Women taking tamoxifen for early-stage breast cancer who developed blood clots were more likely to carry a gene mutation for clotting than women taking tamoxifen who did not develop blood clots, according to an online study published June 16 in The Journal of the National Cancer Institute.

Tamoxifen is a widely-used breast cancer treatment after surgery for pre and post menopausal patients with hormone receptor-positive breast cancer. One of the most serious complications of tamoxifen usage is the development of blood clots, or thromboembolic events (TEs). Previous studies have shown that use of tamoxifen increases the risk of TEs in healthy women twofold, and that in women aged 50 and above, it is associated with even greater risk. The genetic mutation Factor V Leiden (FVL) is the most common inherited clotting factor mutation and also causes increased thrombosis risk.

To determine if having the Factor V Leiden genetic mutation increases the risk of thromboembolisms among women taking tamoxifen, Judy E. Garber, M.D. of the Dana-Farber Cancer Institute, and colleagues at the National Cancer Institute’s Cancer and Leukemia Group B (CALGB) looked at 412 women who received the drug as adjuvant treatment for stage I, II, or IIIA breast cancer, between January 1999 and April 2005. The women, whose median age was 64, included 141 patients who developed TEs and 271 who did not.

The researchers found that women who had experienced a thromboembolism while taking tamoxifen were nearly five times more likely to carry the FVL mutation compared with the women who did not develop a thromboembolism. This result differed from previous studies, which found no associated risk of TEs or an increased presence of FVLs among women at risk of breast cancer, but who did not actually have the disease.

The researchers concluded that the presence of breast cancer may influence the occurrence of TEs among patients taking tamoxifen. Chemotherapy is also thought to increase the risk of TEs by decreasing coagulation inhibitors and damaging vascular endothelium. However, even though half the women in this study had also received chemotherapy, the study showed no statistically significant difference in chemotherapy exposure between the women who developed TEs and those who did not. So chemotherapy, the researchers concluded, was unlikely to explain the prevalence of the FVL mutation among women with TEs in this study. The risk of TE was also associated with smoking and family and personal history of TEs.

The researchers also concluded that: “These data may prove useful to women who must decide between tamoxifen and an effective, essentially non-thrombogenic, alternative adjuvant therapy for breast cancer, such as aromatase inhibitors for postmenopausal women and gonadotropin-releasing hormone analogs or oophorectomy for premenopausal women.”

According to the authors, the study’s limitations include lack of family history data on TE and other hereditary factors leading to coagulopathies. The researchers also did not collect data on other potential TE risk factors, such as body mass index and recent surgery.

In an accompanying editorial, Jack Cuzick, Ph.D., of the Wolfson Institute of Preventive Medicine at Queen Mary University of London, said that why the FVL mutation is associated with TEs among breast cancer patients taking tamoxifen but not among people taking tamoxifen preventively “remains a mystery.”

“Continued follow-up and research on the relationship between the FVL mutation and tamoxifen, especially in the prevention setting, will be the only way to clarify these apparently contradictory settings,” Cuzick said.

Source:
Kristine Crane
Journal of the National Cancer Institute

There have been no health policies in this election campaign offering improved medical care of older Australians living in residential aged care facilities, and that’s a disgrace according to the AMA.

AMA President, Dr Rosanna Capolingua, said today that older Australians should not have to lose easy access to quality health care when they move from their homes to an aged care home.

“Their GP has been with them throughout their lives and that important doctor-patient relationship should be maintained and supported in a person’s old age, especially when they are moving into a new unfamiliar environment,’ Dr Capolingua said.

“Doctors spend a lot of time looking after the complex medical needs of people in residential aged care facilities. More than half of doctors’ time is spent managing patients’ care with families and staff, but this care is not supported by Medicare.

“Many doctors are left with the challenging choice between a waiting room full of patients, or travelling to an aged care facility to visit a patient in need of care at an aged care facility.

“Medicare insufficiently supports the aged care visit, so it is not surprising that just 16 per cent of Australian GPs visit an aged care facility more than once a week.

“Many aged care facilities do not have treatment rooms where doctors can see their patients in private, nor do they have the necessary IT support for prescribing and record keeping.

“It is vital that on-site access to GP services is built into future planning and funding of residential aged care facilities.

It’s not too late for the Coalition and Labor to put this affordable and responsible policy out there for voters to consider,” Dr Capolingua said.

The AMA wants aged care policies that:

– Introduce dedicated Medicare items that improve access to GPs and medical specialists for older Australians and subsequently improve health care delivery, health outcomes and quality of life for older Australians,

– Improve clinical management and the delivery of care in the residential aged care sector by introducing computer systems that facilitate medical records and prescribing, and which connect the GP to the residential aged care facility and to the pharmacy, and

– Make treatment rooms a standard feature of residential aged care facilities.

ama.au

UroToday – The use of PSA screening for the detection and treatment of prostate cancer (CaP) has been controversial. Two articles on this topic appear in the March 18, 2009 online edition of the New England Journal of Medicine. This article by Professor SchГ¶der and associates and the other by Dr. Andriole and colleagues are both reviewed in Urotoday.

Professor Schöder and co-authors participated in the European Randomized Study of Screening for Prostate Cancer (ERSPC), a randomized, multi-center trial of screening for CaP with cause-specific mortality as the primary endpoint. In general, men between the ages of 55-69 were randomized; 82,816 to the screening group and 99,184 to the control group. A PSA cutoff value of 3.0ng/ml was used as an indication for a prostate biopsy. Over the course of the study, an increasing number of prostate biopsy cores were used. For almost all centers, the screening interval was 4 years. Pathology was not centrally reviewed. The study was designed with a power of 86% to show a statistically significant difference of 25% or more in CaP mortality.

The mean age at randomization was 60.8 years, and 82.2% of men in the screened group were screened once or more. An average of 2.1 PSA tests were performed among screened men and overall 16.2% were positive. Compliance with the recommended biopsy was 85.8%. CaP was detected in 5,990 men in the screened group and 4,307 men in the control group, corresponding to a cumulative incidence of 8.2% and 4.8%, respectively. The positive predictive value of a biopsy was 24.1% and the cumulative incidence of localized CaP was higher in the screened group. With an average follow-up time of 8.8 years, there were 214 and 326 CaP deaths in the screened and control groups, respectively. The rates of death in the two groups began to diverge at year 7 and continued to do so. The number of men who would need to be screened to prevent one CaP death is 1,410. There were no deaths reportedly associated with the prostate biopsy.

Thus, the study reports that PSA screening is associated with a significant absolute reduction of 0.71 CaP deaths per 1,000 men an average follow-up of 8.8 years. This corresponds to a relative reduction of 20% in the rate of CaP death among men between the ages of 55 and 69 years. This study differs from the PLCO trial in that the PSA cutoff was lower at 3.0ng/ml, the study was of longer duration and the screening interval greater at 4 years.

Schröder FH, Hugosson J, Roobol MJ, Tammela TL, Ciatto S, Nelen V, Kwiatkowski M, Lujan M, Lilja H, Zappa M, Denis LJ, Recker F, Berenguer A, Määttänen L, Bangma CH, Aus G, Villers A, Rebillard X, van der Kwast T, Blijenberg BG, Moss SM, de Koning HJ, Auvinen A; ERSPC Investigators.
Collaborators: 156
N Engl J Med. 2009 Mar 26;360(13):1320-8

UroToday Contributing Editor Christopher P. Evans, MD, FACS

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Aging disrupts the balance between bone formation and bone destruction, resulting in osteoporosis, which is characterized by reduced bone mass and increased risk of fracture. Recent data have suggested that this imbalance is a result of a decrease in formation of bone forming osteoblast cells from mesenchymal cells upon aging. Instead, these cells form more fat cells. Insight into this age-related switch in cell type generation has now been provided by a team of researchers, led by Hiroshi Takayanagi, at Tokyo Medical and Dental University, Japan, working in mice. The data generated might provide new avenues of research for those developing approaches to treat age-related osteoporosis.

In the study, the gene regulatory protein Maf was found to promote mesenchymal cell generation of osteoblasts and suppress their generation of fat cells. Consistent with this, mice lacking Maf showed delayed bone formation. Furthermore, Maf levels were found to decrease in mouse mesenchymal cells upon aging and to be reduced by increased oxidative stress, something that occurs upon aging. Both the authors and, in an accompanying commentary, Laurie McCauley, at University of Michigan, Ann Arbor, believe these data could lead to new approaches to treat age-related osteoporosis.

Title:
Maf promotes osteoblast differentiation in mice by mediating the age-related switch in mesenchymal cell differentiation.

Accompanying Comentary Title:
c-Maf and you won’t see fat

Source:
Karen Honey

Journal of Clinical Investigation

UCSF scientists have received two grants from the California Institute for Regenerative Medicine to refine their human embryonic stem cell-based strategies for treating neurological diseases and liver failure. The goal of the grants is for researchers to make significant strides toward the development of potential therapies within the next three years.

If the strategies prove successful, they could then be further prepared as potential therapies and submitted as new drug applications to the U.S. Food and Drug Administration, leading toward clinical trials.

One team, led by Arturo Alvarez-Buylla, PhD, UCSF Heather and Melanie Muss Professor of Neurological Surgery, received a $1,752,058 grant to further investigate their novel strategy using embryonic neurons to inhibit the hyperactivity that occurs in the nervous system in several neurological conditions. Maintaining the balance between inhibitory and excitatory signaling in the nervous system is critical to normal neurological function.

The research supported by the grant will focus on epilepsy, but potentially could be used to treat Parkinson’s disease, traumatic brain injury, and spasticity after spinal cord injury.

“In 20 to 30 percent of patients with epilepsy, seizures are unresponsive to drugs, requiring invasive surgical resection of brain regions with aberrant activity,” says Alvarez-Buylla.

“The candidate cells we propose to develop can inhibit hyperactive neural circuits after implantation into the damaged brain. These cells have the unique ability to disperse through the adult brain and become functionally integrated in the neural circuitry. By bringing back a balance between excitation and inhibition in the nervous system, these cells could have important therapeutic benefits.”

Another team, led by Mark Zern, MD, of University of California, Davis, includes UCSF co-principle investigator Holger Willenbring, MD, assistant professor of surgery. The scientists will use their $5,199,767 grant to develop therapeutically effective liver cells, or hepatocytes, from human embryonic stem cells.

“Previous studies have shown that human embryonic stem cell-derived hepatocytes can provide liver function in rodents,” says Willenbring. “We will be seeking to produce human liver cells that stand the test of curing a mouse model of human liver failure, with an eye toward clinical application.”

“The cells could be used in patients suffering acute liver failure and those requiring such large liver resections that the residual hepatocyte mass wouldn’t be able to provide enough liver function until natural regeneration had occurred.”

The projects are among the 19 “translational research” awards announced yesterday by CIRM. The projects are expected to either result in a proposed drug or cell therapy or lead to significant progress in the development of a potential therapy, which could then be further developed for submission to the FDA for clinical trial.

Novel strategy for neurological diseases

The strategy being developed by Alvarez-Buylla, Scott Baraban, PhD, professor of neurological surgery, Arnold Kriegstein, MD, PhD, professor of neurology and director of the Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell research at UCSF, and John Rubenstein, MD, PhD, professor of psychiatry, involves a set of embryonic cells known as medial ganglia eminence (MGE) neurons. These cells mature into so-called GABAergic inhibitory interneurons, which play a key role in maintaining the balance between inhibitory and excitatory signaling in the nervous system.

In previous studies, the team determined that when the embryonic neurons are transplanted into the brains of mice they mature, integrate into neural circuitry and reduce the overactive excitatory signaling that occurs in some neurological diseases.

In mice genetically engineered to have a human form of epilepsy, for instance, the cells decreased the number and severity of seizures. (Proceedings of the National Academy of Science, vol. 106, no. 36, 2009) . In mice genetically engineered to have an illness resembling Parkinson’s disease, the cells improved balance, speed, and length of stride during walking. In healthy “control” rats in which the cells had been transplanted, the animals took longer strides and ran faster on a runway test (Cell Stem Cell (vol. 6, issue 3, 2010),

In the current study, the team will examine at a detailed level what happens to the MGE cells when they are grafted into the mouse brain. They will examine whether the cells mature appropriately and migrate to the intended locations in the brain, how they interact with the native neurons, how many are required to increase inhibition (dose-response information) and whether they have unwanted side-effects.

While the team previously used MGE neurons from the brains of embryonic mice, in the current study they primarily will use human MGE neurons they produced in the culture dish from human embryonic stem cells – work that was funded by a CIRM “Comprehensive” grant to Kriegstein in 2007. The human MGE neurons will be compared to mouse MGE neurons, which remain the “gold standard” for the research.
Regenerating damaged livers

UCD’s Zern and UCSF’s Willenbring will work to develop high quality human liver cells, or hepatocytes, from human embryonic stem cells in the culture dish. They will test the effectiveness and safety of these cells and thus their potential for regenerating human liver in a mouse model of fatal liver disease.

Willenbring previously has shown that hepatocytes derived from reprogrammed skin cells – a type of pluripotent stem cell similar to embryonic stem cells – are in principle capable of curing liver failure in mice. Over the last seven years, Zern has developed protocols for the differentiation of human embryonic stem cells into hepatocytes. “The hepatocytes we are producing provide levels of liver function that are on average within 10-20 percent of that of primary human hepatocytes,” says Willenbring.

Now, the team will refine the process by further maturing the hepatocytes, and develop strategies for “purifying,” or selecting, the cells in the culture dish to make sure that only fully differentiated, or specialized, liver cells are transplanted.

“We have really promising preliminary results. Now we have to put the strategy to the test and develop it further in animal models, with the ultimate goal of rescuing liver function in patients who would otherwise die of liver failure.”

The new awards brings the total funds awarded to UCSF by CIRM to $110,532,518.

UCSF is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care.

Source:
Jennifer O’Brien
University of California — San Francisco

Two-thirds of the difference between death rates among African Americans and Caucasians are now due to causes that could be prevented or cured, according to a new study appearing in the Journal of Epidemiology and Community Health. The study, “Black-White Differences in Avoidable Mortality in the United States, 1980-2005,” found that death from preventable or treatable conditions represented half of all deaths for individuals under age 65 and accounted for nearly 70 percent of the black-white mortality difference.

“People should not be dying prematurely from stroke, hypertension, diabetes, colon cancer, appendicitis or the flu. Our study shows that while much progress has been made, our health care system is still failing to meet the very basic needs of some Americans. Many disparities can be conquered by focusing more on public policies that promote prevention and by ensuring that all Americans have access to good quality health care,” said James Macinko, who conducted the research as a Robert Wood Johnson Foundation Health & Society Scholar at the University of Pennsylvania. He is the lead author of the study.

The major reason for the black-white mortality gap – representing about 30 percent of the gap for men and 42 percent for women – is due to conditions that have effective treatments, the study found. Disparities were most pronounced for conditions or diseases for which deaths can be prevented, such as diabetes, stroke, infectious and respiratory diseases, preventable cancers, and circulatory diseases like hypertension.

The conditions analyzed included premature deaths from common infectious diseases, cervical cancers, appendicitis, maternal deaths, hypertension, stroke, diabetes, peptic ulcers and traffic accidents, all of which could be avoided through medical care or health policy changes. The study suggests that the reinforcement of policies that improve access to quality medical care will be important to reducing death disparities.

“As the nation turns its attention to health care reform, we now know that much can be done to reduce racial and ethnic health care disparities and to improve the health care for all Americans,” said Macinko. “We also have a lot to learn from other health care systems that measure performance based on preventable deaths.”

To analyze the death disparity among African Americans and Caucasians, the scholar used “avoidable mortality,” a commonly used measure of health system performance in Europe. It is defined as premature death under age 65 from conditions responsive to medical care, changes in public policy, or behaviors. Over the last decade, avoidable mortality has declined less rapidly in the United States than in other industrialized nations.

“Avoidable mortality gives us one way to assess the shortcomings of our health care system, particularly in the area of prevention,” said Irma T. Elo, Ph.D., co-author on the report and an associate professor of sociology at the University of Pennsylvania. “It can help to identify where preventable disparities are greatest and aid in directing resources to where they can improve the health of vulnerable populations.”

Elo also serves as an affiliated-faculty member for the RWJF Health & Society Scholars Program at the University of Pennsylvania.

Source:
Jennifer Combs

RWJF Health & Society Scholars Program

Pets may not be the only organisms endangered by some food additives. An arsenic-based additive used in chicken feed may pose health risks to humans who eat meat from chickens that are raised on the feed, according to an article in the April 9 issue of Chemical & Engineering News, the weekly news magazine of the American Chemical Society.

Roxarsone, the most common arsenic-based additive used in chicken feed, is used to promote growth, kill parasites and improve pigmentation of chicken meat. In its original form, roxarsone is relatively benign. But under certain anaerobic conditions, within live chickens and on farm land, the compound is converted into more toxic forms of inorganic arsenic. Arsenic has been linked to bladder, lung, skin, kidney and colon cancer, while low-level exposures can lead to partial paralysis and diabetes, the article notes.

Use of roxarsone has become a topic of increasing controversy. A growing number of food suppliers have stopped using the compound, including the nation’s largest poultry producer, Tyson Foods, according to the article. Still, about 70 percent of the 9 billion broiler chickens produced annually in the U.S. are fed a diet containing roxarsone, the article points out.

Complicating the issue is the fact that no one knows the exact amount of arsenic found in chicken meat or ingested by consumers who frequently eat chicken. “Neither the Food and Drug Administration nor the Department of Agriculture has actually measured the level of arsenic in the poultry meat that most people consume,” according to the article.

The National Chicken Council, a trade association that represents the U.S. chicken industry, claims there is “no reason to believe there are any human health hazards” associated with the use of roxarsone.

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The American Chemical Society – the world’s largest scientific society – is a nonprofit organization chartered by the U.S. Congress and a global leader in providing access to chemistry-related research through its multiple databases, peer-reviewed journals and scientific conferences. Its main offices are in Washington, D.C., and Columbus, Ohio.

Contact: Michael Bernstein
American Chemical Society

Truck drivers who have severe sleep apnea or who sleep less than five hours each night while at home are more likely to suffer from sleepiness, performance impairment and decreased task vigilance while behind the wheel.

The results of this large study of commercial truck drivers appear in the second issue for August 2006 of the American Journal of Respiratory and Critical Care Medicine, published by the American Thoracic Society.

Allan L. Pack, M.B., Ch.B., Ph.D., of the University of Pennsylvania, and six associates tested 247 commercial drivers at high risk for sleep apnea and 159 at lower risk for sleep impairment. They evaluated the role of short sleep duration at home over one week in 340 drivers, with 55 sleeping less than five hours. Of the 406 drivers examined for sleep apnea, 118 had mild to moderate forms of the disease, and 28 had severe sleep apnea.

“In the United States, approximately 5,600 people are killed annually in crashes involving commercial trucks,” said Dr. Pack. “Falling asleep while driving is an important factor in serious crashes involving commercial vehicles, prompting the question, why?” According to the authors, the two culprits are chronically insufficient sleep and obstructive sleep apnea.

The researchers defined mild to moderate sleep apnea as “from 5 to less than 30 temporary breathing pauses per hour of sleep,” a process that decreases the amount of oxygen in the blood. Severe sleep apnea, on the other hand, involves more than 30 breathing pauses per hour.

However, the investigators also found that 77 percent of those with mild sleep apnea and 56 percent of with moderate sleep apnea did not have what could be termed “pathologic sleepiness” as a result of their problem.

The authors used the Epworth Sleepiness Scale to assess subjective sleepiness, the Multiple Sleep Latency Test to objectively determine the driver’s propensity to fall asleep, and the Psychomotor Vigilance Task to assess behavioral alertness and define vigilance lapses. These tests were administered in addition to a normal sleep test (polysomnography) to measure breathing pauses and movement disorders in the sleep laboratory.

“In this study, we showed that both subjective and objective sleepiness, as well as performance impairments are common in our sample of commercial driver’s license holders,” said Dr. Pack. “Our analyses reveal that chronic short sleep duration is a risk factor for subjective sleepiness, objectively measured sleepiness and performance impairments. The results for sleep apnea are less clear.”

The percentage of drivers with two or three performance impairments among those with less than 5 hours of sleep was 49.5 percent.

Of the 406 drivers tested, 93.3 percent were male and were over 45 years old. At the time of the study, 81.6 percent were employed as drivers of a commercial vehicle. All participants had a commercial driver’s license.

“When we examined definitions of impairment for Psychomotor Vigilance Task Performance lapses and Divided Attention Driving Task tracking error based on data comparing results with those produced by alcohol intoxication, we found that slightly over 29 percent for lapses and almost 37 percent for mean tracking error had performance decrements compared to that induced in control subjects, albeit in different populations, after alcohol intoxication,” said Dr. Pack.

The authors noted that these results should encourage the Federal Motor Carrier Safety Administration to reduce sleepiness and potential crash risk in commercial drivers. They suggest that the agency should develop plans to implement ways of identifying “sleep-impaired” drivers through objective testing, to identify and treat individuals with severe sleep apnea and to monitor their adherence to therapy, and to promote increased sleep duration among commercial drivers.

Impaired Performance in Commercial Drivers
Role of Sleep Apnea and Short Sleep Duration
Allan I. Pack, Greg Maislin, Bethany Staley, Frances M. Pack, William C. Rogers, Charles F. P. George and David F. Dinges
American Journal of Respiratory and Critical Care Medicine
Vol 174. pp. 446-454, (2006)
Click Here View Abstract Online

Lymph nodes can be crucial for spreading low doses of infective prion agents — the pathogens responsible for conditions such as scrapie and Creutzfeldt-Jakob disease — into the nervous system, according to new research published in the online open access journal BMC Veterinary Research. While we can show that the regional lymph node plays no pivotal role in the neuroinvasion of prions for high doses of infection, we cannot rule out the possibility that lymph nodes are still involved in the distribution of prions throughout the body to other non-neural tissues.

The research, carried out by scientists in the group of Michael Beekes at the Robert-Koch Institute in Berlin, Germany, sheds new light on the important issue of how prion agents are transmitted from the site of infection to the brain and spinal cord, where they cause irreparable and fatal damage.

Christine Kratzel and colleagues investigated the role of the lymphoreticular system — which comprises the network of lymph nodes that is part of the body’s defence system — in the spread of scrapie infection to nerve tissue in hamsters. The team discovered that if a lymph node close to the site of infection is removed within six days after a high or a medium dose of infective agent has been administered, the animal still develops the disease. However, if the node is removed 4 weeks before infection, a high dose causes the disease while a low dose does not (over the course of the 314 day time period for the study). The results suggest that for low doses of infective agent the lymphoreticular system is important in facilitating neuroinvasion i.e. the spread of prions from the infection site to the central nervous system.

The team also noted that after a node had been removed and the wound not yet healed, prion infection is substantially accelerated.

The findings are important because the role of the lymphoreticular system and inflammatory processes in the spread of prion infectivity through the body has been poorly understood. A clearer understanding of the factors involved in the transport of the agent in the body will help scientists and doctors to develop new ways of preventing and treating prion diseases.

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Article:

Relevance of the regional lymph node in scrapie pathogenesis after peripheral infection of hamsters
Christine Kratzel, Dominique KrГјger and Michael Beekes

BMC Veterinary Research (in press)

BMC Veterinary Research. All articles are available free of charge, according to BioMed Central’s Open Access policy.

For author contact details please contact Susanne Glasmache (Press Office, Robert-Koch Institute):

Source: Charlotte Webber

BioMed Central

The conflicts in Iraq and Afghanistan have left a terrible legacy: more than 1,200 returning American soldiers have lost one or more limbs. To address this growing national need, researchers at Worcester Polytechnic Institute (WPI) are laying the groundwork for a new generation of advanced prosthetic limbs that will be fully integrated with the body and nervous system. These implantable neuroprosthetics will look and function like natural limbs, enabling injured soldiers and the more than 2 million other amputees in the United States lead higher quality, more independent lives.

As part of the recently approved Department of Defense appropriations bill, the U.S. Congress has allocated $1.6 million to the Center for Neuroprosthetics and BioMEMS (CNB), part of WPI’s Bioengineering Institute, to advance this groundbreaking work. Sponsored by Massachusetts Senators John Kerry and Paul G. Kirk Jr and Massachusetts Representative James P. McGovern, the allocation will, in particular, fund work at WPI on neural control for advanced prosthetics. The allocations will be directed by the U.S. Army’s Telemedicine and Advanced Technology Resource Center (TATRC).

“WPI’s involvement with neuroprosthetics began with the encouragement and support of Senator Ted Kennedy, who helped secure the funds that launched our neuroprosthetics center,” said Dennis D. Berkey, WPI president and CEO. “We are grateful for the leadership of Senators Kerry and Kirk and the support of Congressman McGovern, who have made it possible for the important work Senator Kennedy started to continue. These funds will generate extraordinary technological advances that will give hundreds of soldiers, veterans, and other Americans a quality of life they might have thought impossible.”

“These federal investments will not only substantially increase the quality of life of our injured soldiers and veterans, but will also help stimulate the Massachusetts economy by fostering local innovation, expanding our strengths in health care and medical devices, and creating good-paying jobs,” Rep. McGovern said.

In all, 30 WPI researchers, from multiple science and engineering disciplines, including regenerative biology, tissue engineering, surface science and nanotechnology, and biomedical signal processing, are engaged in work related to neuroprosthetics. Their research focuses on two primary goals: regenerating tissue to create a robust soft-tissue seal around an implanted limb to make possible natural movement and deter infection; and using engineered micro-wires as scaffolds for the recruitment of neural stem cells and the regeneration of nerves. Ultimately, by regenerating nerves, it is anticipated that it will be possible to connect the limb directly to the nervous system, enabling it to send feedback to and receive commands from the brain.

“With advances in body armor and battlefield medicine, soldiers are far more likely to survive combat injuries today than during past conflicts,” says W. Grant McGimpsey, Professor of Chemistry and Biochemistry and director of WPI’s Bioengineering Institute and the CNB. “But too often, they return home to find their quality of life curtailed. We owe it to those who have made sacrifices for our country to apply our know-how and expertise to making them whole again. This is the goal that drives everyone engaged in this research.”

WPI’s research in implantable, neurally controlled prosthetics began in 2007 as a result of $1 million Congressional allocation to support CNB, championed by Senators Kennedy and Kerry, and Congressman McGovern. An award from the John Adams Innovation Institute enabled the new center to explore relationships with other research institutions, and to establish the nation’s first symposium series dedicated to advancing the field of neuroprosthetics. The first national symposium was held at WPI in September 2009 and planning is under way for Neuroprosthetics 2010.

Source:
Michael Dorsey
Worcester Polytechnic Institute