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Thursday, May 19, 2011

Discovery Could Change The Way Your Doctor Treats Your Autoimmune Disease or Cancer

Researchers in the Faculty of Medicine & Dentistry at the University of Alberta have made an important discovery that provides a new understanding of how our immune system "learns" not to attack our own body, and this could affect the way doctors treat patients with autoimmune diseases and cancer.

When patients undergo chemotherapy for cancer or as part of experimental therapies to treat autoimmune diseases such as diabetes and lupus, the treatment kills the patients' white blood . What can be done afterwards, is to give these patients blood stem cells through transplantation. Stem cells are taken from patients then injected back into them – with the theory being that the patients' immune system won't attack their own cells, and the  can get to work healing their bodies.
But U of A medical researchers Govindarajan Thangavelu, Colin Anderson and their collaborators discovered that if a particular molecule is not working properly in T-cells, the body will attack itself. This is significant for stem-cell transplantation treatment because it means the immune systems of the patients could consider their own cells "foreign" and initiate an attack.
"So your own cells would be killing you," says Thangavelu, a PhD student specializing in immunology, who was the first author in the research study, which was recently published in the peer-reviewed Journal of Autoimmunity. "What we found is if this molecule is absent in T-cells, if the pathway isn't intact, it will cause severe autoimmunity to the subject's own body. In essence, subjects become allergic to their own cells."
Anderson, an associate professor with the Alberta Diabetes Institute and Principal Investigator added: "The ability of our immune system to attack dangerous microbes while not attacking our own cells or tissues is a delicate balance. Restarting the immune system after wiping it out in patients with autoimmune diseases or cancer requires re-establishing this appropriate balance. We discovered that a particular immune system molecule is critical to prevent the immune system from attacking our own cells or tissues when the immune system is restarted. If that molecule is missing, the  will wreak havoc on the body."
T-cells are supposed to protect people and animals from things invading their bodies. But this research demonstrates if these cells become unregulated because they are missing a molecule, it can lead to autoimmunity – particularly dangerous in scenarios where patients have lost white blood cells when they are being treated for  or cancer.
Thangavelu has won awards for this research. He was invited to present his work at an international conference of immunology in Japan last year. He has also travelled to the United Kingdom to talk about his findings with the medical community.
Provided by University of Alberta (news : web)

Get Pain Relief From An Injectable Gel?

Some 25 million people in the United States alone suffer from rheumatoid arthritis or its cousin osteoarthritis, diseases characterized by often debilitating pain in the joints. Now researchers at Brigham and Women's Hospital (BWH) report an injectable gel that could spell the future for treating these diseases and others.

Among its advantages, the gel could allow the targeted release of medicine at an affected joint, and could dispense that medicine on demand in response to enzymes associated with arthritic flare-ups.
"We think that this platform could be useful for multiple medical applications including the localized treatment of cancer, ocular disease, and ," said Jeffrey Karp, leader of the research and co-director of the Center for Regenerative Therapeutics at BWH.
Karp will present the findings April 15 at the annual meeting of the Society for Biomaterials (SFB) as part of winning the coveted SFB Young Investigator Award for this work. The work was also reported by Karp and colleagues in the May 2011 issue of the Journal of Biomedical Materials Research (JBMR): Part A, and is currently available on the journal's website.
Local Delivery
Arthritis is a good example of a disease that attacks specific parts of the body. Conventional treatments for it, however, largely involve drugs taken orally. Not only do these take a while (often weeks) to exert their effects, they can have additional side effects. That is because the drug is dispersed throughout the body, not just at the affected joint. Further, high concentrations of the drug are necessary to deliver enough to the affected joint, which runs the risk of toxicity.
"There are many instances where we would like to deliver drugs to a specific location, but it's very challenging to do so without encountering major barriers," says Karp, who also holds appointments through Harvard Medical School (HMS), Harvard Stem Cell Institute (HSCI), and the Harvard-MIT Division of Health Sciences and Technology (HST).
For example, you could inject a drug into the target area, but it won't last long--only minutes to hours--because it is removed by the body's highly efficient lymphatic system. What about implantable drug-delivery devices? Most of these are composed of stiff materials that in a dynamic environment like a joint can rub and cause inflammation on their own. Further, most of these devices release medicine continuously--even when it's not needed. Arthritis, for example, occurs in cycles characterized by flare-ups then remission.
Toward the Holy Grail
"The Holy Grail of drug delivery is an autonomous system that [meters] the amount of drug released in response to a biological stimulus, ensuring that the drug is released only when needed at a therapeutically relevant concentration," Karp and colleagues write in JBMR. His coauthors are Praveen Kumar Vemula, Nathaniel Campbell, and Abdullah Syed of BWH, HMS and HSCI; Eric Boilard (now at Université Laval), Melaku Muluneh, and David Weitz of Harvard University; and David Lee of BWH, currently at Novartis. Karp notes the key involvement of Lee, a doctor who is "treating patients with the problem we're trying to solve."
The researchers tackled the problem by first determining the key criteria for a successful locally administered arthritis treatment. In addition to having the ability to release drug on demand, for example, the delivery vehicle should be injectable through a small needle and allow high concentrations of the drug. The team ultimately determined that an injectable gel seemed most promising.
Next step: what would the gel be made of? To cut the time involved in bringing a new technology to market, the team focused only on materials already designated by the Food and Drug Administration as being generally recognized as safe (GRAS) for use in humans.
Ultimately, they discovered a GRAS material that could be coaxed into self-assembling into a drug-containing gel. "The beauty of self-assembly is that whatever exists in solution during the assembly process--in this case, a drug--becomes entrapped," says Vemula, first author of the paper, who also has an appointment at HST.
They further expected that the same material would disassemble, releasing its drug payload, when exposed to the enzymes present during inflammations like those associated with arthritis.
Promising Results
A series of experiments confirmed this. For example, the team created a gel containing a dye as a stand-in for a drug, then exposed it to enzymes associated with arthritis. The drug was released. Further, the addition of agents that inhibited the enzymes stopped the release, indicating that the gel "can release encapsulated agents in an on-demand manner," the researchers write. Although the team has yet to test this in humans, they did find that dye was also released in response to synovial fluid taken from arthritic human joints.
Among other promising results, the researchers found that gel injected into the healthy joints of mice remained stable for at least two months. Further, the gel withstood wear and tear representative of conditions in a moving joint.
Additional tests in mice are underway. The technique has yet to be demonstrated in humans, but the researchers write that it "should have broad implications for the localized treatment of many…diseases" caused by the enzymatic destruction of tissues.
The researchers have applied for a patent on the work, which was sponsored by the Center for Integration of Medicine and Innovative Technology (CIMIT) through the U.S. Army and by the Harvard Catalyst Program.
Provided by Brigham and Women's Hospital

Illusion Can Cut Osteoarthritis Pain in Half

( -- A serendipitous discovery by academics at The University of Nottingham has shown that a simple illusion can significantly reduce -- and in some cases even temporarily eradicate -- arthritic pain in the hand.

By tricking the brain into believing that the painful part of the hand is being stretched or shrunk, the researchers were able to halve the pain felt by 85 per cent of sufferers they tested.
The research could point to new technologies of the future which could assist patients in improving mobility in their hand by reducing the amount of pain they experience while undergoing physiotherapy.
The Nottingham team stumbled on its finding completely by chance during the University’s Community Open Day in April last year.
As part of the event they invited members of the public to experience some of the body distortion illusions they use as part of their every day research using Nottingham’s unique MIRAGE technology — which takes a real-time video capture image of a hand and uses computer manipulations combined with physically pulling or pushing on the hand to fool the brain into believing the hand is stretching or shrinking.
Up until now, the technology has been used for fundamental research into body representation — the way in which our brain puts together what we see and what we feel.
Dr Roger Newport who is leading the research in the School of Psychology said: “The majority of people who come to these fun events are kids — the illusions really capture their imagination and they think it’s a cool trick and can become a bit obsessed with working out how we do it.”
Dr. Catherine Preston, who is now at Nottingham Trent University and collaborated on the study, added: “During the course of the day the grandmother of one of the children wanted to have a go, but warned us to be gentle because of the arthritis in her fingers. We were giving her a practical demonstration of illusory finger stretching when she announced: “My finger doesn’t hurt any more!” and asked whether she could take the machine home with her! We were just stunned — I don’t know who was more surprised, her or us!”
To capitalise on their lucky discovery, the team immediately contacted a local osteoarthritis support group and asked them to take part in a series of tests to confirm the effectiveness of MIRAGE for pain relief.
The study attracted 20 volunteers with an average age of 70, all clinically-diagnosed with arthritic pain in the hands and/or fingers and none medically managing their pain on the day by anything stronger than paracetamol. Before starting the test they were asked to rate their pain on a 21-point scale, with 0 indicating no pain and 20 representing the most unbearable pain imaginable.
The team then compared the MIRAGE body  to just physically pushing and pulling on the painful parts of the volunteers’ hands to test the effect on their pain. Other control tests were conducted by stretching or shrinking a non-painful part of the hand and visually enlarging or reducing the whole hand.
The results, reported in a letter to the latest edition of the journal Rheumatology, showed a marked reduction in pain —on average halving the discomfort for 85 per cent of volunteers. Some reported greater reduction in pain for stretching, some for shrinking and some for both. The pain reduction only worked when painful parts of the hand were manipulated.
Remarkably, stretching or shrinking the painful part of the hand temporarily eliminated pain in one-third of all volunteers. Anecdotally, many volunteers also reported an increased range of movement.
Osteoarthritis is a debilitating and painful inflammatory condition which affects the joints and is one of the most common arthritic conditions. Around one million people consult their GPs about OA every year — mostly people aged over 50 who are more prone to developing the disease.
There is currently no cure for osteoarthritis but the symptoms can be managed by a range of treatments including painkillers and physiotherapy — although pain can be a barrier to sufferers trying to exercise and keep joints mobile.
The Nottingham team are hopeful their finding could be the first step towards new technologies for physiotherapy, allowing health professionals to reduce the pain for sufferers while exercising their joints. Eventually, cheaper technology may allow a low-cost model of the system to be produced which could be small enough for sufferers to keep in their home and offering brief periods of respite from their discomfort.
Dr Newport added: “This research is an excellent example of how fundamental research can often produce unexpected and significant results. In my early career I was lucky enough to receive internal funding to develop the MIRAGE technology which is unique to The University of Nottingham.”
“Without that support we never would have unearthed this surprising and exciting result, which potentially could be extremely important to the millions of people who suffer from this painful and debilitating illness.”
Provided by University of Nottingham (news : web)

Wednesday, May 18, 2011

First Breakthrough in 50 Years For Lupus

(Medical Xpress) -- A Monash researcher has played a crucial role in the first major lupus treatment breakthrough for over 50 years.

Professor Fabienne Mackay Head of the Department of  at Monash University, discovered a new factor in the development of the disease, something known as BAFF - B cell Activating Factor.
It has led directly to the development of a medication called Benlysta, which was approved by the US Food and Drug Authority for release last month.
Professor Mackay explains that B  make  for invaders such as  and other foreign bodies, like pollen.
“BAFF helps B cells survive, which is a good thing. But if there is too much BAFF, then there can be an overproduction of B cells and they hang about for longer than they should - in particular  that are normally meant to die because they are harmful. Autoimmunity will be initiated, and this is how the immune system ends up attacking the body’s own cells,” Professor Mackay said.
Lupus is an autoimmune inflammatory disease affecting about five million people worldwide. An autoimmune problem is one where the body’s immune system attacks the body itself.  In the case of lupus, the  attacks connective tissue in the joints, lungs, kidneys and heart, causing joint and skin diseases in most patients, and organ and blood disorders in about half of lupus sufferers.
Professor Mackay was the first to show that the overproduction of BAFF was driving lupus. In a follow up study, elevated levels of BAFF were discovered in patients with a number of autoimmune diseases including lupus, rheumatoid arthritis and Sj√∂gren’s syndrome.
She said this was an exciting discovery as it implied that if BAFF production can be blocked, the entire cascade effect that resulted in autoimmune disease could be prevented.
Manufacturers of the drug, GlaxoSmithKline designed their clinical trials in line with the insights from Professor Mackay’s experimental data.
Professor Mackay says that one of the reasons for her interest in lupus is its affect on the Indigenous Australian population. Aboriginal Australians suffers from  at a rate double that of the non-Aboriginal population.
“I am very pleased to have created the platform of knowledge from which effective therapies can springboard. In particular, I have long been concerned about the higher incidence of this disease and associated morbidity within Indigenous Australians populations and the limited arsenal of therapies, many very toxic, and it is wonderful news that a medication has been developed which may be able to help them.”
Provided by Monash University (news : web)

Patient Dies In Oral RA Drug Study

(AP) --  Pfizer Inc. confirmed that one patient who was taking its drug candidate tofacitinib, a pill designed to treat rheumatoid arthritis, died during a recent clinical trial and said the death was connected to the drug.
The world's largest drugmaker said the patient died of . Three other patients who were treated with tofacitinib during the study died as well, but those deaths were not determined to be drug-related. Two of those deaths occurred several weeks after the patients stopped taking tofacitinib. Tofacitinib, formerly called tasocitinib, is being tested as a treatment for moderate to severe rheumatoid arthritis, a  that causes inflammation, usually of the hands and feet.
More than 1,000 patients have taken tofacitinib during , and Pfizer said late Thursday that overall death rate for patients in those studies is similar to what has been observed in other biologic treatments for rheumatoid arthritis.
The late-stage trial was called ORAL Sync. Pfizer said in March that tofacitinib met its main goals in the 792-patient study. The patients received either 5 or 10 milligrams of the drug twice per day. Some patients received a placebo. The trials involved patients with moderate to severe active rheumatoid arthritis who have not been helped by an older class of drugs including methotrexate. Pfizer will present full results from the ORAL Sync trial on May 27 at a conference of the European League Against .
Earlier this month Pfizer said the drug met its goals in a separate late-stage trial.
Pfizer said the other deaths included a patient who died of acute , one death caused by brain injury following trauma, and one case of worsening rheumatoid arthritis. The  death occurred 22 days after the patient stopped taking tofacitinib, and the patient who died of worsening rheumatoid arthritis had stopped taking tofacitinib six weeks earlier.

Attention: Scientists Discover 'How to Stop Your Immune System From Killing You'

(Medical Xpress) -- Scientists at the University of Birmingham have discovered a 'molecular hoover' with the potential to prevent autoimmune conditions.

Research findings published today in the journal Science by Dr David Sansom and his team in the MRC Centre for Immune Regulation at Birmingham show how a , called CTLA-4, keeps the  damped down during day-to-day activities and prevents inappropriate aggressive behaviour from T cells, the ‘command centre of our immune response’.

‘Only when we are truly infected with invading microbes is the alarm system allowed to work properly, unleashing the full force of our immune system in the right place and at the correct time,’ says Dr Sansom.
‘We all take our immune system for granted,’ he explains. ‘Every day we are faced with a constant barrage of infectious agents just dying to make our bodies their home. To prevent this invasion, our immune system deploys a range of weapons designed to eat, poison and ultimately kill unwanted and potentially dangerous guests. On the whole, the immune system is remarkably good at its job.’
Why does this potent arsenal of weapons not kill us? ‘The fact is that a number of diseases can be caused by such collateral immune damage, indeed rheumatoid arthritis, Type 1 diabetes and inflammatory bowel syndrome are all thought to be examples of  where the immune system attacks our bodies in some way,’ says Dr Sansom.
One essential component of our immune system is CTLA-4, a protein found on T cells, he says. ‘Without CTLA-4  start to recognise our bodies, leading to the attack of many different organs in a manner which is fatal.’
While immunologists have known for a long time that CTLA-4 is required to prevent immune responses against ourselves, how it works has remained a mystery. The Sansom lab’s work puts in place a critical piece of the puzzle by illustrating that CTLA-4 acts as a hoover removing the alarm signals that can drive unwanted and damaging immune responses against our bodies.
The work was funded by the Biotechnology and Biological Sciences Research Council (BBSRC) and the findings provide a new way of thinking about how to gain better control of our immune response and may help in the design of drugs to treat autoimmune diseases such as arthritis and diabetes.
Dr Sansom adds: ‘Alternatively, by discovering new ways to prevent CTLA-4 working, it may be possible to encourage our immune cells to attack cells of our own bodies which could be desirable in cancers.’
In either case, he says, understanding how CTLA-4 works and learning how to manipulate its behaviour represents a significant step in understanding self-control in the immune system.
Provided by University of Birmingham

Tuesday, May 17, 2011

Adult Arthritis Suffers Have a Poorer Health Quality of Life

A new study reports that the health-related quality of life (HRQOL) for U.S. adults with arthritis is much worse than for those without this condition. Both physical and mental health are affected by arthritis, which poses a significant health and economic burden as the number of those diagnosed continues to climb. Details of this study are now online in Arthritis Care & Research, a journal published by Wiley-Blackwell on behalf of the American College of Rheumatology (ACR).

Approximately, 50 million Americans have doctor-diagnosed , and the Centers for Disease Control and Prevention (CDC) estimates that with the aging U.S. population 67 million adults could be affected by 2030. Arthritis is also the most common cause of disability in the U.S.—limiting activity for 19 million individuals and inhibiting employment for nearly 8 million working-age Americans. According to prior studies, arthritis accounts for 44 million outpatient visits, roughly 1 million hospitalizations, and more than $128 billion in medical expenses and lost earnings in the U.S. annually.
In the present study, Sylvia Furner, MPH, PhD, of the School of Public Health at the University of Illinois at Chicago and colleagues at CDC analyzed data from the Behavioral Risk Factor Surveillance System (BRFSS) to compare HRQOL in U.S. adults with and without arthritis. BRFSS is a telephone survey used by state health departments and CDC to collect HRQOL, demographic, and behavioral risk factor information from a representative sample of U.S. adults 18 years of age and older. Questions related to arthritis are included in the annual survey in odd years, and the current study used data from 2003, 2005, 2007.
More than 1 million respondents were included in the analysis during the 3-year study period. Researchers found 27% of survey respondents with arthritis reported fair or poor health compared to 12% of those without arthritis. The mean number of physically unhealthy days (7 vs.3), mentally unhealthy days (5 vs.3), total unhealthy days (10 vs.5), and activity-limited days (4 vs.1) was greater for individuals with arthritis than for those without. Additionally, those with arthritis who experienced limitations to normal activities reported poorer HRQOL than individuals without arthritis-related restrictions.
"Our analysis showed that the values for all five measures of HRQOL were 2-3 times worse in those with arthritis compared to those without," said Dr. Furner. HRQOL measures used for analysis were demographics (age, gender, race), social factors (education, income, employment), healthcare factors (access to care, cost barrier to care), health behaviors (physical activity, smoking status, alcohol consumption), and health conditions (diabetes, hypertension, body mass index). Having low family income, being unable to work, cost being a barrier to care, and having diabetes were all strongly associated with poor HRQOL.
Individuals who were physically active had significantly better HRQOL compared with those who were inactive. Furthermore, those who had arthritis and remained physically active were less likely to report fair or poor health. "Given the projected high prevalence of arthritis in the U.S. interventions should address both physical health and ," concluded Dr. Furner. "Increasing physical activity, reducing co-morbidities, and increasing access to healthcare could improve then  for adults with arthritis."
More information: "Health-Related Quality of Life of U.S. Adults with Arthritis: Analysis of Data from the Behavioral Risk Factor Surveillance System, 2003, 2005, and 2007." Sylvia E. Furner, Jennifer M. Hootman, Charles G. Helmick, Julie Bolen, Matthew M. Zack. Arthritis Care and Research; Published Online: April 28, 2011 (DOI: 10.1002/acr.20430).
Provided by Wiley (news : web)

The New Structure of An Important Immune System Complex Has Resolved A 10-year Controversy

(Medical Xpress) -- Researchers at the University of Toronto and the University of Bath have resolved a longstanding controversy surrounding an important structure of the immune system that could result in new therapeutic targets for antibody-mediated autoimmune diseases as well as the potential to enhance the efficacy of vaccines.

In a study published in the April 29 issue of Science, Professor David Isenman of biochemistry and Jean van den Elsen of the University of Bath shed light on the complex between complement receptor 2 and its  C3d, both of which are constituents of an  of our body known as complement.
“We recognize that the goal of applying this knowledge to autoimmune therapies and enhanced vaccine efficiency will not be trivial. But the structural scaffold for further discoveries is now in place,” said Isenman.
The detailed knowledge of the receptor-ligand interface provided by the new structure of this complex has implications as both a potential , in the case of antibody-mediated , and as something that may be exploited in enhancing the efficacy of vaccines.
The role of complement in mediating the clearance of microbial pathogens, either directly or in conjunction with , has long been recognized. A key element of the process is the “tagging” of the foreign target by a proteolytically activated fragment of complement component C3. This first C3 split product, as well as its subsequent degradation products, remains covalently attached to the foreign target where they act as ligands (i.e., bridging molecules) for complement receptors present on white blood cells. In turn, these white blood cells can engulf and destroy the tagged microbial target.
New structure of an important immune system complex resolves a 10-year controversy
In more recent years, it has become well established that complement also plays a role in focusing the antibody arm of the adaptive  on an antigen which it has tagged with a C3 split product, the limit one of which is known as C3d. The latter is a ligand for complement receptor 2 (CR2) on B lymphocytes, the very type of cell that, when stimulated by a specific antigen, undergoes clonal expansion and ultimately differentiates into “factory” cells that secrete large amounts of the antibody against the antigen that was initially encountered. As illustrated in the accompanying schematic, both the antigen recognition entity of the B cell (the B cell receptor, BCR), as well as the C3d-binding CR2 molecule, are each associated with other molecules involved in generating intracellular signals that drive B cell clonal expansion. In what is known as the co-ligation model, the C3d-tagged antigen mediates a bridge between the BCR complex and the CR2/CD19/CD81 complex, the effect of which is to greatly enhance the amount of signalling relative to that achieved by antigen binding to the BCR alone. What this does is lower by orders of magnitude the threshold quantity of antigen required to initiate the antibody response of the particular B cell recognizing that particular antigen. There is an additional role for CR2 present on a different cell type, the follicular dendritic cell (FDC) of lymph nodes, in trapping C3d-tagged antigen in the lymph node. This in turn is important in generating stronger binding antibodies and in the induction of long-lived memory B cells that allows one to rapidly mount an antibody response years after the first encounter with a particular antigen. These effects, which are mediated by the CR2-C3d interactions on B cells and FDCs, are collectively referred to as the “molecular adjuvant” effects of complement and this is important in making the antibody response sensitive to the low concentrations of antigen that are present in the early stages of infection. Unfortunately, these same CR2-C3d binding events can sometimes lead to detrimental effects in the case of individuals having B cells that are reactive against self-antigens and which produce the antibodies at the root of antibody-mediated autoimmune diseases such as systemic lupus erythematosus (commonly known as lupus disease or SLE).
Clearly there is a potential to therapeutically exploit the CR2-C3d interaction, either through the rational design of drugs that would inhibit the interaction in the case of some autoimmune conditions or the rational design of small molecule CR2-binding mimetics of C3d, which may be used to decorate antigens in a subunit (i.e,. pathogen surface protein-based, as opposed to whole pathogenic microorganism-based)  situation. Unfortunately, the molecular details of the CR2-C3d interface (represented within the white box of the schematic) necessary to pursue such therapeutic avenues have been mired in controversy for the past decade. Specifically, in 2001 an X-ray crystal structure of the complex consisting of C3d and the first two domains of CR2 [hereinafter denoted CR2(SCR1-2)] was published in Science, however from the start that structure was discordant with much biochemical data in the literature, and over the years the discrepancies have only increased.
“To be clear, there were no errors made in the original structure determination, but it is now apparent from extensive subsequent biochemical work that the 2001 structure represented a non-physiologic complex that resulted from the particular crystallization conditions used,” said van den Elsen.
The structure of the CR2(SCR1-2)-C3d complex from van den Elsen and Isenman was also determined using X-ray crystallography, but under more physiologic crystallization conditions. The new structure (depicted here) is very different from the previous one, but its features do conform to all existing biochemical data. With the controversy regarding atomic level details of the binding interface now finally resolved, the new structure of the CR2(SCR1-2)-C3d complex will hopefully provide the platform for both the design of compounds that may exploit this interface as either a therapeutic target or in enhancing the efficacy of vaccines. While this discovery lays an important foundation, the authors of the current study recognize that neither of these goals will be simple to achieve and will require contributions from medicinal chemists, in addition to complementologists and immunologists.
Provided by University of Toronto (news : web)

Ongoing Relationship With Your Care Provider Is Your Key to Improved Health

(Medical Xpress) -- People with a chronic condition such as diabetes or arthritis may find themselves taking on a more active role in maintaining or improving their own health if there is an ongoing relationship with a primary healthcare (PHC) provider, according to University of British Columbia research.

Appearing in the current issue of , the study is the first in Canada to investigate the links between having a regular primary healthcare provider and patient activation, a growing direction in healthcare that aims to increase people’s skills, confidence and knowledge so they can better manage their own health.
Primary care refers to the first level of contact with healthcare for individuals. These include clinical services from doctors, nurses or nurse practitioners as well as health promotion activities.
“The idea is that we need to do the best we can with our current healthcare dollars to provide sustained quality care for individuals who in some cases are living with one or more chronic conditions,” says Assoc. Prof. Sabrina Wong, lead author and a researcher in the School of Nursing and Centre for Health Services and Policy Research.
“What we’re seeing across North America is a policy direction that links patient-reported outcome measures such as patient activation to the quality of services and care provided by primary healthcare, especially in chronic disease management,” says Wong.
Previous U.S.-based studies have shown that having a strong primary healthcare system in place pays dividends for patients, and ultimately the taxpayer. For example, individuals with one or more chronic conditions experience reduced risk, and reduced duration and effects, of acute and episodic conditions. As well, they report reduced risk and effects of continuing health conditions,
For their study, Wong and the research team looked at relationships between patient activation and multiple dimensions of primary healthcare in B.C. including access, utilization, responsiveness, interpersonal communication and satisfaction for patients, both with and without a chronic condition.
Taking part in the study were 504 B.C. residents with an average age of 46. Fourteen per cent of participants reported their health as being fair or poor, and 44 per cent reported having at least one chronic condition such as , high blood pressure or .
“The results suggest there is a strong relationship between patients’ ability to self-manage their health and having a positive relationship with at least one PHC provider,” says Wong.
With the typical primary care visit lasting between 10 and 12 minutes, one aspect of care especially important to those with a chronic condition was having enough time to talk with their family physician or nurse practitioner.
Other aspects of care such as communication, patient-centered decision-making and being treated as a whole person also appear especially important for those with a chronic condition.
Findings also show that for patients with a , high quality PHC was more about a strong connection with the place of care than whether it was delivered through group practice, solo practice or a walk-in clinic.
What was most important, however, for physically healthy adults – who may visit doctors or clinics less frequently – was the quality of the interpersonal interaction.
Provided by University of British Columbia (news : web)

Monday, May 16, 2011

New Test Could Give Patients With Systemic Lupus Erythematosus A More Tolerable Life

Five million people worldwide suffer from the chronic rheumatic disease SLE, systemic lupus erythematosus. Together with rheumatologists, researchers at Lund University in Sweden are on the way to developing a new test that could resolve a number of question marks surrounding the disease and in the long run improve the lives of SLE patients. Their research is published in the next issue of the respected journal Molecular and Cellular Proteomics.

"At present, it can take up to a year before a patient is diagnosed with SLE. This is because the symptoms are diffuse and are often mistaken for other diseases. However, with this blood-based test, it is possible to determine quickly whether someone has the disease or not", says Christer Wingren, associate professor in Immunotechnology at CREATE Health, Lund University.
The test can also determine how far the disease has progressed. There are three different variants of SLE, and all require different treatment. With current methods, it is often difficult to find out which variant a patient has, which makes it difficult for doctors to prescribe the right medication. A third advantage of the new technique is that it also makes it possible to predict when the disease will become active.
"Characteristic of SLE is that the disease goes in waves, or flares. Without warning, the disease can flare up and put the patient out of action for a long time. With our test, we hope to be able to predict when an episode is about to happen and in this way prevent it using the right medication", explains Christer Wingren.
If all goes well, hospitals could start using the technique in two to three years.
The test itself comprises a small chip, smaller than a little fingernail, on which the researchers create a , known as an array, using specially selected . The antibodies serve as 'capture molecules'; by placing a drop of blood on the chip, the antibodies bind the proteins, or biomarkers, in the body. In this way, a unique 'fingerprint' is produced for each patient, which reflects the disease.
"In our article, we show which pattern of  (the 'fingerprint') to look for. From a technical point of view, we get a large number of data signals that say whether the marker is present and in what quantity. These measurements are then entered into a computer, which can present them to the doctors in a way that is easy to understand. It is this fingerprint which doctors could use in the future in clinical practice", explains Christer Wingren, who has spent most of the past decade developing the technique, and the past two years adapting it for SLE in particular.
According to Christer Wingren, a number of researchers around the world have attempted to develop something similar, but without success. The Lund researchers' success in the task is partly due to them having found a way to make the antibodies stable and thus more functional. The method has also become highly sensitive.
In order for the research to benefit patients, a number of key biomarker signatures, which form the basis for the test, have been patented. The findings have also been transferred to a newly started company, Immunovia, which was founded by Christer Wingren and three of his colleagues at the Department of Immunotechnology.
The research has its origins in the cancer research that Christer Wingren and a number of other researchers at the translational cancer centre CREATE Health work on. Together with Carl Borrebaeck, Dr Wingren uses an equivalent technological platform that can detect and diagnose different types of cancer. They have very promising data for predicting breast cancer recurrence and diagnosing pancreatic cancer.
Provided by Lund University

Conventional medicine finally admits MS caused by vitamin D deficiency

Conventional medicine finally admits MS caused by vitamin D deficiency

(NaturalNews) Is it true that those who suffer from Multiple sclerosis (MS) just need a little sun? Researchers at the University of Oxford seem to think so. In 2006, a study by the Journal of the American Medical Association suggested higher levels of vitamin D might decrease overall risk of developing MS. Now researchers at the University of Oxford are backing that study with further evidence while also suggesting a link between lack of sunlight and how the body responds when faced with an infection. The research concludes that MS is caused by several factors working in combination but clearly correlates to a lack of vitamin D.

Is it really as simple as soaking up some rays?

While the phenomenon of vitamin D deficiency is seen all over the world, countries in the northern hemisphere have been linked to significantly higher rates of MS. Scotland, for example, has one of the largest populations of MS sufferers, while the disease is "virtually unknown" in Africa. Even in sunny areas of the globe, it's not uncommon for people to become vitamin D deficient during the winter, as the sun's rays aren't often high enough to penetrate atmospheric layers.

The research put forth by the University of Oxford suggests that, while those who already have MS may not benefit exponentially simply by increasing levels of vitamin D, getting more sun could be an effective preventative measure against developing the disease and managing symptoms.

More importantly, MS sufferers may be able to boost immunity to other conditions with an increase in vitamin D. A recent study by Anticancer Research affirms that typical adults need much more than the daily dosage recommended by the U.S. Government. According to that research, 4,000-8,000 IUs of vitamin D every day could not only help prevent MS but also several types of cancer and Type 1 diabetes.

The health care industry, of course, won't promote a natural and safe preventative measure for degenerative diseases. Instead, people are warned about the dangers of UV exposure and the risks of vitamin toxicity. With vitamin D deficiency afflicting 90% of the U.S. population, however, it may be time to get a tan. Here are some interesting facts about the relationship between vitamin D and health:

1. It's free. Five to thirty minutes of sunlight a couple of times a week is usually sufficient for helping the body create enough vitamin D

2. Getting enough vitamin D from food is virtually impossible
3. Sunscreens may block the body's ability to generate vitamin D
4. Vitamin D is essential for the absorption of calcium in the body
5. Those who live further from the equator generally require longer periods of sun exposure to generate enough vitamin D
6. A lack of vitamin D can affect bone strength. One theory suggests that women who are deficient in vitamin D can suffer from contracting pelvises, which can result in the death of babies during labor
7. Vitamin D deficiency cannot be reversed quickly. It takes months for the body to increase and regulate vitamin D levels. This is why short periods of sun exposure are not only safe but also necessary for the synthesis of this important substance

For those with MS, increased sun exposure may be an easy and safe preventative measure against further cognitive and physical degeneration. As a direct threat to the medical establishment, however, it remains to be seen whether further government warnings and regulations about vitamin D will eventually ban people from sun bathing.

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Folic Acid Really Doesn't Help Heart and Blood Vessels

The belief that folic acid can reduce the risk of getting cardiovascular diseases took root sixty years ago. Scientists discovered that people with a certain  suffered from cardiovascular diseases and brain hemorrhage already at a young age. These people had a high level of homocysteine in their blood. Subsequently, epidemiologists did research into people without such a disorder, and found that this relationship also exists: the higher the level of homocysteine in the blood, the bigger the chance of cardiovascular diseases. As it is difficult to establish cause and effect In epidemiological studies, the logical next step was to carry out specific experiments. Since vitamins B6,  and folic acid are effective in lowering homocysteine levels, the question was raised as to whether they could do the same for cardiovascular diseases.
This did not seem to be the case for people who had recovered from a  or a . The chance of getting a heart attack a second time did not become less. Perhaps, folic acid only works at an early stage, was the thinking of Wageningen researchers of the Top Institute Food & Nutrition. Together with researchers from the Julius Centre in Utrecht, they began a major study in 1999. More than 800 people between the ages of fifty and seventy who had high levels of homocysteine in their blood - but had almost no cardiovascular diseases - were monitored for three years. Half of them were given a high dose of folic acid daily, while the other half got a placebo. Measurements were taken at the start and after three years of the carotid artery thickness and its elasticity, both of which are indicators of arteriosclerosis and cardiovascular disease.
The folic acid pills appeared to have taken effect: they lowered the homocysteine level in the blood by a quarter. But neither the thickness of the vessel walls nor their elasticity had any significant changes. As such, the chances of getting cardiovascular diseases have not changed too. 'This study confirms that extra folic acid cannot prevent cardiovascular diseases', says Petra Verhoef, now working at Unilever, who was then the project manager of the study. 'Homocysteine is perhaps not the cause of heart and vascular diseases, but an offshoot in a process related to heart and vascular diseases. Luckily, there are other ways to lower the risk of getting heart and vascular diseases.
Provided by Wageningen University