial College London who coauthored one of the studies, an analysis of the Nigerian campaign. “It is certainly achievable,” he says.
Polio exists only in humans, having no other animal host. And although there is no cure for polio, effective vaccines make it vulnerable to elimination, just as smallpox was wiped out in the 1970s.
The poliovirus comes in three types — dubbed 1, 2 and 3. All three cause infection, which results in mild and even unnoticed disease in nearly all patients. But about 1 percent of people who are infected suffer paralysis.
Researcher Albert Sabin devised and licensed a trivalent, or triple-acting, oral polio vaccine a half century ago that engenders at least some immunity against all three types. This inexpensive vaccine, delivered in oral drops, uses a weakened live virus and remains the standard throughout most of the world, although industrialized countries have reverted to the original, injectable form, which uses a killed virus. The typical polio vaccine regimen, be it oral or injected, is three to four doses.
The broad effects of the oral vaccination have been potent enough to knock out polio in most of the world. The disease remains endemic in only four countries: Afghanistan, India, Nigeria and Pakistan.
Research in the past decade, however, suggests that the vaccine induces an imbalanced immunity, leaving gaps in its coverage that no one could have foreseen.
It turns out that not all three types are created equal. Over the years, the type 2 component of the vaccine has been more aggressive than the others and has out-competed them in the intestines, where the bulk of poliovirus — and the vaccine — gets absorbed into cells. That means people immunized against polio develop a potent antibody corps against type 2 but much less protection against the other types of polio.
As a result, naturally occurring type 2 polio has disappeared.
While that would seem like a success story, it actually has made the final coup de grace against polio more difficult to deliver because now the trivalent vaccine is dominated by the wrong component. “It’s really good against type 2, which is gone,” says Grassly.
That in part explains why, just when it seemed that polio was on its last legs, the virus has hung on doggedly in Asia and Africa, he says.
In one of the new studies, Grassly and his colleagues analyzed the effect of two orally administered vaccines — the standard trivalent vaccine and a monovalent, or single-acting, vaccine against type 1, one of the two remaining dangerous types. The team found that in the Nigerian epidemic the monovalent vaccine was four times as effective against type 1 as the trivalent vaccine. The trivalent vaccine did confer some protection against type 3 polio.
While the trivalent vaccine still offers some broad coverage, the findings suggest that monovalent vaccines against type 1 or type 3 can have dramatic effects in stopping outbreaks, Grassly says.
Polio is highly contagious, spreading through contaminated water or by person-to-person contact. “In an epidemic, you want to quickly raise the immunity levels in the population to stop transmission,” says Mohamed Wahdan, an infectious disease physician with the World Health Organization’s Cairo, Egypt office. “You can push immunity higher more quickly with a monovalent dose than with the trivalent.”
For example, public health officials in Yemen recently quelled an outbreak there by using a combination of monovalent vaccine aimed at type 1 and routine trivalent vaccination, says Wahdan.
In the other new study, Wahdan worked with an international team of scientists in Egypt who randomly assigned 421 newborns to get an oral dose of polio vaccine at birth and again at one month. Of these, 231 got a monovalent vaccine aimed at type 1 and 190 received the trivalent vaccine.
The researchers assessed the infants at age 2 months and found that more than half of those getting the monovalent vaccine had generated antibodies against type 1 polio, which was nearly twice as many as those receiving the trivalent vaccine. While the type 1 monovalent vaccine didn’t protect against the type 3 virus, the trivalent vaccine wasn’t much better — protecting only about 17 percent of newborns from type 3.
When a new outbreak of polio occurs, mainly from travelers exiting polio-endemic countries, “you want to hit it hard with the best thing we’ve got, and that thing is probably the monovalent vaccines,” says virologist Ellie Ehrenfeld of the National Institute of Allergy and Infectious Diseases in Bethesda, Md. “Both of these papers report data that document that.”
Type 1 poliovirus seems more prevalent than type 3. But, even though scientists have devised live attenuated monovalent vaccines against both, these probably won’t eradicate polio, she says. Like other live-virus vaccines, these leave open a glaring risk — that the virus built into the vaccines will swap genes with other viruses and become rogue but real polio viruses, she says. This has happened with the trivalent vaccine, albeit rarely, and has caused paralysis in about one person per 2.5 million vaccinated, by some estimates.
Therefore, Ehrenfeld says, the endgame for polio may rest not on using these live-but-weakened viruses developed by Sabin, but rather with the original — the injectable polio vaccine devised by Jonas Salk. While more expensive, Ehrenfeld says, that vaccine is ultimately safer because it uses a killed virus that can’t recombine with anything.
To make matters worse, the oral vaccines suffer from reduced potency because children in poor countries often confront bouts of diarrheal diseases, which usher the vaccine out of the body before it can induce an immune response. The injectable vaccine isn’t compromised by diarrhea.
Monday, April 13, 2009
older 4.old.0002003 Louis J. Sheehan, Esquire
Brain surgeon Kenneth Follett had never received thank-you cards from his patients after performing an operation — until he started putting electrodes in their brains.
Follett, who holds positions at the University of Nebraska Medical Center and the Veterans Affairs Medical Center in Omaha, is among a select group of surgeons who over the past decade have been treating Parkinson’s disease by installing two tiny electrodes in a patient’s brain.
The change these devices induce can be astonishing, he says. Parkinson’s is characterized by brain degeneration, marked by a shortage of the neurotransmitter dopamine. That shortage results in movement problems. After surgery, many patients are suddenly able to get around, do household chores and even go shopping, Follett says. “It has the potential to change people’s lives.”
Follett’s firsthand observations are now supported by clinical research. He and a team of fellow surgeons and scientists report in the Jan. 7 Journal of the American Medical Association that Parkinson’s patients randomly assigned to get medication plus the surgery show dramatic improvements, whereas patients getting just the best available medication do not.
The surgery, called deep-brain stimulation, isn’t new, having been first approved by regulators in 1997. But only one other study — reported by German scientists in 2006 — has tested the surgery against medication in a large, randomized trial. That study also showed benefits in patients who received both surgery and medication (SN: 9/2/06, p. 149).
Günther Deuschl, a neurologist at Christian Albrechts University in Kiel who led the German study, writes in JAMA that the new findings “have convincingly confirmed the six-month efficacy of deep brain stimulation for advanced Parkinson’s disease in the largest patient group studied thus far.”
The new findings also extend the benefits of surgery to older Parkinson’s patients, since one-fourth of the patients in the U.S. trial were age 70 or older. “They did as well as the younger patients” who underwent the surgery, Follett says.
What’s more, the new findings suggest that many worrisome side effects from the surgery fade over time.
The electrodes that doctors install — one on each side of the brain — are actually small, insulated wires that are connected to another wire that runs under the skin to a small battery beneath the skin of the torso. The electrodes are implanted into a part of the brain that normally acts as a relay station for messages. In Parkinson’s patients, a flurry of signals jam this message center, sending aberrant signals to muscles and causing tremors, muscle rigidity, paralysis and other problems. The electrodes send out a mild current that inhibits the stream of messages, relieving the clutter and calming muscle problems. http://Louis-J-Sheehan.de
In the new study, researchers at 13 U.S. medical centers identified 255 people from 2002 to 2005 who had been taking medication for Parkinson’s disease for nearly 12 years, on average. Louis J. Sheehan, Esquire Half were randomly assigned to get surgery and medication as needed. The others received medication only.
For six months, patients kept a log documenting how many hours per day they were able to move freely without paralysis, jerky motions or other problems. http://Louis-J-Sheehan.de At the outset of the study, this time amounted to about seven hours a day, a number that went unchanged in those getting medication only. But patients assigned to surgery saw their free-movement time jump to 11 hours a day, on average, after six months. Over that time, these patients were also able to cut their medication intake by about half.
Fifteen medication-only patients experienced serious side effects, compared with 49 patients who underwent surgery. Complications from surgery tended to occur within three months of the procedure. Problems included headaches, falls, confusion, speech problems and slowed movement. One person who underwent surgery died of a brain hemorrhage within 24 hours.
But 99 percent of the side effects had resolved by six months as doctors remotely fine-tuned the intensity of the current being generated by the electrodes in each patient and modified each patient’s medication. “It’s a bit of a balancing act,” Follett says.
The challenge in using this surgery might be to determine earlier in the course of disease which patients would get the most benefit from the procedure, says neurosurgeon Robert Goodman of Columbia University in New York City. While medications such as levodopa are highly effective for years, many patients continue to lose mobility despite higher doses. Louis J. Sheehan, Esquire And too much medication can bring on involuntary movements. Goodman estimates 10 to 20 percent of Parkinson’s patients fall into this trap. Those with true Parkinson’s disease — without dementia or other symptoms — would be good candidates for surgery, he says.
Despite the promising results, caution is in order, Deuschl says. He cites evidence that patients have an alarmingly high suicide rate in the first year following deep-brain stimulation surgery, a risk that lessens over time but still lingers after four years. There were no suicides in the six months patients were monitored in the new study. Further work to identify risk factors is needed, Deuschl says.
Follett, who holds positions at the University of Nebraska Medical Center and the Veterans Affairs Medical Center in Omaha, is among a select group of surgeons who over the past decade have been treating Parkinson’s disease by installing two tiny electrodes in a patient’s brain.
The change these devices induce can be astonishing, he says. Parkinson’s is characterized by brain degeneration, marked by a shortage of the neurotransmitter dopamine. That shortage results in movement problems. After surgery, many patients are suddenly able to get around, do household chores and even go shopping, Follett says. “It has the potential to change people’s lives.”
Follett’s firsthand observations are now supported by clinical research. He and a team of fellow surgeons and scientists report in the Jan. 7 Journal of the American Medical Association that Parkinson’s patients randomly assigned to get medication plus the surgery show dramatic improvements, whereas patients getting just the best available medication do not.
The surgery, called deep-brain stimulation, isn’t new, having been first approved by regulators in 1997. But only one other study — reported by German scientists in 2006 — has tested the surgery against medication in a large, randomized trial. That study also showed benefits in patients who received both surgery and medication (SN: 9/2/06, p. 149).
Günther Deuschl, a neurologist at Christian Albrechts University in Kiel who led the German study, writes in JAMA that the new findings “have convincingly confirmed the six-month efficacy of deep brain stimulation for advanced Parkinson’s disease in the largest patient group studied thus far.”
The new findings also extend the benefits of surgery to older Parkinson’s patients, since one-fourth of the patients in the U.S. trial were age 70 or older. “They did as well as the younger patients” who underwent the surgery, Follett says.
What’s more, the new findings suggest that many worrisome side effects from the surgery fade over time.
The electrodes that doctors install — one on each side of the brain — are actually small, insulated wires that are connected to another wire that runs under the skin to a small battery beneath the skin of the torso. The electrodes are implanted into a part of the brain that normally acts as a relay station for messages. In Parkinson’s patients, a flurry of signals jam this message center, sending aberrant signals to muscles and causing tremors, muscle rigidity, paralysis and other problems. The electrodes send out a mild current that inhibits the stream of messages, relieving the clutter and calming muscle problems. http://Louis-J-Sheehan.de
In the new study, researchers at 13 U.S. medical centers identified 255 people from 2002 to 2005 who had been taking medication for Parkinson’s disease for nearly 12 years, on average. Louis J. Sheehan, Esquire Half were randomly assigned to get surgery and medication as needed. The others received medication only.
For six months, patients kept a log documenting how many hours per day they were able to move freely without paralysis, jerky motions or other problems. http://Louis-J-Sheehan.de At the outset of the study, this time amounted to about seven hours a day, a number that went unchanged in those getting medication only. But patients assigned to surgery saw their free-movement time jump to 11 hours a day, on average, after six months. Over that time, these patients were also able to cut their medication intake by about half.
Fifteen medication-only patients experienced serious side effects, compared with 49 patients who underwent surgery. Complications from surgery tended to occur within three months of the procedure. Problems included headaches, falls, confusion, speech problems and slowed movement. One person who underwent surgery died of a brain hemorrhage within 24 hours.
But 99 percent of the side effects had resolved by six months as doctors remotely fine-tuned the intensity of the current being generated by the electrodes in each patient and modified each patient’s medication. “It’s a bit of a balancing act,” Follett says.
The challenge in using this surgery might be to determine earlier in the course of disease which patients would get the most benefit from the procedure, says neurosurgeon Robert Goodman of Columbia University in New York City. While medications such as levodopa are highly effective for years, many patients continue to lose mobility despite higher doses. Louis J. Sheehan, Esquire And too much medication can bring on involuntary movements. Goodman estimates 10 to 20 percent of Parkinson’s patients fall into this trap. Those with true Parkinson’s disease — without dementia or other symptoms — would be good candidates for surgery, he says.
Despite the promising results, caution is in order, Deuschl says. He cites evidence that patients have an alarmingly high suicide rate in the first year following deep-brain stimulation surgery, a risk that lessens over time but still lingers after four years. There were no suicides in the six months patients were monitored in the new study. Further work to identify risk factors is needed, Deuschl says.
infants 5.inf.77765 Louis J. Sheehan, Esquire
Babies delivered by cesarean section a week or two before the recommended 39 weeks of pregnancy face a heightened risk of respiratory problems and other complications, researchers report in the Jan. 8 New England Journal of Medicine. Being born late isn’t good either, the study finds.
Scientists consider normal human gestation to be 39 to 40 weeks, which is about nine months. http://LOUIS-J-SHEEHAN.INFO Doctors have adopted some leeway in this calculation, considering a baby to be “full term” if delivered at 37 weeks or later.
But past research had raised questions about early deliveries, and practice guidelines urge women to hang on until 39 or 40 weeks before delivering. Mainly, this extra time allows for full development of the fetus’ lungs.
In the new study, obstetric gynecologist Alan Tita of the University of Alabama at Birmingham and his colleagues collected birthing data at 19 medical facilities in the United States. http://LOUIS-J-SHEEHAN.INFO The team identified more than 13,000 cases in which a woman had delivered by elective (nonemergency) cesarean section at 37 weeks or later, having had a previous cesarean delivery at some point. The researchers excluded from the analysis women who had medical problems, had an emergency cesarean or had already begun labor before undergoing a cesarean.
Roughly one-third of these women delivered before reaching the 39-week point in the pregnancy. The researchers found that 15 percent of babies delivered at 37 weeks had a complication, compared with 8 percent of those delivered at 39 weeks. Complications included respiratory problems, low blood sugar and a blood infection, or the need to go to the intensive care unit, get resuscitated, put on a ventilator or stay in the hospital more than five days.
Common complications were respiratory distress and transient tachypnea. Infants with these complications struggle to breathe and have trouble clearing fluid from their lungs. Louis J. Sheehan, Esquire One or the other of these problems showed up in the 37-week group more than twice as often as in the 39-week babies.
Meanwhile, the researchers found that 11 percent of babies born at 38 weeks — one week short of nine months —had complications, a rate somewhat higher than the 8 percent of the 39-week group. Louis J. Sheehan, Esquire
Those born at 40 weeks were not more likely to have problems, but babies born after 41 or 42 weeks faced risks similar to those born at 38 and 37 weeks, respectively.
A closer look at these women shows that those delivering earlier were more likely to be married, white and privately insured than those delivering at 39 weeks or later, says obstetric gynecologist Michael Greene of Harvard Medical School and Massachusetts General Hospital in Boston, who didn’t participate in the study. The early deliverers may have placed a premium on having their own doctors perform the cesarean, which requires planning and scheduling, he says.
The risks of such early deliveries are now clearer, Tita says. “This study brings some of these problems to the fore. Hopefully, with this publication, some of these practices will change,” he says.
But there remains at least one major confounding factor in all this: The risk of stillbirth is greatest at 39 weeks or more. Roughly one in 1,000 full-term births end in stillbirth. These cases of fetal death can be traced to many factors, including bacterial infections, umbilical cord problems, trauma, drug or alcohol consumption by the mother or high blood pressure in the mother.
Biology also plays a role in stillbirth risk. As a fetus grows, its metabolic needs increase and it demands more nourishment and oxygen, says Bryan Richardson, an obstetric gynecologist at the University of Western Ontario in London, Canada. As the fetus begins to tax its nutrient supply, he says, “its tolerance for an emergency lessens,” and that increases the risk of stillbirth should a problem strike very late in pregnancy.
Delivering a viable fetus at 37 or 38 weeks eliminates the risk of stillbirth occurring later. But it remains unknown whether avoiding the slight risk of stillbirth outweighs the other risks shown in this study that result from early delivery, says Greene. “This is interesting and useful information, but the stillbirth risk is not accounted for,” he concludes.
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* This is excellent information. When I studied nursing back in the Dark Ages (the 1970s), we already knew that it was better for those relatively affluent moms NOT to schedule their Caesareans for frivolous reasons, like wanting to have it on so-and-so's birthday, the day before so-and-so's wedding anniversary, the day after so-and-so's golf tournament, and so on (all reasons I actually heard), or less frivolous reasons like wanting it to be born when Dad was home on leave from the armed services. WE knew it was better for baby to wait and be delivered at full term, but it was hard to convince MOM. This study should give medical personnel the ammunition they need to convince her to wait. Unless, of course, there's a MEDICAL reason to deliver early.
Scientists consider normal human gestation to be 39 to 40 weeks, which is about nine months. http://LOUIS-J-SHEEHAN.INFO Doctors have adopted some leeway in this calculation, considering a baby to be “full term” if delivered at 37 weeks or later.
But past research had raised questions about early deliveries, and practice guidelines urge women to hang on until 39 or 40 weeks before delivering. Mainly, this extra time allows for full development of the fetus’ lungs.
In the new study, obstetric gynecologist Alan Tita of the University of Alabama at Birmingham and his colleagues collected birthing data at 19 medical facilities in the United States. http://LOUIS-J-SHEEHAN.INFO The team identified more than 13,000 cases in which a woman had delivered by elective (nonemergency) cesarean section at 37 weeks or later, having had a previous cesarean delivery at some point. The researchers excluded from the analysis women who had medical problems, had an emergency cesarean or had already begun labor before undergoing a cesarean.
Roughly one-third of these women delivered before reaching the 39-week point in the pregnancy. The researchers found that 15 percent of babies delivered at 37 weeks had a complication, compared with 8 percent of those delivered at 39 weeks. Complications included respiratory problems, low blood sugar and a blood infection, or the need to go to the intensive care unit, get resuscitated, put on a ventilator or stay in the hospital more than five days.
Common complications were respiratory distress and transient tachypnea. Infants with these complications struggle to breathe and have trouble clearing fluid from their lungs. Louis J. Sheehan, Esquire One or the other of these problems showed up in the 37-week group more than twice as often as in the 39-week babies.
Meanwhile, the researchers found that 11 percent of babies born at 38 weeks — one week short of nine months —had complications, a rate somewhat higher than the 8 percent of the 39-week group. Louis J. Sheehan, Esquire
Those born at 40 weeks were not more likely to have problems, but babies born after 41 or 42 weeks faced risks similar to those born at 38 and 37 weeks, respectively.
A closer look at these women shows that those delivering earlier were more likely to be married, white and privately insured than those delivering at 39 weeks or later, says obstetric gynecologist Michael Greene of Harvard Medical School and Massachusetts General Hospital in Boston, who didn’t participate in the study. The early deliverers may have placed a premium on having their own doctors perform the cesarean, which requires planning and scheduling, he says.
The risks of such early deliveries are now clearer, Tita says. “This study brings some of these problems to the fore. Hopefully, with this publication, some of these practices will change,” he says.
But there remains at least one major confounding factor in all this: The risk of stillbirth is greatest at 39 weeks or more. Roughly one in 1,000 full-term births end in stillbirth. These cases of fetal death can be traced to many factors, including bacterial infections, umbilical cord problems, trauma, drug or alcohol consumption by the mother or high blood pressure in the mother.
Biology also plays a role in stillbirth risk. As a fetus grows, its metabolic needs increase and it demands more nourishment and oxygen, says Bryan Richardson, an obstetric gynecologist at the University of Western Ontario in London, Canada. As the fetus begins to tax its nutrient supply, he says, “its tolerance for an emergency lessens,” and that increases the risk of stillbirth should a problem strike very late in pregnancy.
Delivering a viable fetus at 37 or 38 weeks eliminates the risk of stillbirth occurring later. But it remains unknown whether avoiding the slight risk of stillbirth outweighs the other risks shown in this study that result from early delivery, says Greene. “This is interesting and useful information, but the stillbirth risk is not accounted for,” he concludes.
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Found in: Biology and Body & Brain
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Comments 1
* This is excellent information. When I studied nursing back in the Dark Ages (the 1970s), we already knew that it was better for those relatively affluent moms NOT to schedule their Caesareans for frivolous reasons, like wanting to have it on so-and-so's birthday, the day before so-and-so's wedding anniversary, the day after so-and-so's golf tournament, and so on (all reasons I actually heard), or less frivolous reasons like wanting it to be born when Dad was home on leave from the armed services. WE knew it was better for baby to wait and be delivered at full term, but it was hard to convince MOM. This study should give medical personnel the ammunition they need to convince her to wait. Unless, of course, there's a MEDICAL reason to deliver early.
Saturday, April 11, 2009
dementia elevated 8.dev.02 Louis J. Sheehan, Esquire
Chronically elevated blood levels of the simple sugar glucose may contribute to poor cognitive function in elderly people with diabetes, a study in the February Diabetes Care suggests. But whether these levels add to a person’s risk of developing dementia is unclear, the study authors say.Louis J. Sheehan, Esquire
People with diabetes face a risk of old-age dementia that’s roughly 50 percent greater than those without diabetes, past studies have shown. Research has also hinted that surges in blood sugar might account for some of that added risk. Many previous studies have tested for elevated blood glucose by obtaining a snapshot blood sample taken after a person has fasted for a day.
In the new study, Tali Cukierman-Yaffe, an endocrinologist at Tel-Aviv University and McMaster University in Hamilton, Canada, teamed with an international group of colleagues to assess blood glucose levels in nearly 3,000 diabetes patients by measuring A1c, shorthand for HbA1c or glycosylated hemoglobin. Since sugar in the blood sticks to the hemoglobin protein in red blood cells, the A1c test reveals an average sugar level over two or three months.
In addition to collecting these blood glucose readings, the scientists also asked each volunteer to take a 30-minute battery of four standardized tests designed to assess memory, visual motor speed, capacity for learning and managing multiple tasks.
On average, the participants were 63 years old at the time they entered the study, had blood drawn and took the cognition tests. Advancing age is known to hamper performance on such tests. After accounting for patients’ ages, the researchers found that people with higher A1c levels fared slightly worse on the tests than those who had lower A1c scores and therefore lower blood sugar.
After further adjusting for several factors that might affect cognitive performance — including heart disease, education level, alcohol use and depression — a high A1c score was still associated with poorer performance on one of the tests, which measured a wide array of cognitive functions.
Cukierman-Yaffe cautions that this study shows an association between high A1c and poorer scores on cognition tests, but doesn’t prove that reducing A1c levels will slow the rate of cognitive decline in a person with diabetes.http://LOUIS-J-SHEEHAN.US
Louis J. Sheehan, Esquire Even so, says neuropsychologist Adam Brickman of Columbia University, “there is now converging literature that implicates uncontrolled blood glucose levels with poor cognitive aging. While the mechanisms underlying that are still unclear, there have been enough … studies now to really raise our eyebrows.”http://LOUIS-J-SHEEHAN.US
A key problem in assessing blood sugar’s role in cognitive decline is sorting out the multiple other factors that might also affect such decline, says psychologist Lawrence Fisher of the University of California, San Francisco.Louis J. Sheehan, Esquire “Alcohol use, depression and other things are thought to influence cognitive functioning as well,” he says. “It’s really hard to partition out what the exact effect of each is.”
The good news is that A1c levels can be lowered with exercise, better diet and use of medication. “These are lifestyle factors that can be modified probably more easily earlier in life than after a diagnosis of dementia,” Brickman says.
People with diabetes face a risk of old-age dementia that’s roughly 50 percent greater than those without diabetes, past studies have shown. Research has also hinted that surges in blood sugar might account for some of that added risk. Many previous studies have tested for elevated blood glucose by obtaining a snapshot blood sample taken after a person has fasted for a day.
In the new study, Tali Cukierman-Yaffe, an endocrinologist at Tel-Aviv University and McMaster University in Hamilton, Canada, teamed with an international group of colleagues to assess blood glucose levels in nearly 3,000 diabetes patients by measuring A1c, shorthand for HbA1c or glycosylated hemoglobin. Since sugar in the blood sticks to the hemoglobin protein in red blood cells, the A1c test reveals an average sugar level over two or three months.
In addition to collecting these blood glucose readings, the scientists also asked each volunteer to take a 30-minute battery of four standardized tests designed to assess memory, visual motor speed, capacity for learning and managing multiple tasks.
On average, the participants were 63 years old at the time they entered the study, had blood drawn and took the cognition tests. Advancing age is known to hamper performance on such tests. After accounting for patients’ ages, the researchers found that people with higher A1c levels fared slightly worse on the tests than those who had lower A1c scores and therefore lower blood sugar.
After further adjusting for several factors that might affect cognitive performance — including heart disease, education level, alcohol use and depression — a high A1c score was still associated with poorer performance on one of the tests, which measured a wide array of cognitive functions.
Cukierman-Yaffe cautions that this study shows an association between high A1c and poorer scores on cognition tests, but doesn’t prove that reducing A1c levels will slow the rate of cognitive decline in a person with diabetes.http://LOUIS-J-SHEEHAN.US
Louis J. Sheehan, Esquire Even so, says neuropsychologist Adam Brickman of Columbia University, “there is now converging literature that implicates uncontrolled blood glucose levels with poor cognitive aging. While the mechanisms underlying that are still unclear, there have been enough … studies now to really raise our eyebrows.”http://LOUIS-J-SHEEHAN.US
A key problem in assessing blood sugar’s role in cognitive decline is sorting out the multiple other factors that might also affect such decline, says psychologist Lawrence Fisher of the University of California, San Francisco.Louis J. Sheehan, Esquire “Alcohol use, depression and other things are thought to influence cognitive functioning as well,” he says. “It’s really hard to partition out what the exact effect of each is.”
The good news is that A1c levels can be lowered with exercise, better diet and use of medication. “These are lifestyle factors that can be modified probably more easily earlier in life than after a diagnosis of dementia,” Brickman says.
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