Humans, Not Climate, Driving Increased Dengue Risk In Australia

‘Drought-proofing’ Australia’s urban regions by installing large domestic
water tanks may enable the dengue mosquito Aedes aegypti to regain its
foothold across the country and expand its range of possible infections,
according to a new study published May 5 in the open-access journal PLoS
Neglected Tropical Diseases.

Dr Nigel Beebe and colleagues from the University of Queensland, CSIRO
Entomology, the Australian Army Malaria Institute, and the Communicable
Diseases Branch of Queensland Health, Brisbane, challenge the common
assumption that climate change will drive the spread of this mosquito,
suggesting
instead that the real driver is human behavior.

The study combines current and forecasted climate change conditions with
historical epidemics to reveal the risk of dengue infections in all
capital
cities around Australia by 2050. Beebe and colleagues developed and
critically assessed their models to project the distribution of the
mosquito in
2030 and 2050. Currently, dengue fever occurs in Queensland only. However,
the implementation of new water tanks, combined with already warm summer
temperatures, could enable the mosquito to re-emerge and further its
current reach.

“Dengue risks will not be driven directly by warmer temperatures or
changes in rainfall patterns,” Beebe said. “Our summers already provide
ideal conditions for dengue transmission around the country, but the
introduction of government-subsidized water storage devices now adds the
ideal
breeding ground for the dengue mosquito to re-emerge.”

“While research is properly focused on the impact of anthropogenic climate
change, this study highlights the need to look also at our responses to
those changes and the outcomes they generate,” he said.

The current dengue fever epidemic in far north Queensland is approaching
1,000 reported cases over the summer of 2008-2009.

Beebe and colleagues are continuing this research under the auspices of
the CSIRO Climate Change Adaption National Research Flagship.

FINANCIAL DISCLOSURE: This work was supported by a jointly funded position
at the University of Queensland and the CSIRO Climate Adaptation Flagship.
The funders had no role in study design, data collection and analysis,
decision to publish, or preparation of the manuscript.

Citation:
“Australia’s Dengue Risk Driven by Human Adaptation to Climate Change.”
Beebe NW, Cooper RD, Mottram P, Sweeney AW (2009)
PLoS Negl Trop Dis 3(5): e429. doi:10.1371/journal.pntd.0000429

Source
PLoS
Neglected Tropical Diseases

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Liver Transplantation After Drug Induced Acute Liver Failure Examined By Study

Liver transplantation offers a good chance for survival for patients with drug induced acute liver failure, however, certain pre-transplant factors are associated with worse outcomes. Patients who are on life support, who have elevated serum creatinine, and children whose liver failure was caused by antiepileptic drugs did not fare as well after transplantation. These findings are in the July issue of Liver Transplantation, a journal published by John Wiley & Sons. The article is also available online at Wiley Interscience.

Drug induced acute liver failure is very rare, but can be life-threatening. Acetaminophen is the most common cause, accounting for nearly half of cases in adults, but other drugs can also be responsible. For patients who are unlikely to recover spontaneously, liver transplantation is the only treatment.

Researchers, led by Ayse L. Mindikoglu, M.D., M.P.H. of the University of Maryland School of Medicine and VA Maryland Health Care System, examined the United Network for Organ Sharing (UNOS) database which contains information about outcomes of nearly all liver transplants performed in the U.S. since 1987. They planned to analyze all of the drugs associated with acute liver failure and subsequent liver transplantation, determine survival rates after transplantation, and develop a model that would predict the risk of death after transplantation for these patients.

They included 661 patients – 567 adults and 94 children under age 18 – who were transplanted for drug induced acute liver failure between October 1, 1987, and December 31, 2006. For each case, they collected twenty recipient and six donor demographic and clinical variables from the database.

They found that the leading drug groups causing liver failure that required transplantation were acetaminophen (40 percent), antituberculosis drugs (8 percent), antiepileptics (7 percent) and antibiotics (6 percent). For the entire cohort of transplant recipients, median survival time was 14.4 years. One year estimated survival probabilities were 76 percent, 82 percent, 52 percent, 82 percent, and 79 percent for acetaminophen, antituberculosis, antiepileptics, antibiotics and others, respectively.

“Among the patients who had acute liver failure due to antiepileptics, one-year survival was only 27 percent in patients less than 18 years old compared to 75 percent in patients 18 years old or older,” the authors report. Interestingly, these patients were least likely to be listed as status 1 and spent the most time waiting for an organ. Also, the warm and cold ischemia times were longest for this group of patients. “The relatively low survival probability persisted after controlling for these variables in multivariate analysis,” the authors report. The reasons for the decreased survival in this group could not be elucidated based on the available data.

Examining the different demographic and clinical factors for each patient and donor, the researchers noted that, “elevated serum creatinine, being on life support, and drug-induced acute liver failure due to antiepileptics (at age less than 18) were found to be independent pretransplant predictors of poor survival.”

Using the entire study population, the researchers developed a prognostic model which showed strong predictive ability.

An accompanying editorial by Paul B. Watkins of the Institute for Drug Safety at the Hamner Institutes of Health Sciences, Research Triangle, NC and Paul H. Hayashi of the University of North Carolina , commends the authors for adding valuable information about acute liver failure caused by drugs. In particular, “the identification of poorer outcome for children with anti-epileptic drug induced acute liver failure is intriguing and points out the need for more focused research on drug induced liver injury in pediatric populations.”

Drug induced liver injury has wide implications for all of us who take and prescribe medications, they write. And they look forward to future advances in our understanding of the issue, as researchers investigate hypotheses about preventive factors and genetic predisposition.

Notes:

Article: “Outcome of Liver Transplantation for Drug Induced Acute Liver Failure in the United States. Analysis of the United Network for Organ Sharing Database.” Mindikoglu, Ayse L.; Magder, Laurence S.; Regev, Arie. Liver Transplantation; July 2009.

Editorial: “Progress in Our Understanding of Severe Drug Induced Liver Injury.” Hayashi, Paul H. Watkins, Paul B.; Liver Transplantation; July 2009.

Source:
Sean Wagner

Wiley-Blackwell

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Embryonic Stem Cell State Sustained By Molecular Alliance

One of the four ingredients in the genetic recipe that scientists in Japan and the U.S. followed last year to persuade human skin cells to revert to an embryonic stem cell state, is dispensable in ES cells, thanks to the presence of a molecular alliance between a specific group of key proteins known as transcription factors, a research team led by the Genome Institute of Singapore (GIS) under the Agency for Science, Technology and Research (A*STAR) reports in the current issue of Nature Cell Biology.

The reprogramming factor – Klf4, one of the transcription factors that determine whether a cell’s genes are active or silent – has at least two other sibling molecules that will substitute Klf4 to maintain a pluripotent embryonic stem (ES) cell state, the GIS-led team said.

Klf4 (also known as gut-enriched KrГјppel-like factor or Gklf) belongs to the KrГјppel-like factor (Klf) family of transcription factors that regulate numerous biological processes including proliferation, differentiation, development and apoptosis, or programmed cell death.

Since reprogramming mature cells to the ES state may provide a ready source of tissue for biomedical research and clinical treatment of diseases such as Parkinson’s and diabetes, several laboratories, including GIS, are trying to better understand and finely tune the reprogramming process.

The team looks for clues for what these reprogramming ingredients are doing in ES cells.

“Klf4 has been a mysterious player among the four reprogramming factors. As taking out Klf4 in ES cells did not have any apparent effects, it is difficult to reconcile why such a potent reprogramming factor has no role in ES cell biology,” said GIS scientist Ng Huck Hui, Ph.D., who headed the research team. Other members of the team include researchers from the National University of Singapore and University of Illinois at Urbana-Champaign.

The GIS research team found that when Klf4 was depleted, Klf2 and Klf5 took over Klf4′s role. To understand the molecular basis of the Klf4 redundancy, the scientists studied the DNA binding and transcription activation properties of the three Klfs and found that the profiles of the three Klfs were strikingly similar.

“Most important, the data showed that the other Klfs were bound to the target sites when one of them was depleted.” said Dr. Ng. “These KrГјppel-like factors form a very powerful alliance that work together on regulating common targets. The impact of losing one of them is masked by the other two sibling molecules.”

For example, Klfs were found to regulate the Nanog gene and other key genes that must be active for ES cells to be pluripotent, or capable of differentiating into virtually any type of cells. Nanog gene is one of the key pluripotency genes in ES cells.

“We suggest that Nanog and other genes are key effectors for the biological functions of the Klfs in ES cells,” Dr. Ng said.

“Together, our study provides new insight into how the core Klf circuitry integrates into the Nanog transcriptional network to specify gene expression unique to ES cells.

The way these factors network with key genes in ES cells suggest a way of how Klf4 (along with the other three reprogramming factors) can jump-start the ES cell gene expression engine in adult cells,” he noted.

Although these three Klfs are involved in diverse biological roles, their redundant roles have not been previously appreciated.

“Dr. Ng and his colleagues at the Genome Institute of Singapore again have unraveled another intricacy of what makes a stem cell,” said Edison Liu, M.D., Executive Director of GIS. “This work brings us closer to a detailed understanding of the genetic components of stemness.”

Alan Colman, Ph.D., internationally recognized leader in stem cell research, said, “Klf4 is a transcription factor that came to prominence recently because it was one of four factors used to reprogram somatic cells back to the pluripotent state seen in embryonic stem cells.

“The mystery of the role of Klf4 has been revealed in studies by Huck Hui and colleagues,” added Colman, Executive Director of the Singapore Stem Cell Consortium, which like GIS, is part of Singapore’s A*STAR. “They show for the first time that Klf4 itself is not needed for the maintenance of the pluripotent state in ES cells; however, this is because the cells have a number of other Klf-like transcription factors that can substitute for Klf4.”

###

Contact:
Genome Institute of Singapore
Winnie Serah Lim
Asst Manager, Corporate Communications

Source: Cathy Yarbrough

Agency for Science, Technology and Research (A*STAR), Singapore

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Nicotine Creates Stronger Memories, Cues To Drug Use

Ever wonder why former smokers miss lighting up most when they are in a bar or after a meal with friends?

Researchers at Baylor College of Medicine say nicotine, the addictive component in cigarettes, “tricks” the brain into creating memory associations between environmental cues and smoking behavior. The findings appear in the current issue of the journal Neuron.

“Our brains normally make these associations between things that support our existence and environmental cues so that we conduct behaviors leading to successful lives. The brain sends a reward signal when we act in a way that contributes to our well being,” said Dr. John A. Dani, professor of neuroscience at BCM and co-author of the study. “However, nicotine commandeers this subconscious learning process in the brain so we begin to behave as though smoking is a positive action.”

Dani said that environmental events linked with smoking can become cues that prompt the smoking urge. Those cues could include alcohol, a meal with friends, or even the drive home from work. To understand why these associations are so strong, Dani and Dr. Jianrong Tang, instructor of neuroscience at BCM and co-author of the report, decided to record brain activity of mice as they were exposed to nicotine, the addictive component of tobacco.

The mice were allowed to roam through an apparatus with two separate compartments. In one compartment, they received nicotine. In the other, they got a benign saline solution. Later, the researchers recorded how long the mice spent in each compartment. They also recorded brain activity within the hippocampus, an area of the brain that creates new memories.

“The brain activity change was just amazing,” Dani said. “Compared to injections of saline, nicotine strengthened neuronal connections – sometimes up to 200 percent. This strengthening of connections underlies new memory formation.”

Consequently, mice learned to spent more time in the compartment where the nicotine was administered compared to the one where saline was given to them.

“We found that nicotine could strengthen neuronal synaptic connections only when the so called reward centers sent a dopamine signal. That was a critical process in creating the memory associations even with bad behavior like smoking.”

Dani said understanding mechanisms that create memory could have implications in future research and treatments for memory disorders, such as Alzheimer’s disease, and for dopamine signaling disorders, such as Parkinson’s disease.

This study was supported by the National Institute of Neurology Disorders and Stroke and the National Institute of Drug Abuse.

Source:
Graciela Gutierrez

Baylor College of Medicine

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Major Grant To Support Rapid, Accurate, Affordable Test For Tuberculosis

Dr. Antonio Campos-Neto, head of the department of Cytokine Biology at The Forsyth Institute, has received a major grant from the internationally renowned Foundation for Innovative New Diagnostics (FIND) to continue his work to develop a test to diagnose active Tuberculosis (TB), the world’s second deadliest infectious disease. Dr. Campos-Neto aims to create a rapid, sensitive, non-invasive and accurate TB diagnostic test, modeled after a pregnancy test, which would identify the TB bacterium’s molecules present in a patient’s urine.

TB is a leading cause of death worldwide, with 1.7 million deaths and 9 million new active cases annually. TB cases are already at epidemic levels in Africa and are on the rise in developing countries throughout the world, particularly among HIV/AIDS patients. This resurgence – combined with the ease of transmission through coughing, sneezing and other common activities, and the emergence of drug resistant TB strains – is leading to a growing fear of a global spread of the disease.

Among the main barriers to preventing the spread of TB are the shortcomings of existing diagnostic tests, including: inaccurate diagnoses, limited test sensitivity, invasive sample collection, time-consuming testing and most importantly, failure to distinguish between active and latent cases.

“We are in the preliminary stages of establishing a methodology that allows us to detect minute traces of the TB antigens that are excreted in the urine by a TB-infected patient. What is so exciting about this project is that if we are successful it will contribute tremendously to the control of a disease that kills close to two million people every year,” says Dr. Campos-Neto.

The research has already detected molecules produced by TB in the urine of infected mice and humans. Establishing a test that can be used in a clinical setting offers several potential benefits:
confirming the diagnosis of active TB, not latent or dormant infection

the test does not require expensive equipment and can be performed anywhere in the world, including the most remote locations

the test result is easy to read and obtained in less than five minutes, enabling the immediate initiation of treatment

urine is a far easier sample to collect and, unlike current sample collection, is completely non-invasive

the presence of TB antigens in urine may be detectable earlier than through other samples, leading to earlier treatment and increased survival rates

Philip Stashenko, President and CEO of The Forsyth Institute, says, “Dr. Campos-Neto’s research offers a tremendous opportunity to address a critical worldwide public health problem, and extends the Institute’s mission to study systemic disease. This would be an important breakthrough in the diagnosis and treatment of TB.”

Recent studies show that an improved TB diagnostic test could save as many as 625,000 lives every year. Without a new, more efficient and more reliable diagnostic test, TB will continue to spread at alarming rates.

###

About The Foundation for Innovative New Diagnostics:

FIND is dedicated to the development of rapid, accurate and affordable diagnostic tests through public-private partnerships. Its mission is driven by the conviction that good health is central to winning the war against poverty and that correct diagnosis is a crucial first step towards establishing health and efficient use of resources.

About The Forsyth Institute:

Founded in 1910 as a dental infirmary for disadvantaged children, The Forsyth Institute is the world’s leading independent organization dedicated to scientific research and education in oral health and related biomedical sciences.

Source: Matt Ellis

Forsyth Institute

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B Vitamins And The Aging Brain Examined

B vitamins B-6, B-12 and folate all nourish the brain. But much remains to be discovered about the relation between these essential nutrients and our brainpower.

U.S. Department of Agriculture (USDA) nutritionist Lindsay H. Allen has collaborated in ongoing research that has taken a closer look at the role these nutrients may play in preventing decline in brain function. The investigations, led by Mary N. Haan of the University of California-San Francisco, are part of the multiyear Sacramento (Calif.) Area Latino Study on Aging, or “SALSA.” Begun in 1996, the study attracted nearly 1,800 Hispanic seniors, ages 60 to 101, as volunteers.

According to Allen, the research is needed because many studies of B vitamins and brain function have given inconsistent or conflicting results. Allen is director of the Agricultural Research Service (ARS) Western Human Nutrition Research Center in Davis, Calif. ARS is the chief intramural scientific research agency of USDA. Scientists from the University of California-Davis (UCD) and the UCD Medical Center also are collaborating in the research.

An analysis of volunteers’ blood samples showed that lower levels of one B vitamin, folate, were associated with symptoms of dementia and poor brain function, also called “cognitive decline,” as determined by standard tests of memory and other factors. The impairments were detectable even though less than 1 percent of the volunteers were actually deficient in folate.

In women, but not men, low levels of folate were associated with symptoms of depression. In fact, female volunteers whose plasma folate levels were in the lowest third were more than twice as likely to have symptoms of depression as volunteers in the highest third. That finding provided new evidence of an association between lower blood folate and depression. Depression is already known to affect brain function.

In research with vitamin B-12, the SALSA team determined that a protein known as holoTC, short for holotranscobalamin, might be key to a new approach for detecting cognitive decline earlier and more accurately.

The researchers have published these and other findings, beginning in 2003 and continuing through this year, in the American Journal of Clinical Nutrition, Clinical Chemistry and Laboratory Medicine, The European Journal of Clinical Nutrition, The Journal of Nutrition, and The Journal of Nutrition, Health, and Aging.

Source: USDA, Office of Research, Education, and Economics

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Othopaedists Say Biomarker Could Make Diagnosing Knee Injury Easier, Less Costly

A recently discovered biomarker could help doctors diagnose a common type of knee injury, according to a new study.

A team of researchers led by Gaetano Scuderi, MD, clinical assistant professor of orthopaedic surgery at Stanford University School of Medicine and an orthopaedic surgeon at Stanford Hospital & Clinics, has confirmed that a particular protein complex appears in patients with painful meniscal tears. The finding, to be published Feb. 16 in /i>The Journal of Bone and Joint Surgery, could be used to prevent needless surgery and to save billions of dollars in medical-imaging costs.

The menisci are two crescent-shaped pieces of cartilage in each knee joint. Contact sports, such as football, as well as sports that involve lot of pivoting, such as basketball and tennis, increase the risk of the cartilage tearing. It is also prone to tear as a result of natural degeneration, meaning older people are at increased risk. Meniscal tears are painful and usually accompanied by swelling and stiffness. Sometimes the knee joint feels as though it is locked in place.

Patients are generally advised to elevate and apply ice to the knee, as well as to take a break from physical activity that could aggravate the injury. These measures might not be enough, however, so patients can undergo a minimally invasive procedure, arthroscopic surgery, to trim away or repair the meniscus.

But identifying whether a patient’s knee pain stems from a meniscal tear, as opposed to joint arthritis or another type of leg injury, is difficult. For example, in an older patient, magnetic-resonance imaging might reveal an abnormal-looking meniscus that doctors mistake as evidence of a painful tear, even though it is just due to natural degeneration from lots of wear over the years. For such a patient, who is perhaps really suffering from joint arthritis, meniscal surgery would offer no relief.

Knee pain also can stem from other parts of the body. For example, a young athlete who complains of symptoms similar to those of a torn meniscus may undergo a costly MRI that reveals no cartilage abnormalities. In reality, an injured hip ligament could be causing the knee to hurt. “It’s like someone with heart disease feeling pain in his left shoulder,” Scuderi said.

In the study, Scuderi and his co-authors found that the biomarker appeared in the knee fluid of 30 patients who had suffered a painful meniscal tear. It was not present in the knees of 10 asymptomatic patients. The biomarker, a fibronectin-aggrecan complex, holds out the promise of allowing orthopaedists to quickly and accurately diagnose whether the source of a patient’s discomfort is a meniscal tear, as opposed to another type of injury or abnormality, simply by taking a sample of knee fluid. It could thus obviate the need for expensive medical scans and help to prevent surgery that does not address the true cause of a patient’s pain.

“The challenge is not identifying molecular markers of cartilage degeneration, dozens of which are now known,” said co-author Raymond Golish, MD, PhD, who recently completed a fellowship in spine surgery at Stanford. “The difficulty is in finding markers that correlate with painful injuries, as opposed to age-related degeneration that is painless. This study is a big step in that direction.”

Scuderi and his colleagues undertook the prospective study to validate their findings from an earlier study in which they first noted the presence of the protein complex in patients with torn menisci and knee pain. (Those results were published in the July 2010 issue of Clinical Biochemistry.)

The researchers are now running experiments to confirm that the biomarker does not show up in other types of knee injuries, such as ACL tears unaccompanied by meniscal tears. They also are studying whether the protein complex, which is implicated in knee inflammation, could serve as a therapeutic target. “We could envision several things, such as blocking the fibronectin and aggrecan protein fragments from coming together to form a complex, or interfering with the activation of white blood cells at the site,” Scuderi said.

Notes:

The research was supported by Cytonics Inc., a Florida-based company founded by Scuderi in 2006 to pursue possible clinical applications of the fibronectin-aggrecan complex. Researchers from the Jupiter Medical Center, the New York University Hospital for Joint Diseases, the University of Pittsburgh and Cytonics Inc. were also co-authors of the study. Stanford’s Department of Orthopaedic Surgery also supported this work.

Source:
John Sanford
Stanford University Medical Center

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A Special Night To Help The Stroke Association

Celebrity Style Expert Nick Ede once again hosts his annual charity event with the help of Xtra Factor presenter Konnie Huq, to raise awareness for The Stroke Association. The night’s success has been driven by Nick, whose mother died sadly from a stroke some years ago

The following celebrities have confirmed to attend this years event Sarah Harding, Meg Mathews, Jamie Winstone, Patsy Palmer, Jenni Falconer, Kristina Rhianoff, Louie Spence, Tamara Beckwith, Ali Bastien, Camilla Dallarup, Brenda Cole, Michelle Williams, Tina O’ Brien, Andrea McLean, Sinitta, Michelle Mone, Angelica Bell, Zoe Salmon, Jennifer Ellison and Jason Gardiner.

This year’s event on 30 November 2010 is at the Swarovski Crystallized Lounge, 24 Great Marlborough Street, London from 7pm to 10pm, with an exclusive after party hosted by Mark Fuller at Sanctum Soho Hotel.

“The Stroke Association is a charity which is very close to my heart” says Nick, “We need to do everything possible to raise awareness of the charity to help the estimated one million people in the UK who are living with the devastating affects of a stroke. I hope that the party will be a memorable night for everyone who comes but, most crucially, together we raise thousands of pounds for The Stroke Association!”

Elspeth McAusland from The Stroke Association said, “Every five minutes someone in the UK has a stroke but with the right help and support many people can make a good recovery. The kind generosity of supporters like Nick means we can work towards our goal of fewer strokes and for all those touched by stroke to get the help they need.”

Source:

The Stroke Association

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Researchers Unite To Provide Tools To Speed Stem Cell Research

Engineers at Rensselaer Polytechnic Institute have developed tools to help solve two of the main problems slowing the progress of stem cell research — how to quickly test stem cell response to different drugs or genes, and how to create a large supply of healthy, viable stem cells to study from only a few available cells.

The researchers have created methods to study millions of stems cells on devices the size of a standard microscope slide. The techniques enable thousands of individual stem cell experiments to be carried out quickly and in parallel on one small device.

“Rensselaer is quickly establishing itself as leader in the development of stem cell technology that hastens the speed and accuracy of stem cell research,” Provost Robert Palazzo said. “Our scientists and engineers are filling a vital niche in the global scientific effort to develop medical therapies using stem cells. Tools like these, which enable high-throughput study of stem cells, will quickly advance stem cell research in medical labs around the world.”

The two groups of researchers used microarrays to develop miniaturized stem cell laboratories. With this technique researchers can perform high-throughput analysis of the material or cells on a single slide, analyzing tens of thousands of samples in one experiment. Each of the teams developed separate specialized microarray platforms.

Helping Develop Stem Cell Drugs


A team led by Jonathan Dordick, the Howard P. Isermann Professor of Chemical and Biological Engineering, and visiting doctoral student Tiago Fernandez and Professor Joaquim M.S. Cabral from the Instituto Superior TГ©chinco-Lisbon in Portugal developed a platform that will enhance the speed of drug discovery by revealing how different molecules help or hinder stem cell function. Their research was presented at the 234th American Chemical Society (ACS) National Meeting in Boston.

The platform will serve as a tool in the discovery of new drugs that target stem cells, Dordick said. He explained that although this three-dimensional system can be used to discover materials that support stem cell development and growth, not all stem cells are worth saving. “New research is showing that some stem cells could be the precursor for cancer and the reason that cancer reappears after having been totally eradicated by chemotherapy,” he said. “With this platform we may be able to rapidly screen new drug candidates that target and kill these stem cells. Instead of going for the mature liver cell that spreads cancer, we can catch a liver stem cell before it can kick off cancer development.”

The device will enable drug researchers to quickly screen thousands of small molecules (the basic element of many modern drugs) for their impacts on the fate of stem cells.

Dordick’s group was able to prepare up to 1,000 drops as small as 20 nanoliters on a chemically modified slide. The drops contained a mixture of mouse embryonic stem cells encased in a specialized gel. The researchers discovered that in this mixture, the cells remained viable and could be used in various forms of cell-based screening.

Helping Understand Gene Function in Stem Cells


A separate team led by Professor of Chemical and Biological Engineering Ravi Kane and Rensselaer doctoral student Randolph Ashton created a platform that will allow researchers to quickly understand how different genes impact stem cell function or development. Their research will be published in upcoming edition of the journal Stem Cells.

“There are millions of DNA bases and tens of thousands of genes within the human genome,” Kane said. “In order to screen how all these different DNA sequences affect stem cell function you need an extremely high throughput method.”

In order to become a specialized organ, tissue, or neural cell, a stem cell needs to be pointed in the right direction, and that guidance is believed to be provided by a highly complex arrangement of genes. If researchers can isolate the specific genetic sequences that cause a stem cell to transform into a neural cell, the example that Kane used in his research, they can begin to develop medical treatments for common diseases like Parkinson’s disease using specially programmed stem cells infected with the correct arrangement of genes to produce healthy neural cells.

Kane and his team developed a specialized stamping technique that can be used to quickly understand how different genetic sequences affect stem cell development. The stamp is covered with thousands of mircoscale prongs, similar to the surface of a LEGO®. Those prongs imprint the surface of the corresponding slide, creating a microarray platform with thousands of individual cell-adhesive divots — the perfect mircoscale Petri dishes. The master stamp can create thousands of stamped surfaces without the needs for a clean room or sophisticated machinery.

To develop the stem cell mixture added to the stamped surface, the researchers first created a stem cell library. Each stem cell within this library would overexpress a different genetic sequence. Cells from the library are then dropped onto the micropatterned surface, such that each divot contains only one type of cell. Those seeded populations then divide to form individual clonal populations of cells. A stamped surface the size of a microscope slide can contain 3,500 clonal cell populations. These populations can then be screened at the same time for researchers to determine which cells exhibit a desired behavior (i.e. the development of healthy neural cells). The researcher then immediately knows what DNA sequence is responsible for the observed behavior.

To exhibit the effectiveness of their technology, Kane and his group screened clonal populations of rat neural stem cells to identify a sequence that promoted neural stem cell proliferation.

###

Dordick and Fernandez were assisted in their research by Seok Joon Kwon, Moo-Yeal Lee, Maria M. Diogo, and Claudia Lobata de Silva. Kane and Ashton were assisted by Joseph Peltier, Analeah O’Neill, Joshua Leonard, and David Schaffer of the University of California at Berkley and Christopher Fasano and Sally Temple of Albany Medical College.

About Rensselaer


Rensselaer Polytechnic Institute, founded in 1824, is the nation’s oldest technological university. The university offers bachelor’s, master’s, and doctoral degrees in engineering, the sciences, information technology, architecture, management, and the humanities and social sciences. Institute programs serve undergraduates, graduate students, and working professionals around the world. Rensselaer faculty are known for pre-eminence in research conducted in a wide range of fields, with particular emphasis in biotechnology, nanotechnology, information technology, and the media arts and technology. The Institute is well known for its success in the transfer of technology from the laboratory to the marketplace so that new discoveries and inventions benefit human life, protect the environment, and strengthen economic development.

Source: Gabrielle DeMarco

Rensselaer Polytechnic Institute

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Food-Density Dependent Inefficiency In Animals With A Gut As A Stabilising Mechanism In Trophic Dynamics

This work indicates that the conventional simulation of the transfer of energy and resources through trophic systems may on occasion be seriously over estimated.

This is because of a failure to consider adequately the operation of the gut within consumers when consumers are confronted with food in excess or of inferior quality.

Under such conditions, assimilation efficiency declines, resulting in food-density dependent inefficiency. In consequence oscillations in food production, during good or bad years, are moderated as they pass through the food chain.

Proceedings of the Royal Society B: Biological Sciences

Proceedings B is the Royal Society’s flagship biological research journal, dedicated to the rapid publication and broad dissemination of high-quality research papers, reviews and comment and reply papers. The scope of journal is diverse and is especially strong in organismal biology.

Proceedings of the Royal Society B: Biological Sciences

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