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A study of 84,285 women seeking care in Dutch family physician offices between 1985 and 2003 revealed that breast symptoms were reported in about 3 percent of all visits.

Of the women complaining of breast symptoms, 3 percent of those women were subsequently diagnosed with breast cancer. Notably, those patients reporting a breast mass had a markedly elevated likelihood of breast cancer (15.04 likelihood ratio), suggesting that clinicians should aggressively work up such complaints regardless of patient age.
BY : Angela Sharma

DEFINITION AND VARIETIES OF YOGA :
What, then, is Yoga and what is Pranayama ? if anything abnormal is done by a person, anything beyond the capacity of an ordinary individual, it is generally said to have been done by the Science of Yoga. Before we are initiated into the mystery of this Science of Yoga, it is well to know what Yoga means. The word ‘Yoga’ is derived from the root “Yuja” to join or to weld together. Just a in welding, two pieces of the same metal are made to become one by the process of heating and harming, so also in the Yoga of Indian Philosophy, the embodied spirit of Jivatma, which is a part of the Universal Spirit Pranayama, is made to become one with the Universal Spirit by certain physical and mental exercises. There are good many ably written works on Yoga, both in the vernaculars and in English, and each has tried to define Yoga in its own particular way, and I will mention a dew definitions. Some have defined Yoga as “self concentration with a view to seeing the soul as it looks when it is abstracted from mind and matter.” Patanjali describes Yoga as ‘suppression of thought’. Here the word ‘thought’ must not be understood in the usual narrower sense of reflection, but should be taken to mean consciousness which includes sensibility, imagination and dreams.
A simple definition of Yoga is found in the Bhagwad-Gita, where it is described as equanimity of mind in thought and deed, resulting in efficiency of action, done as service dedicated to God. But the following is a more or less comprehensive definition of the term Yoga. “Yoga is the science, which raises the capacity of the human mind to respond to higher vibrations, and to perceive, catch and assimilate the infinite conscious movements going on around us in the universe.” In fact it makes one transmitting as well as receiving station of radio activity with the mind as the aerial. One can catch and receive the unspoken thoughts of others from any distance. One can also broadcast one’s own thoughts to assist others in spiritual upliftment or guide them when they are in difficulty. It is claimed that all the miracles performed by the long line of saints, saviours and sages of all times and in all climes, were due to the knowledge of this, the grandest of all sciences. From the definition given above, we can see that Yoga means the union or the linking together of man with God; or, more correctly, the disunion or separation of man from objects of sense, i.e., from the phenomenal world. It is the science which leads the initiate by easy gradations to the loftiest height of Self-realisation till he stands face to face with the objects of his search. This object of his search can be obtained by a variety of ways, either by dedicating all the fruits of work to God – Karma-Yoga – or the absolute surrender of all our hopes and aspirations including the self also to God, in the belief that His grace is our highest good – Bhakti-Yoga. The highest form of Yoga is that in which the soul does not see itself except as infilled by and made identical with the Absolute God – Jnyana-Yoga. This is enough for our purpose. I need not go deeper into the mysteries of Yoga, but a few words regarding its achievement will not be out of place.

Woman, 35, Suffers Rare Orgasm-Related Stroke
Sex- and orgasm-triggered strokes in relatively young women and men are rare, but not unheard of. They require a combination of factors and events not unusual in themselves, but which are highly unlikely to occur at the same time.

The 35-year-old woman’s symptoms were typical of this unusual kind of “cryptogenic” stroke, says Jose Biller, MD, professor and chair of the neurology department at Loyola University, Chicago.

“This young woman … while having intercourse had numbness on the left side of her face, slurred speech, and weakness in her left arm,” Biller tells WebMD. “When she was transferred to our care six hours after onset, she was completely unable to move her left arm, her face was paralyzed, her speech was garbled, and she was in a state of panic.”

It was too late to inject the woman with the clot-busting drug tPA, which must be given within three hours of a stroke. So Biller’s team quickly ran a catheter from an artery in the woman’s groin up into her brain to find the blood clot by angiography. Once it was found, they had only one option: to apply tPA directly to the clot.

It was a risky decision. “We did this with a lot of sweat,” Biller says.

The woman’s symptoms began to improve almost immediately; within an hour she was out of the woods and within 12 hours the symptoms were almost gone. Today she is well, with only an almost imperceptible fold in the skin under her nose and slight loss of dexterity in her left hand.
Stroke From Sex

Why did sex trigger this young woman’s stroke? She shared one thing in common with six other young people who suffered sex-related strokes: a small opening in the wall between the two upper chambers of her heart.

One in four adults has this minor heart defect, called a patent foramen ovale or PFO. A PFO allows some blood to flow from the right side of the heart to the left side. This blood bypasses the lung and goes straight to the brain.

Most people with a PFO have no symptoms and don’t know they have it. But 40% of people who suffer a cryptogenic stroke — stroke of no known cause — have a PFO.

Blood flow through a PFO increases when a person strains, such as bearing down during a bowel movement or breathing out with the mouth closed and nostrils pinched shut.
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Public health authorities say the 28-year-old man died Sept. 3, a day after he checked into a hospital.

People typically get infected while sweeping up rodent droppings without a mask, and the Utah Department of Health attributed the man’s death to that activity.

But a local health official said that fact had yet to be determined.

TriCounty Health Department spokeswoman Jeramie Tubbs said investigators were still trying to determine what the man was doing when he got infected.

Tubbs didn’t know if the man was able to offer any information before dying
by : foxnews

The National Center for Complementary and Alternative Medicine (NCCAM), part of the National Institutes of Health (NIH), has launched Time to Talk, an educational campaign to encourage –particularly seniors–and their health care providers to openly discuss the use of complementary and alternative medicine (CAM ). CAM is a group of diverse medical and health care systems, practices, and products that are not presently considered to be part of conventional medicine, such as herbal supplements, meditation, naturopathy, and acupuncture.

According to a national consumer survey conducted by NCCAM and AARP, almost two-thirds of people age 50 or older are using some form of CAM, yet less than one-third of these CAM users talk about it with their providers. The NCCAM/AARP survey revealed some reasons why this doctor-patient dialogue about CAM does not occur. The most common reasons survey respondents cited were:

• That the physician never asked
• They did not know they should discuss CAM
• There was not enough time during the office visit

More than one-half of respondents who had talked about CAM with their physician said they (not their physician) initiated the CAM discussion. The telephone survey was administered to a nationally representative group of 1,559 people age 50 or older.

“In an era of genomics and personalized medicine, we need to remember that a key ingredient to good health care is the dialogue you, as a patient, have with your providers,” said Elias A. Zerhouni, M.D., NIH Director. “And talking about what CAM therapies you use is an important part of that discussion. This is important for people of all ages.”

The Time to Talk campaign is aimed at addressing the need for this dialogue to help ensure safe, coordinated care among all conventional and CAM therapies. Talking not only allows integrated care, it also minimizes risks of interactions with a patient’s conventional treatments. When patients tell their providers about their CAM use, they can more effectively manage their health. When providers ask their patients about CAM use, they can ensure that they are fully informed and can help patients make wise health care decisions.

“As frequent users of CAM, people 50 and older need to understand the importance of discussing CAM use with their providers to ensure coordinated, safe care. Simply put, it’s time to talk,” said Josephine P. Briggs, M.D., NCCAM Director. “Giving your health care providers a full picture of what you do to manage your health helps you stay in control.”

NCCAM’s Time to Talk campaign encourages patients to tell their providers about CAM use and providers to ask about it by offering tools and resources—such as wallet cards, posters, and tip sheets—all of which are available for free on the NCCAM Web site or can be ordered from NCCAM’s information Clearinghouse (1-888-644-6226). NCCAM is reaching out to professional associations and consumer organizations to help educate their members about the importance of this dialogue and the availability of NCCAM’s campaign materials. As the Federal government’s lead agency for scientific research on CAM, NCCAM is committed to educating both consumers and health care providers about the importance of discussing CAM and providing evidence-based information to help with health care decision making.

Patient Tips for Discussing CAM with Providers

• When completing patient history forms, be sure to include all therapies and treatments you use. Make a list in advance.
• Tell your health care providers about all therapies or treatments—including over-the-counter and prescription medicines, as well as herbal and dietary supplements.
• Take control. Don’t wait for your providers to ask about your CAM use.
• If you are considering a new CAM therapy, ask your health care providers about its safety, effectiveness, and possible interactions with medicines (both prescription and over-the-counter)

Provider Tips for Discussing CAM with Patients

• Include a question about CAM use on medical history forms.
• Ask your patients to bring a list of all therapies they use, including prescription, over-the-counter, herbal therapies, and other CAM practices.
• Have your medical staff initiate the conversation

Genetic variation in the DNA of mitochondria – the “power plants” of cells – contributes to a person’s risk of developing age-related macular degeneration (AMD). The study is the first to examine the mitochondrial genome for changes associated with AMD, the leading cause of blindness in Caucasians over age 50.

“Most people don’t realize that we have two genomes,” said lead author Jeff Canter, M.D., M.P.H., an investigator in the Center for Human Genetics Research. “We have the nuclear genome – the “human genome” – that makes the cover of all the magazines, and then we also have this tiny genome in mitochondria in every cell.”

Canter teamed with Jonathan Haines, Ph.D., and Paul Sternberg, M.D., experts in AMD genetics and treatment, to examine whether a particular variation in the mitochondrial genome is associated with the disease. The genetic change occurs in about 10 percent of Caucasians, referred to as mitochondrial haplogroup T.

“We suspect that this variant will be one of a small group of important genetic variations that underlie AMD,” Canter said. “By knowing this, we have a better chance of predicting accurately who will get the disease.”

AMD affects as many as 10 million people in the United States, robbing them of the sharp central vision necessary for everyday activities like reading, driving, watching television, and identifying faces. The toll of the disease is expected to mount as the U.S. population ages.

The genetics of AMD has been a “hot” area lately, Canter said. Haines led a team that identified a variant in the Complement Factor H (CFH) gene as accounting for up to 43 percent of AMD. Variations in ApoE2 and a gene called LOC387715 on chromosome 10 have also been linked to the disease, and Haines and colleagues demonstrated an interaction between the chromosome 10 gene and smoking in raising AMD risk.

The current study also examined variation in these nuclear genes in 280 cases and 280 age-matched controls, and demonstrated that the mitochondrial genome variation was independent of the known nuclear factors.

“We’re at the stage where we can use genetic information to predict who is likely to develop AMD well before they actually develop it,” said Haines, director of the Center for Human Genetics Research. “Now we can conduct trials of preventive treatments – something’s that never been possible before.”

Sternberg, G.W. Hale Professor and Chairman of the Vanderbilt Eye Institute, is leading a trial to test preventive measures in AMD.

Variation in the mitochondrial genome reflects human migrations and different environmental exposures. Changes in the mitochondrial DNA can alter the efficiency of energy generation and lead to over-production of “reactive oxygen species” – free radicals that can damage the cell.

“By identifying genetic changes associated with the mitochondria, our results lend additional confirmatory evidence for the role of oxidative stress in AMD,” Sternberg said. “This supports study of interventions that attempt to bolster our antioxidant defenses.”

“I can see a day when physicians order genotyping on patients at a certain age to determine risk for AMD and put things in place – dietary changes, antioxidants, increased screening – that could prevent the disease,” Canter added. “This would be truly personalized medicine.”

Canter emphasized that variation in the mitochondrial genome has been linked to a wide variety of diseases including neurodegenerative diseases like Parkinson’s and Alzheimer’s as well as breast cancer and trauma survival.

“It’s important to realize that there’s another genome in the mitochondria, and even though there are not many genes there, they’re important,” Canter said.

The developing nervous system makes far more nerve cells than are needed to ensure target organs and tissues are properly connected to the nervous system. As nerves connect to target organs, they somehow compete with each other resulting in some living and some dying.

Now, using a combination of computer modeling and molecular biology, neuroscientists at Johns Hopkins have discovered how the target tissue helps newly connected peripheral nerve cells strengthen their connections and kill neighboring nerves.

“It was hard to imagine how this competition happens because the signal that leads cells to their targets also is responsible for keeping them alive, which begs the question: How do half of them die?” says David Ginty, Ph.D., a professor of neuroscience and investigator of the Howard Hughes Medical Institute.

Target tissues innervated by so-called peripheral neurons coax nerves to grow toward them by releasing nerve growth factor protein, or NGF. Once the nerve reaches its target, NGF changes from a growth cue to a survival factor.  In fact, when some populations of nerve cells are deprived of NGF they die.  To further investigate how this NGF-dependent survival effect works the researchers looked for genes that are turned on by NGF in developing nerve cells.

They found hundreds of genes that respond to NGF genes, some of which are involved in enhancing NGF’s effect. With the observation that NGF seems to control genes that improve NGF effectiveness, Ginty’s team hypothesized that this could be the way in which nerve cells compete with one another for survival. To test this idea the team turned to colleagues at the Mind/Brain Institute at Hopkins who specialize in computer modeling of such problems.

The computer model they built assigns each nerve cell its own mathematical equation that take into account how much NGF the cell encounters or how effective NGF can be to simulate a cell’s drive to survive. When they plugged in the model, it showed that over time-about 100 days or so-about half of the cells manage to survive, while the other half die.

But, in the developing mouse embryo, nerve cells that die do so over the course of two to three days just before birth. “So then we considered whether these nerves compete like other systems in the body, where those with stronger connections punish the weaker ones,” says Ginty. The team turned their attention to other genes they found to be NGF dependent; two of which code for proteins that kill neighboring nerve cells and another is the receptor for these death proteins.

According to Ginty, nerves that connect to muscles undergo a similar process called synapse elimination where stronger connections stay connected and weaker ones are eliminated. The team wondered if this is also true of peripheral nerve cells competing for NGF availability and ultimate cell survival.  To test this idea they plugged these three additional genes into their computer model, assuming that the stronger connected nerve cell punishes its neighbors by releasing the two proteins capable of killing. The computer model showed again, that half the nerve cells die over time, but this time the death occurred over two to three days rather than 100 days, just as in living animals.

To confirm that the model is accurate, the team went back to genetically altered mice. They predicted that removal of the punishment signals should delay cell death as observed in their early computer simulations. Indeed, nerve cells in mice lacking the receptor protein for the death signals died much slower than in mice with the receptor protein intact.

“I never would have believed that these three genes could speed up competition so much,” says Ginty. “But there it was in front of us-it was amazing.”

The research was funded by the National Institutes of Health, a Woodrow Wilson Undergraduate Research Fellowship, and the Howard Hughes Medical Institute.

Authors on the paper are Christopher Deppmann,

Being resistant to aspirin makes patients four times more likely to suffer a heart attack, stroke or even die from a pre-existing heart condition, according to a recent study. The study relates to patients who are prescribed aspirin long term as a way of preventing clots from forming in the blood.

Patients who are labelled “aspirin resistant” have blood cells (platelets) that are not affected in the same way as those of patients who are responsive to the drug, ie people who are “aspirin sensitive.”

There is currently no agreed method of accurately determining who is and isn’t aspirin resistant and the reasons why someone might be aspirin resistant are currently a cause of controversy.

Relatively few studies have looked at whether aspirin resistance has any impact on clinical outcome so the Canadian authors carried out a review of all the available data to better understand the relationship between the two.

They identified 20 studies, involving 2,930 patients with cardiovascular disease, all of whom had been prescribed aspirin as a way of preventing clots from forming in the blood. 28% were classified as aspirin resistant.

They found that all aspirin resistant patients, regardless of their underlying clinical condition, were at greater risk of suffering a heart attack, stroke or even dying. In particular they found that 39% of aspirin resistant patients compared to 16% of aspirin sensitive patients suffered some sort of cardiovascular event.

They also found that taking other drugs to thin the blood, such as Clopidogrel or Tirofiban, did not provide any benefit to these patients.

The authors conclude that there needs to be further studies on aspirin resistance to identify the most useful test to determine the condition. They also say aspirin resistance: “is a biological entity that should be considered when recommending aspirin as antiplatelet therapy.”

The study was published in the online edition of British Medical Journal.

Two tiny genetic variations may provide the best clues yet for finding more precise ways to estimate prostate cancer risk and improve screening and early detection for men of African descent, report researchers from the University of Chicago and the Translational Genomics Research Institute, Phoenix, AZ, in the December 2007 issue of Genome Research, published early online.

The researchers set out to determine whether results from four previous studies that linked genetic variations on one region of chromosome 8 to increased prostate cancer risk among Caucasians were also valid for men of African heritage. In the process, however, they found an additional genetic variation among African American men that was an even stronger marker for cancer risk for these men. That variation is located within a gene that plays a role in DNA repair. A malfunction in DNA repair could contribute to cancer development.

“This finding emphasizes the importance of ancestry in studying genetics,” said study author Rick Kittles, associate professor of medicine at the University of Chicago Medical Center. “Previous studies led us to one specific region of chromosome 8,” he said. “Then this approach—which took advantage of genetic differences among African American men, who are at very high risk for this type of cancer—led us to a different locus within that region and directly to a gene of interest.”

Prostate cancer is the most common male malignancy and the second leading cause of cancer death in men. According to the American Cancer Society, it will affect nearly 220,000 men in the United States in 2007 and claim the lives of more than 27,000. It disproportionately affects African Americans who “exhibit the highest rate worldwide,” Kittles said.

In this study, research groups lead by Kittles and by John Carpten of the Translational Genomics Research Institute analyzed the region of chromosome 8 highlighted by the earlier studies done on Caucasian men. But this time they searched for tiny genetic differences between 490 African American men who had been diagnosed with prostate cancer at Howard University Hospital in Washington, DC, and 567 African American men without cancer.

The researchers were able to replicate the linkage between one of the markers detected by previous studies and increased risk. More important, they found a new genetic marker, known as rs7008482, that was even more strongly associated with prostate cancer in African Americans. This marker was located within a gene that is involved in DNA replication, recombination and repair.

Altering this gene could confer an “inherited predisposition to genetic instability,” Kittles said. “This could lead to increased cancer risk. By studying this region, we may be able to develop molecular targets for improved screening, early detection, and possibly treatment.”

Multiple studies, the authors conclude, strongly support the existence of several independent genetic variants that could increase prostate cancer risk within this small region of chromosome 8. They have already begun to look closer at this region and to study the function of nearby genes.

The study also reinforces the need to keep ancestry in mind when looking at disease-gene genetics. “Since African Americans vary significantly in genetic ancestral proportions and the prevalence of prostate cancer is almost two-fold higher among African Americans compared to European Americans,” Kittles said, “the use of ancestry-informative markers for association with prostate cancer is quite powerful.”

The National Institutes of Health and the Department of Defense supported this research. Additional authors include Jada Benn Torres, Stanley Hooker, and Wenndy Hernandez of the University of Chicago; Christiane Robbins and Angel Candreva from the Translational Genomics Research Institute; Carolina Bonilla of the University of Oxford (UK), and Chiledum Ahaghotu of Howard University Hospital.

Source: University of Chicago Medical Center

The U.S. Food and Drug Administration (FDA) today announced it has cleared for marketing the first rapid blood test for the drug-resistant staph bacterium known as MRSA (methicillin-resistant Staphylococcus aureus), which can cause potentially deadly infections.

Methicillin is an antibiotic that has been used successfully to treat infections from the Staphylococcus aureus bacterium. Over the years, the staph bacterium mutated and spawned MRSA, a strain of staph bacterium that is resistant to methicillin and which has a higher rate of being fatal.

The BD GeneOhm StaphSR Assay uses molecular methods to identify whether a blood sample contains genetic material from the MRSA bacterium or the more common, less dangerous staph bacterium that can still be treated with methicillin.

“The BD GeneOhm test is good news for the public health community. Rather than waiting more than two days for test results, health care personnel will be able to identify the source of a staph infection in only two hours, allowing for more effective diagnosis and treatment,” said Daniel G. Schultz, M.D., director, FDA’s Center for Devices and Radiological Health.

Staph infections occur most frequently among persons in hospitals and health care facilities (such as nursing homes and dialysis centers) who have weakened immune systems. Both types of bacteria also can infect healthy people.

Distinguishing between the two sources of infection is critical to successful treatment.
The more common, less dangerous strain of staph results in infections that are generally mild and affect the skin with pimples or boils that can be swollen, painful and drain pus.

However, the MRSA staph bacterium is difficult to treat with ordinary antibiotics. It can cause potentially life-threatening conditions such as blood stream infections, surgical site infections or pneumonia.

FDA cleared the BD GeneOhm StaphSR assay based on the results of a clinical trial at five locations. The new assay identified 100 percent of the MRSA-positive specimens and more than 98 percent of the more common, less dangerous staph specimens.

In order to preserve the integrity of positive test results, this test should be used only in patients suspected of a staph infection. The test should not be used to monitor treatment for staph infections because it cannot quantify a patient’s response to treatment. Test results should not be used as the sole basis for diagnosis as they may reflect the bacteria’s presence in patients who have been successfully treated for staph infections. Also, the test will not rule out other complicating conditions or infections.

The BD GeneOhm StaphSR test is manufactured by BD Diagnostics, a subsidiary of BD of Franklin Lakes, N.J.