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Though hormone therapy has proven useful in treating late-stage prostate cancer, it often results in the development of fatal secondary tumors that are resistant to such therapy.

Now, however, researchers working with mice believe they have uncovered a mechanism by which the secondary tumors gain their resistance — a finding that eventually might help prolong the lives of men with prostate cancer.

Substances secreted during the body’s inflammatory response to the hormone therapy appear to play a role in creating resistance to hormone therapy, according to the study, published in the March 11 issue of Nature.

Doctors might be able to delay the onset of hormone-resistant tumors by two to three years if subsequent research finds a way to control the effects of inflammation, according to the research team, which included scientists from the University of California, San Diego (UCSD), the Scripps Research Institute in Florida and the Engelhardt Institute of Molecular Biology in Moscow.

Hormone therapy for prostate cancer, also known as androgen deprivation therapy or androgen ablation therapy, involves the reduction of male hormones in the body, according to the American Cancer Society. These male hormones, called androgens, promote the growth of prostate cancer cells. Reducing androgen levels can cause prostate tumors to shrink or can retard their growth, making them easier to remove surgically or treat with radiation.

“That therapy usually works, but in too many patients it leads to the appearance of castration-resistant cancer — cancer that no longer responds to androgen ablation therapy,” said Michael Karin, one of the UCSD researchers. “That form of prostate cancer is more aggressive, more metastatic and more difficult to treat with traditional chemotherapy and radiation therapy.”

By studying prostate cancer in mice, the researchers figured out that, as the prostate tumor shrinks, the dying cancer cells apparently send off signals that activate the body’s immune response.

“What we think is going on is, when you kill the tumor, the body doesn’t know it’s the tumor being killed,” Karin said. “It responds to it like there is tissue injury, a wound or something like that.”

White blood cells called B-cells infiltrate the tumor and release a substance called lymphotoxin, a protein that kills infected cells. The research team found that exposure to lymphotoxin promoted the development of cancer cells resistant to hormone therapy. Interfering with the inflammatory response delayed the development of castration-resistant cancer.

“It’s somewhat counterintuitive, that the death of these androgen-resistant cells somehow contributes to androgen resistance,” said Dr. Durado Brooks, director of prostate and colorectal cancer for the American Cancer Society.

The finding could be key in developing a means to delay or stop the development of therapy-resistant secondary tumors. Until now, research into this resistance has focused on the role that the cells’ androgen receptors play in the process. But researchers now can also consider controlling inflammation as another way to delay resistance.

Don’t expect anything useful for humans anytime soon. Researchers will have to first make sure that human prostate cancer responds in the same way that the cancer did in mice.

“There’s going to have to be a lot more work done to clarify that the mechanisms in humans are the same as those they have identified in mouse prostate cancer,” Brooks said. “It’s going to be quite a while before this mouse model moves to the bedside and actual clinical practice, if it ever does.”

But if the findings do transfer to humans, this new understanding of the role of inflammation in prostate cancer treatment could help extend lives.

“Androgen resistance is often one of the complications that occurs in later stages of prostate cancer management that often precedes death related to prostate cancer,” Brooks said. “If there was a way to prolong the time between treatment and development of androgen resistance, we could prolong a man’s life.”

SOURCES: Michael Karin, Ph.D., professor, pharmacology, University of California, San Diego; Durado Brooks, M.D., director, prostate and colorectal cancer, American Cancer Society, Atlanta;  2010, Nature

Strength training improves hand grip and arm function in people who have suffered a stroke without causing increased muscle spasticity or pain, according to combined data from multiple studies.

Stroke commonly weakens muscles and may temporarily cause muscle spasm and pain.

There is some controversy surrounding strength training in stroke patients, as some rehabilitation groups feel that strengthening stroke-weakened muscles will also increase spasticity and pain. But that’s not what Dr. Janice J. Eng and Dr. Jocelyn E. Harris, of University of British Columbia in Vancouver, Canada, found.

They pooled results from 13 studies that recorded how strength training exercises, versus no strengthening intervention, affected overall arm strength and function in 517 stroke patients with mild to moderately impaired movement of the upper limbs.

On average, strength training lasted for about one hour on 2 to 3 days a week for 4 weeks, although some of the training periods extended as long as 19 weeks. Most interventions used small weights, resistance bands, and gym-type pulley weights to build muscle.

The combined results suggest, “strengthening does not increase spasticity on a permanent basis,” Eng told Reuters Health in an email. Rather, strengthening may actually reduce muscle spasticity, she added.

None of the studies analyzed reported side effects and those that measured spasticity prior to strength training reported no increase in spasticity over the course of training.

In six studies (a total of 306 participants), strength training led to moderate or large improvement in hand grip strength, Eng and Harris report.

In 11 studies (a total of 465 participants) training resulted in a small improvement in arm function.

However, five studies involving 210 participants showed no improvement in activities of daily living, for example picking up a small object. This finding, Eng said, calls for a re-examination of stroke rehabilitation efforts to “ensure that strength training not only improves function, but also activities of daily living.”

SOURCE: Stroke

Scientists have linked a chemical used in consumer goods like non-stick pans and water-resistant fabrics with thyroid disease, raising questions about the potential health risks of exposure to the substance.

A study by British researchers found that people with high levels of the chemical perfluorooctanoic acid (PFOA) in their blood have higher rates of thyroid diseases — conditions which affect the body’s metabolism.

PFOA is a common chemical, used in industrial and consumer products including non-stick cooking pans, stain-proof carpet coatings and waterproofing for fabrics.

The study, published in the Environmental Health Perspectives journal, did not establish whether PFOA was causing higher levels of thyroid disease.

The researchers said the link might be complex and indirect, and added that their work highlighted a need for further studies of the human health effects of low-level exposures to chemicals like PFOA.

“We need to know what they (these chemicals) are doing,” said Tamara Galloway, a professor of ecotoxicology at Exeter University, who led the research.

Previous studies of people living near sites where PFOA is manufactured have not found an association between exposure to these chemicals and thyroid function, and some other scientists advised caution about drawing conclusions from the study.

INDIRECT LINK?

“Studies like this cannot tell us that the two things are definitely linked,” said Ashley Grossman, professor of neuroendocrinology at Queen Mary, University of London.

“We also don’t know whether this chemical is directly affecting the thyroid. Thyroid disease is often caused by the body’s own immune system attacking the thyroid gland so perhaps this chemical is having some effect on the immune system, rather than directly on the thyroid.”

The thyroid, located in the neck, is a kind of master gland, secreting hormones affecting metabolism. People with low thyroid function may lose hair, gain weight and feel sluggish, while those with overactive thyroids may lose weight and feel their hearts race. Both conditions can be treated.

The British researchers looked at 3966 American adults aged 20 and above whose blood serum was sampled between 1999 and 2006 for PFOA. They found that those with the highest PFOA concentrations (above 5.7 nanograms per milliliter) were more than twice as likely to report current thyroid disease than individuals with the lowest levels (below 4.0ng/ml).

Thyroid diseases are much more common in women than men, but in terms of the link between PFOA and thyroid disease, the researchers found no difference between the sexes.

Galloway and colleagues stressed the need for more work but said their study suggested it is “plausible that the compounds could disrupt binding of thyroid hormones in the blood or alter their metabolism in the liver.”

“This new evidence does not rule out the possibility that having thyroid disease changes the way the body handles PFOA,” they added, and its presence “might also prove to be simply a marker for some other factor associated with thyroid disease.”

A nationwide program to get faster treatment for people with the most severe kind of heart attack has dramatically reduced the time between hospital arrival and lifesaving angioplasty.

More than three-quarters of people with STEMI heart attacks — so called because of the electrocardiogram pattern that shows major blockage of a heart artery — were receiving artery-opening angioplasty within 90 minutes of reaching a hospital in 2008, said a report released online Wednesday in advance of print publication Dec. 15 in the Journal of the American College of Cardiology.

Before the campaign began, in 2005, only half of those patients met the 90-minute deadline recommended for emergency angioplasty.

“It is a remarkable leap in performance, a tangible improvement in how people are being treated around the country,” said Dr. Harlan M. Krumholz, professor of medicine at Yale University School of Medicine and an author of the journal report.

When the American College of Cardiology and 38 partner organizations set up what is called the Door-to-Balloon (D2B) Alliance, there were doubts that it could succeed, Krumholz said. The name is based on the angioplasty procedure, in which a thin, balloon-tipped catheter is threaded into a blocked heart artery, and the balloon is expanded to restore blood flow.

“There were warnings that we were setting up a situation where we all could fail,” Krumholz said. “But all of a sudden people were saying, ‘We can do this.’”

The report on 831 hospitals showed the 90-minute door-to-balloon deadline for STEMI heart attacks being met in 52.5 percent of cases in 2005. That number increased to 76.4 percent of cases in 2008.

And the improvement has continued, said the American College of Cardiology. Its most recent data, from June 2009, shows 81.7 percent of patients getting 90-minute door-to-balloon time. Also, the average time for start of angioplasty decreased from 121 minutes in 2005 to 80 minutes in 2009.

“I think we can say that in this country, the speed with which you are treated for a heart attack has improved no matter where you are,” said Elizabeth H. Bradley, professor of public health at Yale and lead author of the journal report.

And while the study does not measure the effect of quicker treatment on outcome, “in the past couple of years, several studies have shown that reduction of door-to-balloon time is associated with improved patient survival,” Bradley said.

Most of the changes prompted by the program were simple: Having ambulance attendants call the hospital to alert them that a heart attack victim was on the way, alerting the catheterization laboratory where angioplasty is done and the interventional cardiologists who do the procedure to be ready to go to work, and getting the patient to the catheter laboratory as quickly as possible, Bradley said.

But a key ingredient was a change in the mindset of the hospital personnel dealing with heart attacks, Krumholz said. “The important thing is that everyone felt they were working hard and fast before this,” he said. “But the numbers showed they weren’t. Then people came together and reworked the process by which these procedures were done.”

Data on how much the program has improved survival might not be easy to obtain, because statistics do not separate out STEMI heart attacks — “the crushing heart attacks that kill you,” Bradley said.

But overall figures show “a marked reduction in heart attack mortality over this period,” Krumholz said, and it can be assumed that the D2B program has a role in that reduction.

Women who take low-dose aspirin to protect their heart might be helping their eyes as well.

A new study by Harvard University researchers found what they described as a modest benefit for aspirin in preventing age-related macular degeneration (AMD), an eye disease that destroys sharp, central vision.

“The data indicate that long-term treatment with low-dose aspirin has no large beneficial or harmful effect on risk of AMD,” said the study’s lead researcher, Dr. William G. Christen, an epidemiologist at Brigham and Women’s Hospital in Boston and an associate professor of medicine at Harvard Medical School.

“But, the data could not rule out a possible modest benefit,” he said.

Researchers have been looking at aspirin to see if it helps or hurts the eyes. Some believe its blood-thinning quality would be helpful in letting more blood reach the capillaries in the eyes. But others have proposed that, in a common form of AMD called wet AMD, in which blood leaks in the back of the eye and results in rapid vision loss, aspirin might increase the risk of bleeding.

For the study, reported in the December issue of Ophthalmology, Christen’s group collected data on 39,421 women who took part in the Women’s Health Study, which originally focused on heart disease and cancer. None of the women had AMD. They were randomly assigned to take either low-dose aspirin or a placebo.

During the next 10 years, 111 women who took aspirin developed AMD, compared with 134 women who took the placebo. That equates to an 18 percent lower risk for AMD among those who took aspirin, “but the rate difference was not statistically significant,” Christen said.

Dr. Stephen G. Schwartz, an associate professor of clinical ophthalmology at the University of Miami’s Bascom Palmer Eye Institute, said there have been similar results with aspirin in other eye diseases, such as diabetic retinopathy.

“This also fits in with common clinical experience,” he said.

However, Schwartz said he did not think that people should be taking aspirin to try to prevent AMD. The fact that aspirin had little or no effect on AMD is good news, he said.

“If you need to be on aspirin, you should take it and not worry about AMD,” he said. “If you don’t need to be on aspirin, you probably shouldn’t take it.”

Another report in Ophthalmology found that common cholesterol-lowering drugs called statins do not stop advanced AMD.

The study’s lead researcher, Maureen G. Maguire, from the department of ophthalmology at the University of Pennsylvania, said in a prepared statement that the data “did not support a large effect for statins in decreasing advanced AMD risk in patients who already had large drusen in both eyes.”

Drusen are whitish deposits, commonly found in the eyes of people over 60, that could be a sign of AMD. People who used statins were at slightly higher risk for developing advanced AMD than were non-users, she said.