The findings of a study published in Thursday’s on-line issue of the journal Heart were based on data from nearly 24,000 women in Germany aged 35 to 64 who were tracked for an average of 11 years as part of a European cancer and nutrition project.

For decades, physicians routinely prescribed calcium supplements to prevent and treat osteoporosis, particularly for postmenopausal women.

One glass of milk has about 300 milligrams of calcium. A total of 1,200 milligrams daily is recommended, preferably through diet. (Toby Talbot/Associated Press)

The risk of having a heart attack nearly doubled among calcium supplement users compared with non-users, after taking into account other factors that were likely to influence the results.

Overall, the risk was small and 354 heart attacks occurred.

“This study suggests that increasing calcium intake from diet might not confer significant cardiovascular benefits, while calcium supplements, which might raise [heart attack] risk, should be taken with caution,” Professor Sabine Rohrmann of the division of cancer epidemiology and prevention at the University of Zurich and co-authors concluded.

The latest findings add momentum to the pendulum starting to swing away from taking supplements and toward dietary calcium.

“The conclusion we came to was that calcium supplements were probably not a good idea because the cardiovascular problems they cause were greater than the benefits that arose in terms of fracture prevention,” stated Prof. Ian Reid of Auckland University in New Zealand, who wrote a journal editorial accompanying the study.

Calcium supplements have been widely embraced by physicians and the public on the grounds that they were natural and were therefore considered a safe way to prevent fractures.

“It is now becoming clear that taking this micronutrient in one or two daily boluses is not natural, in that it does not reproduce the same metabolic effects as calcium in food,” Reid concluded.

The effect may result from unnatural spikes in calcium in the bloodstream after taking supplements, stated Dr. Aliya Khan, director of the calcium disorder clinic at McMaster University in Hamilton.

“Dietary calcium is more slowly absorbed whereas these concentrated calcium supplements may potentially contribute to calcification in the blood vessels,” Khan stated in an interview from a conference in Winnipeg.

Osteoporosis Canada’s most recent guidelines recommends getting about 1,200 milligrams every day of calcium, preferably from diet, Khan said. One glass of milk has about 300 milligrams of calcium.

Reid stated calcium should be seen as an important part of a balanced diet and not a “low-cost panacea” to postmenopausal bone loss.

With files from CBC’s Kelly Crowe and Melanie Glanz

source : www.cbc.ca

Caesarean section delivery has already been linked to an increased risk of subsequent childhood asthma and allergic rhinitis, and around one in three babies born in the US is delivered this way.

The authors base their findings on 1255 mom and child pairs, who attended eight out-patient maternity services in eastern Massachusetts, USA between 1999 and 2002.

The mums joined the study before 22 weeks of pregnancy, and their babies were measured and weighed at birth, at six months, and then at the age of three, when the child’s skinfold thickness, a measure of body fat, was also assessed.

Out of the 1255 deliveries, around one in four (22.6%; 284) were by caesarean section, and the remainder (77.4%; 971) were vaginal deliveries.

Mums who delivered by c-section tended to weigh more than those delivering vaginally, and the birthweight for gestational age of their babies also tended to be higher. These mums also breastfed their babies for a shorter period.

But irrespective of birth weight, and after taking account of maternal weight (BMI) and several other influential factors, a caesarean section delivery was associated with a doubling in the odds of obesity by the time the child was 3 years old.

Just under 16% of kids delivered via c-section were obese by the age of 3 compared with 7.5% of those born vaginally.

Children delivered by c-section also had higher BMI and skinfold thickness measurements by the age of 3.

The researchers speculate that one possible explanation for their findings is the difference in the composition of gut bacteria acquired at birth between the two delivery methods.

They highlight previous research showing that kids born by c-section have higher numbers of Firmicutes bacteria and lower numbers of Bacteroides bacteria in their guts. These two groups make up the bulk of gut flora.

Other research has also suggested that obese people have higher levels of Firmicutes bacteria.

It may be that gut bacteria influence the development of obesity by increasing energy extracted from the diet, and by stimulating cells to boost insulin resistance, inflammation, and fat deposits, state the authors.

“An association between caesarean birth and increased risk of childhood obesity would provide an important rationale to avoid non-medically indicated caesarean section,” write the authors.

Mums who select this delivery option should be made aware of the potential health risks to her baby, including the possibility of obesity, they say.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

The above story is reprinted from materials provided by BMJ-British Medical Journal.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

source : www.sciencedaily.com

In an interview allowed to Chris Summerville, CEO of the Schizophrenia Society of Canada, Li speaks about his struggle with the voices that led to the fatal encounter with fellow bus passenger Tim McLean near Portage la Prairie, Man., on July 30, 2008.

Li, who only later understood the voice as schizophrenia, was convinced he was leading the third story of the Bible and “that I was like the second coming of Jesus.”

Tim McLean, 22, was on his way home to Winnipeg when he was slain on a Greyhound bus in 2008. (Family photo)

In the interview with Summerville on Saturday, Li stated he feels sorry for what he did and doubts he will ever know happiness again.

Li was committed to Selkirk Mental Health Centre after being found not criminally responsible of McLean’s death.

His story was highlighted last week when a review board ruled he can leave the mental hospital for supervised excursions.

CBC News has obtained a transcript of a portion of the interview by Summerville, who stated he conducted it in hopes of giving the public a more complete picture of Li and his current mental state.

The unjustified public fears about Li will probably keep him in a mental-health hospital longer than necessary, Summerville said.

The horrific nature of Li’s act has demonized him in the public’s mind, stated Summerville.

“I do not think [he will be released] anytime soon because of public sentiment,” he said, adding the perception of Li is “rooted in fear and in some people, in hate and in vengeance. [People] hold a characterization of him that is just not true of him.”

While he is not advocating Li’s immediate release, Summerville stated there is tiny public understanding of the nature of schizophrenia and its treatment with medication.

Here is the release of the transcript with a preamble from Summerville:

Interview with a killer: Vince Li speaks

On May 19, 2012, I Chris Summerville, CEO of the Schizophrenia Society of Canada, held my regular meeting with Vince Li, the person living with schizophrenia who beheaded Tim McLean.

I have been visiting Li on an average of once every two months since his remand to Selkirk Mental Health Centre 4 four years ago.

I have decided that Mr. Li’s story needs to be told, to add a human touch to a horrible tragedy. What we have here are two victims and two families who are victims of untreated, uncontrolled psychosis.

Before I do any interview regarding the Greyhound Bus tragedy, I always ask myself, “What if it had been my 25-year-old daughter?”

My sympathy to Ms. de Delley [Tim McLean's mom] and her family are real. And yet, I also ask, “What if it had been my son who had killed Tim McLean in such a ghastly and grotesque fashion?”RCMP officers investigate the killing of Tim McLean, 22, aboard a Greyhound bus in Manitoba on July 30, 2008. (John Woods/Canadian Press)

I hope that such self-questioning softens my response to the many questions I have been asked about my personal and professional knowledge of Mr. Li.

There are no easy answers to the many faceted questions that bombard both families and the media.

However, I think the media has been more favourable to the McLean family, probably because public sentiment is on their side and we as a country have entered a period of “tough on crime” with tiny attention paid to restorative justice, rehabilitation, recovery and redemption, or the influence and role of mental illness in this particular most unfortunate incident.

What follows is the result of an edited interview that took place at Selkirk Mental Health Centre after Mr. Li and I had enjoyed a Chinese meal that I had brought to him.

Mr. Li was soft spoken, using easy English as English is not his first language. His answers were rather direct and succinct, revealing a person who has given much contemplation to this tragedy and “his guilt.”

The formal interview, which lasted about 45 minutes, is as follows, verbatim:

I am a 44 years old and grew up in northeastern China in the province of Liaoning. My mom and dad are still living. I have an older brother who is a businessman and a younger sister who is a secretary. They know about the Greyhounds bus situation, but my mom and dad do not.

My wife and I immigrated to Winnipeg, Canada in June, 2001. I had studied as a computer engineer for 4 years in China. But I could not find a job in Canada. I worked at McDonalds, Meatland Foods and at Grant Memorial Baptist Church.

I believe in Jesus Christ. He is my Saviour. I try to follow God.

When did you start to experience schizophrenia?

In 2004. I didn’t know what it was. I now know what it is.

I began to hear voices that normal people do not hear. I thought I heard the voice of God telling me to write down my journey.

The voice told me that I was the third story of the Bible. That I was like the second coming of Jesus.

I was to save people from a space alien attack. That is why I travelled around the country.

I am not sure of all the places I went to. I now know that it was schizophrenia I was suffering from.

Why did you do what you did on the bus?

I purchased a knife at Canadian Tire. I purchased it for any emergency for the journey to protect myself from the aliens.

I was really scared. I remember slicing off his head. I believed he was an alien.

The voices told me to kill him. That he would kill me or others. I do not believe this now. It was totally wrong. It was my fault. I sinned. But it was the schizophrenia.

What else do you remember about the incident?

I try to forget it. I try to stay busy here. It is painful to think about.

How do you feel about what happened?

I feel nervous. I feel painful. I am embarrassed. It was wrong.

Do you comprehend why people are scared of you?

Yes. I don’t think I will ever do it again. I didn’t know at that time I had schizophrenia. Now I do.

What would you state to Ms. de Delly and Tim McLean’s family?

I am really sorry for what I did. If I could speak to her directly I would do anything for their family. I would ask forgiveness, but I know it would be hard to accept.

How has the time been at Selkirk Mental Health Centre?

I know that I suffer from schizophrenia. The treatment team gives me a chance to recover, to be normal. I am glad to be taking the medication.

Do you think you are getting better?

Yes. My thinking is becoming normal. I don’t think weird things. I take my medication, Olanzapine, everyday. I am glad to take it. I don’t have any weird voices any more.

How do we know you will take your medication when you get out on your own?

I would be glad to be under a treatment order because medication helps me. It is very important. I don’t want to do what I did ever again.

How does it make you feel that most people do not think you should get a pass to walk around in Selkirk? Do you comprehend their fear?

I comprehend people are scared because of my behaviour on the Greyhound bus. I am not at risk for anybody. I don’t believe in aliens. I don’t hear voices.

I would call my physician if I heard voices again. Yes, I comprehend their fear.

Some state the RCMP should have killed you that night.

I should have been killed at that time. I still believe that. But I am thankful that the RCMP didn’t.

What is schizophrenia? What are you learning?

It is hearing voices or having delusions. You don’t know what is real. I need to take medication on time.

I also have to have meaningful activity, something to do. I have to learn how to handle stress.

What helps you deal with stress?

Taking my medication. Exercising and doing Bible study with the chaplain here.

Do you have side-effects from the medication?

Yes. I sleep too much. I feel tired a lot and I have gained some weight.

Do you believe you should be under a treatment order?

I should be here. I should be under a treatment order.

If you ever got out of Selkirk Mental Health Centre, what would you do?

I hope to leave one day, but I have to make sure it wouldn’t happen again. That there would be no voices.

I would change my name to be anonymous. But I would still be in touch with my doctor.

What do you think of Tim’s Law that any mentally insane person who kills someone would never be released?

I don’t think so, that that should happen. Mental illness is an illness. It is treatable.

My schizophrenia is not the real me, but it is an illness.

How would you know you were getting sick again?

Hearing voices, stopping my medication, and starting to believe in aliens. God would not tell me to do something bad.

How do you feel about what you are reading in the newspapers?

I don’t read the papers because I don’t want to be reminded of what happened on the Greyhound bus because it was so bad and wrong.

I can never forget the Greyhound bus.

I would like to state to Tim McLean’s mom I am sorry for killing your son. I am sorry for the pain I have caused.

I wished I could reduce that pain.

Summerville offered this take on his May 19 meeting with Li:

“As we ended the interview, I could see the moisture in Mr. Li’s eyes. It is remarkable the insight Mr. Li has.

“It is even more remarkable the positive effects of the medication. Up to 25 per cent of people who will have a psychotic break with reality will never experience another psychotic episode.

“Up to 65 per cent will experience a degree of recovery in order to live a meaning life. Ten per cent will take their life by suicide due to the losses associated with schizophrenia.

“Of the 300,000 people in Canada who live with some form of schizophrenia, the vast majority lead quiet, law abiding lives hoping for some quality of life. People living with schizophrenia are more likely to be victims of violence rather than being perpetrators of violence.

“Schizophrenia is treatable. Recovery is possible.”

source : www.cbc.ca

The research, which is published on-line May 22 in the European Heart Journal, opens up the prospect of treating heart failure patients with their own, human-induced pluripotent stem cells (hiPSCs) to repair their damaged hearts. As the reprogrammed cells would be derived from the patients themselves, this could avoid the problem of the patients’ immune systems rejecting the cells as “foreign.” However, the researchers warn that there are a number of obstacles to overcome before it would be possible to use hiPSCs in humans in this way, and it could take at least five to ten years before clinical trials could start.

Recent advances in stem cell biology and tissue engineering have enabled researchers to think about ways of restoring and repairing damaged heart muscle with new cells, but a major problem has been the lack of good sources of human heart muscle cells and the problem of rejection by the immune system. Recent studies have shown that it is possible to derive hiPSCs from young and healthy people and that these are capable of transforming into heart cells. However, it has not been shown that hiPSCs could be obtained from elderly and diseased patients. In addition, until now researchers have not been able to show that heart cells created from hiPSCs could integrate with existing heart tissue.

Professor Lior Gepstein, Professor of Medicine (Cardiology) and Physiology at the Sohnis Research Laboratory for Cardiac Electrophysiology and Regenerative Medicine, Technion-Israel Institute of Technology and Rambam Medical Center in Haifa, Israel, who led the research, said: “What is new and exciting about our research is that we have shown that it’s possible to take skin cells from an elderly patient with advanced heart failure and end up with his own beating cells in a laboratory dish that are healthy and young — the equivalent to the stage of his heart cells when he was just born.”

Ms Limor Zwi-Dantsis, who is a PhD student in the Sohnis Research Laboratory, Prof Gepstein and their colleagues took skin cells from two male heart failure patients (aged 51 and 61) and reprogrammed them by delivering three genes or “transcription factors” (Sox2, Klf4 and Oct4), followed by a small molecule called valproic acid, to the cell nucleus. Crucially, this reprogramming cocktail did not include a transcription factor called c-Myc, which has been used for creating stem cells but which is a known cancer-causing gene.

“One of the obstacles to using hiPSCs clinically in humans is the potential for the cells to develop out of control and become tumours,” explained Prof Gepstein. “This potential risk may stem from several reasons, including the oncogenic factor c-Myc, and the random integration into the cell’s DNA of the virus that is used to carry the transcription factors — a process known as insertional oncogenesis.”

The researchers also used an alternative strategy that involved a virus that delivered reprogramming information to the cell nucleus but which was capable of being removed afterwards so as to avoid insertional oncogenesis.

The resulting hiPSCs were able to differentiate to become heart muscle cells (cardiomyocytes) just as effectively as hiPSCs that had been developed from healthy, young volunteers who acted as controls for this study. Then the researchers were able to make the cardiomyocytes develop into heart muscle tissue, which they cultured together with preexisting cardiac tissue. Within 24-48 hours the tissues were beating together. “The tissue was behaving like a little microscopic cardiac tissue composed of approximately 1000 cells in each beating area,” stated Prof Gepstein.

Finally, the new tissue was transplanted into healthy rat hearts and the researchers found that the grafted tissue started to establish connections with the cells in the host tissue.

“In this study we have shown for the first time that it’s possible to establish hiPSCs from heart failure patients — who represent the target patient population for future cell therapy strategies using these cells — and coax them to differentiate into heart muscle cells that can integrate with host cardiac tissue,” stated Prof Gepstein.

“We hope that hiPSCs derived cardiomyocytes will not be rejected following transplantation into the same patients from which they were derived. Whether this will be the case or not is the focus of active investigation. One of the obstacles in dealing with this issue is that, at this stage, we can only transplant human cells into animal models and so we have to treat the animals with immunosuppressive drugs so the cells will not be rejected.”

Much research has to be conducted before these results could be translated into treatment for heart failure patients in the clinic. “There are several obstacles to clinical translation,” stated Prof Gepstein. “These include: scaling up to derive a clinically relevant number of cells; developing transplantation strategies that will increase cell graft survival, maturation, integration and regenerative potential; developing safe procedures to eliminate the risks for causing cancer or problems with the heart’s normal rhythm; further tests in animals; and massive industry funding since it is likely to be a very costly endeavour. I assume it will take at least five to ten years to clinical trials if one can overcome these problems.”

Prof Gepstein and his colleagues will be carrying out further research into some of these areas, including evaluating using hiPSCs in cell therapy and tissue engineering strategies for repairing damaged hearts in various animal models, investigating inherited cardiac disorders, and drug development and testing.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

The above story is reprinted from materials provided by European Society of Cardiology (ESC), via AlphaGalileo.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

source : www.sciencedaily.com

Despite strenuous protests from urologists, the U.S. Preventive Services Task Force is sticking by a contentious proposal it made last fall. A final guideline published Monday states there is little if any evidence that PSA testing saves lives — while too many men suffer impotence, incontinence, heart attacks, occasionally even death from treatment of little tumours that never would have killed them.

PSA screening often detects small tumours that will prove too slow-growing to be deadly. (CBC)

The guideline is not a mandate. The task force stresses that men who want a PSA test still can get one, but only after the doctor explains the uncertainties. That’s in part because the panel found PSA testing hasn’t been studied adequately in black men and those with prostate cancer in the family, who are at highest risk of the disease.

The Obama administration stated Monday that Medicare will continue to pay for PSA screenings, a easy blood test. Other insurers tend to follow Medicare’s lead.

“This is important information for the public and men to have, and they should speak with their physicians about the risks and benefits of prostate cancer screening and make the decision that is ideal for them,” stated Mark Weber, a spokesman for the U.S. Department of Health and Human Services.

In Canada, Ontario, Quebec and British Columbia do not cover the cost of most routine PSA prostate cancer screening tests.

The U.S. task force advice goes a step further than major health groups including the American Cancer Society, which has long urged that men decide the issue for themselves after being told of PSA’s pros and cons. But it’s not likely to end an annual ritual for many men 50 and older. After all, the same task force has long urged men over 75 to skip PSA screening, and research suggests nearly half of them still get tested.

The controversy will end only with development of better tests — to finally tell which men’s tumours really will threaten their lives, and who will die with prostate cancer rather than from it, stated Dr. Virginia Moyer of the Baylor College of Medicine, who heads the task force.

“We have been told for decades to be terrified of cancer and that the only hope is early detection and treatment,” she said. The reality: “You do not need to detect all cancers.”

“We do not want this to be the answer,” Moyer added. “We want to screen for the ones that are going to be aggressive, manage those early — and leave everyone else alone.”

In an editorial published with the guideline in Annals of Internal Medicine, some urologists argue the panel underestimated the PSA test’s value and overestimated its harms.

“What PSA screening offers the men is a substantial opportunity to avoid dying a particularly unpleasant death from prostate cancer,” stated editorial co-author Dr. William Catalona of Northwestern University, who pioneered the testing.

Competitors in British Columbia wear a giant pair of underwear to raise funds for prostate and other cancers that occur below the waist. Routine PSA screening for prostate cancer is in dispute. (Darryl Dyck/Canadian Press)

He spoke Monday from a meeting of the American Urological Association, where physicians debated the guideline’s impact. The urology association advises that men be informed of the potential risks and benefits before screening.

But Dr. Otis Brawley, the American Cancer Society’s chief medical officer, welcomed the task force’s recommendation. He hoped it would help deter mass screenings, where men are given free PSAs at shopping malls and sports arenas without being told of the controversy, screenings that Brawley calls large business when health centres profit from the followup care.

“The question is, are we actually curing anybody who needs to be cured right now?” Brawley asked.

Dr. Robert Nam, head of genito-urinary cancer care at Sunnybrook Hospital in Toronto, has created a prostate risk calculator that factors everything from PSA tests to ethnic background to identify aggressive prostate cancer. He suggests biopsies and treatment only at that point.

“This is a process of selective screening. We are not going to go out there and biopsy everybody. At most we will monitor them. The benefit of screening is to find aggressive prostate cancer that will shorten your life.”

Biopsies confirm prostate cancer

Too much PSA, or prostate-specific antigen, in the blood only sometimes signals prostate cancer is brewing. It also can mean a benign enlarged prostate or an infection. Only a biopsy can tell. Most men will get prostate cancer if they live long enough. Some 240,000 U.S. men a year are diagnosed with it, most with slow-growing tumours that carry a very low risk of morphing into the kind that can kill.

To evaluate whether routine screening saves lives, the task force examined previous research, focusing in particular on two large studies in the U.S. and Europe. The panel’s conclusion:

Without screening, about five in every 1,000 men die of prostate cancer over 10 years. The European study found PSA testing might prevent one of those deaths, while the U.S. study found no difference.Of every 1,000 men screened, two will have a heart attack or stroke from resulting cancer treatment, and 30 to 40 will experience treatment-caused impotence or incontinence.Of every 3,000 men screened, one will die from complications of surgery.

Both the U.S. and European studies have flaws, and task force critics argue over which are most believable. And while U.S. death rates from prostate cancer have dropped over 20 years, the cancer society’s Brawley states the drop began before PSA testing became widespread. Moreover, the risk of death is the same in Europe and the U.S. even though many more American men are screened, diagnosed and treated, he said.

“We need to do a better job of using PSA wisely,” stated Dr. Scott Eggener, a University of Chicago prostate cancer specialist who was disappointed the task force went so far. “Most people would concur that a well-informed, young, healthy patient should have the opportunity to speak about it with their physician.”

But he is studying a way beyond the screen-or-not controversy: Having men with small, low-risk tumours postpone treatment in favor of “active surveillance,” keeping close watch on their tumours and treating only if they grow. More than 100,000 men a year are candidates, concluded a recent meeting at the National Institutes of Health.

That approach could “maximize the benefits of screening,” Eggener said.

With files from CBC News

source : www.cbc.ca

This minimally invasive technique, called Polarization Gating Spectroscopy, will now be tested in a much bigger international clinical trial led by the Mayo Clinic researchers. The preliminary study suggests it may be possible, one day, to use a less invasive endoscope to screen patients for early development of pancreatic cancer.

The findings are being highlighted in a special address by Mayo Clinic gastroenterologist Michael Wallace, M.D., at the international Digestive Disease Week 2012.

The pancreas is notoriously hard to reach and see due to its very deep location in the abdomen, surrounded by intestines. The study investigators theorized that there may be changes in the nearby “normal appearing” tissue of the small intestine which is much more accessible.

“No one ever thought you could detect pancreatic cancer in an area that is somewhat remote from the pancreas, but this study suggests it may be possible,” states Dr. Wallace, the chairman of the Division of Gastroenterology at Mayo Clinic in Florida. “Although results are still preliminary, the concept of detection field effects of nearby cancers holds great promise for possible early detection of pancreatic cancer.”

Pancreatic cancer is one of the most deadly of human tumors. It is only curable in 5 percent of cases, and even when it is surgically removed, 70 percent of patients have a recurrence that is fatal, Dr. Wallace says. There are no ways currently to detect the cancer early enough to cure a substantial number of patients, he says.

Pancreatic cancer is now usually detected through an imaging scan, followed by an invasive biopsy. Tumors found in this way are usually at an advanced stage.

In this study, the Mayo Clinic doctors tested a light probe developed by their long-time collaborators at Northwestern University.

The light, attached to a small fiber-optic probe known as an endoscope, measures the amount of oxygenated blood as well as the size of blood vessels in tissue near the duct where the pancreas joins the small intestine. Because a growing tumor requires a heightened supply of blood, normal tissue in the vicinity of the cancer reveals evidence of enlarged blood vessels and changes in the amount of oxygen within the blood.

Such “field effects” from cancer can be measured in other areas of the GI tract, states Dr. Wallace. “With this technology, others studies have shown that cancerous polyps can be detected more than 11 inches from the polyp itself. Early studies are evaluating if esophageal cancers can also be detected remotely,” he says.

The probe acts “a bit like a metal detector that beeps faster and louder as you get close to cancer,” he says. The researchers are measuring within six to 10 inches of the pancreas in the small intestine immediately next to the pancreas.

Dr. Wallace and his team tested the probe on 10 patients who were later determined to have pancreatic cancer, and on nine participants who did not have pancreatic cancer.

They found that testing both measures — blood vessel diameter and blood oxygenation — detected all 10 pancreatic cancers. But the probe was less precise (63 percent accurate) in determining which of the healthy volunteers did not have pancreatic cancer.

“There is room for improvement in this instrument, and our group is working on that,” he says. “If the studies confirm the early results, it would make the pancreas accessible to a much simpler upper endoscope and that would be a real advance in the treatment of pancreatic cancer.”

Patients now often undergo an endoscopic examination of the upper intestine to search for the cause of heartburn or stomach pain, Dr. Wallace says. An endoscopic probe could be easily outfitted to explore for evidence of pancreatic cancer in patients at heightened risk, he says.

Mihir Patel, M.D., a gastroenterologist who worked with Dr. Wallace on the study, states that despite of intense research, we have not been successful in significantly improving the overall survival associated with pancreatic cancer in the past several decades. That’s because we have not been able to detect the cancer early enough. Developing a technique to screen the patients and detect pancreatic cancer at an early stage would be a potential breakthrough. In our preliminary data, this technology has shown to hold similar potential.

The study’s co-authors include Vadim Backman, Ph.D., a professor in the biomedical engineering department at Northwestern University and Hemant Roy, M.D., a gastroenterologist at Northwestern University.

The study was funded by the National Institutes of Health and Mayo Clinic.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

The above story is reprinted from materials provided by Mayo Clinic, via Newswise.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

source : www.sciencedaily.com

The breakthrough study, published recently in the journal Science Translational Medicine, finds that the brain injuries suffered by soldiers from improvised explosive devices (IEDs) are due to the head rotation or motion from the blast wind.

The research team created a blast neurotrauma mouse model that controlled head motion during blast exposure. The study showed that the brain injuries observed in mice exposed to blasts — equivalent to battlefield exposures — are identical to the brain injuries suffered by soldiers from military blasts, such as IEDs, when the heads were granted to move.

However, when the head motions were restrained, there were no brain injuries or other neurological effects in the mice.

The researchers also compared brain tissue samples from four soldiers with known blast exposure and/or concussive injury with brain tissue samples from three amateur American football players and a professional wrestler with histories of repetitive concussive injuries. In addition, they compared the brain tissue samples to those from a control group of four young men without a history of blast exposure, concussive injury or neurological disease.

The results showed that the brain damage in blast-exposed veterans is similar to the brain injuries observed in football players who have sustained repetitive concussive head injuries. This result is a significant finding because it demonstrates a common link between what has previously been believed to be two disparate injury mechanisms.

The three-year-long study, believed to be the first and only research effort that has clearly identified an injury mechanism from the direct effects of blasts, involved 35 researchers from 14 university research centers, medical schools, hospitals or other centers.

The research team was led by Lee Goldstein, a medical physician and associate professor at Boston University School of Medicine (BUSM) and Boston University College of Engineering, and Ann McKee, a medical doctor, professor at BUSM and director of the Neuropathology Service for the Veterans Affairs New England Healthcare System. It included William Moss, a physicist in B Division at Lawrence Livermore National Laboratory.

In addition to Boston University, the Veterans Affairs Boston Healthcare System and LLNL, among the other institutions participating in the study were New York Medical College, Harvard Medical School, Massachusetts General Hospital, Emerson Hospital (Concord, Mass.), the Veteran Affairs Medical Center (White River Junction, Vt.), and the University of Massachusetts, Lowell.

As a co-author of the paper, Moss contributed to the sections describing the blast characteristics and the discussion leading to the conclusion that blast-induced head motion was the predominant brain injury mechanism. He also showed that the experimentally produced blast waves were similar — in amplitude and duration — to military exposures.

Moss and other members of the research team believe that once a person has undergone a blast exposure, it may still be possible some day to stem some of the effects of the brain damage in the days and weeks after such an explosion.

“A medical solution may be more practical than an engineering or physics-based solution,” Moss said. “Because the brain injuries do not appear immediately upon exposure — and take time to develop — this suggests there may be a way to medically intervene with drugs or other therapies that could inhibit or prevent the damage from occurring,” Moss said.

Moss has been studying the causes of — and ways to mitigate — TBI in soldiers for more than five years.

Last year, Moss and colleague Mike King, an LLNL mechanical engineer, concluded a one-year study that found that soldiers using military helmets one size bigger and with thicker pads could reduce the severity of TBI from blunt and ballistic impacts. Their research was funded by the U.S. Army and the Joint IED Defeat Organization.

In an article published in September 2009 in Physical Review Letters, Moss and King found that non-lethal blasts may induce sufficient skull rippling to generate potentially damaging forces in the brain without a head impact.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

The above story is reprinted from materials provided by Lawrence Livermore National Laboratory.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

source : www.sciencedaily.com

A Yale Child Study Center research team that includes postdoctoral fellow Ilanit Gordon and Kevin Pelphrey, the Harris Associate Professor of Child Psychiatry and Psychology, will present the results on May 19 at the International Meeting for Autism Research.

“Our findings provide the first, critical steps toward devising more effective treatments for the core social deficits in autism, which may involve a combination of clinical interventions with an administration of oxytocin,” stated Gordon. “Such a treatment approach will fundamentally improve our understanding of autism and its treatment.”

Gordon stated that while a great deal of progress has been made in the field of autism research, there remain few effective treatments and none that directly target the core social dysfunction. Oxytocin has recently received attention for its involvement in regulating social capabilities because of its role in many aspects of social behavior and social cognition in humans and other species.

To assess the impact of oxytocin on the brain function, Gordon and her team conducted a first-of-its-kind, double-blind, placebo-controlled study on kids and adolescents aged 7 to 18 with ASD. The team members gave the kids a single dose of oxytocin in a nasal spray and used functional magnetic resonance brain imaging to observe its effect.

The team found that oxytocin increased activations in brain regions known to process social information. Gordon stated these brain activations were linked to tasks involving multiple social information processing routes, such as seeing, hearing, and processing information relevant to understanding other people.

Other authors on the study include Randi H. Bennett, Brent C. vander Wyk, James F. Leckman, and Ruth Feldman.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

The above story is reprinted from materials provided by Yale University. The original article was written by Karen N. Peart.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

source : www.sciencedaily.com

“We are extremely concerned over the health impacts that this will have on the most vulnerable members of our society, many of whom will eventually become Canadian citizens,” the letter to Jason Kenney states.

It is signed by the heads of eight prominent healthcare groups:

Currently, under a long-standing program called the Interim Federal Health Program, the federal government provides basic health care, dental and vision care, medications and medical devices as needed to refugee claimants until they become eligible for coverage under provincial health care.

But under the new government plan, which is due to take effect June 30, some refugee claimants would only be entitled to urgent care; others would be denied all care unless they have a disease that would be a risk to the public, such as tuberculosis.

Download costs to provinces and charities

Kenney stated the plan is to ensure refugees do not get better health care than ordinary Canadians. He stated it’s also meant to deter fraudulent refugee claimants from coming to Canada for free health and dental care.

The plan would also save the government about $100 million over the next five years, he said.

But the medical professionals state it won’t save money in the long run because people who are sick will only get worse and take up more resources down the line.

They argue the plan will download costs to provincial governments, charitable groups and community organizations, which they state are already struggling to provide adequate healthcare services to the overall community.

And they state the move will hurt not only refugees, it will endanger the public.

“These changes will have deleterious effects to the public health and safety of all Canadians. For instance, tuberculosis, which is still quite prevalent in various regions of the world, may go unnoticed by health professionals, inevitably putting the greater public in harm’s reach,” the letter states.

The health professionals are also concerned that there is no grandfathering provision. That means people who currently have medications provided to them for serious illnesses such as heart disease and diabetes will be cut off or forced to pay for it themselves.

Doctors in Toronto staged a sit-in to protest proposed cuts to health care for refugees and refugee claimants. (Maureen Brosnahan/CBC)

“The health implications of slicing off individuals who are already receiving necessary health care could be catastrophic,” the health professionals wrote.

Jeff Morrison, director of government relations and public affairs for the Canadian Pharmacists Association, told CBC News in an interview Friday that the government should think about other ways to save money without compromising the health of refugees.

“We would be more than happy to work with them in improving efficiencies in other areas,” he said.

So far, the group has not had a response from Kenney or his office to their letter.

source : www.cbc.ca

“I knew there would be rare variation but had no idea there would be so much of it,” stated the senior author of the research, John Novembre, an assistant professor of ecology and evolutionary biology and of bioinformatics at UCLA.

A team of life scientists studied 202 genes in 14,002 people. The human genome contains some 3 billion base pairs; the scientists studied 864,000 of these pairs. While this is only a small part of the genome, the sample size of 14,002 people is one of the largest ever in a sequencing study in humans.

“Our results suggest there are many, many places in the genome where one individual, or a few individuals, have something different,” Novembre said. “Overall, it is surprisingly common that there is a rare variant in the population.

“This study doesn’t tell us how to cure a particular disease but suggests that disease in general may be caused by rare variants, and if you are trying to find the genetic basis of disease, it’s important to focus on those variants. Understanding the genetic basis of disease provides clues to how the diseases work and clues about how to treat them.”

The scientists discovered one genetic variant every 17 bases, which was a dramatically higher rate than they expected, stated Novembre, a population geneticist who is a member of UCLA’s interdepartmental program in bioinformatics.

Most of the time, only one person has the genetic variant and the other 14,001 do not.

“We saw lots of that,” he said. “We discovered there are many places in these 202 genes where there is variation and only a few individuals differ from the whole group, or only one differs. We also see evidence that a substantial fraction of these rare genetic variants appear to be deleterious in a long-term evolutionary sense and might impact disease.”

The research team included Daniel Wegmann, a former UCLA postdoctoral scholar in Novembre’s laboratory and a co-first author of the study; Darren Kessner, a UCLA graduate student in the bioinformatics interdepartmental Ph.D. program; colleagues from the University of Michigan, Ann Arbor (in fields including human genetics and biostatistics); and geneticists from international health care company GlaxoSmithKline, including project leader Matthew Nelson. The UCLA life scientists were involved in the population genetic analysis of the data.

In the study, 10,621 people had one of 12 diseases, including coronary artery disease, multiple sclerosis, bipolar disorder, schizophrenia, osteoarthritis and Alzheimer’s disease; 3,381 did not have any of the diseases.

“The massive sample size grants us to see patterns with more clarity than ever before,” Novembre said. “If rare variants are like distant stars, this kind of massive sample size is like having the Hubble Telescope; it’s allowing us to see more than before. We see a ton of rare variation, and these rare variants more often make changes to proteins than not. In that way, this study has important implications for the genetic basis of disease in humans. It’s consistent with the idea that many diseases may be partly caused by rare variants.”

Human population growth helps to explain the massive number of genetic variants, the scientists said.

“The fact that we see so many rare variants is in part due to the fact that human populations have been growing very rapidly,” Novembre said. “Because the human population has grown so much, the opportunity for mutations to occur has also grown. Some of the variants we are seeing are very young, dating to population growth since the invention of agriculture and even the Industrial Revolution; this growth has created many opportunities for mutation in the genome because there are so many transmissions of chromosomes from parent to child in massive populations.”

The scientists isolated and sequenced the pieces of DNA from the 202 genes.

They estimated mutation rates from population genetic data, which has only rarely been done before.

“We have been able to estimate mutation rates for each of the genes, which has been difficult to do with smaller sample sizes,” Novembre said. “In future research, we can study mutation rates not just in these 202 genes, but genome-wide.”

Sequencing technologies are advancing rapidly, he said. “What seemed like science fiction in the past is science today.”

Rare genetic variants would not have been detectable in most previous studies, whose samples usually had fewer than 1,000 people.

Typically, in population genetics, it is difficult to estimate mutation rates separately from population sizes, but when you get to very massive sample sizes, you can estimate the two separately, Novembre said.

“We estimate 202 mutation rates, one for each gene,” he said. “We show that the mutation rate varies from gene to gene. Follow-up studies may be able to reveal more about what factors affect mutation rates.”

Rare genetic variants are frequently geographically localized to small pockets around the globe rather than being widespread, Novembre said.

In the image accompanying this release, each vertical line represents one of the 202 genes. For each gene, the scientists plotted, at the top of the image, the number of genetic variants that have a frequency greater than 0.5 percent. When variants are greater than 0.5 percent, previous studies have been able to find most of them.

“With our massive sample size, we can detect variants at a frequency less than 0.5 percent, and we see all of these, which have never been seen before,” Novembre said. “Previous studies have analyzed the tip of the iceberg of genetic variation, but there is all this rare variation that has been below the surface, below our threshold of detection. Now, with massive sample sizes, we can see a more complete picture of human genetic diversity.”

The genetic code has changes that are “nonsynonymous” (they change the meaning of a protein) and “synonymous” (they do not change the meaning of a protein).

“We see many nonsynonymous changes amongst the rare variants, and these are plausibly affecting disease in humans, though in ways that are not yet well understood,” Novembre said

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

The above story is reprinted from materials provided by University of California – Los Angeles. The original article was written by Stuart Wolpert.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

source : www.sciencedaily.com