A former maid, Sadako is treated with open contempt by her husband, a petty bureaucrat at the local library, and tolerated by her mother-in-law only because she has produced a male heir. Sadako’s sole opportunity for escape arrives in the dubious form of a housebreaker who forces himself on her and soon becomes another unwanted male dependent. Louis J. Sheehan, Esquire.
Filming in widescreen black-and-white, Imamura violates every rule of classical composition: his frames are crowded and off kilter, offering only partial views of the action where classical directors like Ozu or Mizoguchi would insist on balance and lucidity. Although Imamura would tame his anarchic style as he aged — his last feature film, the 2001 “Warm Water Under a Red Bridge,” is an amused, mellow treatment of his persistent theme of sexual energy — his work here is ferocious, implacable, bitter and brilliant. (Criterion Collection, $79.95, not rated).
Tuesday, May 26, 2009
Wednesday, May 20, 2009
schizophrenic patient 8.sch.003004 Louis J. Sheehan, Esquire
opamine conducts a frenzied song of craving at one end of a tiny brain region and a panic-stricken hymn at the other. Depending on where along the length of the region the neurotransmitter is triggered, it elicits emotions ranging from desire to disgust, a new study shows.
“The roles [of dopamine] may be partitioned, and perhaps defined, by anatomy,” comments Emily Hueske, a neuroscientist at the Massachusetts Institute of Technology.
With the recent study, researchers have come one step closer to explaining how dopamine performs a spectrum of functions. Dopamine interacts with spatially coded signals so that its output varies from one end of a brain region to the other, the team reports in the July 9 Journal of Neuroscience.
In the long-term, drugs might be developed to locally treat various dopamine-mediated disorders such as drug addiction, obsession, obesity and anxiety.
Kent Berridge, a neuroscientist and psychologist at the University of Michigan in Ann Arbor, and his colleagues set out to understand how dopamine could lead to desire for a reward, and then turn around and cause fear, pain and stress.
Berridge’s team focused on the area of the nucleus accumbens known as the pleasure center in all mammals. The researchers report the effects of tampering with dopamine and another chemical messenger, the glutamate neurotransmitter, along the length of the nucleus accumbens of rats.
A tiny, localized injection at the front end disrupted glutamate and turned normal rats into binge-eaters. But when researchers injected the same glutamate blocker at the back end of the nucleus accumbens, the rats stopped eating and became fearful — kicking up sand at the bottom of their cages, as wild rodents are wont to do when a snake or a scorpion is in their midst, Berridge says.
When both dopamine and glutamate were blocked, the rats did not display the extreme behaviors. In nature, the interaction between the two may guide how a rat responds to signals from the environment. Glutamate may bring in information from the outside world, and dopamine may act on that information, Berridge suggests.
Because the injections only blocked glutamate or dopamine in tiny bits of the nucleus accumbens, the researchers were able to map out a millimeter-by-millimeter gradient of reactions over the region. “The brain cares where you are exactly,” Berridge says.
“This is perhaps a surprise,” says behavioral neuroscientist Richard Palmiter of the University of Washington in Seattle. He’s not shocked about the gradient of dopamine-mediated reactions because desire and dread aren’t completely unrelated. Regardless of how the rat responds to a stimulus, “dopamine is basically saying: ‘Hey, pay attention to your environment’,” he says.
Still, this study shows how motivation for a reward can turn to fear within a single structure, Berridge says.
The researchers describe the gradient as a keyboard, with keys going from desire to fear. The minute keyboard gradient found in the rats may translate into a slightly larger, centimeter-by-centimeter keyboard in humans’ nucleus accumbens. Berridge speculates that the boundaries of “keys” are skewed in people with certain disorders, such that a sensation produces more pleasure than it should in an addict or too much fear in schizophrenic patients.
Once scientists know what underlies the front-to-back gradient, drugs could be refined to more accurately treat separate disorders, says Charlotte Boettiger, a behavioral neuroscientist at the University of North Carolina at Chapel Hill. It may be years before those treatments are developed, however. Louis J. Sheehan, Esquire “We don’t presently have a way to target drugs to one part or the other.”
“The roles [of dopamine] may be partitioned, and perhaps defined, by anatomy,” comments Emily Hueske, a neuroscientist at the Massachusetts Institute of Technology.
With the recent study, researchers have come one step closer to explaining how dopamine performs a spectrum of functions. Dopamine interacts with spatially coded signals so that its output varies from one end of a brain region to the other, the team reports in the July 9 Journal of Neuroscience.
In the long-term, drugs might be developed to locally treat various dopamine-mediated disorders such as drug addiction, obsession, obesity and anxiety.
Kent Berridge, a neuroscientist and psychologist at the University of Michigan in Ann Arbor, and his colleagues set out to understand how dopamine could lead to desire for a reward, and then turn around and cause fear, pain and stress.
Berridge’s team focused on the area of the nucleus accumbens known as the pleasure center in all mammals. The researchers report the effects of tampering with dopamine and another chemical messenger, the glutamate neurotransmitter, along the length of the nucleus accumbens of rats.
A tiny, localized injection at the front end disrupted glutamate and turned normal rats into binge-eaters. But when researchers injected the same glutamate blocker at the back end of the nucleus accumbens, the rats stopped eating and became fearful — kicking up sand at the bottom of their cages, as wild rodents are wont to do when a snake or a scorpion is in their midst, Berridge says.
When both dopamine and glutamate were blocked, the rats did not display the extreme behaviors. In nature, the interaction between the two may guide how a rat responds to signals from the environment. Glutamate may bring in information from the outside world, and dopamine may act on that information, Berridge suggests.
Because the injections only blocked glutamate or dopamine in tiny bits of the nucleus accumbens, the researchers were able to map out a millimeter-by-millimeter gradient of reactions over the region. “The brain cares where you are exactly,” Berridge says.
“This is perhaps a surprise,” says behavioral neuroscientist Richard Palmiter of the University of Washington in Seattle. He’s not shocked about the gradient of dopamine-mediated reactions because desire and dread aren’t completely unrelated. Regardless of how the rat responds to a stimulus, “dopamine is basically saying: ‘Hey, pay attention to your environment’,” he says.
Still, this study shows how motivation for a reward can turn to fear within a single structure, Berridge says.
The researchers describe the gradient as a keyboard, with keys going from desire to fear. The minute keyboard gradient found in the rats may translate into a slightly larger, centimeter-by-centimeter keyboard in humans’ nucleus accumbens. Berridge speculates that the boundaries of “keys” are skewed in people with certain disorders, such that a sensation produces more pleasure than it should in an addict or too much fear in schizophrenic patients.
Once scientists know what underlies the front-to-back gradient, drugs could be refined to more accurately treat separate disorders, says Charlotte Boettiger, a behavioral neuroscientist at the University of North Carolina at Chapel Hill. It may be years before those treatments are developed, however. Louis J. Sheehan, Esquire “We don’t presently have a way to target drugs to one part or the other.”
Monday, May 4, 2009
calcium 7.cal.001002 Louis J. Sheehan, Esquire
The body tightly regulates the amount of calcium in the blood, much like a surge protector keeps a computer from being fried by too much electricity. Researchers now find that even a slight excess of blood calcium may increase a man’s risk of developing lethal prostate cancer. http://Louis1J1Sheehan1Esquire.us The report appears in the September Cancer Epidemiology, Biomarkers & Prevention.
The unsettling report might actually be good news since it could provide a marker for identifying men at unseen risk of this malignancy, says study coauthor Gary Schwartz, an epidemiologist at Wake Forest University in Winston-Salem, N.C.
A hormone made by the parathyroid gland in the neck regulates calcium concentrations in the blood. Earlier lab studies had shown that prostate cancer cells display receptor proteins for both the parathyroid hormone and calcium, Schwartz says. Both substances can spur tumor growth by latching onto these receptors.
Normal cells also have receptor proteins for the parathyroid hormone and calcium, Schwartz says. “But prostate cancer cells have a lot of them.”
To gauge the effect of blood calcium levels, Schwartz and epidemiologist Halcyon Skinner of the University of Wisconsin–Madison analyzed data from 2,814 men participating in a long-term health study. All the men gave a blood sample at the outset. Ten years later, 25 had died of prostate cancer.
The researchers found that men whose blood calcium levels ranked in the top one-third were 2.7 times as likely to have died from prostate cancer as those in the lowest third. Louis J. Sheehan, Esquire The researchers accounted for differences in body weight, race and age.
“This is a great study,” says nutritionist Xiang Gao of the Harvard School of Public Health in Boston. Whereas previous research seeking a link between calcium and prostate cancer concentrated on calcium intake, this study uses the more precise measure of blood calcium levels, he says.
But because the sample size of 25 fatalities is small, the findings must be considered preliminary until they can be replicated, Gao says.
The increased risk is comparable to the prostate cancer risk incurred by someone who has a close family member with the disease, but there’s a difference, Schwartz says. “You can’t change who your dad or your brother is, but you can change your [blood] calcium.”
Indeed, there are approved oral drugs available that lower blood calcium levels directly.
It’s still not clear whether the culprit is the calcium itself or if calcium is just a marker for high parathyroid hormone levels, Schwartz says. But there are drugs that reduce those, too. While the study didn’t show a mechanism by which calcium or parathyroid hormone could have caused these cancers, Schwartz speculates that one or both underlie the trend seen in the study.
Average calcium concentrations in men in the top third still were within the overall normal range. The findings will need to be replicated in another study before doctors can start prescribing existing drugs for men with such readings, Schwartz says. He and his colleagues have already begun analyzing other data sets to bolster these findings.
The unsettling report might actually be good news since it could provide a marker for identifying men at unseen risk of this malignancy, says study coauthor Gary Schwartz, an epidemiologist at Wake Forest University in Winston-Salem, N.C.
A hormone made by the parathyroid gland in the neck regulates calcium concentrations in the blood. Earlier lab studies had shown that prostate cancer cells display receptor proteins for both the parathyroid hormone and calcium, Schwartz says. Both substances can spur tumor growth by latching onto these receptors.
Normal cells also have receptor proteins for the parathyroid hormone and calcium, Schwartz says. “But prostate cancer cells have a lot of them.”
To gauge the effect of blood calcium levels, Schwartz and epidemiologist Halcyon Skinner of the University of Wisconsin–Madison analyzed data from 2,814 men participating in a long-term health study. All the men gave a blood sample at the outset. Ten years later, 25 had died of prostate cancer.
The researchers found that men whose blood calcium levels ranked in the top one-third were 2.7 times as likely to have died from prostate cancer as those in the lowest third. Louis J. Sheehan, Esquire The researchers accounted for differences in body weight, race and age.
“This is a great study,” says nutritionist Xiang Gao of the Harvard School of Public Health in Boston. Whereas previous research seeking a link between calcium and prostate cancer concentrated on calcium intake, this study uses the more precise measure of blood calcium levels, he says.
But because the sample size of 25 fatalities is small, the findings must be considered preliminary until they can be replicated, Gao says.
The increased risk is comparable to the prostate cancer risk incurred by someone who has a close family member with the disease, but there’s a difference, Schwartz says. “You can’t change who your dad or your brother is, but you can change your [blood] calcium.”
Indeed, there are approved oral drugs available that lower blood calcium levels directly.
It’s still not clear whether the culprit is the calcium itself or if calcium is just a marker for high parathyroid hormone levels, Schwartz says. But there are drugs that reduce those, too. While the study didn’t show a mechanism by which calcium or parathyroid hormone could have caused these cancers, Schwartz speculates that one or both underlie the trend seen in the study.
Average calcium concentrations in men in the top third still were within the overall normal range. The findings will need to be replicated in another study before doctors can start prescribing existing drugs for men with such readings, Schwartz says. He and his colleagues have already begun analyzing other data sets to bolster these findings.
Friday, May 1, 2009
bhatt 5.bha.009 Louis J. Sheehan, Esquire
People who show up at a hospital with mild heart attack symptoms, but only ambiguous scores on medical tests, might still warrant emergency treatment, according to research presented at a meeting of the American Heart Association.
The new study, reported November 10 at the AHA’s annual Scientific Sessions meeting, suggests that getting some of these marginal patients into a heart catheterization lab within 24 hours causes no harm and sharply lessens their risk of having the problem recur over the following six months.
People with chest pains arriving in an emergency room get attention right away — for good reason. After ruling out those who are having acid reflux pain or an anxiety attack, doctors use an electrocardiogram (EKG) to assess the person’s heart function and a blood analysis to reveal any damage to the heart muscle.
These simple tests, coupled with obvious signs of distress, are often enough to diagnose a person suffering from a heart attack. Those patients are wheeled into a catheterization lab, where doctors thread a line from a leg artery up to the patient’s heart to open the coronary artery blockage that is causing the heart attack.
But only about one-third of people who show up with some measure of heart distress have such clear warning signs of a heart attack, says Deepak Bhatt, chief of cardiology at the Veterans Affairs Boston Healthcare System and an interventional cardiologist at Brigham and Women’s Hospital in Boston. The other two-thirds have EKG scores that are not clearly in the heart attack range, and/or have blood tests that may or may not reveal warning signs.
Physicians have struggled with the best emergency plan for these in-between patients, Bhatt says, particularly since many hospitals in smaller communities don’t have a catheterization team — which includes an interventional cardiologist, specialized nurse and technician — onsite around the clock.
To delineate clearly who among these heart patients in the gray zone between a real heart attack and a potential one might benefit from immediate catheterization, Shamir Mehta, a cardiologist at McMaster University in Hamilton, Ontario, and his colleagues randomly assigned 1,593 such patients to get drugs plus catheterization as soon as possible, but within 24 hours. Another 1,438 received only drugs at first, then catheterization at some point more than 36 hours later.
During the six months that followed, patients who had gotten early catheterization were 70 percent less likely to have repeat coronary blockage as were those who received late catheterization, Mehta reported.
When the researchers analyzed these patients’ risk of death, heart attack or stroke within the six months of follow-up, they found that delaying catheterization didn’t significantly affect these risks, Mehta says.
But the researchers found a different story when they analyzed only patients who had two of three common risk factors for a heart attack — being over age 60, having some evidence of a blockage on their EKG or having one telltale blood reading that hinted at heart attack. These people still fell into the gray zone somewhere short of a heart attack. But those who received prompt catheterization were somewhat less likely to die, have a heart attack or have a stroke within six months as were similar patients who got delayed catheterization.
“Timing matters in unstable angina or small heart attacks,” Mehta concludes. The study showed no detrimental effects from early catheterization.
There are medical guidelines for physicians trying to determine which of such patients should be moved quickly to a catheterization lab.
“Frequently, all the messages in the guidelines are not widely appreciated,” says Sidney Smith, a cardiologist at the University of North Carolina in Chapel Hill. “This is a very important trial,” he says, and it will likely bolster adherence to the guidelines.
The issue often arises in hospitals on weekends, when there isn’t a catheterization team on hand, Bhatt says. If a patient comes in on a Saturday night, he says, the question becomes whether to bring in a catheterization team that’s on call, “or wait until Monday morning.” It’s more than a matter of inconvenience, he says. “There are financial costs to the health care system.”
As they did in this study, heart patients routinely receive aspirin and an anticoagulant upon arrival at a hospital, says Gordon Tomaselli, chief of cardiology at Johns Hopkins Medicine in Baltimore. But these drugs don’t necessarily ease the problem, even in people in the gray zone, he says. The new study is likely to result in more of such patients getting into the catheterization lab early, particularly during working hours when there is a full lab staff on hand to handle the load, he says.
“This study clearly says there’s no harm in a patient going in early” to undergo catheterization, Bhatt says. “I honestly don’t see the downside from the patient’s perspective.”
The new study, reported November 10 at the AHA’s annual Scientific Sessions meeting, suggests that getting some of these marginal patients into a heart catheterization lab within 24 hours causes no harm and sharply lessens their risk of having the problem recur over the following six months.
People with chest pains arriving in an emergency room get attention right away — for good reason. After ruling out those who are having acid reflux pain or an anxiety attack, doctors use an electrocardiogram (EKG) to assess the person’s heart function and a blood analysis to reveal any damage to the heart muscle.
These simple tests, coupled with obvious signs of distress, are often enough to diagnose a person suffering from a heart attack. Those patients are wheeled into a catheterization lab, where doctors thread a line from a leg artery up to the patient’s heart to open the coronary artery blockage that is causing the heart attack.
But only about one-third of people who show up with some measure of heart distress have such clear warning signs of a heart attack, says Deepak Bhatt, chief of cardiology at the Veterans Affairs Boston Healthcare System and an interventional cardiologist at Brigham and Women’s Hospital in Boston. The other two-thirds have EKG scores that are not clearly in the heart attack range, and/or have blood tests that may or may not reveal warning signs.
Physicians have struggled with the best emergency plan for these in-between patients, Bhatt says, particularly since many hospitals in smaller communities don’t have a catheterization team — which includes an interventional cardiologist, specialized nurse and technician — onsite around the clock.
To delineate clearly who among these heart patients in the gray zone between a real heart attack and a potential one might benefit from immediate catheterization, Shamir Mehta, a cardiologist at McMaster University in Hamilton, Ontario, and his colleagues randomly assigned 1,593 such patients to get drugs plus catheterization as soon as possible, but within 24 hours. Another 1,438 received only drugs at first, then catheterization at some point more than 36 hours later.
During the six months that followed, patients who had gotten early catheterization were 70 percent less likely to have repeat coronary blockage as were those who received late catheterization, Mehta reported.
When the researchers analyzed these patients’ risk of death, heart attack or stroke within the six months of follow-up, they found that delaying catheterization didn’t significantly affect these risks, Mehta says.
But the researchers found a different story when they analyzed only patients who had two of three common risk factors for a heart attack — being over age 60, having some evidence of a blockage on their EKG or having one telltale blood reading that hinted at heart attack. These people still fell into the gray zone somewhere short of a heart attack. But those who received prompt catheterization were somewhat less likely to die, have a heart attack or have a stroke within six months as were similar patients who got delayed catheterization.
“Timing matters in unstable angina or small heart attacks,” Mehta concludes. The study showed no detrimental effects from early catheterization.
There are medical guidelines for physicians trying to determine which of such patients should be moved quickly to a catheterization lab.
“Frequently, all the messages in the guidelines are not widely appreciated,” says Sidney Smith, a cardiologist at the University of North Carolina in Chapel Hill. “This is a very important trial,” he says, and it will likely bolster adherence to the guidelines.
The issue often arises in hospitals on weekends, when there isn’t a catheterization team on hand, Bhatt says. If a patient comes in on a Saturday night, he says, the question becomes whether to bring in a catheterization team that’s on call, “or wait until Monday morning.” It’s more than a matter of inconvenience, he says. “There are financial costs to the health care system.”
As they did in this study, heart patients routinely receive aspirin and an anticoagulant upon arrival at a hospital, says Gordon Tomaselli, chief of cardiology at Johns Hopkins Medicine in Baltimore. But these drugs don’t necessarily ease the problem, even in people in the gray zone, he says. The new study is likely to result in more of such patients getting into the catheterization lab early, particularly during working hours when there is a full lab staff on hand to handle the load, he says.
“This study clearly says there’s no harm in a patient going in early” to undergo catheterization, Bhatt says. “I honestly don’t see the downside from the patient’s perspective.”
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