(HealthDay News) -- Women who know they should get regular Pap smears but dread the stirrups that go along with the test may finally get a reprieve.
New research shows that Pap results are just as accurate when the screen is performed with the patient keeping her feet on the examining table.
There was a real bonus in terms of comfort, too.
"There's about a 50 percent reduction in physical discomfort if women did not use the stirrups," said lead researcher Dr. Dean Seehusen, a family physician at the Eisenhower Army Medical Center at Fort Gordon, in Augusta, Ga. Women also said they felt psychologically less vulnerable, he said.
Seehusen, who published his findings recently in the British Medical Journal, remains hopeful that the practice of giving women a choice -- stirrups or no stirrups -- will catch on.
It could even boost women's health by inspiring them to have the exam more regularly, he added.
Seehusen said he had long suspected that one reason some women avoid potentially lifesaving Pap smears, and the accompanying pelvic exam, is due to the anxiety and discomfort of the stirrups position.
It can raise real anxiety in some women, he said, because "when your feet are in the stirrups you cannot easily get out." Women with mobility problems can also have an especially difficult time, he said. On top of those issues, many stirrups are cold to the touch, as well.
The study involved 197 women, ages 18 and up, who had come to the medical clinic for their annual pelvic exams. They were assigned to undergo the Pap test either in the stirrups or not.
After the tests, the women answered questions about their physical comfort, as well as their psychological sense of vulnerability and loss of control.
The result: The quality and accuracy of the Pap smears were similar, regardless of whether stirrups were used or not.
Seehusen's advice: "If a woman thinks she wants to try this method, she should ask her provider," he said.
Another women's health expert agreed.
"If a doctor can do without using the stirrups and you are more comfortable, by all means ask," said Dr. Celeste Robb-Nicholson, editor-in-chief of the Harvard Women's Health Watch and assistant professor of medicine at Harvard Medical School, Boston.
"If this alternative is offered," she said, "it could result in higher screening rates" for pap smears.
But your doctor may still prefer to do some exams with the stirrups, for better stability, she cautioned. While a simple Pap test may be no problem to perform when a woman's legs are not in the stirrups, more complicated procedures -- such as getting an endometrial biopsy -- might be better conducted with a woman's legs stabilized by the stirrups, Robb-Nicholson explained.
And some doctors may still prefer to do the Pap smear while a woman's feet are in stirrups.
But for those women who are uncomfortable in the stirrups, "It is reasonable to ask" to skip them, Robb-Nicholson said.
More information
There's more on the Pap smear at the National Women's Health Information Center.
The facts and detailed information about Yeast Infection. Also Pictures on the condition. Symptoms, Diagnosis, Treatment and much more.
Monday, June 25, 2007
Friday, June 22, 2007
Fighting Ancient Virus May Have Left Humans Vulnerable to HIV
(HealthDay News) -- Humans' distant ancestors beat back a now-extinct virus 4 million years ago, but that victory left the species vulnerable to HIV today, scientists believe.
The finding may also explain why chimpanzees, gorillas and other primates resist infection with the virus that causes AIDS, while humans are much more easily infected.
The difference lies in a human gene called TRIM5alpha, which, in lab experiments, effectively blocked infection from a reconstructed portion of the ancient retrovirus, called PtERV1. That virus probably flourished 4 million or 5 million years ago but is extinct today.
Writing in the June 22 issue of Science, the researchers say PtERV1 left behind telltale traces of its DNA inside the genomes of many primates -- with the notable exception of humans, suggesting it never gained a foothold there.
In fact, when geneticists first compared the genomes of humans against those of chimps, "the biggest difference is the presence [in nonhuman primates] of this virus, PtERV1," said study senior author Michael Emerman, a member of the Human Biology and Basic Sciences divisions at the Fred Hutchinson Cancer Research Center, in Seattle.
"There are about 130 copies in the genomes of chimps and gorillas, and maybe other primates, but it's not present at all in the genome of humans," Emerman said.
That could mean one of two things, he said: Either the ancestors of Homo sapiens already carried the TRIM5alpha gene and couldn't be infected by PtERV1, or PtERV1 wiped out all but a few individuals who were lucky enough to carry the gene. Those individuals might then have passed the gene on through their progeny, right up to the humans of today.
However, that early antiviral victory may have a darker legacy.
The experts found that various primate species carry slightly different versions of TRIM5alpha, one of a class of infection-blocking genes called "cellular restriction factors." In the case of Homo sapiens, the gene's ability to block infection against PtERV1 does not seem to extend to another dangerous retrovirus, HIV.
"We know that the human version of TRIM5alpha isn't good at all against HIV," Emerman said.
On the other hand, the TRIM5alpha found in chimps and gorillas appears to be very effective in denying HIV access to cells. It probably wasn't much good against PtERV1, however.
This type of "either/or" situation often happens in genetics, Emerman said. Genes change so that species "get better at something -- but they get worse at something else," he said.
The end result in this case is that "the human type of TRIM5alpha does not restrict HIV, and yet the TRIM5alpha in other primates can restrict HIV infection," explained Rowena Johnston, vice president for research at the Foundation for AIDS Research (amfAR) in New York City. "The critical question is, what do they have that we don't have?" she said.
She and Emerman agreed that the Hutchinson discovery isn't of immediate practical benefit to the fight against AIDS. But Johnston said research focused on cellular restriction factors such as TRIM5alpha remains "one the most promising and interesting areas of research that we have going on in the HIV world right now."
"Is there a way for us to be able to use that information to make our TRIM5alpha more potent against HIV, or at least to work out how it is that TRIM5alpha works in other animals?" she asked. "Or, to see if we can come up with some kind of mimic that would do something similar in humans?"
Advances along those lines are likely to be a "long way off," Johnston cautioned.
"What we are really talking about here are millions of years of human evolutionary history that's made us how we are today," she said. "As the paper says, we've ended up with this trade-off.
We have this great protection against PtERV1, and none of the protection against HIV."
More information
There's more on HIV/AIDS at the U.S. National Institute of Allergy and Infectious Diseases.
The finding may also explain why chimpanzees, gorillas and other primates resist infection with the virus that causes AIDS, while humans are much more easily infected.
The difference lies in a human gene called TRIM5alpha, which, in lab experiments, effectively blocked infection from a reconstructed portion of the ancient retrovirus, called PtERV1. That virus probably flourished 4 million or 5 million years ago but is extinct today.
Writing in the June 22 issue of Science, the researchers say PtERV1 left behind telltale traces of its DNA inside the genomes of many primates -- with the notable exception of humans, suggesting it never gained a foothold there.
In fact, when geneticists first compared the genomes of humans against those of chimps, "the biggest difference is the presence [in nonhuman primates] of this virus, PtERV1," said study senior author Michael Emerman, a member of the Human Biology and Basic Sciences divisions at the Fred Hutchinson Cancer Research Center, in Seattle.
"There are about 130 copies in the genomes of chimps and gorillas, and maybe other primates, but it's not present at all in the genome of humans," Emerman said.
That could mean one of two things, he said: Either the ancestors of Homo sapiens already carried the TRIM5alpha gene and couldn't be infected by PtERV1, or PtERV1 wiped out all but a few individuals who were lucky enough to carry the gene. Those individuals might then have passed the gene on through their progeny, right up to the humans of today.
However, that early antiviral victory may have a darker legacy.
The experts found that various primate species carry slightly different versions of TRIM5alpha, one of a class of infection-blocking genes called "cellular restriction factors." In the case of Homo sapiens, the gene's ability to block infection against PtERV1 does not seem to extend to another dangerous retrovirus, HIV.
"We know that the human version of TRIM5alpha isn't good at all against HIV," Emerman said.
On the other hand, the TRIM5alpha found in chimps and gorillas appears to be very effective in denying HIV access to cells. It probably wasn't much good against PtERV1, however.
This type of "either/or" situation often happens in genetics, Emerman said. Genes change so that species "get better at something -- but they get worse at something else," he said.
The end result in this case is that "the human type of TRIM5alpha does not restrict HIV, and yet the TRIM5alpha in other primates can restrict HIV infection," explained Rowena Johnston, vice president for research at the Foundation for AIDS Research (amfAR) in New York City. "The critical question is, what do they have that we don't have?" she said.
She and Emerman agreed that the Hutchinson discovery isn't of immediate practical benefit to the fight against AIDS. But Johnston said research focused on cellular restriction factors such as TRIM5alpha remains "one the most promising and interesting areas of research that we have going on in the HIV world right now."
"Is there a way for us to be able to use that information to make our TRIM5alpha more potent against HIV, or at least to work out how it is that TRIM5alpha works in other animals?" she asked. "Or, to see if we can come up with some kind of mimic that would do something similar in humans?"
Advances along those lines are likely to be a "long way off," Johnston cautioned.
"What we are really talking about here are millions of years of human evolutionary history that's made us how we are today," she said. "As the paper says, we've ended up with this trade-off.
We have this great protection against PtERV1, and none of the protection against HIV."
More information
There's more on HIV/AIDS at the U.S. National Institute of Allergy and Infectious Diseases.
Monday, June 18, 2007
Overworked Medical Interns a Danger to Patients
(HealthDay News) -- Extended work shifts pose a threat to the health and safety of medical interns and the patients they treat, according to a U.S. study of more than 2,700 interns.
The interns took part in a nationwide Internet survey and completed more than 17,000 monthly reports.
Study author Laura Barger of Brigham and Women's Hospital in Boston analyzed the data to determine the association between extended duration shifts (24 hours or more at a time), reported medical errors, and the interns' self-reported levels of stress.
Compared to months where no extended duration shifts were worked, interns who worked five or more extended duration shifts in a month were seven times more likely to report at least one fatigue-related significant medical error that harmed a patient, and 300 percent more likely to report fatigue-related errors that caused the death of a patient.
Interns who reported a medical error that caused harm to a patient were more than three times as likely to report high stress in that month, the study found.
"These results suggest that extended duration shifts negatively impact patient safety and the well-being of medical interns. (The findings) have important public policy implications for post-graduate medical education and suggest the need for counseling or other care for interns who make medical errors," Barger noted.
The study was presented Wednesday in Minneapolis at SLEEP 2007, the annual meeting of the Associated Professional Sleep Societies.
More information
Two studies funded by the U.S. Agency for Healthcare Research and Quality and the National Institute for Occupational Safety and Health found that shorter shifts for medical interns reduced medical errors.
The interns took part in a nationwide Internet survey and completed more than 17,000 monthly reports.
Study author Laura Barger of Brigham and Women's Hospital in Boston analyzed the data to determine the association between extended duration shifts (24 hours or more at a time), reported medical errors, and the interns' self-reported levels of stress.
Compared to months where no extended duration shifts were worked, interns who worked five or more extended duration shifts in a month were seven times more likely to report at least one fatigue-related significant medical error that harmed a patient, and 300 percent more likely to report fatigue-related errors that caused the death of a patient.
Interns who reported a medical error that caused harm to a patient were more than three times as likely to report high stress in that month, the study found.
"These results suggest that extended duration shifts negatively impact patient safety and the well-being of medical interns. (The findings) have important public policy implications for post-graduate medical education and suggest the need for counseling or other care for interns who make medical errors," Barger noted.
The study was presented Wednesday in Minneapolis at SLEEP 2007, the annual meeting of the Associated Professional Sleep Societies.
More information
Two studies funded by the U.S. Agency for Healthcare Research and Quality and the National Institute for Occupational Safety and Health found that shorter shifts for medical interns reduced medical errors.
Friday, June 08, 2007
More Proof That Breast Cancer Rates Are Declining
(HealthDay News) -- More statistics from U.S. health officials confirm that rates of breast cancer have fallen since many women stopped using hormone-replacement therapy five years ago.
The trend was first reported in April in the New England Journal of Medicine, in a study that showed an 8.6 percent drop in breast cancer among postmenopausal women from 2001 to 2004. That decline coincided with a significant drop, starting in 2002, in the number of prescriptions for HRT, which had been linked to an increased risk for breast cancer.
Now, a new report in the June 8 issue of the U.S. Centers for Disease Control and Prevention's Morbidity and Mortality Weekly Report confirms these findings, using a much larger set of data.
Combining statistics from the U.S. National Cancer Institute's Surveillance, Epidemiology, and End Results program with the CDC's National Program of Cancer Registries program, the CDC was able to produce data that accounts for approximately 86 percent of the U.S. population.
The analysis showed that rates for invasive breast cancer dropped each year from 1999 to 2003. The greatest decrease (6.1 percent) occurred between 2002 and 2003. Moreover, women over age 50 had a significant decrease in breast cancer during this period.
In 2002, the Women's Health Initiative study reported that hormone-replacement therapy for menopausal and postmenopausal women was linked to a greater risk of breast cancer.
The new CDC statistics revealed a decrease in breast cancer from 2002 to 2003 in all women over 50 years of age, with women aged 60 to 69 showing the largest decrease. Also, women of all racial and ethnic groups had a significant decrease in breast cancer rates from 2002 to 2003, except for American Indian/Alaska Native women, whose breast cancer rates were stable.
At first glance, the new study appears to suggest that the drop in breast cancer rates is directly related to the drop in HRT use.
A study of California women aged 50 to 74 found that rates of HRT dropped by 68 percent from 2001 to 2003. During the same time, breast cancer rates dropped by 10 percent among the women in the study and 11 percent among all women in California.
But, since the rate of breast cancer started dropping before 2002 -- before the decrease in HRT use -- there may be other factors that might have contributed to the decline in breast cancer. These factors might include diet and lifestyle changes, according to an editorial note that accompanied the MMWR report.
More studies are need to confirm these findings, the editorial authors said.
More information
For more on preventing breast cancer, visit the American Cancer Society.
The trend was first reported in April in the New England Journal of Medicine, in a study that showed an 8.6 percent drop in breast cancer among postmenopausal women from 2001 to 2004. That decline coincided with a significant drop, starting in 2002, in the number of prescriptions for HRT, which had been linked to an increased risk for breast cancer.
Now, a new report in the June 8 issue of the U.S. Centers for Disease Control and Prevention's Morbidity and Mortality Weekly Report confirms these findings, using a much larger set of data.
Combining statistics from the U.S. National Cancer Institute's Surveillance, Epidemiology, and End Results program with the CDC's National Program of Cancer Registries program, the CDC was able to produce data that accounts for approximately 86 percent of the U.S. population.
The analysis showed that rates for invasive breast cancer dropped each year from 1999 to 2003. The greatest decrease (6.1 percent) occurred between 2002 and 2003. Moreover, women over age 50 had a significant decrease in breast cancer during this period.
In 2002, the Women's Health Initiative study reported that hormone-replacement therapy for menopausal and postmenopausal women was linked to a greater risk of breast cancer.
The new CDC statistics revealed a decrease in breast cancer from 2002 to 2003 in all women over 50 years of age, with women aged 60 to 69 showing the largest decrease. Also, women of all racial and ethnic groups had a significant decrease in breast cancer rates from 2002 to 2003, except for American Indian/Alaska Native women, whose breast cancer rates were stable.
At first glance, the new study appears to suggest that the drop in breast cancer rates is directly related to the drop in HRT use.
A study of California women aged 50 to 74 found that rates of HRT dropped by 68 percent from 2001 to 2003. During the same time, breast cancer rates dropped by 10 percent among the women in the study and 11 percent among all women in California.
But, since the rate of breast cancer started dropping before 2002 -- before the decrease in HRT use -- there may be other factors that might have contributed to the decline in breast cancer. These factors might include diet and lifestyle changes, according to an editorial note that accompanied the MMWR report.
More studies are need to confirm these findings, the editorial authors said.
More information
For more on preventing breast cancer, visit the American Cancer Society.
Saturday, June 02, 2007
Gene Therapy Shows Promise Against Chronic Pain
(HealthDay News) -- Animal studies suggest that gene therapy might block tough-to-treat neuropathic pain.
Neuropathic pain -- a type of chronic pain in people for which there are few effective treatments -- is the result of injury- or disease-related damage to nerve fibers. Even after surrounding tissue has healed, the damaged nerve fibers continue to send pain signals to the brain, according to background information in the article.
For some people, neuropathic pain causes long-term disability and dependence on pain medications.
In this study with rats, researchers at the University of Pittsburgh introduced the gene for part of the human glycine receptor (GlyR). This gene is found primarily on the surface of nerve cells in the spinal cord and the lower brain but not in the nerves in the limbs.
The researchers used an engineered herpes simplex virus (HSV) to deliver the gene into the paws of some rats, while other rats received only the HSV vector without the inserted gene. All the rats were then injected with an irritant that simulated symptoms of neuropathic pain, followed by injections of glycine to activate the GlyR receptor.
The glycine injection halted pain response in GlyR-HSV-treated rats but not in the rats that received only the HSV vector.
The findings suggest that targeted use of GlyR-HSV and activation with glycine may help treat humans with neuropathic pain and other chronic pain disorders, the study authors said.
The study was presented at the annual meeting of the American Society of Gene Therapy, in Seattle.
More information
The National Pain Foundation has more about neuropathic pain.
Neuropathic pain -- a type of chronic pain in people for which there are few effective treatments -- is the result of injury- or disease-related damage to nerve fibers. Even after surrounding tissue has healed, the damaged nerve fibers continue to send pain signals to the brain, according to background information in the article.
For some people, neuropathic pain causes long-term disability and dependence on pain medications.
In this study with rats, researchers at the University of Pittsburgh introduced the gene for part of the human glycine receptor (GlyR). This gene is found primarily on the surface of nerve cells in the spinal cord and the lower brain but not in the nerves in the limbs.
The researchers used an engineered herpes simplex virus (HSV) to deliver the gene into the paws of some rats, while other rats received only the HSV vector without the inserted gene. All the rats were then injected with an irritant that simulated symptoms of neuropathic pain, followed by injections of glycine to activate the GlyR receptor.
The glycine injection halted pain response in GlyR-HSV-treated rats but not in the rats that received only the HSV vector.
The findings suggest that targeted use of GlyR-HSV and activation with glycine may help treat humans with neuropathic pain and other chronic pain disorders, the study authors said.
The study was presented at the annual meeting of the American Society of Gene Therapy, in Seattle.
More information
The National Pain Foundation has more about neuropathic pain.
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