Philips Collaborates To Develop New Clinical Tools To Aid Patients Suffering From Complex Heart Rhythm Disorders
Challenging heart rhythm disorders, or arrhythmias, require electrophysiology (EP) technologies to pinpoint and ultimately fix problem areas within the heart’s electrical circuitry during an interventional procedure. As EP procedure volume increases worldwide, clinicians are requesting intuitive, advanced tools to help shorten procedure times and gain detailed visualizations for interventions. Recognizing this, Royal Philips Electronics (NYSE: PHG, AEX: PHI) today announced an agreement with Bard Electrophysiology, a division of C. R. Bard, Inc., to co-develop new clinical tools that will be designed to help electrophysiologists meet these needs and aid patients suffering from arrhythmias.
Cardiac arrhythmia can lead to serious health risks, including heart failure or stroke. Atrial fibrillation – a heart rhythm disorder characterized by irregular, rapid beating of the atrial chambers – is found in about 2.2 million Americans and 4.5 million Europeans. With robust EP technologies, clinicians may be better able to evaluate and diagnose abnormalities in the heart’s electrical activity.
The goal of the combination of Bard’s LabSystemTMPRO EP Recording System and Philips’ EP navigator and the Allura Xper FD series is to provide electrophysiologists a faster and easier way to integrate image guidance with mapping and analysis of complex arrhythmias, while offering insights for more accurate interventional navigation. EP physicians and lab staff may also benefit from improved workflow in the EP lab due to integration and compatibility between Philips and Bard technologies.
“Providing simpler and more intuitive approaches to the management of complex arrhythmias is something that fascinates me. Significant advancement in science and technology is frequently made when two seemingly dissimilar techniques are merged. The collaboration between Bard Electrophysiology and Philips is very promising, and I am looking forward to learning more about the potential for these new technologies in my practice,” commented Michael V. Orlov, M.D., Ph.D., director of Arrhythmia Service at Caritas St. Elizabeth’s Medical Center of Boston and an associate professor of Medicine at Tufts University School of Medicine.
“Philips is dedicated to simplifying heart rhythm care. The relationship with Bard exemplifies our strategy of collaborating with best-in-class companies to develop solutions that address the needs of the electrophysiologists and their patients,” said Gerard Winkels, vice president and general manager, Electrophysiology, for Philips Healthcare. “The collaboration with Bard Electrophysiology will allow us to bring new clinical tools to market aiming to enable our joint customers to perform EP procedures faster and more simply and allow them to provide enhanced care offerings for their patients.”
Dave Hemink, vice president and general manager, Bard Electrophysiology said, “This alliance will provide us the opportunity to fundamentally impact the way that we analyze and diagnose complex arrhythmias. We recognize that current solutions are complex and time consuming. Together with Philips, we will innovate towards simpler approaches to these clinical challenges, with a focus on helping healthcare providers’ EP labs achieve greater business potential through expanded functionality and improved efficiencies.”
About Royal Philips Electronics
Royal Philips Electronics of the Netherlands (NYSE: PHG, AEX: PHI) is a diversified Health and Well-being company, focused on improving people’s lives through timely innovations. As a world leader in healthcare, lifestyle and lighting, Philips integrates technologies and design into people-centric solutions, based on fundamental customer insights and the brand promise of “sense and simplicity”. Headquartered in the Netherlands, Philips employs approximately 128,000 employees in more than 60 countries worldwide. With sales of $42 billion (EUR 27 billion) in 2007, the company is a market leader in cardiac care, acute care and home healthcare, energy efficient lighting solutions and new lighting applications, as well as lifestyle products for personal well-being and pleasure with strong leadership positions in flat TV, male shaving and grooming, portable entertainment and oral healthcare. News from Philips is located at http://www.philips.com/newscenter.
About Bard Electrophysiology
Bard Electrophysiology, a division of C. R. Bard, Inc., is a global company focused on the development and delivery of a broad range of devices for the diagnosis and treatment of cardiac arrhythmias. We offer the electrophysiologist a product portfolio including advanced RF ablation and mapping catheters, diagnostic catheters, EP recording systems and stimulators, and intracardiac access products. Through our rich history of commitment to innovative products, unparalleled support, and a dedication to education worldwide, Bard Electrophysiology continues to be a leader in the field of EP. For more information about Bard Electrophysiology, please visit us at http://www.bardep.com.
Royal Philips Electronics
Childhood Obesity Linked To Newly Discovered Genes
Scientists studying the gene maps of thousands of Europeans found three new genetic variations that increase the risk for obesity and said
that together with what we already know about genes and obesity the findings could help to develop tools that can predict which young children are at
risk of becoming obese.
The study was the work of researchers from Imperial College London, UK, the French National Research Institute CNRS, and other research centres in
Europe and Canada, and was published online in Nature Genetics on 18th January.
Ten per cent of children under six in the UK are obese, according to figures from the Department of Health’s National Child Measurement Programme
2007/08.
Co-author Professor Philippe Froguel, from the Department of Genomic Medicine at Imperial College London said:
“When young children become obese, their lives can be affected in a very negative way. Sadly, obese children are often unfairly stigmatised and they
can suffer heart and lung problems, painful joints, diabetes and cancer as they grow up.”
The variants discovered in this 10-year study could be responsible for up to 50 per cent of cases of severe obesity, said the researchers.
For the study, they did a genome-wide association study of 1,380 European obese children under six and severely obese adults, and 1,416 age-matched
normal weight controls. Most of the obese adults had been obese since childhood or their teenage years.
The researchers found 38 genetic markers with a strong link to a higher than normal body mass index (BMI). They then investigated these in another
14,186 Europeans and found three mutations that are significantly linked to obesity.
The variant that they found to be most strongly linked with childhood obesity and adult morbid obesity is sited near the PTER gene. Nobody knows
what this gene does, but the researchers estimated that the variant probably accounts for up to one third of all childhood obesity and one fifth of all
severe adult obesity cases.
The second mutation that was strongly linked to childhood and adult obesity was found in the NPC1 gene, which mouse studies have shown to play a
role in appetite control (mice without this gene don’t eat much and suffer late-onset weight loss). The researchers estimated that this second variant
accounts for about 10 per cent of all childhood obesity and 14 per cent of all cases of severe adult obesity.
The third variant was found near the MAF gene, which controls the making of insulin and glucagon, plus chains of amino acids known as glucagon-like peptides, all of which are important for metabolizing glucose and carbohydrates and in controlling feelings of fullness after eating. The
researchers estimated that this variant accounts for about 6 per cent of childhood obesity and 16 per cent of severe adult obesity.
Although the researchers said that more research was needed to see whether these genes are acting independently (it might be the case that they only
work together), the joint effect of these new variants could account for up to 50 per cent of all cases of severe adult and childhood obesity.
As Froguel explained, understanding the genetic basis of obesity is the first step, and once we know which genes are responsible:
“We can develop ways to screen children to find out who is most at risk of becoming obese.”
“Hopefully we can then intervene with measures such as behavioural therapy, to make sure a child forms healthy eating habits and does not develop a
weight problem,” he added.
The study was sponsored by the Medical Research Council, the Agence Nationale de la Recherche, the Conseil Regional Nord-Pas de Calais / Fonds
européen de développement économique et régional, Genome Quebec / Genome Canada and the German Research Council (for the German
cohorts).
“Genome-wide association study for early-onset and morbid adult obesity identifies three new risk loci in European
populations.”
David Meyre, Jerome Delplanque, Jean-Claude Chevre, Cecile Lecoeur, Stephane Lobbens et al.
Nature Genetics Published online 18 Jan 2009.
doi: 10.1038/ng.301
Click here for
Abstract.
Sources: Journal abstract, Imperial College London.
Written by: Catharine Paddock, PhD
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today
Research!America Selects Ambassador To Join Distinguished Health Experts In Seeking Greater US Investment In Global Health
Research!America honored Dr. Keith C. Norris, the executive vice president for Research and Health Affairs at Charles Drew University of Medicine and Science, by naming him an “ambassador” for the nonprofit organization’s Paul G. Rogers Society for Global Health Research.
The Rogers Society, named for the late Florida Congressman Paul G. Rogers (1921-2008), a champion for health research and Research!America chair emeritus, advocates for greater U.S. investment in research to fight diseases that disproportionately affect the world’s poorest nations.
Norris is among 25 new ambassadors for the Rogers Society. They will join 50 of their peers in Research!America’s Rogers Society in a united effort to build a national conversation around the value and importance of U.S.-funded global heath research.
These prominent advocates include experts in pediatrics, nursing and dentistry and specialize in critical areas, such as neglected and emerging tropical diseases, tuberculosis and polio. They were selected by an advisory council comprised of renowned leaders in science, public policy and communications, including four Nobel Laureates.
Together with their peers, they will meet with policymakers to make the case for an increased U.S. investment in global health research.
“These ambassadors will be exceptional leaders in advocacy. Their example will serve as an inspiration for every global health researcher,” said the John Edward Porter, chair of the Rogers Society Advisory Council and Research!America board. “Paul Rogers’ spirit lives on through the work of each of these ambassadors. As he often said, without research, there is no hope.”
Dr. Norris is the second Rogers Society ambassador from Charles Drew University. Dr. Eric Bing, CDU’s director of International HIV programs, served in the same capacity two years ago.
“I see our nation reasserting itself as a global leader in unity with other nations through the promotion of health and wellness,” Dr. Norris said. “Ultimately, it is service informed by research and driven by passion that will be the key to our success.”
Dr. Norris is board certified by the American Boards of Internal Medicine and Nephrology and certified as a specialist in clinical hypertension by the American Society of Hypertension. He is a fellow of the American College of Physicians and the American Society of Nephrology and an active member of the National Kidney Foundation. He is also a member of the National Institutes of Health Study Sections (NCRR & NIDDK) and the NIH-NCRR Clinical Research Working Group.
Dr. Norris’ research interests focus on the prevention and early treatment of chronic kidney disease, with an emphasis on improving outcomes for African-American and Latino populations. Other areas include the role of vitamin D in chronic kidney disease, calcium management in end-stage renal disease and hypertension. He is currently a principal investigator on four National Institutes of Health (NIH) grants and co-investigator on several others.
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Article adapted by Medical News Today from original press release.
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ABOUT CHARLES DREW UNIVERSITY OF MEDICINE AND SCIENCE (CDU)
CDU is a private nonprofit, nonsectarian, minority-serving medical and health sciences institution. Located in the Watts-Willowbrook area of South Los Angeles, CDU has graduated over 550 medical doctors, 2,500 post-graduate physicians, more than 2,000 physician assistants and hundreds of other health professionals. The only dually designated Historically Black Graduate Institution and Hispanic Serving Health Professions School in the U.S. CDU is recognized as a leader in health inequities and translational research, specifically with respect to heart disease, diabetes, cancer, mental health, and HIV/AIDS. The University is among the top 7% of National Institutes of Health (NIH)-funded institutions and rated one of the top 50 private universities in research in the U.S. Recently, the CDU/UCLA medical program was named the “best performer” in the University of California System with respect to producing outstanding underrepresented minority physicians. For more information, visit http://www.cdrewu.edu/.
ABOUT PAUL G. ROGERS SOCIETY FOR GLOBAL HEALTH RESEARCH
The Society was established in 2006 by Research!America with funding from the Bill & Melinda Gates Foundation. Research!America works with the Ambassadors to maximize the effectiveness of their outreach to policy makers, opinion leaders and the media.
Research!America is the nation’s largest not-for-profit public education and advocacy alliance working to make research to improve health a higher national priority. Founded in 1989, it is supported by 500 member organizations, which represent more than 125 million Americans. For more information, visit http://www.researchamerica.org.
Source: John Mitchell
Charles Drew University of Medicine and Science
The Long (And Sticky) Arms Of The Law: SQUID Technology Catches Them By The Axles
What’s possible when a group of scientists are inspired by a famous superhero and a giant creature from the sea? How about a new technology for stopping drivers in their tracks?
Fleeing drivers are a common problem for law enforcement. They just won’t stop unless persuaded – persuaded by bullets, barriers, spikes, or snares. Each option is risky business.
Shooting up a fugitive’s car is one possibility. But what if children or hostages are in it? Lay down barriers, and the driver might swerve into a school bus. Spike his tires, and he might fishtail into a van – if the spikes stop him at all. Existing traps, made from elastic, may halt a Hyundai, but they’re no match for a Hummer. In addition, officers put themselves at risk of being run down while setting up the traps.
But what if an officer could lay down a road trap in seconds, then activate it from a nearby hiding place? What if – like sea monsters of ancient lore – the trap could reach up from below to ensnare anything from a MINI Cooper to a Ford Expedition? What if this trap were as small as a spare tire, as light as a tire jack, and cost under a grand?
Thanks to imaginative design and engineering funded by the Small Business Innovation Research (SBIR) Office of the U. S. Department of Homeland Security’s Science and Technology Directorate (S&T), such a trap may be possible by 2010. It’s called the Safe Quick Undercarriage Immobilization Device, or SQUID. When closed, the current prototype resembles a cheese wheel full of holes. When open (deployed), it becomes a mass of tentacles entangling the axles. By stopping the axles instead of the wheels, SQUID may change how fleeing drivers are, quite literally, caught.
The 1.5-foot-wide disc was conceived and developed by Engineering Science Analysis Corporation (ESA) of Tempe, Arizona. S&T’s Borders and Maritime Security Division manages the project.
“SQUID was inspired by a sea creature and a superhero,” says ESA president Martín Martínez. Like its oceanic namesake, SQUID ensnares its prey with sticky tendrils. Like Spiderman’s webbing, these tendrils stretch to absorb the kinetic energy of their fleeing target.
Huge amounts of such counterforce are necessary to stop a heavy, swift vehicle: Think Spiderman II, where Spidey stretched his webbing for blocks to halt a runaway passenger train. The force nearly killed him. Martínez took a different approach that would have made Spidey proud: Don’t fight the Force; just stop the axles from turning. Do that and you can stop (almost) anything with wheels.
Can it really work? Martínez and DHS think so. In testing, a SQUID prototype safely stopped a 35 mph pickup truck (see video). That’s a good start, but before SQUID can be marketed, law enforcement officers need proof that it has the fiber to stop a 5,000-pound vehicle – about the heft of a Ford F-150 pickup – speeding at 120 miles per hour.
Beyond performance, SQUID will need to satisfy other demands of law enforcement.
“We must make it lighter,” says Mark Kaczmarek, the S&T SQUID program manager. “Also, more affordable, so it becomes the stopper of choice, regardless of budget.” Finally, SQUID must be rugged, reliable, and capable of being reloaded. These goals will be pursued in 2009, as ESA teams with Pacific Scientific Energetic Materials Corporation (PSEMC) of Chandler, Arizona.
Meanwhile, the spidery disc has lured the interest of state and local police as well as federal agencies such as Customs and Border Protection (CBP) and Immigration and Customs Enforcement (ICE). In response to concerns about whether criminals will see the disc, SQUID may be reborn as a centipede – that happens to look like a speed bump.
Martínez and Kaczmarek hope their spidery cephalopod will spawn a generation of offspring – in this case, a family of nonlethal stopping devices for land, sea, and air…all based on the same sticky principle, less is more.
“If bad guys need ‘inspiration’ to comply,” says a smiling Martínez, “we’ll be glad to inspire them.”
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Article adapted by Medical News Today from original press release.
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Source: John Verrico
US Department of Homeland Security – Science and Technology
Determination Of 3-D Structure Of TIGAR, An Enzyme Whose Presence In The Body Can Warn Doctors That Cancer May Follow
Two Brown University researchers have determined the three-dimensional structure of an enzyme whose presence in the body could help doctors detect cancer earlier or develop more targeted treatments.
Hua Li and Gerwald Jogl detail their progress with the enzyme known as TIGAR in a paper published Jan. 16, 2009, in The Journal of Biological Chemistry.
“It will help us to understand where else we should be looking for good [anti-cancer] targets,” said Jogl, assistant professor of biology in the Department of Molecular Biology, Cell Biology and Biochemistry at Brown. Jogl is the study’s principal investigator and corresponding author. Li is a fifth-year Ph.D. student based in Jogl’s lab and is the lead author.
Jogl and Li wanted to determine the structure of TIGAR. After more than a year of research, they discovered that it is has a more substantive active site than they had expected. To map the structure, the pair used a method called X-ray crystallography.
The process involved using intensive X-ray light produced at the National Synchroton Light Source in Brookhaven, N.Y., to analyze crystals grown from samples of the TIGAR enzyme.
A separate study by researchers from St. Jude’s Children’s Research Hospital first identified the existence of TIGAR. Those results were published in CELL in 2006.
TIGAR, which helps regulate energy production in the cell, is activated after cell damage. Because of this, the presence of the enzyme can indicate potential problems that may lead to cancer. But TIGAR itself is positive. Once activated, TIGAR slows all processes in the cell, allowing time to repair cell damage. This process is also intended to prevent further damage that could lead to cancer.
Jogl and Li believe their finding may suggest that TIGAR has additional functions in the cell.
Understanding TIGAR is important, Jogl said, because the enzyme is “one of the good guys” in the battle against cancer. Because its presence can come in tandem with cellular damage, TIGAR is an important clue for scientists that could indicate cancer may follow. Knowing more about TIGAR could lead to earlier cancer detection or even preventative treatments.
“We are looking at the good guys,” Jogl said. “Studying the good guys will lead us to the bad guys and where the places are to interfere.”
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Article adapted by Medical News Today from original press release.
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A National Institutes of Health grant helped support the study.
Source: Mark Hollmer
Brown University
African-Americans Have Worse Prognosis At Colorectal Cancer Diagnosis
African-American patients with colorectal cancer were more likely to present with worse pathological features at diagnosis and to have a worse five-year survival rate compared to Caucasian patients, according to a study conducted by researchers at Thomas Jefferson University.
The results were presented at the 2009 American Society of Clinical Oncology (ASCO) Gastrointestinal Cancers Symposium. The study was led by Edith Mitchell, M.D., a clinical professor in the Department of Medical Oncology at Jefferson Medical College of Thomas Jefferson University. Dr. Mitchell is also associate director of Diversity Programs for the Kimmel Cancer Center at Jefferson.
“One possible explanation could be the socioeconomic factors that are often associated with African-American patients,” Dr. Mitchell said. “For example, research has shown that African-Americans are less likely than Caucasian patients to have health insurance, and thus they may not receive the screening necessary to detect colorectal cancer at an earlier stage.”
Dr. Mitchell and colleagues obtained data from the tumor registry of Thomas Jefferson University Hospital on 2,500 patients treated for colorectal cancer from 1988 to 2007. They compared those data with data obtained from the National Cancer Institute’s Surveillance, Epidemiology and End Results (SEER) database on 244,701 patients with colorectal cancer treated from 1988 to 2005. The researchers collected data on location, stage and histologic grade of the cancer.
In both patient groups, more African-American patients presented with advanced disease (defined as stage III or stage IV) at diagnosis. African-American patients were also more likely to have proximal – on the right side of the colon – disease. Among patients diagnosed with early-stage disease, the risk for nodal involvement was greater in African-American patients.
African-American patients also had a worse five-year survival, both overall and when stratified by cancer stage.
“Right now, we cannot definitely explain why there are such differences between the African-American and the Caucasian patients,” Dr. Mitchell said. “We need to do more studies on prognostic factors related to tumor biology, molecular markers and genetics to account for the racial disparities.”
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Article adapted by Medical News Today from original press release.
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Source: Emily Shafer
Thomas Jefferson University
Progress Made In Understanding Causes And Treatment Of Endometriosis
Endometriosis is a poorly understood chronic disease characterized by infertility and chronic pelvic pain during intercourse. It affects between 5 to 10 million women in the U.S.
Serdar Bulun, M.D., George H. Gardner Professor of Clinical Gynecology at Northwestern University’s Feinberg School of Medicine, has spent the past 15 years investigating and identifying the causes of this disease. Bulun, and colleagues in his lab, discovered key epigenetic abnormalities in endometriosis and identified existing chemicals that now help treat it.
Bulun describes his lab’s findings over the past 10 years in the Jan. 15 issue of the New England Journal of Medicine.
One of the abnormalities he discovered is the presence of the enzyme aromatase — which produces estrogen — in endometriosis, the diseased tissue that exists on pelvic organs and mimics the uterine lining. (Normal endometrium, located in the uterine cavity, does not contain aromatase.) As a result, women with endometriosis have excessive estrogen in this abnormal tissue found on surfaces of pelvic organs such as the ovaries. Bulun found the protein SF1 that produces aromatase, which is supposed to be shut down, is active in endometriosis.
“Estrogen is like fuel for fire in endometriosis,” Bulun said. “It triggers the endometriosis and makes it grow fast.”
As a result of the aromatase finding, Bulun launched clinical trials in 2004 and 2005 testing aromatase inhibitors — currently used in breast cancer treatment — for women with endometriosis. The drug blocks estrogen formation and secondarily improves progesterone responsiveness.
“We came up with a new treatment of choice for post-menopausal women with endometriosis,” Bulun said. Moreover, treatment with an aromatase inhibitor is a very good option for premenopausal women with endometriosis not responding to existing treatments, he noted.
Another molecular abnormality Bulun found is that women with endometriosis have a progesterone receptor that is inappropriately turned off. Normal progesterone action would be beneficial because it blocks the growth of endometriosis. In the absence of appropriate progesterone action, endometriosis tissue remains inflamed and continues to grow.
Bulun believes that these abnormalities result from epigenetic defects that occur very early on during embryonic development and may be the result of early exposure to environmental toxins. In fact, other investigators have implicated the environmental pollutant dioxin and the synthetic estrogen DES in the etiology of endometriosis.
“This may be a disease that women are born with,” Bulun said. “Perhaps when a baby girl is born, it has already been determined that she is predisposed to have endometriosis. Maybe research can now be directed toward the fetal origins of the disease and raise the awareness of how the disease develops.”
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Article adapted by Medical News Today from original press release.
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Source: Marla Paul
Northwestern University
Identification Of Key Protein That May Cause Cancer Cell Death
Researchers at A*STAR’s Institute of Molecular and Cell Biology (IMCB) have become the first to discover and characterize a human protein called Bax-beta (Baxβ), which can potentially cause the death of cancer cells and lead to new approaches in cancer treatment. The finding is published in the 16 Jan. report of Molecular Cell.
Detection of Baxβ has eluded scientists until now. Said Dr Victor Yu, principal investigator of the IMCB research team, “Our research findings reveal that Baxβ protein levels are normally kept at essentially undetectable levels in healthy cells by the protein degradation machine in cells known as proteasomes.
Proteasomes are “protein-digesting machines” that regulate cellular levels of various proteins including that of the lethal Baxβ, by breaking them into smaller components within the cell.
“Thus, the proteasomes are there to keep the lethal Baxβ in check,” he added. “This is exciting – if the proteasome-mediated degradation of Baxβ could be inhibited specifically in cancer cells, it could cause the harmful cancer cells to go through apoptosis”. In apoptosis, unwanted, damaged and infected cells are eliminated.
Until the discovery of Baxβ by Dr. Yu’s team, only one single protein called Bax-alpha (Baxα) had been extensively studied in cells. Earlier evidence had suggested that more than one protein was encoded by the Bax gene.
However, only a single protein called Baxα had ever been detected and extensively studied in cells. Bax is known to be a key gene needed for the execution step of apoptosis, or programmed cell death.
The researchers also found that Baxβ is able to associate with, and promote, Baxα activation, and that Baxβ, in its native form, is 100 times more potent than its sibling Baxα in triggering a key step in apoptosis.
The future development of novel compounds that can selectively elevate levels of Baxβ or stimulate its interaction with Baxα could also lead to new drug approaches to cancer treatment, as these compounds are likely to enhance the apoptotic signals triggered by many conventional cancer drugs, which frequently cause toxic side effects in patients when higher doses of drugs are needed.
Dr. David Andrews, Professor of Biochemistry and Biomedical Sciences at McMaster University, Canada added, “The beta-isoform4 of Bax has been enigmatic for several years. Although earlier research had hinted at its existence, the protein has proven extremely difficult to detect or examine functionally. Even attempts to produce the protein in the laboratory have been largely unsuccessful. In this study the Yu group resolves these issues by demonstrating that in cells Baxβ is normally rapidly degraded and kept at low levels, and when it is not degraded, it is profoundly apoptotic on its own and works in concert with Baxα. These studies provide information necessary for the elucidation of the importance of Baxβ in cell physiology.”
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Article adapted by Medical News Today from original press release.
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For more information, please contact:
Wang Yunshi
Corporate Communications
Agency for Science, Technology and Research (A*STAR)
The research findings are reported in the article, “Baxβ: A Constitutively Active Human Bax Isoform that is under Tight Regulatory Control by the Proteasomal Degradation Mechanism,” in the Jan. 16, 2009 print issue of Molecular Cell.
Authors: Nai Yang Fu, Sunil K. Sukumaran, Sze Yen Kerk and Victor C. Yu*.
Corresponding author: Victor Yu
Institute of Molecular and Cell Biology (IMCB):
The Institute of Molecular and Cell Biology (IMCB) is a member of Singapore’s Agency for Science, Technology and Research (A*STAR) and is funded through A*STAR’s Biomedical Research Council (BMRC). It is a world-class research institute that focuses its activities on six major fields: Cell Biology, Developmental Biology, Structural Biology, Infectious Diseases, Cancer Biology and Translational Research, with core strengths in cell cycling, cell signalling, cell death, cell motility and protein trafficking. Its recent achievements include leading an international consortium that successfully sequenced the entire pufferfish (Fugu) genome. The IMCB was awarded the Nikkei Prize 2000 for Technological Innovation in recognition of its growth into a leading international research centre and its collaboration with industry and research institutes worldwide. Established in 1987, the Institute currently has 35 independent research groups with more than 400 staff members. For more information about IMCB, please visit http://www.imcb.a-star.edu.sg.
Agency for Science, Technology and Research (A*STAR):
A*STAR is Singapore’s lead agency for fostering world-class scientific research and talent for a vibrant knowledge-based Singapore. A*STAR actively nurtures public sector research and development in Biomedical Sciences, Physical Sciences and Engineering, with a particular focus on fields essential to Singapore’s manufacturing industry and new growth industries. It oversees 22 research institutes, consortia and centres, and supports extramural research with the universities, hospital research centres and other local and international partners. At the heart of this knowledge intensive work is humancapital. Top local and international scientific talent drive knowledge creation at A*STAR research institutes. The agency also sends scholars for undergraduate, graduate and post-doctoral training in the best universities, a reflection of the high priority A*STAR places on nurturing the next generation of scientific talent. For more information about A*STAR, please visit http://www.a-star.edu.sg/
Source: Cathy Yarbrough
Agency for Science, Technology and Research (A*STAR), Singapore
Medical News From Weill Cornell, December 2008 – January 2009
Gene Therapy Studied for Preeclampsia – New Clues to a Mysterious Pregnancy Condition
To better understand preeclampsia, a sudden rise in maternal blood pressure and onset of kidney disease during pregnancy, researchers from Cornell University and Weill Cornell Medical College are studying mice that have the same affliction. Preeclampsia is the leading cause of both maternal and fetal death – killing more than 500,000 women worldwide each year and causing 15 percent of all premature births – yet the condition is not well understood.
Dr. Robin Davisson, Dr. Shari Gelber, and their team of researchers have developed an experimental gene therapy technique that lessens preeclampsia in mice, with the hope of someday applying their promising findings to humans. Dr. Davisson is a professor of cell and developmental biology at Weill Cornell Medical College and professor of molecular physiology at Cornell University’s College of Veterinary Medicine, in Ithaca, New York. Dr. Shari Gelber is a clinical fellow in maternal-fetal medicine in the department of obstetrics and gynecology at Weill Cornell Medical College in New York City.
To test their therapy, Dr. Davisson and Dr. Gelber have identified a type of mouse, called the BPH/5 mouse, that demonstrates features similar to those seen in humans with preeclampsia.
They have observed that these mice have a blood pressure spike late in the second trimester or early in the third trimester of pregnancy, as well as high protein found in the urine because of impaired kidney function – all of which mimic the clinical signs of preeclampsia in humans. They also have smaller litters of pups, both in number and in birth weight.
Currently, it is a mystery as to who is at a greater risk for preeclampsia, because the disease does not show symptoms until late in gestation. What experts do know is that there is a shallow invasion, or weak connection, between the placenta and the mother’s uterus – which is also seen in the BPH/5 mice. The research team is studying the BPH/5 mice with the hope of understanding the disease in early gestation, and to test a gene therapy technique that boosts a growth factor and improves blood circulation between the mother and fetus.
To administer the gene therapy, Dr. Davisson and her colleagues have injected mice with a harmless virus that contains a gene that, when taken up by the body, raises secretions of VEGF endothelial growth factor. The molecule helps blood vessel growth in the placenta, creating a better connection between the mother and fetus. The research team was encouraged to find that the experimental mice did not have a blood pressure spike or high levels of protein in the urine, compared with normal mice that received a virus injection that lacked the VEGF-producing gene. The experimental mice also have more normal litter sizes and the mouse pups weigh more.
During pregnancy, a preeclamptic mother suffers from elevated blood pressure, which can develop into eclampsia, causing stroke, liver failure, internal bleeding, postpartum hemorrhage, seizure, coma and death. The only known way to treat the condition is to deliver the fetus, usually before term. There is a risk of fetal death and low birth weight, which raises the risk of childhood seizures, blindness and pediatric asthma.
Busted Spine-Discs? Grow New Ones! Researchers Are Bioengineering Intervertebral Discs (IVD)
Each year, 40 to 60 percent of American adults suffer from chronic back pain. For patients diagnosed with severe degenerative disc disease, neurosurgeons must perform surgery called discectomy – removing the IVD – followed by a fusion of the vertebrate bones to stabilize the spine. Even after all that effort, the patient’s back will likely not feel the same as before their injury. But collaboration between physician-scientists at Weill Cornell Medical College and basic science researchers at Cornell University has led to the creation of bioengineered IVDs, in the laboratory, for transplantation into the spines of rats.
To create new spine discs, Dr. Roger Härtl and Dr. Lawrence Bonassar are using cells from IVD tissue of human patients who have had their spinal discs removed. Dr. Härtl is a noted neurological surgeon at NewYork-Presbyterian Hospital/Weill Cornell Medical Center, and the Leonard and Fleur Harlan Clinical Scholar and assistant professor of neurological surgery at Weill Cornell Medical College, and Dr. Bonassar is an associate professor in the departments of biomedical engineering and mechanical and aerospace engineering at Cornell University in Ithaca, New York.
Dr. Härtl harvests tissue from the removed discs and sends it to Dr. Bonassar. Cells are then isolated from this tissue and grown in an incubator that simulates the environment in the body. Once developed, they are placed on a bioengineered scaffold, enabling the assembly of the cells and scaffold into an IVD-shaped implant. The research team then surgically implants the discs inside a rat’s spine in order to see how the tissue reacts to the mechanical and biological demands. So far, results are promising. The researchers hope to soon test the bioengineered discs in human subjects in a clinical trial, so that someday people can receive spare parts for their aging or injured backs.
The Genetic Fingerprint of Prostate Cancer – How Estrogen Might Play a Role
One in six American men are diagnosed with prostate cancer within their lifetime and 186,000 will be diagnosed this year. For most men, their disease is confined to the prostate gland, making it easier to treat and less lethal. However, some unfortunate patients suffer from a more aggressive cancer that metastasizes, or spreads beyond the boundaries of the prostate gland. Physician-scientists are trying to uncover part of the disease’s molecular fingerprint, with the hope of explaining why some forms metastasize. Their findings may help physicians provide tailored, and therefore, more effective treatments for patients.
Dr. Mark A. Rubin, professor of pathology and laboratory medicine, and vice chair for experimental pathology at Weill Cornell Medical College, and attending pathologist at NewYork-Presbyterian Hospital/Weill Cornell Medical Center, believes that the common joining of two genes to form a new fusion gene influences a certain type of prostate cancer that is more aggressive and sensitive to hormones. In a recent article published in the Journal of the National Cancer Institute, Dr. Rubin describes how in addition to the male hormone testosterone, estrogen – typically thought of as a female hormone – can stimulate this fusion gene. Dr. Rubin’s group is currently exploring how this mechanism may help us understand how aggressive prostate cancer progresses in the absence of male hormones.
Currently, Dr. Rubin and his colleague Dr. Francesca Demichelis, assistant professor in pathology and laboratory medicine and computational biomedicine at the Institute of Computational Biomedicine at Weill Cornell Medical College, are testing blood samples and comparing the DNA of over 2,500 men with and without prostate cancer. They hope to discover clear genetic indicators of prostate cancer, especially its aggressive forms. Their findings will potentially lead to the development of diagnostic tests and preventive drugs for prostate cancer.
NewYork-Presbyterian Hospital/Weill Cornell Medical Center
NewYork-Presbyterian Hospital/Weill Cornell Medical Center, located in New York City, is one of the leading academic medical centers in the world, comprising the teaching hospital NewYork-Presbyterian and Weill Cornell Medical College, the medical school of Cornell University. NewYork-Presbyterian/Weill Cornell provides state-of-the-art inpatient, ambulatory and preventive care in all areas of medicine, and is committed to excellence in patient care, education, research and community service. Weill Cornell physician-scientists have been responsible for many medical advances – from the development of the Pap test for cervical cancer to the synthesis of penicillin, the first successful embryo-biopsy pregnancy and birth in the U.S., the first clinical trial for gene therapy for Parkinson’s disease, the first indication of bone marrow’s critical role in tumor growth, and, most recently, the world’s first successful use of deep brain stimulation to treat a minimally conscious brain-injured patient. NewYork-Presbyterian, which is ranked sixth on the U.S.News & World Report list of top hospitals, also comprises NewYork-Presbyterian Hospital/Columbia University Medical Center, Morgan Stanley Children’s Hospital of NewYork-Presbyterian, NewYork-Presbyterian Hospital/Westchester Division and NewYork-Presbyterian Hospital/The Allen Pavilion. Weill Cornell Medical College is the first U.S. medical college to offer a medical degree oversees and maintains a strong global presence in Austria, Brazil, Haiti, Tanzania, Turkey and Qatar. For more information, visit http://www.nyp.org and Weill Cornell Medical College.
Source: Andrew Klein
New York- Presbyterian Hospital/Weill Cornell Medical Center/Weill Cornell Medical College
Bird Flu Kills Second Woman In China
A second Chinese woman infected with the bird flu virus died in Shandong province on Saturday 17 January, the second person to die from the
virus ths year, and in the meantime a 2-year old girl is also confirmed to be infected with the deadly H5N1 strain of avian flu.
The victim, whose surname was Zhang, was a 27-year old woman from Jinan, the capital of the northern coastal province of Shandong; she fell ill on
5th January.
According to Xinhua, the state run news agency, the 2-year old toddler, who is from the northern province of Shanxi, and whose surname is Peng, fell
ill on 7th January while visiting the more southerly province of Hunan and was taken back to Shanxi by her grandparents on the 11th. Local officials
said yesterday that the child is in a critical condition and that 67 people who have been in contact with her have been kept under close observation but
have not shown any symptoms of bird flu.
The Chinese national Center for Disease Control and Prevention (CDC) confirmed yesterday, Sunday 18 January, that Zhang had contracted the H5N1
strain of the virus and the health authorities in Shandong province said that people who had been in close contact with her have undergone medical
tests but none was found to have symptoms of bird flu, reported the state-run English newspaper China Daily.
The 19-year old woman who died earlier this month was from Beijing, and is thought to have contracted the virus from handling poultry bought at a
market. The authorities have not said how the latest two victims are thought to have contracted the virus.
China’s Ministry of Agriculture (MOA) said yesterday that no bird flu epidemics were detected in Shanxi and Hunan following tests carried out in
poultry farms and markets near to where the toddler had been. However, they urged local veterinary departments in the two provinces to increase
checks on poultry markets and disinfect them thoroughly, reported Xinhua.
Poultry trading is usually brisk in the weeks leading up to Spring Festival, or Chinese New Year, which this year falls on the 26th January, said the
MOA, and coupled with the threat of frequent outbreaks in neighbouring countries it means China now faces a “grim situation” in bird flu prevention.
It will be especially difficult to implement prevention measures at what Xinhua describes as “loosely managed household farms”.
In the meantime, the nationwide network for testing of bird flu has been established following the death of the first woman in Beijing. Vice director
of virus control and prevention at China’s CDC, Shu Yuelong, told the state press that the network links up 63 labs in 31 provinces, autonomous
regions and municipalities. Another 21 new labs will follow over the course of this year, said Shu, adding that:
“Every lab has the ability to test and identify virus of avian influenza and some in provincial disease control centers are capable of analyzing the
virus.”
Worldwide, 394 laboratory confirmed cases of the deadly H5N1 bird flu have been reported to the World Health Organization, including 248 deaths
(WHO, 14 January). Experts believe that it is only a matter of time before the virus mutates into a form where it can pass from human to human, and
when it does, there will be a worldwide pandemic that will kill millions of people. The more outbreaks that occur, the greater the opportunity for the
virus to mutate.
At present people can only catch the virus from infected birds.
Click here for more information on Avian
Influenza (WHO).
Sources: China Daily, Xinhua, WHO.
Written by: Catharine Paddock, PhD
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today
