GoogleNews.com, May 20, 2009, by Maggie Fox — WASHINGTON, (Reuters) – U.S. health officials said on Wednesday they are considering starting the vaccination campaign for seasonal flu earlier this year to make room for a possible second round of shots against the new H1N1 flu.
The United States also reported its eighth death from the new swine flu virus, in a patient in Arizona.
“If possible we do want to have an earlier rollout of seasonal vaccine,” Dr Daniel Jernigan of the U.S. Centers for Disease Control and Prevention told reporters in a telephone briefing.
He said the CDC would work with manufacturers of influenza vaccines and a committee of doctors that advises on vaccination policy to see if that would be possible and desirable. Flu vaccination usually starts in September in the United States and peaks in November.
Vaccine experts agree it would be better to launch a second round of vaccinations against the new H1N1 strain instead of trying to add it to the seasonal flu vaccine or replacing one of its three components with the new H1N1 virus.
“The production of seasonal flu vaccine is nearly complete,” Jernigan said.
On Wednesday, the CDC reported 5,710 confirmed and probable cases of the new H1N1 strain in 48 states, with eight deaths. Globally, more than 10,000 cases have been confirmed with 80 deaths, most in Mexico.
Jernigan said it is clearly still affecting younger people more in the United States — 40 percent of the 247 people who have been hospitalized with serious illness from the new H1N1 strain are aged 19 to 49, he said.
Seasonal influenza puts 200,000 Americans in the hospital every year and is a factor in 36,000 deaths, but 90 percent are over 65 or have chronic diseases such as asthma and heart disease that make them more vulnerable. With the new H1N1 flu, Jernigan said, 70 percent of hospitalized patients have an underlying condition.
AGE 50 ADVANTAGE
Only 13 percent of people who have been hospitalized with swine flu are over 50, Jernigan said, and he said tests of blood among the general population may eventually show whether people born before 1957 may have been infected with an older H1N1 strain that was close to the swine flu strain. They may then have some lifetime resistance to the new strain, he said.
In 1957, a new flu strain called H2N2 caused a pandemic and became the predominant strain of flu circulating globally. There is a seasonal H1N1 strain that still circulates but it is only a very distant relative of the new swine flu strain.
Seasonal flu is also still infecting people but Jernigan said 78 percent of U.S. cases tested for influenza are the new H1N1 strain. The CDC and state health departments are only doing targeted testing and say the true number of flu cases across the country is likely more than 100,000.
Jernigan said many flu patients are getting antibiotics — which prevent so-called secondary infections — but not enough are getting the antiviral drugs Tamiflu and Relenza, which are known to help symptoms.
The new flu seems to be about as contagious as seasonal flu, Jernigan said.
He was unable to say why so many more people are infected in the United States than in countries such as Britain, which reports 102 cases, but said there may have been more U.S. travelers to Mexico and more time for the virus to spread.
(Editing by Eric Beech)
Pre-1957 Flu Exposure May Protect Against H1N1 Swine Flu
Reviewed by Louise Chang, MD
CDC researchers have detected antibodies in the blood of older people that neutralize the new flu bug now sweeping the nation, Daniel Jernigan, MD, MPH, deputy director of the CDC’s flu division, said today in a news conference.
“We infer from that, there is some level of protection,” Jernigan said. “But to prove protection, we look at the effect [the virus has] on the population, and at this point we don’t have that information.”
Why is 1957 a key year? Every flu season after it first appeared, the deadly 1918 pandemic H1N1 flu bug circled the globe. Each year, the virus acquired changes that made it different from the original virus. But in 1957 there was a new pandemic, this time with an H2N2 virus. The new virus took the place of the old H1N1 bug.
“And so when we talk about the pre-1957 exposures, we are referring to those exposed to the past H1N1 virus that went away in 1957,” Jernigan said. “The farther back you go in time, the more likely you are to have been exposed to an H1N1 virus before 1957 — and exposure to that virus many years ago may allow you to have some reaction to the new H1N1.”
The new H1N1 swine flu bug is much different from the 1918 H1N1 virus. It’s also much different from the H1N1 seasonal flu virus that still circulates. But something about that pre-1957 bug seems to have left older people with antibodies that neutralize the new flu — and might offer some protection against it.
Swine Flu Hits Youths Hardest
Whether or not ancient antibodies are protective, many older people are getting sick from the new flu. Some of these illnesses are severe: 13% of people hospitalized with swine flu are 50 or older. And the number of H1N1 cases among older people is increasing.
But H1N1 swine flu is hitting young people hardest. More than 60% of cases are in 5- to 24-year-olds.
Remarkably — since this is usually the healthiest age group — 37% of people hospitalized with swine flu are 19 to 49 years old. The median age of a person hospitalized with the new flu is 19.
Those aged 5 to 18 make up 29% of swine flu hospitalizations. Because so many cases of H1N1 swine flu have been transmitted in schools, it’s possible that older people only seem to be protected because they’ve had less contact with younger people.
In past flu pandemics, however, the same pattern has emerged: the illness tended to strike young people hardest.
Jernigan said that the CDC will soon release a detailed report on the neutralizing antibody study.
Meanwhile, the new flu continues its spread while the seasonal flu wanes. Jernigan said that nearly 80% of people who test positive for flu now turn out to have the new H1N1 bug.
Window, please: The model shows the flow of fluid particles from two contaminated passengers during a sneezing simulation. The path of the particles from one passenger is shown in blue, the other in green.
A new study suggests that single particle detectors should be used to help control pandemics.
MIT Technology Review, May 20, 2009, by Brittany Sauser — Each year, an estimated 600 million passengers fly in the United States, and of those, roughly 350,000 are international travelers, according to the Bureau of Transportation Statistics. This leaves commercial airliners vulnerable to biological contamination and makes the spread of disease a real threat.
Now researchers at the MITRE Corporation have conducted a study that, for the first time, looks at the particle distribution of exhaled breath to better understand how airborne pathogens spread in aircraft cabins, and how best to detect the particles that could contain viruses.
“The most important point is that if you want to detect infectious viruses from exhaled breath, you need a biosensor with single particle detection,” says Grace Hwang, principal investigator of the study and a lead biosensors scientist at MITRE. “Most commercially available biosensors need 10 million viruses before they can inform the user that a virus of concern has been caught, and usually diagnosis takes three to four hours.” This is problematic, adds Hwang, since most viruses are found in low concentrations when expelled from an infected person, and many flights do not last more than 90 minutes.
In addition, the researchers determined that most particles stayed suspended in the aisle, so when booking a trip, take a window seat, says Michael Harkin, a member of the MITRE team, who presented the research at the 2009 IEEE Conference on Technologies for Homeland Security. Particles also did not travel far outside the contaminated row, and if they did, it was across the row. Previously, it was thought that contaminants would travel front to back, or back to front. “There was minimal exposure to the row in front of, and to the window passengers in, [the contaminated row],” says Harkin. Thus, the researchers concluded that biosensors should be placed at the ceiling of the aircraft cabin, about every four rows.
“Our goal is to capture the infected cases coming into the U.S. before people are symptomatic,” says Hwang. “That will buy time to defend against a pandemic spread, and the economic benefits would be enormous.”
The need for such sensors was evident in the 2003 outbreak of Severe Acute Respiratory Syndrome (SARS), which originated in an Air China flight from Hong Kong to Beijing, spread through 18 countries, and resulted in 774 fatalities. Asian economies suffered $11 billion in damages. “If you have an appropriate device to detect pathogens on aircraft, which is a huge challenge, then you are prepared for a deadly outbreak,” says Byron Jones, associate dean for research and graduate programs at Kansas State University, and director of its engineering experiment station. “We have seen how the swine flu spreads, and while it has turned out to be a mild disease, if it were something deadly and contagious like typhoid fever, it could be a different story.” Jones is also part of a team of experts at the Air Transportation Center for Excellence currently looking into the healthfulness of aircrafts.
The first case of H1N1 occurred in April, and since then, there have been close to 80,000 flights within North America and only one air-travel case under investigation. The risk of catching H1N1 via airliners is low but present, adds Mark Gendreau, a senior staff physician and vice chair of emergency medicine at Lahey Clinic, in Burlington, MA, and an associate professor of emergency medicine at Tufts University School of Medicine, in Boston.
To conduct the study, MITRE researchers used a computational fluid dynamics model to investigate the extreme coughing and sneezing situations of seven passengers known as “super spreaders.” (Super spreaders cough and sneeze at a rate of 50 times per hour.) The software modeled the aircraft ventilation of a Boeing 767 airliner cabin, as many prior studies have done to determine the optimal sensor placement. But that does not tell you anything about the number of particles exhaled, says Hwang. The researchers found the fluid volume in saliva and divided it by the number of particles from a sneeze and a cough to get a distribution of particles. This, coupled with the data from the computational fluid dynamics model, allowed the researchers to compute the number of collectable bioparticles, says Hwang.
The researchers found that contamination traveled farther in sneezing than in coughing cases, and that particles from the two window-seat passengers entered the outlet vents quickly and were the least circulated in the cabin. In contrast, particles from the three passengers in the center row lingered and were not transported as effectively as particles exhaled from passengers in the two aisle seats of the aircraft’s two outside rows.
For the purposes of the study, the researchers assumed that they had approximately 90 minutes to detect a virus. That’s about the length of time that it takes to fly from Vancouver to San Francisco–a flight that often carries passengers who have just arrived from Asia.
Gendreau cautions that while the study did use sophisticated modeling techniques, the researchers did make assumptions about the super spreaders: “We don’t have a good idea of super spreaders’ characteristics.” However, the Center for Disease Control is putting a lot of money into addressing such knowledge gaps, and MITRE’s study is a nice start, says Gendreau.
The MITRE researchers also determined that to detect the presence of viruses, ultrasensitive biosensors are necessary. “The particles are small and dispersed, so you need detection down to the single particle level,” says Harkin. Currently, there are no commercial biosensors that can do that. Hwang and researchers at the University of California, San Diego, are building a novel surface plasmon polariton biosensor that has performed single molecule resolution in the laboratory. The sensor uses a plasmonic substrate with a gold surface that is perforated with nanometer-wide holes. A glycoprotein is attached to the gold surface inside each hole, and the researchers monitor the resonance of the photons that get transmitted through the gold nanohole. When a pathogen like H1N1 or H1N5 binds to the glycoprotein, the resonance changes. The work was featured in Nature earlier this year.
By Michael Smith, North American Correspondent, MedPage Today
Published: May 20, 2009
Reviewed by Zalman S. Agus, MD; Emeritus Professor
University of Pennsylvania School of Medicine.
TORONTO, May 19 — Pneumonia associated with community-acquired methicillin-resistant staphylococcus aureus (MRSA) often appears after a bout of influenza-like illness, Atlanta researchers said.
The disease manifests itself as a severe, necrotizing pneumonia with substantial morbidity and mortality, according to Alicia Hidron, M.D., of Emory University School of Medicine and colleagues.
Patients from the community who have sepsis and multilobar infiltrates, are coughing blood, and have a low white cell count are suspects for the condition, Dr. Hidron and colleagues wrote in the June edition of The Lancet Infectious Diseases.
Based on two case studies and a literature review, the researchers concluded that the standard treatment for community-acquired pneumonia will probably be “inappropriate.”
Instead, they said, treatment should include an antibiotic with activity against MRSA, such as vancomycin (Vancocin) or linezolid (Zyvox), as part of the empirical therapy until culture results are available.
In addition, clinicians may find — as the researchers did in the two reported cases — that patients fail to improve until the addition of a drug geared to toxin suppression, such as clindamycin (Cleocin).
But, they noted, “the best treatment of this partly toxin-mediated disease has not been clearly defined.”
In both cases that Dr. Hidron and colleagues described, the patients presented with shortness of breath, fever, chills, and cough. Both had suffered an influenza-like illness a week before the onset of symptoms…………………………….
Points Worth Noting
Methicillin-resistant staphylococcus aureus (MRSA) infection — long associated with acquisition in healthcare settings — is more and more often acquired in the community.
This study suggests that one of the manifestations of the infection is a severe form of pneumonia that should be treated differently than commonly seen community-acquired pneumonia.
Primary source: The Lancet Infectious Diseases
Hidron AI, et al “Emergence of community-acquired methicillin-resistant Staphylococcus aureus strain USA300 as a cause of necrotising community-onset pneumonia” Lancet Infect Dis 2009; 9: 384-92.
Characteristics of Hospitalized Swine Flu Patients Revealed
By Todd Neale, Staff Writer, MedPage Today
Published: May 19, 2009
LITTLE FALLS, N.J., May 19 — Fever, vomiting, pneumonia, and underlying health issues are all common findings in patients hospitalized with 2009 H1N1 (swine) flu, according to the CDC.
At latest count, there were 5,469 confirmed or probable cases of infection with the new virus in the U.S., with six deaths, but only a very small percentage have required hospitalization, the agency said.
To explore the characteristics of those who are need to be hospitalized, CDC researchers and public health officials from California examined all 30 patients admitted in that state as of May 17.
The cases spanned a wide range of ages — from 29 days to 89 years (median 27.5 years) — and spectrum of disease severity, according to the report presented in a Morbidity and Mortality Weekly Report early release.
All but one patient presented with fever. Other common symptoms included cough and shortness of breath.
Nearly half (46%) presented with vomiting, which is unusual for infection with seasonal influenza viruses, according Anne Schuchat, M.D., interim deputy director of the CDC’s science and public health program. She discussed the MMWR report on a conference call with reporters.
Evidence of pneumonia was seen on lung X-rays of 60% of the hospitalized patients, 20% required admission to the intensive care unit, and 13% were placed on mechanical ventilation.
Only half received antiviral treatment with oseltamivir (Tamiflu).
Dr. Schuchat said the CDC is recommending that all patients hospitalized with the new H1N1 virus receive antiviral treatment, even if they are admitted more than 48 hours after symptom onset.
Nearly two-thirds (64%) of the patients had at least one underlying medical condition that put them at risk for complications from the flu.
These conditions included chronic lung disease, conditions associated with immunosuppression, chronic heart disease, diabetes, and obesity………………………
|Free flow: These images show a patient’s left ventricle before treatment (on the left) and after (on the right). The top images were captured after exercise and the bottom ones show the ventricle at rest. Increased blood flow is indicated by more orange.
Credit: Leiden University Medical Center
A new treatment may help angina sufferers who are resistant to surgery and medication.
MIT Technology Review, May 20, 2009, by Michael Day — Injecting the hearts of angina sufferers with cells extracted from their own bone marrow can reverse the condition and relieve its symptoms, a new study suggests.
The Dutch cardiologists behind the placebo-controlled study say that the results may lead to radical new treatments for patients for whom surgery and medication bring little or no relief from this painful and debilitating condition, which results from narrowed arteries that cannot supply enough blood to the heart during exercise. All 50 subjects involved in the study were resistant to existing treatments.
Three months after being given the injections, patients’ hearts were less starved of blood, and they were able to exercise more, researchers report in the latest issue of the Journal of the American Medical Association.
Lead researcher Douwe Atsma, a cardiologist at Leiden University Medical Center, in the Netherlands, hopes that follow-up studies, which are currently in progress, will also reveal lower death rates among those who received the treatment.
Atsma’s team first fed catheters through patients’ femoral veins, up into the aorta, and then into the heart’s left ventricle–the chamber that pumps oxygen-rich blood back in the circulation. By touching an electro-sensitive tip around the chamber’s surface, the researchers were able to locate areas of low electrical activity, where diminished blood supply had caused cells to die. They built up a “map” of the left ventricular surface of all 50 patients.
The researchers then took bone marrow from participants’ hips and extracted the mass of mononuclear cells–an ill-defined mix of stem cells and progenitor cells.
In 25 of the patients, the researchers injected around 100,000 cells into angina-affected areas on the ventricular surface, using a modified form of the same catheter. The remaining 25 patients received a placebo injection of saline.
Three months after the treatment, more catheter tests showed that the average number of diseased grid areas in the hearts of treated patients had fallen from 4.2 to 1.8, or 57 percent. In patients given the placebo, the number fell from 3.8 to 3.1–a significantly smaller 18 percent reduction.
Bone-marrow recipients were also able to expend more energy on an exercise bike after three months: 114 kilocalories, compared with 107–a small but significant change. Placebo patients experienced an improvement of just 101 kilocalories compared with 99.
Earlier trials in which researchers sought to treat heart-attack victims with their own bone-marrow cells produced mixed results. Some studies found moderate improvements in a few measures of heart function, but none showed a clear health benefit.
Atsma notes, however, that angina is very different from a heart attack. “People who’ve just had a heart attack need instant methods to remove blockages, as tissue starts to die and all sorts of inflammatory processes are being unleashed,” he says. “It may be that cell injections are best suited to the treatment of chronic heart conditions such as angina. In using this method to treat angina, you are treating the underlying cause of a chronic condition over weeks and months.”
Atsma hopes that follow-up research will demonstrate that angina patients who receive the treatment are less at risk from associated conditions, particularly abnormal heartbeats, or arrhythmias, which kill thousands every year. He says that the small but significant improvement in blood supply seen in the placebo group suggests that the act of pricking the heart lining may encourage growth of new blood vessels.
The researchers are now investigating which types of bone-marrow cell best help repair the heart. One theory is that a type of progenitor cell called a mesenchymal cell, which gives rise to muscle and bone tissue, might encourage the growth of new blood vessels by releasing growth factors. “But the truth is we don’t really know which cells–or which combination of cells–are having the effect,” Atsma says.
Stefan Janssens, a cardiologist and research scientist at University Hospital Gasthuisberg, in the Netherlands, is also investigating bone-marrow treatment for heart disease, and he says that the study succeeded in demonstrating that cell injections increase blood supply to the heart. “This is a good study, and it’s important that it’s randomized and double-blinded,” he says.
But Janssens also notes that it sheds little light on the exact mechanism of the treatment. “The injected cells are probably encouraging the growth of new blood vessels indirectly by producing growth factors. But it’s not possible to rule out that they are improving the condition of old vessels.”
Janssens says that boosting blood supply alone would not help the huge number of patients with heart failure, a deadlier condition in which injured hearts swell and pump blood less effectively. “For these patients, we need to know which cells will allow them to grow new heart muscle,” he says.
Promise for Parkinson’s: Twelve months after receiving an experimental gene therapy for Parkinson’s disease developed by Neurologix, this patient has reduced metabolic activity (indicated in blue) in the brain area most damaged by the disease.
Credit: The Lancet
More-invasive therapies show promise for treating Parkinson’s.
MIT Technology Review, May 20, 2009, by Emily Singer — The brain has long presented a special challenge to drug developers: tightly enclosed by the blood brain barrier, it remains locked to many therapies delivered orally or intravenously.
However, thanks to more-precise methods of targeting the brain, advances in brain imaging, and the growing popularity of implanted stimulators for treating neurological diseases, the brain is no longer off limits. This is highlighted by a number of new clinical trials involving Parkinson’s patients, in which a therapeutic gene or another treatment is delivered directly to a specific part of the brain.
“My belief is that we’re entering into an era where instrumentation in the brain will become routine, not just for Parkinson’s, but for myriad central nervous system disorders,” says Howard Federoff, a neurologist and executive dean of the School of Medicine at Georgetown University, in Washington, DC. “I anticipate that delivery technologies will drive the development of new therapeutics and the repurposing of existing treatments, where they could be delivered directly to the part of the brain where it’s needed at the appropriate dose.”
Drugs that replace the chemical messenger dopamine have been very effective in treating Parkinson’s disease, but the benefits of these medications frequently decline over time. About a third of the more than half a million Parkinson’s patients in the United States are in the later stages of the disease and resistant to medication. One option for these patients is deep brain stimulation (DBS)–a surgical procedure in which an electrode is implanted directly into the brain. While the exact mechanism underlying the benefits of DBS is unknown, scientists believe that the electrical pulses sent to the damaged part of the brain override the abnormal neural signaling that triggers tremors, rigidity, and other symptoms of Parkinson’s.
More than 40,000 people worldwide have undergone the procedure–a figure that reflects its relative safety and efficacy, as well as a growing acceptance of more-invasive treatments for neurological disease. Many academic researchers and some startup companies are now searching for new alternatives that also directly target the brain, but which involve shorter surgical time and a better prognosis. While DBS is effective in reducing the symptoms of Parkinson’s disease, it does not cure it.
One approach is to correct abnormal activity with gene therapy rather than with electricity. Neurologix, a biotechnology company based in Fort Lee, NJ, has developed a novel gene-therapy treatment that is now being tested in clinical trials. The therapeutic gene involved, called GAD, codes for an enzyme that catalyzes production of the chemical messenger GABA. (Dopamine is a chemical precursor to GABA, and the cells that produce it are lost in Parkinson’s.) “By delivering the gene, you can bypass the area affected by cell death,” said John Mordock, the company’s chief executive officer, at the Neurotechnology Industry conference in San Francisco last week. “It’s taken up into the cells, allowing them to express GABA, restoring balance to the circuit.”
As with DBS, surgeons first drill a small hole in the skull, then insert an electrode to search for a small brain area called the subthalamic nucleus, which emits a characteristic pattern of electrical activity. But the electrode is then removed, and a small catheter is inserted, and a small pump infuses the genetic material into the brain. The specialized drug-delivery device was developed by Medtronic, a medical-device company that also markets DBS systems. Mordock says that Neurologix plans to market the device and the gene-therapy treatment together.
In a small trial in which every Parkinson’s patient received the same treatment, they showed a 29 percent improvement in motor function. Researchers have begun a larger, blinded trial and expect to have preliminary results later this month.
A second approach is to use gene therapy to slow or prevent cell death in the brain area ravaged by Parkinson’s. Federoff is overseeing an academic consortium planning human tests of a gene therapy that codes for a protein called GDNF (glia-derived neurotropic factor), which enhances neuronal survival. The therapy is also delivered via a catheter in the brain, but the infusion is driven by a small pressure gradient, a technique known as convection-enhanced delivery. Federoff, who is also the founder of Canadian startup MedGenesis Therapeutix, which is commercializing the technology, says that this allows for more-targeted delivery.
In addition to convection-enhanced delivery, surgeons will use real-time neuroimaging to make sure that the gene therapy is delivered as precisely as possible. Scientists can add a labeled marker to the gene-therapy solution, which can then be seen on CT or MRI scans and used to visualize the diffusion of the molecules in the brain. Researchers have already used this technique to deliver therapies to patients with brain cancer.
In addition to cancer, Parkinson’s disease will likely be the first to be treated using these approaches: scientists know which part of the brain is most damaged and can design therapies accordingly. (Alzheimer’s disease, in contrast, has a much more diffuse effect on the brain.)
Success with Parkinson’s could pave the way for treating other disorders. “As we learn more about the biology of these disorders and develop more treatment compounds, opportunities will expand with the ability to deliver drugs locally,” says Russell Lonser, chair of the Surgical Neurology Branch of the National Institute for Neurological Disorders and Stroke, in Bethesda, MD.
Gene therapy does have its downsides compared with DBS, however. “DBS can be turned off, catheters can be removed, and patients can then be brought back to their basal state,” says Federoff. “We believe that gene delivery is lifelong.”
Pain relief: Scientists at MicroTransponder are developing a novel neuro stimulator to treat chronic pain. Small electrodes (blue circles) are injected near the spinal cord, and a PDA controls an external coil on the surface of the skin, powering the electrodes.
RFID technology allows neural stimulators to get really small
MIT Technology Review, May 20, 2009, by Emily Singer — A tiny injectable implant, smaller than a grain of rice, might one day take the place of large neural stimulators used to treat chronic pain and other neurological disorders. The novel device, under development by MicroTransponder, a Dallas-based startup, owes its small size to the use of RFID (radio-frequency identification) technology like that used to tag clothes to prevent shoplifting.
The device works similarly to spinal-cord stimulators for managing chronic pain. The idea is that the electrical jolts delivered by the device override the neural pain signals being transmitted to the spinal cord. However, the precise mechanism is not yet clear.
Existing devices have a battery and controller implanted beneath the skin, which delivers electrical pulses to a connected set of leads placed near the spinal cord. The MicroTransponder device, in contrast, is wireless and has no batteries. The implanted portion consists of small electrodes and a small coil, which is powered by an external battery-powered coil worn like a cuff on the arm or leg. The stimulation parameters are programmed via laptop or PDA and would be tailored to the individual patient.
Like some cochlear implants and other medical devices, the implant is powered with radio-frequency transmission: radio waves transmitted by the external coil generate a magnetic field in the internal coil, which powers the electrodes. Adopting technologies from the rapidly advancing RFID world has allowed the researchers to further shrink the device. “Instead of trying to transfer energy from two coupled antennas to do telemetry, which is a common approach for medical devices, RFID is geared to have very small transponders, so you don’t need a large coil,” says Joseph Pancrazio, a program director at the National Institute for Neurological Disorders and Stroke, a government funding agency, in Bethesda, MD, that has given the company small business loans.
The research is still in a very early stage. Researchers have developed a prototype device, which they are testing in rats. The device can effectively stimulate peripheral nerves in rats, although it’s not yet clear whether the electrical stimulation alleviates chronic pain. (Scientists assess chronic pain in rats by recording how much the animals eat; a rat in pain won’t eat as much.)
Some scientists are skeptical that the device will be powerful enough to deliver a therapeutic level of stimulation. “The main limitation of any electronic device small enough to be injected into the body is that it must receive enough power to operate its circuitry and provide the required stimulation parameters,” says Gerald Loeb, director of the Medical Device Development Facility at the University of Southern California, in Los Angeles. Loeb has also developed an injectable radio-powered microstimulator, which he says has encountered substantial limitations in range and power.
“We believe we can do it with less power,” says Scott Armstrong, MicroTransponder’s chief technical officer. However, he declined to give further details of the technology for proprietary reasons.
If it does prove successful, the device could have a number of applications. Researchers at MicroTransponder plan to test it as a treatment for tinnitus, a perceived ringing in the ears that is particularly common among veterans with head injuries.
|Credit: Technology Review|
America needs a Human Genome Project for personalized health care
MIT Technology Review, May 2009, by David Ewing Duncan — Recently, I discovered that my heart-attack risk is frighteningly high over the next 10 to 20 years. This alarming prognosis was achieved using technology that could potentially be good news for the health-care reform effort being attempted in Washington. Amid bailouts and numbing deficits, this kind of personalized medicine might even help save billions or possibly trillions of dollars over the next decade or two.
My heart, the nation’s economy, and health-care reform are connected through an experimental test that I took last year that delivered my dire forecast. Created by Entelos, a company that performs computer simulations to make predictions about a person’s health, the test gathered data on my cholesterol levels, a heart CT scan, a genetic profile, and more, and fed the results into a powerful computer.
What popped out is a prediction that the company claims is not only customized to my own genes and physiology, but also factors in far more variables than traditional heart-risk tests.
Entelos was on track to raise money to refine and launch its test commercially within a year or two. But in the current economic climate, sources of funding have become more difficult, delaying the final development and launch of the test.
The company is hardly alone. Other potentially promising discoveries almost ready for prime time include protein markers that can target and trace therapies for cancer, and new discoveries in fields ranging from neurological disorders to diabetes. Likewise, thousands of gene markers associated with diseases have been identified by researchers. Companies such as 23andme, deCODEme, and Navigenics offer tests for some of them, although the approach has yet to be validated by clinical testing.
What’s missing is a comprehensive plan to push these efforts to the next stage, not only in terms of science and medicine, but also in terms of patent law, regulation, ethics, and finance. What’s needed is a Human Genome Project level of focus on personalized and preventive medicine for major diseases. Let’s call it the Personalized Health Project.
The Human Genome Project cost $2.7 billion and took more than a decade to complete. A Personalized Health Project would similarly cost in the low billions and take between 10 and 20 years, although unlike the genome project, which was completed only at the end of a long process, the personalized project could begin producing results almost from the start.
The endeavor would link up genetics with promising research on the impact of environmental factors affecting disease. The Entelos model is one example of how scientists are attempting to combine these different disciplines in order to provide personalized profiles of an individual’s health future–not only risk factors for disease, but also alternative scenarios based on diet and lifestyle that can increase or decrease the likelihood of cancer, diabetes, or heart disease.
In my case, the heart-attack model provided me with three distinct scenarios over the next 20 years. First was a heart-stopping risk factor of 40 percent in 10 years that I will have a heart attack and a nearly 70 percent risk factor in 20 years. But this dire forecast only happens if I gain a modest amount of weight: about a pound a year, the average weight gain for a man over age 40. If my weight flatlines, the risk falls to only about 2 percent. If I take cholesterol-lowering statins, my risk falls to zero.
I took the Entelos test seriously enough that I dropped 10 pounds, having gained a pound a year since turning 40 (I’m now 51).
Whether my new leanness will actually save me from a heart attack has yet to be determined. Nor can I be sure that the Entelos model is accurate, because the company hasn’t run the extensive clinical trials with the thousands of patients needed to validate the test.
Once funded, Entelos would like to offer its test for less than $1,000 as volume increases. This price tag might seem high, but not if it substantially delays or prevents the need for, say, a diagnostic cardiac catheterization that costs $25,322 or a heart bypass operation that runs $85,633. The cost also has to be weighed against the $448 billion spent last year in direct and indirect costs for heart disease among the 80 million Americans who suffer from this malady.
Would a $1,000 test given to, say, people over 50 with borderline high cholesterol put off or eliminate debilitating and costly treatments?
No one knows. Nor will we know for sure unless we provide the organized push needed to find out.
David Ewing Duncan is the author of Experimental Man: What one man’s body reveals about his future, your health, and our toxic world.