New Method Could Enable Reprogramming Of Mammalian Cells

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Main Category: Genetics
Also Included In: Biology / Biochemistry;  Stem Cell Research
Article Date: 04 Aug 2012 - 0:00 PDT Current ratings for:
New Method Could Enable Reprogramming Of Mammalian Cells

Through the assembly of genetic components into "circuits" that perform logical operations in living cells, synthetic biologists aim to artificially empower cells to solve critical problems in medicine, energy and the environment. To succeed, however, they'll need far more reliable genetic components than the small number of "off-the-shelf" bacterial parts now available.

Now a new method developed by Boston University biomedical engineers Ahmad S. Khalil and James J. Collins -- and collaborators at Harvard Medical School, Massachusetts General Hospital and MIT -- could significantly increase the number of genetic components in synthetic biologists' toolkit and, as a result, the size and complexity of the genetic circuits they can build. The development could dramatically enhance their efforts not only to understand how biological organisms behave and develop, but also to reprogram them for a variety of practical applications.

Described in the August 2 online edition of Cell, the method offers a new paradigm for constructing and analyzing genetic circuits in eukaryotes -- or organisms whose cells contain nuclei, which include everything from yeasts to humans. Instead of constructing these circuits with off-the-shelf parts from bacteria and porting them into eukaryotes, as most synthetic biologists do, Khalil and his collaborators have engineered these circuits using modular, functional parts from the eukaryotes themselves.

With funding from the Howard Hughes Medical Institute, the Defense Advanced Research Projects Agency and other sources, the research team built their synthetic genetic circuit parts from a class of proteins, known as zinc fingers, which can be programmed to bind desired DNA sequences. The modularity of the new parts enables a wide range of functions to be engineered, the construction of much larger and more complex genetic circuits than what's now possible with bacteria-based parts, and ultimately, the development of much more powerful applications.

"Our research may lead to therapeutic applications, such as the dynamic modification and control of genes and genetic networks that are important in human disease," said Khalil. Potential medical applications include stem cell therapeutics for a wide variety of injuries and diseases and in-cell devices and circuits for diagnosing early stages of cancer and other diseases. The new method may also equip groups of cells to perform higher-order computational tasks for processing signals in the environment in sensing applications.

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Swarms Of Bees Could Unlock Secrets To Human Brains

Main Category: Neurology / Neuroscience
Article Date: 13 Dec 2011 - 0:00 PST

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Scientists at the University of Sheffield believe decision making mechanisms in the human brain could mirror how swarms of bees choose new nest sites.

Striking similarities have been found in decision making systems between humans and insects in the past but now researchers believe that bees could teach us about how our brains work.

Experts say the insects even appear to have solved indecision, an often paralysing thought process in humans, with scouts who seek out any honeybees advertising rival nest sites and butt against them with their heads while producing shrill beeping sounds.

Dr James Marshall, of the University of Sheffield's Department of Computer Science, who led the UK involvement in the project and has also previously worked on similarities between how brains and insect colonies make decisions, said: "Up to now we've been asking if honeybee colonies might work in the same way as brains; now the new mathematical modelling we've done makes me think we should be asking whether our brains might work like honeybee colonies.

"Many people know about the waggle dance that honeybees use to direct hive mates to rich flower patches and new nest sites. Our research published in the journal Science (on December 9), shows that this isn't the only way that honeybees communicate with each other when they are choosing a new nest site; they also disrupt the waggle dances of bees that are advertising alternative sites."

Biologists from Cornell University, New York, University of California Riverside and the University of Bristol set up two nest boxes for a homeless honeybee swarm to choose between and recorded how bees that visited each box interacted with bees from the rival box. They found that bees that visited one site, which were marked with pink paint, tended to inhibit the dances of bees advertising the other site, which were marked with yellow paint, and vice versa

Tom Seeley of Cornell University, author of the best-selling book Honeybee Democracy said "We were amazed to discover that the bees from one nest box would seek out bees performing waggle dances for the other nest box and butt against them with their heads while simultaneously producing shrill beeping sounds. We call this rough treatment the 'stop signal' because most bees that receive this signal will cease dancing a few seconds later."

Dr Patrick Hogan of the University of Sheffield, who constructed the mathematical model of the bees, added: "The bees target their stop signal only at rivals within the colony, preventing the colony as a whole from becoming deadlocked with indecision when choosing a new home. This remarkable behaviour emerges naturally from the very simple interactions observed between the individual bees in the colony."

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Researchers Say Scar Findings Could Lead To New Therapies

Main Category: Dermatology
Also Included In: Immune System / Vaccines
Article Date: 13 Dec 2011 - 0:00 PST

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Researchers at the Stanford University School of Medicine report that they have identified the molecular pathway through which physical force contributes to scarring in mice.

"Our study exposes one of the fundamental mechanisms by which the mechanical environment can directly increase inflammation, which is strongly implicated in scarring," said Geoffrey Gurtner, MD, professor and associate chair of surgery.

Mice genetically engineered to lack an enzyme that is activated by mechanical force demonstrated less inflammation and fibrosis - the formation of excess fibrous connective tissue - in their incisions than mice in a control group, the study found. Inflammation and scar formation also were reduced among mice injected with an organic compound, a small molecule called PF-573228, that blocks this enzyme, which helps cells sense changes in the mechanical environment.

While further testing is needed to determine the validity of the findings in humans, the researchers say they hope their work will pave the way for new treatments of fibrotic diseases - disorders caused by excess scarring, such as pulmonary fibrosis (the buildup of scar tissue in the lungs) - as well as inflammatory diseases, such as rheumatoid arthritis.

The study was published online in Nature Medicine. Gurtner is the senior author. The lead author is postdoctoral scholar Victor Wong, MD.

Inflammation, an important part of healing, occurs when white blood cells and the chemicals they release try to kill bacteria and eat up damaged tissue at the site of an injury. However, inflammation is also linked to scarring. Excessive scarring is known as fibrosis. And while there are chemical mechanisms that lead to inflammation, mechanical forces generally have been overlooked as a key stimulator of this biological response and as a possible therapeutic target, the researchers say. An example of such a force would be the pulling on an incision when a patient moves; it's the reason stitches are sometimes needed.

"We just haven't taken the physical environment - the environment of mechanical forces that hold all our cells together - seriously enough as a source of inflammation and fibrosis," Gurtner said.

Previous studies have implicated the enzyme, known as focal adhesion kinase, in cellular responses to force, but whether it played a role in inflammation and scarring remained unclear. When the researchers had it genetically engineered out of mice for the current study, incisions in those mice healed normally but scarring was markedly diminished. Ten days after the mice sustained a skin incision, 48 percent fewer scar-tissue cells had formed around it compared with incisions in a control group, according to the study.

The researchers found that the enzyme appears to modulate protein molecules often used by cells to communicate with one another. In test tube studies, mouse scar tissue missing the enzyme did not respond normally to mechanical stimuli and released far lower levels of inflammatory mediators.

The researchers also tested the effects of the enzyme-inhibiting molecule (PF-573228) on human cells that play a key role in wound healing and found that the molecules that stimulate inflammation were not released.

Tests on humans are needed before researchers can evaluate whether this approach could serve as the basis for a valid therapy. The researchers said they hope their findings can eventually be used to develop treatments for diseases that involve excess scarring throughout the body. "These results suggest that targeted strategies to uncouple mechanical force from inflammation and fibrosis may prove clinically successful across diverse organ systems," they concluded.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our dermatology section for the latest news on this subject. Other Stanford co-authors were Michael Longaker, MD, MBA, the Deane P. and Louise Mitchell Professor at the School of Medicine; Satoshi Akaishi, MD, a visiting surgeon from Japan; postdoctoral fellows Michael Sorkin, MD, Kemal Levi, MD, and Jason Glotzbach, MD; bioinformatics student Michael Januszyk, MD; and medical students Emily Nelson, Kristine Rustad, Josemaria Paterno and Ivan Vial.
The study was funded by grants from the Armed Forces Institute of Regenerative Medicine and the Oak Foundation. Information about Stanford's Department of Surgery, which also supported the work, is available at http://surgery.stanford.edu.
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Clues To Development Of The Pancreas Provided By Rare Genetic Disorder Could Lead To Diabetes Therapy

Main Category: Diabetes
Also Included In: Genetics
Article Date: 13 Dec 2011 - 0:00 PST

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A rare genetic disorder has given researchers at the University of Exeter a surprising insight into how the pancreas develops. The finding provides a clue to how it may be possible to 'programme' stem cells - master cells in the body that can develop into specialised cells - to become pancreatic cells.

Pancreatic agenesis is a rare condition in which the body is unable to produce a pancreas. The pancreas plays an essential role in regulating levels of sugar (glucose) in the blood. It does this by the release of the hormone insulin, which is generated and released by cells known as pancreatic beta cells. It also produces enzymes to help digest and absorb food.

Rare mutations in the genes PDX1 and PTF1A have previously been shown to cause pancreatic agenesis, but have only been identified in a handful of families affected by the condition. Until now, the underlying causes of most cases have been unknown.

In a paper published in Nature Genetics, an international team of researchers led by scientists from the Peninsula College of Medicine and Dentistry at the University of Exeter report a mutation in the gene GATA6 found in fifteen out of twenty-seven individuals with pancreatic agenesis. The study, funded by organisations including the Wellcome Trust, Diabetes UK and the National Institute for Health Research, establishes a key role for GATA6 in the development of pancreatic cells.

The finding was particularly surprising as switching off the GATA6 gene in mouse models appeared to make no difference to the development of the pancreas.

Professor Andrew Hattersley from the Peninsula College of Medicine and Dentistry, said: "This rare genetic condition has provided us with a surprising insight into how the pancreas develops. What is it that programmes cells to become pancreatic beta cells? Our study suggests that GATA6 plays a very important role in this process and we hope this will help the crucial work to try and make beta-cells for patients with type 1 diabetes."

Whilst pancreatic agenesis is an extreme form of pancreatic dysfunction, far more common is diabetes. In type 1 diabetes, which generally develops in childhood, the immune system attacks and destroys pancreatic beta cells and the body is unable to regulate glucose levels, whilst in type 2 diabetes, the beta cells gradually decline until, usually during adulthood, they cease to function.

Professor Sian Ellard, also from Peninsula College of Medicine and Dentistry, added: "This discovery was possible because new sequencing approaches meant we could test all the genetic information in one go and because with the help of doctors throughout the world we were able to study 27 patients with a very rare condition."

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Hospital Room Cleaning Could Be Revolutionized By New Disinfection Technique

Main Category: Infectious Diseases / Bacteria / Viruses
Also Included In: MRSA / Drug Resistance;  Public Health
Article Date: 12 Dec 2011 - 1:00 PST

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A Queen's University infectious disease expert has collaborated in the development of a disinfection system that may change the way hospital rooms all over the world are cleaned as well as stop bed bug outbreaks in hotels and apartments.

"This is the future, because many hospital deaths are preventable with better cleaning methods," says Dick Zoutman, who is also Quinte Health Care's new Chief of Staff. "It has been reported that more than 100,000 people in North America die every year due to hospital acquired infections at a cost of $30 billion. That's 100,000 people every year who are dying from largely preventable infections."

Dr. Zoutman has also used this disinfection technology to kill bed bugs. A major U.S. hotel chain has already expressed interest in the technology because of its potential to save the company millions of dollars in lost revenue and infected furniture.

Dr. Zoutman worked in collaboration with Dr. Michael Shannon of Medizone International at laboratories located in Innovation Park, Queen's University. Medizone is commercializing the technology and the first deliveries are scheduled for the first quarter of 2012.

The new technology involves pumping a Medizone-specific ozone and hydrogen peroxide vapour gas mixture into a room to completely sterilize everything - including floors, walls, drapes, mattresses, chairs and other surfaces. It is far more effective in killing bacteria than wiping down a room.

Dr. Zoutman says the technique is similar to what we now know Mother Nature uses to kill bacteria in humans. When an antibody attacks a germ, it generates ozone and a minute amount of hydrogen peroxide producing a new highly reactive compound that is profoundly lethal against bacteria, viruses and mold.

"It works well for Mother Nature and is working very well for us," says Dr. Zoutman

There are other disinfecting technologies that involve pumping gas into a room, but Medizone's method is the only one that sterilizes as well as surgical instrument cleaning. It also leaves a pleasant smell and doesn't affect any medical equipment in the room. The entire disinfection process is also faster than other methods - it takes less than one hour.

Dr. Zoutman says the technology could also be used in food preparation areas and processing plants after outbreaks such as listeria and to disinfect cruise ships after an infection outbreak.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our infectious diseases / bacteria / viruses section for the latest news on this subject. Study results on the process are published in the December issue of the American Journal of Infection Control.
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Football Could Contribute To Strokes In Adolescents

Main Category: Stroke
Also Included In: Sports Medicine / Fitness;  Pediatrics / Children's Health
Article Date: 12 Dec 2011 - 1:00 PST

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Young football players may be at higher risk for stroke, according to a new study released in Journal of Child Neurology (JCN), published by SAGE.

Researchers Dr. Jared R. Brosch and Dr. Meredith R. Golomb looked at various case studies of football players in their teens that suffered a stroke and found some potential causes for strokes in young football athletes. Some of those potential risks include: an increase of hyperventilation, repeated neurological injury, use of anabolic steroids, use of highly caffeinated energy drinks an increase in obesity of young players The authors point out the increase in obesity presents a two-fold risk as it not only increases the force of impacts among the players, but also the likelihood for other stroke risk factors such as hypertension.

"Two of our subjects had mild hypertension, but were too young to have had the many years of exposure that would lead to chronic vascular injury," wrote the researchers.

Looking at the previous research, the authors did conclude that even more investigation was needed to better draw conclusions and best practices for dealing with head trauma and football in children.

"Organized childhood tackle football in the United States can begin at age 5 years, leading to potentially decades of repeated brain injuries. In addition, the body mass index of the United States pediatric football-playing population continues to increase, so the forces experienced by tackled pediatric players continues to increase," wrote Brosch and Golomb. "Further work is needed to understand how repeated high-impact large-force trauma from childhood football affects the immature central nervous system."

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Visit our stroke section for the latest news on this subject. "American Childhood Football as a Possible Risk Factor for Cerebral Infarction," in Journal of Child Neurology - available free for a limited time at http://jcn.sagepub.com/content/26/12/1493.full.pdf+html.

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Changing The Locks: HIV Discovery Could Allow Scientists To Block Virus's Entry Into Cell Nucleus

Main Category: HIV / AIDS
Article Date: 11 Dec 2011 - 0:00 PST

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Scientists have found the 'key' that HIV uses to enter our cells' nuclei, allowing it to disable the immune system and cause AIDS The finding, published today in the open access journal PLoS Pathogens, provides a potential new target for anti-AIDS drugs that could be more effective against drug-resistant strains of the virus.

HIV is transmitted through bodily fluids, primarily infected blood or semen. Once inside the bloodstream, the virus infects key components of the immune system including cells known as macrophages. It works its way into the nucleus of the macrophages, where it integrates itself into the cell's DNA, allowing it to replicate and spread throughout the body.

To access the DNA, the HIV must pass through the Nuclear Pore Complex, a gateway into the nucleus. Until now, the mechanism that allows the virus to pass through this gateway was unknown. Now, a team of scientists from UCL (University College London), the University of Pennsylvania School of Medicine and the Laboratory of Molecular Biology in Cambridge, has identified a vital component of this mechanism. A part of the HIV virus called the capsid protein, acting like a key, binds to Nup358, a protein on the nuclear pore complex, unlocking the gateway and granting the virus access to the DNA.

Professor Greg Towers, a Wellcome Trust Senior Research Fellow at UCL, who led the research, says: "It's thirty years since the first cases of AIDS were reported and whilst great progress has been made in developing and improving antiretroviral drugs for treating HIV infection, the virus often develops resistance against these drugs making it very difficult to treat. It's very important that we stay one step ahead with new therapeutic strategies.

"In our research, we have found the 'lock and key' that allow HIV to enter a cell's nucleus. Once inside, the virus can begin to replicate itself, spreading almost unchecked throughout the body. If we were able to block this entry with a drug - in effect, to change the locks - then we could stop this spread."

Targeting proteins in the host, rather than in the virus itself, has added benefits, explains first author Dr Torsten Schaller.

"Almost all HIV treatments target the virus itself," he explains. "We know that HIV can easily evolve and change, which means that the virus can become immune to the effects of the drugs, rendering them ineffective. But if we can develop drugs which target proteins in the infected person's body, the virus will struggle to evolve to get around this."

According to the World Health Organization, 33.3 million people were living with HIV in 2009, of which 2.6 million were newly infected. Without treatment, the virus causes potentially fatal damage to the immune system, leading to opportune infections. Deaths from AIDS-related illnesses are the third most common cause of death in low-income countries, killing around 1.8 million people a year worldwide.

The research was funded by the Wellcome Trust, the National Institute of Health Research and the Medical Research Council in the UK, and the National Institutes of Health, the University of Pennsylvania Center for AIDS Research, and the Pennsylvania Department of Health in the US.

Professor Danny Altmann, Head of Pathogens, Immunology and Population Health at the Wellcome Trust, said: "This is exciting work into somewhat uncharted territory. Professor Towers and colleagues have taken a big step towards modelling how HIV enters and integrates itself into the cell's DNA and then uses it to replicate. It offers the prospect of novel ways to try and combat HIV infection."

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Similar Blood Pressure Drugs Could Have Different Impacts On Dialysis Patients' Heart Health

Main Category: Blood / Hematology
Also Included In: Cardiovascular / Cardiology;  Hypertension;  Urology / Nephrology
Article Date: 11 Dec 2011 - 0:00 PST

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Two seemingly similar blood pressure - lowering drugs have different effects on the heart health of dialysis patients, according to a study appearing in an upcoming issue of the Journal of the American Society Nephrology (JASN). The results indicate that certain dialysis patients may benefit more from one drug while some should opt for the other.

About 20% of kidney disease patients die within one year after they start dialysis and more than half die after five years - mostly from heart disease. Two classes of drugs, called angiotensin converting enzyme inhibitors (ACE inhibitors) and angiotensin receptor blockers (ARBs), act in a similar way to prevent and treat heart disease in the general population. Studies of the drugs in dialysis patients are scarce.

ACE inhibitors and ARBs primarily lower blood pressure, but they also decrease inflammation and can produce other beneficial effects for patients. T. Alp Ikizler, MD (Vanderbilt University Medical Center) and his colleagues looked to see if there is a difference between ACE inhibitor and ARB treatments on dialysis patients' heart health.

The researchers randomized 15 dialysis patients to receive an ACE inhibitor, an ARB, or a placebo for one week. Then patients received no treatment for three weeks, after which they were again randomized to receive an ACE inhibitor, an ARB, or a placebo for one week. This wash-out/treatment cycle was then conducted once more. Tests were conducted after each treatment cycle.

The investigators found that ARBs were more effective at fighting inflammation while ACE inhibitors were better at preventing blood vessel damage. Both of these properties could help prevent heart disease. The results suggest that ACE inhibitors and ARBs have different effects on dialysis patients' heart health that go beyond their similar blood pressure - lowering capabilities.

"The implication is that the choice of each of the drugs in dialysis patients could depend on the profile of each individual considered for treatment, which would be a more personalized approach to therapy," said Dr. Ikizler. This implies that different dialysis patients might respond to each drug differently and that some would get the most benefit from ACE inhibitors while others would benefit more from ARBs. The findings emphasize the need for a long-term randomized clinical trial to compare the effects of ARBs and ACE inhibitors on different aspects of heart health in dialysis patients.

Study co-authors include Jorge Gamboa MD, Mias Pretorius MD, Deanna Todd-Tzanetos MD, James M. Luther MD, Chang Yu, PhD, and Nancy J. Brown MD (Vanderbilt University Medical Center).

Disclosures: Dr. Ikizler is a consultant to Abbott Renal, Abbott Nutrition, Renal Advantage, Inc., AMGEN, Novartis, Bristol Myers Squibb, and Baxter Renal. Dr. Brown is a consultant for Novartis, Merck, and Boehringer-Ingelheim.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our blood / hematology section for the latest news on this subject. "Comparative Effects of Angiotensin-Converting Enzyme Inhibition and Angiotensin-Receptor Blockade on Inflammation during Hemodialysis" online at http://jasn.asnjournals.org/ December 8, 2011, doi: 10.1681/ASN.2011030287.

The content of this article does not reflect the views or opinions of The American Society of Nephrology (ASN). Responsibility for the information and views expressed therein lies entirely with the author(s). ASN does not offer medical advice. All content in ASN publications is for informational purposes only, and is not intended to cover all possible uses, directions, precautions, drug interactions, or adverse effects. This content should not be used during a medical emergency or for the diagnosis or treatment of any medical condition. Please consult your doctor or other qualified health care provider if you have any questions about a medical condition, or before taking any drug, changing your diet or commencing or discontinuing any course of treatment. Do not ignore or delay obtaining professional medical advice because of information accessed through ASN. Call 911 or your doctor for all medical emergencies.

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Similar Blood Pressure Drugs Could Have Different Impacts On Dialysis Patients' Heart Health

Main Category: Heart Disease
Also Included In: Urology / Nephrology
Article Date: 09 Dec 2011 - 2:00 PST

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Two seemingly similar blood pressure lowering drugs have different effects on the heart health of dialysis patients, according to a study appearing in an upcoming issue of the Journal of the American Society Nephrology (JASN). The results indicate that certain dialysis patients may benefit more from one drug while some should opt for the other.

About 20% of kidney disease patients die within one year after they start dialysis and more than half die after five years mostly from heart disease. Two classes of drugs, called angiotensin converting enzyme inhibitors (ACE inhibitors) and angiotensin receptor blockers (ARBs), act in a similar way to prevent and treat heart disease in the general population. Studies of the drugs in dialysis patients are scarce.

ACE inhibitors and ARBs primarily lower blood pressure, but they also decrease inflammation and can produce other beneficial effects for patients. T. Alp Ikizler, MD (Vanderbilt University Medical Center) and his colleagues looked to see if there is a difference between ACE inhibitor and ARB treatments on dialysis patients' heart health.

The researchers randomized 15 dialysis patients to receive an ACE inhibitor, an ARB, or a placebo for one week. Then patients received no treatment for three weeks, after which they were again randomized to receive an ACE inhibitor, an ARB, or a placebo for one week. This wash-out/treatment cycle was then conducted once more. Tests were conducted after each treatment cycle.

The investigators found that ARBs were more effective at fighting inflammation while ACE inhibitors were better at preventing blood vessel damage. Both of these properties could help prevent heart disease. The results suggest that ACE inhibitors and ARBs have different effects on dialysis patients' heart health that go beyond their similar blood pressure lowering capabilities.

"The implication is that the choice of each of the drugs in dialysis patients could depend on the profile of each individual considered for treatment, which would be a more personalized approach to therapy," said Dr. Ikizler. This implies that different dialysis patients might respond to each drug differently and that some would get the most benefit from ACE inhibitors while others would benefit more from ARBs. The findings emphasize the need for a long-term randomized clinical trial to compare the effects of ARBs and ACE inhibitors on different aspects of heart health in dialysis patients.

Article adapted by Medical News Today from original press release. Source: American Society of Nephrology
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