Research

Gene test can help recommend best psychiatric medications for patients

Psychiatrists can use a simple genetic test to determine which psychoactive medications will be most easily metabolized by their patients. And a third clinical study has confirmed that this test has a positive effect on treatment outcome.

The Pine Rest study, published in Discovery Medicine, showed that when psychiatrists have their patients use GeneSite, those in the group whose treatment is guided by the technology showed a greater than two-fold response and remission rate.

GeneSite only requires swabbing the inside of the cheeks and sending the swab into a central lab. Basically, the test segments medications into “green” (use as directed), “yellow” (use with caution) or “red” (use with increased caution) categories, depending on the way a patient’s unique genomic makeup will interact with psychiatric medicines.

Psychiatrists who used GeneSite in the study were twice as likely to switch medications or adjust dosages of medications. In fact, 100 percent of clinicians using GeneSite made such changes, whereas only 50 percent of clinicians without the guidance did so.

The results of the Pine Rest study are similar to those of the La Crosse Study, published in July 2013 in Pharmacogenetics and Genomics. In that study of 227 participants, the GeneSite-guided group experienced a more than two-fold improvement in symptoms and likelihood to achieve remission.

Given the repeated success of GeneSite in these trials, I now use it frequently to help tailor medication treatment for patients. I suggest that you speak with your psychiatrist about it, as well.

Source: top news today

Vitamin C – A Powerful Cancer Cure?

A 2008 Vitamin C – End All Disease study conducted by the National Institute of Health found that, when injected into mice, Vitamin C could slow the growth of tumours. Despite the long history of research into vitamin C and cancer with many of the same findings, the research paper presented its findings as new. Curative health affects using vitamin C therapy have been known for a long time.

Studies on Vitamin C and Cancer

* A study conducted in 1969 found that Vitamin C would selectively kill cancer cells without harming normal cells. These scientific findings were largely ignored by the medical establishment.
* Clinical trials conducted by 2x Nobel Prize winner Linus Pauling and surgeon Ewan Cameron were able to prolongue the lives of cancer patients 6x longer than they would have lived without Vitamin C.1
* A 1994 study conducted by Dr. Art Robinson found that mice with cancer fed a diet of raw vegetables and given high-dose vitamin C lived up to 20 times longer than the control mice.2
* After reviewing the existing literature, Steve Hickey, Ph.D and Hilary Roberts, Ph.D found that in high enough doses, Vitamin C acts as an anti-cancer medicine.3

How Does Vitamin C Work to Kill Tumours?

In healthy tissues, Vitamin C works as an antioxidant to clean up and remove free radicals, and in cancer cells it acts as an oxidant which kills abnormal cells and generates free radicals.

When blood levels of Vitamin C are maintained at a consistently high level, it is absorbed into tumour tissues, where it generates hydrogen peroxide, killing cancer cells.

If you want to understand why Vitamin C can detoxify ANY known chemical, here’s what you need to know:

* All toxins are pro-oxidant in the body, which means they take electrons away from cells unless neutralized with antioxidants. This oxidative stress damages cells.
* Increasing your body’s blood levels of the antioxidant Vitamin C will give the toxins something to consume so that they cannot negatively effect your cells, and they are then removed from the body.

Source: end all disease

How brain balances learning new skills while retaining old ones

Researchers have developed a new computational model that explains how the brain maintains the balance between plasticity and stability, and how it can learn very similar tasks without interference between them.

To learn new motor skills, the brain must be plastic: able to rapidly change the strengths of connections between neurons, forming new patterns that accomplish a particular task. However, if the brain were too plastic, previously learned skills would be lost too easily.
The key, the neuroscientists at MIT said, is that neurons are constantly changing their connections with other neurons. However, not all of the changes are functionally relevant- they simply allow the brain to explore many possible ways to execute a certain skill, such as a new tennis stroke.

“Your brain is always trying to find the configurations that balance everything so you can do two tasks, or three tasks, or however many you’re learning. There are many ways to solve a task, and you’re exploring all the different ways,” lead author Robert Ajemian said.

As the brain learns a new motor skill, neurons form circuits that can produce the desired output- a command that will activate the body’s muscles to perform a task such as swinging a tennis racket. Perfection is usually not achieved on the first try, so feedback from each effort helps the brain to find better solutions.

This works well for learning one skill, but complications arise when the brain is trying to learn many different skills at once. Because the same distributed network controls related motor tasks, new modifications to existing patterns can interfere with previously learned skills.

That connectivity offers an advantage, however, because it allows the brain to test out so many possible solutions to achieve combinations of tasks. The constant changes in these connections, which the researchers call hyper plasticity, is balanced by another inherent trait of neurons- they have a very low signal to noise ratio, meaning that they receive about as much useless information as useful input from their neighbors.

The MIT team said noise is a critical element of the brain’s learning ability. They found that it allows the brain to explore many solutions, but it can only be utilized if the network is hyper plastic.

The study was published in the National Academy of Sciences

Source: news track india

New technique identifies pathogens in patient samples faster, in great detail

A team of Danish investigators has shown how to identify pathogens faster, directly from clinical samples. The research appears in the Journal of Clinical Microbiology.
The investigators used a technique known as whole genome sequencing to identify and completely characterize bacteria causing urinary tract infections. In just 18 hours, they identified the culprit microorganisms, characterized the pathogens’ patterns of antibiotic susceptibility, and identified specific strains.

“Using conventional methodologies this would have taken several days to weeks, and even using whole genome sequencing on cultured bacteria would have taken an extra day,” says Frank M Aarestrup of the Technical University of Denmark, Lyngby, an author on the study.

According to the researchers, their work will help patients heal more quickly and avoid unnecessarily prolonged illness and even death. It will also help prevent outbreaks of hospital-acquired disease, and identify emerging infections.

“Rapid identification of the causative agent, and of any antibiotic resistance is crucial to choosing the correct treatment for individual patients,” says Aarestrup. “Choosing the wrong antibiotic will lead to longer infections and in the worst case, deaths.”

The investigators also identified bacteria in the patient samples that they did not detect using conventional techniques. “Lactobacillus iners, Gardnerella vaginalis, Prevotella, and A. urinae have all been implicated in [urinary tract infections], even though their precise roles as pathogens and normal colonizers of the genital tract have not been firmly established,” write the researchers. They note that by conventional methods A. urinae is rarely identified but frequently misclassified.

The ability to identify strains in patients with repeated infections enables the doctor to know whether the patient’s infection is new, or recurrent. And the typing of bacterial strains enables rapid comparison of bacteria from different patients, so that doctors can detect the spread of infections within the hospital, and identify emerging infections.

“Whole genome sequencing may still be too expensive for routine use in most clinical microbial laboratories,” the researchers write. But they predict that rapidly falling prices and automation will render it a standard technology for infection detection and control, in and out of the hospital.

Source: India Medical Times

New laser procedure treats gum disease with less pain

Years ago, 78-year-old Florence Lee underwent surgery for periodontitis, a severe form of gum disease. And her experience was horrible.

“I had pain during the procedure, I had pain after the procedure and I was frightened,” Lee said.

When Lee learned she might need to be treated again, she was fearful of the procedure, which involves cutting into the gums in order to remove the bacteria that leads to bone loss.

Luckily, Lee learned about a new treatment for gum disease, called laser-assisted new attachment procedure (LANAP). During the procedure, doctors place a tiny fiber in the pocket between the gum and the tooth, delivering the same results with less pain.

“What it does is it targets specifically the inflamed tissue, the infected tissue and the bacteria associated with causing the periodontal destruction,” said Dr. Sam Morhaim, a periodontist at the Great Neck & Mid-Island Dental Associates in New York.

Morhaim said patients typically come in for two visits, each of which last about two hours. Comparatively, traditional surgery can take four or more sessions.

If LANAP catches on, Morhaim said it could do for dentistry what LASIK surgery did for ophthalmology. Other benefits of LANAP include reduced pain, swelling and sensitivity, in addition to the fact that no cutting or sutures are involved in the procedure. Furthermore, it offers great results.

“”We’re starting to see regeneration of the lost tissues, which is very exciting for us, because now we can offer

Lee decided to undergo the LANAP procedure and said that after the surgery, she didn’t experience any pain. She was even able to drive herself home afterwards, because the procedure requires only local anesthesia. technology that is super conservative compared to our conventional means with less downtime,” Morhaim said.

“I would recommend anyone who was having (periodontitis) and (was) fearful of it would have laser (treatment) and not any other procedure,” Lee said.

While insurance plans typically cover LANAP, only a few doctors in the country are performing the procedure.

Source: inagist

Hide and seek: Brain cancer cells ‘lose’ mutations to evade cancer drugs

Brain cancer can play a deadly game of hide and seek.

A new study published in the journal Science has revealed that brain cancer cells can actually evade many current cancer drugs – by temporarily scaling down a certain genetic mutation that the drugs target. Additionally, once therapy has stopped, the cancer cells can then intensify the mutation once again.

According to the researchers, this study has huge implications for the future treatment of glioblastoma multiforme (GBM) – a brain cancer that is in desperate need of effective therapies.

“It’s one of the most common types of adult brain cancer and one of the most lethal of all types of human cancers,” study author Dr. Paul Mischel, a member of the Ludwig Institute for Cancer Research and a professor in the department of pathology at the University of California, San Diego, told FoxNews.com. “And there are a number of real challenges [in treatment]. There are no good early detections for the disease, and the tumor cells invade through the brain, so it’s almost completely impossibly to surgically remove the entire tumor.”

Mischel also noted that GBM becomes resistant to modern chemotherapy and radiation treatments relatively quickly.

Recently, alternative cancer drugs have emerged that are capable of targeting specific genetic mutations in cancer cells. About 60 percent of GBM cells express a mutated variant of the epidermal growth factor receptor – also called EGFRvIII.  Found in the extrachromosomal DNA of these cancer cells, EGFRvIII helps to promote tumor growth and proliferation, and many targeted therapies work by targeting and suppressing this specific mutation.

However, these drugs ultimately haven’t translated to better outcomes for GBM patients.

“You would think that drugs that are used to target that receptor would be effective, but the results have been very disappointing,” Mischel said.

In order to better understand why, Mischel and his research team analyzed the genetic makeup of GBM tumors. When they treated the cancer cells with targeted therapies, they found that the pieces of mutant EGFRvIII DNA, which normally float outside the cancer’s chromosomes, temporarily jumped onto an obscure chromosome — where they could “hide” from the drugs. Then, once they ceased treatment, the DNA pieces removed themselves from the chromosome and floated freely once again, promoting cancer cell proliferation.

So in essence, the cancer cells were able to “shut down” the expression of the mutation while the cancer drugs were present in the body.

“This was a real surprise,” Mischel said. “…Those pieces of extra chromosomal DNA ‘disappeared’ when treated with the drug. It’s truly a hide-and-seek mechanism, because when the drug was removed, it jumped back off the chromosome.”

Mischel said it is still not understood exactly how the cancer can detect the presence of the drugs in the body, but the researchers have a few preliminary ideas.

“The mechanism by which the DNA is sensing the drug is really not understand,” Mischel said. “But the theory is that the DNA is sensing the signals that are being sent indirectly by the drug.”

The study’s findings help better explain why GBM becomes resistant to targeted therapies and it may help doctors determine a better course of treatment for patients. Mischel argued that the discovery could completely change how physicians treat patients with other types of cancer as well.

“It’s really a complete paradigm shift in how we begin to think about treating people with targeted therapies,” Mischel said. “…This find has big implications for this disease, because other types of cancers have these mutations present on extra chromosomal DNA….How we dose these tumors could change. The data we have in hand would suggest a very different type of dosage for targeted cancer treatment.”

Source: all voices

New Artificial hearts won’t beat

The human heart beats 60 to 100 times a minute, more than 86,000 times a day, 35 million times a year. A single beat pushes about 6 tablespoons of blood through the body.

An organ that works that hard is bound to fail, says Dr. Billy Cohn, a heart surgeon at the Texas Heart Institute. And he’s right. Heart failure is the leading cause of death in men and women, killing more than 600,000 Americans every year.

For a lucky few, a heart transplant will add an average of 10 years to their lives. For others, technology that assists a failing heart — called “bridge-to-transplant” devices — will keep them alive as they wait for a donor heart.

Unfortunately, more often than not, the new heart doesn’t arrive in time.

That’s why Cohn and his mentor — veteran heart surgeon Dr. O.H “Bud” Frazier — are working to develop a long-term, artificial replacement for the failing human heart. Unlike existing short-term devices that emulate the beating organ, the new machine would propel blood through the body at a steady pace so that its recipients will have no heartbeat at all.

The concept of a pulseless heart is difficult to fathom. Cohn often compares it to the development of the airplane propeller. When people started to develop flying machines, he says, they first tried to emulate the way birds fly — by flapping the wings aggressively.

“It wasn’t until they decided, ‘We can’t do this the way Mother Nature did,’ and came up with the rapidly spinning propeller that the Wright Brothers were able to fly,” Cohn says.
The idea of an artificial heart goes back decades.

Frazier began medical school in what he describes as “the Kennedy Era.”

“We were going to the moon; we were going to achieve world peace,” and Frazier wanted to develop the first artificial heart. In 1968, he left for Vietnam as a flight surgeon. Thirteen months later, his helicopter was shot down, and he nearly died.

“That experience convinced me I should stick to something more meaningful for the rest of my life.”
That he did. The veteran surgeon, inventor and researcher has devoted the last half century to developing technologies to fix or replace the human heart, the most notable of which is the newest generation of continuous flow Left Ventricular Assist Devices, known as LVADs.

Modeled after an Archimedes Screw, a machine that raises water to fill irrigation ditches, the continuous flow LVAD is a pump that helps failing hearts push additional blood through the body with a rapidly spinning impeller.

Today, the continuous flow LVAD has been implanted in 20,000 people worldwide, including former Vice President Dick Cheney before he received a heart transplant nearly two years later.

In some cases, the LVAD’s turbine has essentially taken over the pumping process entirely from the biological heart. In these instances, the implant recipient barely has any pulse at all.

Observing what happened in these patients led Frazier to one compelling question: If the LVAD can take
over for a weakened heart, could it replace the organ entirely?

In 2004, Frazier asked Cohn to collaborate on a new research project. Cohn’s interest in heart surgery dates back to when he was a young boy reading articles about world-renowned heart surgeons Dr. Michael E. Debakey and Dr. Denton Cooley, who developed and played a role in the transplant of the first artificial heart in a human in 1969.

Now the holder of some 70-odd U.S. patents, Cohn says his work with Frazier to build an artificial heart is the most ambitious project of his career.

The surgeons set out to combine two LVADs to replicate the functions of the heart’s right and left ventricles. Using two commercially available LVAD turbines, Frazier and Cohn combined the devices with plastics and other material used for implants: hernia mesh, Dacron cardiovascular patches and medical silicone. Everything met FDA standards, but Cohn describes the final product as “rather kludged together.”

The surgeons tested their invention by installing it in around 70 calves. All of the cows produced a flat line on an EKG, which measures heart electrical activity, yet they stood, ate and walked around, paying seemingly no notice to a small technicality: They had no heartbeat.

In order for the FDA to approve the device for clinical trials, the calves needed to live for at least one month. Cohn and Frazier’s device trumped these standards, with many calves living healthily for full 90-day studies.

Cohn and Frazier were encouraged, and in March 2011, put their artificial heart into a human patient.
Craig Lewis, 55, was admitted to the Texas Heart Institute with amyloidosis, a rare autoimmune disease that fills internal organs with a viscous protein that causes rapid heart, kidney and liver failure. Without some intervention, Lewis would have been dead in days. Frazier and Cohn decided it was the right moment to test their device and the surgeons undertook the lengthy procedure.

Less than 48 hours later, Lewis was sitting up, talking and using his laptop. When doctors put the stethoscope to Lewis’s heart, all they heard was a steady whir of what sounded like a boat propeller. Lewis survived for six weeks until his failing kidneys and liver got the best of him and his family asked doctors to unplug the device.

Source: CNN

Now, ‘biopen’ to draw new bones inside body

Australian scientists have developed a hi-tech handheld ‘biopen’ that can enable surgeons to draw new bone material onto seriously injured people.

The ‘bio pen’ contains stem cells and growth factors, and could eliminate the need to harvest cartilage and grow it for weeks in a lab.

The pen-like device developed at the University of Wollongong (UOW) will allow surgeons to design customised implants on-site and at the time of surgery.

The BioPen will give surgeons greater control over where the materials are deposited while also reducing the time the patient is in surgery by delivering live cells and growth factors directly to the site of injury, accelerating the regeneration of functional bone and cartilage, scientists say.

The BioPen works similar to 3D printing methods by delivering cell material inside a bio-polymer such as alginate, a seaweed extract, protected by a second, outer layer of gel material.

The two layers of gel are combined in the pen head as it is extruded onto the bone surface and the surgeon ‘draws’ with the ink to fill in the damaged bone section.

A low powered ultra-violet light source is fixed to the device that solidifies the inks during dispensing, providing protection for the embedded cells while they are built up layer-by-layer to construct a 3D scaffold in the wound site.

Once the cells are ‘drawn’ onto the surgery site they will multiply, become differentiated into nerve cells, muscle cells or bone cells and will eventually turn from individual cells into a thriving community of cells in the form of a functioning a tissue, such as nerves, or a muscle.

The device can also be seeded with growth factors or other drugs to assist regrowth and recovery, while the hand-held design allows for precision in theatre and ease of transportation.

The BioPen prototype was designed and built using the 3D printing equipment in the labs at Wollongong and was handed over to clinical partners at St Vincent’s Hospital Melbourne, led by Professor Peter Choong, who will work on optimising the cell material for use in clinical trials.

The BioPen will help build on recent work by researchers where they were able to grow new knee cartilage from stem cells on 3D-printed scaffolds to treat cancers, osteoarthritis and traumatic injury.

“This type of treatment may be suitable for repairing acutely damaged bone and cartilage, for example from sporting or motor vehicle injuries,” Choong, Director of Orthopaedics at St Vincent’s Hospital Melbourne said.

Source: Deccan Chroicle

 

New affordable way to stabilize haemoglobin discovered

A research team has found a way to stabilize hemoglobin, the oxygen carrier protein in the blood, a discovery that could lead to the development of stable vaccines and affordable artificial blood substitutes.

The new approach by UConn research team involves wrapping the polymer poly (acrylic acid) around hemoglobin, protecting it from the intense heat used in sterilization and allowing it to maintain its biological function and structural integrity.

In addition to having potential applications in the stabilization of vaccines and development of inexpensive artificial blood, the stabilizing polymer also allows vaccines and other biomedical products to be stored for longer periods without refrigeration. It could also have applications in biomaterials, biosensors, and biofuels.

‘Protein stability is a major issue in biotechnology,’ says Challa V. Kumar, UConn professor of chemistry and biochemistry and the primary investigator on the project. ‘What we’ve done is taken this protein molecule and wrapped it up in a polymer chain in order to stabilize it. In thermodynamics terms, we have restricted the entropy of the denatured state of the protein and stabilized it beyond our expectations.’

‘The system also exhibits a high degree of reversibility. The protein can be denatured and renatured many, many times. This is the very first example of its kind in the literature of all protein science. No one has ever been able to achieve this kind of stability for proteins.’

As part of its research, the team chose to examine the feasibility of using hemoglobin as an artificial blood substitute. Hemoglobin, when extracted from blood, breaks down and is toxic in its pure form.

Since hemoglobin is the critical oxygen carrier protein in blood, Kumar and his team are looking at ways of stabilizing hemoglobin in its natural form so that it retains its activity and stays harmless when administered as a transfusion agent. This could lead to a new substitute for human blood, which is frequently in short supply. Blood shortages are expected to get worse in coming years, as more and more people in the world are likely to need blood transfusions, Kumar said

Source: Health India

 

Monthly injection to prevent Alzheimer’s in five years

Scientists are hopeful of a breakthrough in dementia within five years – with drugs that could be given to prevent disease

Scientists are hopeful of a breakthrough in dementia within five years – with drugs that could be given preventively to delay the onset of disease.

Researchers say a new drug has shown some promise in patients with mild dementia, and might be yet more effective if given to those at risk of disease long before they show any symptoms.

Dr Eric Karran, director of research at Alzheimer’s Research UK, said scientists were “full of hope” that a breakthrough in drug therapy to prevent dementia could come within five years.

If further trials on the drug succeed, it could mean that those with a family history of dementia are given monthly injections of the drug a decade before any signs of disease show – in the same way that millions of people now take statins to ward off heart disease, he said.
Speaking ahead of a G8 summit next week on dementia, Dr Karran said trials have suggested that a drug called solanezumab may delay the onset of disease, halting problems with brain function and behaviour in those with mild dementia.

The studies originally tested the drug on patients with mild to moderate dementia, where the treatement did not achieve effective results.
But when analysis examined the impact of the drug only on those with mild dementia, researchers found it had an effect both on their daily behaviour and the functioning of their brain and memory.
Now researchers in the US are recruiting to a new study which will examine the impact only on patients with mild dementia.

If the trials prove that the drugs work, it would be “logical” to prescribe them to patients preventively, Dr Karran said, given that changes in the brain associated with dementia occur as far as a decade before symptoms are shown.
Dr Karran said the promise from the drug, and from two other treatments now undergoing trials, left him optimistic that a breakthrough is on the horizon, despite years of disappointment in the field of dementia research.

He said: “I am full of hope that we are going to have a breakthrough in five years.”
If trials on sufferers with mild dementia succeed, “there is a logic” to use the drug therapies at least a decade earlier, to prevent the onset of dementia, he said, in the same way that statins have been widely prescribed for those at risk of heart attacks and strokes.

“That’s exactly the path that blood pressure-lowering agents have taken – people taking them before they have a stroke,” he said. “It’s the path that’s been taken with statins which first showed efficacy against the disease and then you go earlier. That has to be the pathway we take. There is very very good human genetic data which shows that if you can effect this amyloid early on – and only modestly – you have the potential to dealy the onset of that disease very significantly indeed.”

Currently, the only drugs used for dementia can mask symptoms, but do not delay the onset of disease.
Brain scans have found that changes in the brains of patients with diseases such as Alzheimer’s can occur a decade before you have symptoms.

Providing people with anti-body drugs five or 10 years before the condition would otherwise develop could have a “drastic impact” on prevalence of disease, he said.
Dr Doug Brown, director of research and development for the Alzheimer’s Society, said: “If we can delay the onset by five years we could probably cut the numbers with dementia in yhalf – and recent research evidence suggests this could be a possibility.”

Prof Nick Fox, from the Institute of Neurology, at University College London, said that preventing disease before symptoms were present offered the best “window of opportuntity” to halt the impact of disease.

He said: “Let’s just hope that we can slow the devastation at the stage when there is much to save … rather then when we are bed bound or mute – because that is the end result of these dreadful diseases.”
Next week science and health ministers from G8 countries will meet in London for the first ever G8 dementia summit.

Charities called on them to draw up a shared global plan to tackle dementia, and invest heavily in research, which currently receives a fraction of the funds devoted to cancer in this country.
David Cameron has said he will use the UK’s presidency of the G8 to lead coordinated international action.

Source: Telegraph