Cell Phone/Brain Tumor Connection Remains Inconclusive – But They Pose Neurological Health Risks
There has been much speculation over the last few years about whether cell phones increase the risk of developing a brain tumor. Research has not conclusively answered this question, which has left consumers confused. The majority of studies that have been published in scientific journals do not have sufficient evidence to show that cell phones increase the risk of brain tumors. The problem is that cell phone technology is in its infancy, so none of these studies could analyze long-term risks. This unknown is a particular issue for children, who will face a lifetime of cell phone usage. While the cell phone/brain tumor connection remains inconclusive, the American Association of Neurological Surgeons (AANS) cautions that cell phones present plenty of other risks to people’s neurological health.
Several studies show cell phones are a leading cause of automobile crashes. It is estimated that drivers distracted by cell phones are four times more likely to be in a motor vehicle accident. The following are some sobering statistics:
~According to a Harvard University study, an estimated 2,600 people die and 12,000 suffer serious to moderate injuries each year in cell phone-related accidents.
~A Canadian study analysis of 26,798 cell phone calls made during the 14-month study period showed that the risk of an automobile accident was four times higher when using a cell phone.
~National statistics indicate that an estimated 50,000 traumatic brain injury-related deaths occur annually in the United States, 25,000-35,000 of which are attributed to motor vehicle accidents.
A few recent cases treated in U.S. hospital emergency rooms:
~A 29-year-old male was talking on his cell phone while on an escalator, fell backwards, and lacerated his head.
~A 25-year-old male was talking on his cell phone and walked into a street sign, lacerating his head.
~A 43-year-old female fell down 13-14 steps while talking on her cell phone, after drinking alcohol. She suffered a neck sprain and contusions to her head, back, shoulder, and leg.
~A 50-year-old female suffered nerve damage which was related to extensive cell phone usage. She felt pain in her fingers and the length of her arm while holding her cell phone, and was diagnosed with cervical radiculopathy.
~A 39-year-old man suffered a head injury after crashing into a tree on his bicycle while texting
~A 16-year-old boy suffered a concussion because he was texting and walked into a telephone pole.
Cell Phone Injury Prevention Tips
~Talk hands free by using an earpiece or on speaker mode whenever possible.
~Follow all cell phone laws applicable to your city and state – these vary greatly.
~Use your cell phone only when safely parked, or have a passenger use it.
~Do not dial the phone or take notes while driving, cycling, skateboarding, rollerblading, etc.
~Never text message while driving, walking, cycling, skateboarding, rollerblading, etc.
~Never text message or use a cell phone while performing any physical activities that require attention.
~If your phone rings while driving, let the call go into voice mail and respond later when you are safely parked.
Wednesday, November 19, 2008
Mathematics Students Make Prime Discovery
Westfield State College senior mathematics majors Jeffrey P. Vanasse and Michael E. Guenette, working under the direction of Mathematics Department faculty members Marcus Jaiclin and Julian F. Fleron, have made a significant new discovery in the mathematical field of number theory. They have discovered the first known example of a 3 by 3 by 3 generalized arithmetic progression (GAP).
Most easily thought of as a 3 by 3 by 3 cube (similar to a Rubik’s cube puzzle) made up of 27 primes, their discovery begins with 929 as its smallest prime ends with 27917 as its largest prime. The intervening 25 primes are constructed by adding combinations of the numbers 2904, 3150, and 7440 in an appropriately structured method.
“Such an object was known to exist and its approximate size had been loosely estimated,” Fleron said. “However, a blind search would require checking more cases than can be feasibly checked by all existing modern computers each running for the next million years. Instead, the group used knowledge of the structural relationships between the potential candidates to greatly reduce the potential candidates to be checked.”
An algorithm to check the necessary cases – still easily hundreds of trillions of cases – was programmed using a Linux version of the computer language C++.
“This breakthrough is another indication that our Mathematics Department is working on a world-class level,” said Evan S. Dobelle, president of Westfield State College. “The college is very proud of these students and their professors for taking the initiative to practice cutting-edge mathematics.”
“We were worried that it might take months to run based on our estimates,” Guenette said. “Yet initial tests showed the algorithm running at a hopeful speed.”
“We were always optimistic, but the first tests got us really excited that our method would be successful,” Vanasse said.
The team broke the search up into groups of cases for each of the researchers to run on separate computers. Within days the first known example of a 3 by 3 by 3 GAP was found – one with largest prime of 197,957.
Having succeeded in finding the first known example, and now having a strict bound on the size of the largest prime, the group set to work finding other 3 by 3 by 3 GAPs – in particular, the smallest such. They were successful, showing there are exactly three 3 by 3 by 3 GAPs of primes with largest prime less than 50,000, the smallest example being that described above.
The students and faculty members are hopeful that their work will aid number theorists who continue to work on elusive patterns that lurk within the mystery of the prime numbers.
With estimates for the largest prime in a 4 by 4 by 4 or 3 by 3 by 3 by 3 GAP being near 5 quadrillion (that’s a 5 followed by 15 zeroes) the group is fairly certain that their record for finding the highest dimensional GAP will stand for quite some time, Fleron said.
Guenette of Easthampton, Mass., and Vanasse of Chicopee, Mass., both plan on attending graduate school in mathematics following graduation. Their work on this problem has provided them with a valuable introduction to the efforts of a working research mathematician.
For Jaiclin and Fleron, and the rest of the Westfield State Mathematics Department, it is another opportunity to share with and involve undergraduates what they love best: doing significant mathematics and advancing the frontier of human knowledge.
Fleron said the team’s work was inspired by the recent discoveries of the young Australian mathematician Terence Chi-Shen Tao, now a professor at the University of California, Los Angeles. “Many prominent number theorists are working simply to understand the implications of these discoveries,” he said. “Now Westfield State College students are playing a role, as well.”
British mathematician Andrew Granville, now on the faculty of the Université de Montréal, also inspired the group. Granville’s paper, “Prime Number Patterns,” was published in the April edition of American Mathematical Monthly.
Ironically, Granville just gave a lecture on “Patterns in the Primes” as part of the Distinguished Lecture Series of the Mathematical Association of America (MAA). This series, sponsored by the National Security Agency, took place at the MAA Carriage House Conference Center in Washington D.C. on Thursday, Nov. 13. This was the day before the Westfield State group’s discovery.
Westfield State College senior mathematics majors Jeffrey P. Vanasse and Michael E. Guenette, working under the direction of Mathematics Department faculty members Marcus Jaiclin and Julian F. Fleron, have made a significant new discovery in the mathematical field of number theory. They have discovered the first known example of a 3 by 3 by 3 generalized arithmetic progression (GAP).
Most easily thought of as a 3 by 3 by 3 cube (similar to a Rubik’s cube puzzle) made up of 27 primes, their discovery begins with 929 as its smallest prime ends with 27917 as its largest prime. The intervening 25 primes are constructed by adding combinations of the numbers 2904, 3150, and 7440 in an appropriately structured method.
“Such an object was known to exist and its approximate size had been loosely estimated,” Fleron said. “However, a blind search would require checking more cases than can be feasibly checked by all existing modern computers each running for the next million years. Instead, the group used knowledge of the structural relationships between the potential candidates to greatly reduce the potential candidates to be checked.”
An algorithm to check the necessary cases – still easily hundreds of trillions of cases – was programmed using a Linux version of the computer language C++.
“This breakthrough is another indication that our Mathematics Department is working on a world-class level,” said Evan S. Dobelle, president of Westfield State College. “The college is very proud of these students and their professors for taking the initiative to practice cutting-edge mathematics.”
“We were worried that it might take months to run based on our estimates,” Guenette said. “Yet initial tests showed the algorithm running at a hopeful speed.”
“We were always optimistic, but the first tests got us really excited that our method would be successful,” Vanasse said.
The team broke the search up into groups of cases for each of the researchers to run on separate computers. Within days the first known example of a 3 by 3 by 3 GAP was found – one with largest prime of 197,957.
Having succeeded in finding the first known example, and now having a strict bound on the size of the largest prime, the group set to work finding other 3 by 3 by 3 GAPs – in particular, the smallest such. They were successful, showing there are exactly three 3 by 3 by 3 GAPs of primes with largest prime less than 50,000, the smallest example being that described above.
The students and faculty members are hopeful that their work will aid number theorists who continue to work on elusive patterns that lurk within the mystery of the prime numbers.
With estimates for the largest prime in a 4 by 4 by 4 or 3 by 3 by 3 by 3 GAP being near 5 quadrillion (that’s a 5 followed by 15 zeroes) the group is fairly certain that their record for finding the highest dimensional GAP will stand for quite some time, Fleron said.
Guenette of Easthampton, Mass., and Vanasse of Chicopee, Mass., both plan on attending graduate school in mathematics following graduation. Their work on this problem has provided them with a valuable introduction to the efforts of a working research mathematician.
For Jaiclin and Fleron, and the rest of the Westfield State Mathematics Department, it is another opportunity to share with and involve undergraduates what they love best: doing significant mathematics and advancing the frontier of human knowledge.
Fleron said the team’s work was inspired by the recent discoveries of the young Australian mathematician Terence Chi-Shen Tao, now a professor at the University of California, Los Angeles. “Many prominent number theorists are working simply to understand the implications of these discoveries,” he said. “Now Westfield State College students are playing a role, as well.”
British mathematician Andrew Granville, now on the faculty of the Université de Montréal, also inspired the group. Granville’s paper, “Prime Number Patterns,” was published in the April edition of American Mathematical Monthly.
Ironically, Granville just gave a lecture on “Patterns in the Primes” as part of the Distinguished Lecture Series of the Mathematical Association of America (MAA). This series, sponsored by the National Security Agency, took place at the MAA Carriage House Conference Center in Washington D.C. on Thursday, Nov. 13. This was the day before the Westfield State group’s discovery.
Sunday, November 02, 2008
Simple Chemical Procedure Augments Therapeutic Potential of Stem Cells
Adult stem cells resemble couch potatoes if they hang out and divide in a dish for too long. They get fat and lose key surface proteins, which interferes with their movement and reduces their therapeutic potential. Now, via a simple chemical procedure, researchers have found a way to get these cells off the couch and over to their therapeutic target.
To do this, they simply added a molecule called SLeX to the surface of the cells. The procedure took just 45 minutes and restored an important biological function.
“Delivery remains one of the biggest hurdles to stem cell therapy,” explains senior author Jeffrey Karp, an instructor at the Harvard-MIT Division of Health Sciences and Technology. “The blood stream offers a natural delivery vehicle, but stem cells don’t move through blood vessels normally after being expanded in culture. Our procedure promises to overcome this obstacle.”
These findings will be published online in the journal Bioconjugate Chemistry on Oct. 31.
In order for cells injected into the blood stream to be therapeutically useful, they need to take initiative to reach target tissues. But instead, cultured stem cells go with the flow. They move through the body quickly, carried by the current, which means they seldom contact the sides of blood vessels. Thus, they have fewer opportunities to escape into the surrounding tissue by squeezing between cells of the vessel wall. Adult stem cells must escape before they can colonize surrounding tissue and rebuild damaged structures.
In February of 2008, HMS associate professor Robert Sackstein (at Brigham and Women’s Hospital) and colleagues showed they could correct this problem by adding a particular molecule to the surface of adult stem cells. This molecule—a cousin of SLeX—formed temporary connections with proteins on the blood vessel wall, serving as a kind of weak tape. But Sackstein’s method involved enzymes, which made the chemistry complicated. Karp’s team achieved the same result without enzymes.
Karp lab postdoc Debanjan Sarkar simply flooded a dish of cells with three molecules—biotin, streptavidin, and SLeX—one after the other. The biotin and streptavidin anchored SLeX to the cell surface. Sarkar tweaked the concentrations of each molecule to maximize the cell’s ability to roll along the interior of the blood vessel, rather than getting lost in the flow. He also confirmed that the altered cells were still viable.
“The method is very simple,” says Sarkar, who is first author on the paper. “Plus, biotin and streptavidin work with many molecules, so labs can use this universal anchor we discovered to tackle other problems. They’re not limited to sticking SLeX on cells.”
The team worked with human cells extracted from the bone marrow. The cultures included mesenchymal stem cells (MSCs), which can form fat cells, cartilage, bone, tendon and ligaments, muscle cells, and even nerve cells. When injected into the bloodstream of patients, MSCs can home to the site of an injury and replace damaged tissue. But just a fraction of cultured MSCs currently reach their target in clinical trials. Karp’s procedure might improve their homing abilities.
Karp cautions that his lab’s discovery must be validated in animals, before doctors can apply it in the clinic. He’s collaborating with another lab to test the homing ability of the SLeX-dotted cells in mice.
“We need to confirm that this rolling behavior translates into increased homing and tissue repair,” explains Karp. “We may need to tweak the cells further.”
“This is definitely an approach that should be tried,” adds Pamela Robey, chief of the Craniofacial and Skeletal Diseases Branch of the National Institute of Dental and Craniofacial Research. Robey is working to reconstruct three-dimensional tissues with MSCs. “Jeff hasn’t tested the altered MSCs inside animals, and that’s really the gold-standard, but his in vitro data looks promising.”
This research is supported by Brigham and Women’s Hospital. The authors report no conflicts of interest.
The Harvard-MIT Division of Health Sciences and Technology (HST) brings together the Massachusetts Institute of Technology (MIT), Harvard Medical School (HMS), Harvard University, the Boston area teaching hospitals and an assortment of research centers in a unique collaboration that integrates science, medicine and engineering to solve problems in human health.
Adult stem cells resemble couch potatoes if they hang out and divide in a dish for too long. They get fat and lose key surface proteins, which interferes with their movement and reduces their therapeutic potential. Now, via a simple chemical procedure, researchers have found a way to get these cells off the couch and over to their therapeutic target.
To do this, they simply added a molecule called SLeX to the surface of the cells. The procedure took just 45 minutes and restored an important biological function.
“Delivery remains one of the biggest hurdles to stem cell therapy,” explains senior author Jeffrey Karp, an instructor at the Harvard-MIT Division of Health Sciences and Technology. “The blood stream offers a natural delivery vehicle, but stem cells don’t move through blood vessels normally after being expanded in culture. Our procedure promises to overcome this obstacle.”
These findings will be published online in the journal Bioconjugate Chemistry on Oct. 31.
In order for cells injected into the blood stream to be therapeutically useful, they need to take initiative to reach target tissues. But instead, cultured stem cells go with the flow. They move through the body quickly, carried by the current, which means they seldom contact the sides of blood vessels. Thus, they have fewer opportunities to escape into the surrounding tissue by squeezing between cells of the vessel wall. Adult stem cells must escape before they can colonize surrounding tissue and rebuild damaged structures.
In February of 2008, HMS associate professor Robert Sackstein (at Brigham and Women’s Hospital) and colleagues showed they could correct this problem by adding a particular molecule to the surface of adult stem cells. This molecule—a cousin of SLeX—formed temporary connections with proteins on the blood vessel wall, serving as a kind of weak tape. But Sackstein’s method involved enzymes, which made the chemistry complicated. Karp’s team achieved the same result without enzymes.
Karp lab postdoc Debanjan Sarkar simply flooded a dish of cells with three molecules—biotin, streptavidin, and SLeX—one after the other. The biotin and streptavidin anchored SLeX to the cell surface. Sarkar tweaked the concentrations of each molecule to maximize the cell’s ability to roll along the interior of the blood vessel, rather than getting lost in the flow. He also confirmed that the altered cells were still viable.
“The method is very simple,” says Sarkar, who is first author on the paper. “Plus, biotin and streptavidin work with many molecules, so labs can use this universal anchor we discovered to tackle other problems. They’re not limited to sticking SLeX on cells.”
The team worked with human cells extracted from the bone marrow. The cultures included mesenchymal stem cells (MSCs), which can form fat cells, cartilage, bone, tendon and ligaments, muscle cells, and even nerve cells. When injected into the bloodstream of patients, MSCs can home to the site of an injury and replace damaged tissue. But just a fraction of cultured MSCs currently reach their target in clinical trials. Karp’s procedure might improve their homing abilities.
Karp cautions that his lab’s discovery must be validated in animals, before doctors can apply it in the clinic. He’s collaborating with another lab to test the homing ability of the SLeX-dotted cells in mice.
“We need to confirm that this rolling behavior translates into increased homing and tissue repair,” explains Karp. “We may need to tweak the cells further.”
“This is definitely an approach that should be tried,” adds Pamela Robey, chief of the Craniofacial and Skeletal Diseases Branch of the National Institute of Dental and Craniofacial Research. Robey is working to reconstruct three-dimensional tissues with MSCs. “Jeff hasn’t tested the altered MSCs inside animals, and that’s really the gold-standard, but his in vitro data looks promising.”
This research is supported by Brigham and Women’s Hospital. The authors report no conflicts of interest.
The Harvard-MIT Division of Health Sciences and Technology (HST) brings together the Massachusetts Institute of Technology (MIT), Harvard Medical School (HMS), Harvard University, the Boston area teaching hospitals and an assortment of research centers in a unique collaboration that integrates science, medicine and engineering to solve problems in human health.
World's Rarest Big Cat Gets a Check-UpThe world’s rarest big cat is alive and well. At least one of them, that is, according to researchers from the Wildlife Conservation Society (WCS) who captured and released a female Far Eastern leopard in Russia last week.
The capture was made in Primorsky Krai along the Russian-Chinese border by a team of scientists from WCS and the Russian Academy of Sciences Institute of Biology and Soils (IBS). The team is evaluating the health and potential effects of inbreeding for this tiny population, which experts believe contains no more than 10-15 females. Other collaborators include: Wildlife Vets International, National Cancer Institute, and the Zoological Society of London.
The Far Eastern leopard is perhaps the world’s most endangered big cat, with an estimated 25-40 individuals inhabiting a narrow strip of land in the far southeastern corner of the Russian Federation.
The leopardess, nicknamed “Alyona” by the researchers who captured her, was in good physical condition, weighing a healthy 85 pounds (39 kilograms). A preliminary health analysis revealed that she is he is believed to be between 8-10 years old. The animal has since been released unharmed.
Specialists are continuing to analyze blood samples as well as an electrocardiogram, which will reveal genetic information to assess levels of inbreeding. Three leopards captured previously (2 males and 1 female) in 2006 and 2007 all exhibited significant heart murmurs, which may reflect genetic disorders.
“We are excited by the capture, and are hopeful that ongoing analysis of biomedical information will confirm that this individual is in good health,” said Alexey Kostyria, Ph.D., senior scientist at IBS and manager for the WCS-IBS project. “This research is critical for conservation of the Far Eastern leopard, as it will help us to determine the risks posed by inbreeding and what we can do to mitigate them.”
One of the options scientists are considering is trans-locating leopards from other areas to increase genetic diversity -- similar to what happened with Florida panthers when animals from Texas were brought in to supplement the remaining population. Today, Florida panthers have risen from less than ten individuals to a population of approximately 100.
The leopard capture and release was overseen by representatives of the Russian federal agency “Inspection Tiger,” a special department of the Ministry of Natural Resources.
“This project has been ongoing for just over two years, and scientific work to capture Amur tigers and Far Eastern leopards in this part of Primorsky Krai has always been distinguished by the participation of world-class specialists and use of the best equipment and methodologies,” said Sergei Zubtsov, the head of Inspection Tiger. “I want to note that the leopard captured for medical analysis and released represents another achievement for this highly-qualified team, and that one of the most important things is that she was not harmed at any point in the capture process. I hope that such fruitful collaboration will continue in the future.”
Over the last 100 years, Far Eastern leopard numbers have been reduced by poaching combined with habitat loss. However, both camera-trapping and snow-tracking surveys indicate that the population has been stable for the last 30 years, but with a high rate of turnover of individuals. If inbreeding or disease can be kept in check, WCS and its partners believe there is great potential for increasing survival rates and habitat recovery in both Russia and Northeast China.
The Wildlife Conservation Society’s work to protect Far Eastern leopards receives funding by the following U.S. government agencies: U.S. Fish & Wildlife Service’s Rhinoceros and Tiger Conservation Fund, National Fish and Wildlife Foundation’s Save the Tiger Fund, and U.S. Forest Service International Program.
The Far Eastern leopard is listed under CITES (Convention on International Trade in Endangered Species), which protects it against illegal trade for fur and medicinal purposes.
Around the world, large carnivores are faced with a variety of threats including habitat loss, depletion of prey, conflicts with people, poaching, and disease. The U.S. Congress is currently considering legislation called the Great Cats and Rare Canids Act, which would directly benefit the Far Eastern leopard and over a dozen big cat and rare dog species by creating a fund for research and monitoring, law enforcement training, and other conservation efforts. This bill has received support from several leaders in the U.S. Congress – notably Senators Joe Lieberman (CT-I), Barbara Boxer (CA-D) and Sam Brownback (KS-R) and Representatives Tom Udall (NM-D), John Tanner (TN-D), Hal Rogers (KY-R) and Ed Royce (CA-R). Timely action by the U.S. Senate would ensure passage of this important legislation.
Tuesday, October 14, 2008
Landmark Study Unlocks Stem Cell, DNA Secrets to Speed Therapies
In a groundbreaking study led by an eminent molecular biologist at Florida State University, researchers have discovered that as embryonic stem cells turn into different cell types, there are dramatic corresponding changes to the order in which DNA is replicated and reorganized.
The findings bridge a critical knowledge gap for stem cell biologists, enabling them to better understand the enormously complex process by which DNA is repackaged during differentiation -- when embryonic stem cells, jacks of all cellular trades, lose their anything-goes attitude and become masters of specialized functions.
As a result, scientists now are one significant step closer to the central goal of stem cell therapy, which is to successfully convert adult tissue back to an embryo-like state so that it can be used to regenerate or replace damaged tissue. Such therapies hold out hope of treatments or cures for cancer, Parkinson’s disease, multiple sclerosis, spinal cord injuries and a host of other devastating disorders.
Using mouse and human embryonic stem cells, FSU researchers employed advanced imaging techniques and state-of-the-art genomics technology to demonstrate, with unprecedented resolution along long stretches of chromosomes, which sequences are replicated first, and which occur later in the process of differentiation.
“Understanding how replication works during embryonic stem cell differentiation gives us a molecular handle on how information is packaged in different types of cells in manners characteristic to each cell type,” said David M. Gilbert, the study’s principal investigator. “That handle will help us reverse the process in order to engineer different types of cells for use in disease therapies.” Internationally renowned for his body of cutting-edge research on chromosomal structure and reproduction that he began as a doctoral student at Stanford University in the 1980’s, Gilbert joined the FSU faculty and was appointed as the first J. Herbert Taylor Distinguished Professor of Molecular Biology in 2006.
Results from the FSU study, which includes contributions from researchers at three other institutions, are described in a paper published in the October 7, 2008, edition of PLoS (Public Library of Science) Biology, a peer-reviewed journal that showcases biological science research of exceptional significance. So prodigious were the findings that the current paper -- “Global Reorganization of Replication Domains During Embryonic Stem Cell Differentiation” -- is focused solely on results observed in the mouse embryonic stems cells; data on the human cells will be detailed in a future report.
“We know that all the information (DNA) required to take on the identity of any tissue type is present in every cell, because we already can, albeit very inefficiently, create whole animals from adult tissue through cloning,” Gilbert said. “We also can make a kind of artificial embryonic stem cells, called induced pluripotent stem cells, out of many adult cell types, but there are two major hurdles remaining. First, the methods currently used rely on the unnatural retroviral insertion of genes into patients’ cells, and these genes are capable of forming tumors. Second, this method is very inefficient as well because only one in 1,000 cells into which the genes are inserted becomes pluripotent. We must learn how cells lose pluripotency in the first place so we can do a better job of reversing the process without risks to patients.
“The challenge is, adult cells are highly specialized and over the course of their family history over many generations they’ve made decisions to be certain cell types rather than others,” he said. “In doing so, they have tucked away the information they no longer need on how to become other cell types. Hence, all cells contain the same genetic information in their DNA, but during differentiation they package it with proteins into ‘chromatin’ in characteristic ways that define each cell type. The rules that determine how cells package DNA are complicated and have been difficult for scientists to decipher.”
But, Gilbert noted, one time that the cell “shows its cards” is during DNA replication.
“During this process, which was the focus of our FSU research, it’s not just the DNA that replicates,” he said. “All the packaging must be replicated as well in each cell division cycle.”
He explained that embryonic stem cells have many more, smaller “domains” of organization than differentiated cells, and it is during differentiation that they consolidate information.
“In fact, ‘domain consolidation’ is what we call the novel concept we discovered,” he said.
Gilbert likened the concept of domain consolidation to the undeclared or “undifferentiated” college student who then consolidates her literature resources during the course of declaring a major and specialization. “From a student with books on all subjects on all of her bookshelves comes a student who has placed all texts pertaining to her major on the eye-level shelf and moved the distantly-related, potentially distracting texts to the hard-to-reach bottom or top shelves,” he said.
“Now, our challenge as scientists,” said Gilbert, “is to build on what we’ve learned about domain consolidation so that we can efficiently and safely create patient-specific induced pluripotent stem cells or even coax the body’s cells to change their specialization in response to medications.”
Friday, October 10, 2008
Invasive Papaya Pest Discovered in AsiaThanks to efforts by scientists in a Virginia Tech-led program, the papaya mealybug — an emerging threat from India to Indonesia — is being identified and contained.
Attacks by the papaya mealybug are a serious threat. In Indonesia, India, countries in the Caribbean and South America, the Hawaiian Islands, and Florida, papaya means millions of dollars for farmers, middlemen, and processors. In West Java, the scourge has wiped out most of the papaya plantations.
In May, 2008, a team from the Integrated Pest Management Collaborative Research Support Program (IPM CRSP), managed by Virginia Tech’s Office of International Research, Education, and Development, identified papaya mealybug on papaya trees at the Bogor Botanical Gardens in West Java, Indonesia.
It was the first reported occurrence of papaya mealybug in Indonesia and Southeast Asia.
A specialist in mealybug taxonomy at the California Department of Agriculture confirmed the identification as papaya mealybug — an unarmored scale insect found in moist, warm climates.
Two months later, on a trip to Tamil Nadu Agricultural University in Coimbatore, India, Muni Muniappan, director of the IPM CRSP at Virginia Tech, recognized the telltale sticky residue on papayas he saw there as papaya mealybug.
In each case, IPM scientists alerted government authorities and advised them on appropriate actions to take. These discoveries are crucial; the sooner authorities can arrest the spread of the papaya mealybug, the better their chances of saving this lucrative tropical crop.
While papaya is an exotic fruit in the northern hemisphere, papain, a product of papaya, is used in a variety of ways every day, including the production of chewing gum, shampoo, and toothpaste and tooth whiteners; as a meat tenderizer; and in the brewing and textile industries. In many tropical countries, papaya is an important commercial crop and a key component of the daily diet.
The papaya mealybug originated in Mexico, where it developed alongside natural enemies and was first identified in 1992. It wasn’t until it jumped countries and started proliferating in places where it had no natural enemies that it began to pose problems. In 1995, it was discovered on the Caribbean island of St. Martin. By the year 2000, it had spread to 13 countries in the Caribbean, to Florida in the United States, and to three countries each in Central and South America.
The papaya mealybug is a particularly devastating pest because it is polyphagous—it feeds on many things. The insect’s host range includes more than 60 species of plants: cassava, papaya, beans, eggplant, melons, hisbiscus, plumeria, pepper, sweet potato, tomato, citrus, mango, and sour sop.
On papaya plants, the mealybug infests all parts of the young leaves and fruits, mostly along the veins and midrib of the older leaves. Young leaves become crinkly and older leaves turn yellow and dry up. Terminal shoots become bunchy and distorted. Affected trees drop flowers and fruits. To add insult to injury, the mealybug secretes a honeydew-like substance that turns into a thick sooty mold growth, making the fruit inedible and unusable for the production of papain.
The good news is that the U.S. Department of Agriculture’s Animal and Plant Health Inspection Service (APHIS) has developed a biological control program to tackle the pest. Biological control is an integrated pest management tactic that pits natural enemies against pests. APHIS has identified three parasitoids including parasitic wasps that are highly effective at containing the mealybug. These natural enemies are being cultured in a laboratory in Puerto Rico and are offered free to countries that request them.
The IPM CRSP, funded by the U.S. Agency for International Development, is a consortium of integrated pest management scientists working to raise the standard of living in developing countries. The IPM CRSP team that traveled to Indonesia included Robert Hedlund, Cognizant Technical Officer for the USAID-funded program; Muniappan; Clemson University entomology Professors Merle Shepard and Gerry Carner; Clemson economics Professor Mike Hammig; Yulu Xia, assistant director of the NSF Center for IPM at North Carolina State; and Aunu Rauf, professor of entomology at Bogor Agricultural University in Indonesia.
While the challenge of reclaiming the papaya plantations from the papaya mealybug seems daunting, Muniappan is optimistic. “The use of parasitoids has been very effective in Caribbean and Latin American countries, and in Florida, Guam, and Palau,” he said. “But we need to be vigilant.”
Monday, September 29, 2008
Complement enhances tumour evasion
A seemingly illogical link between activation of immune sensors and the ability of tumours to escape the immune system. The unexpected result reveals a new drug target for cancer treatment.
The complement system comprises a cascade of proteins that act as a fire alarm to alert the immune system to the presence of infection. In a bizarre twist, Lambris and colleagues show that tumour activation of one of the complement proteins – C5 – in fact leads to suppression of the anti-tumour immune response.
The surprising outcome is explained by the observation that the activated protein recruits ‘suppressor’ cells to the site. These act to disarm other immune cells and stop them from killing the tumour. Importantly, the authors show that blocking the activity of C5 slows tumour growth in mice and this treatment is as effective as taxol, a commonly used anti-cancer drug.
Author contact:
John Lambris (University of Pennsylvania, Philadelphia, PA, USA)
Tel: +1 215 746 5765; E-mail: lambris@mail.med.upenn.edu
A seemingly illogical link between activation of immune sensors and the ability of tumours to escape the immune system. The unexpected result reveals a new drug target for cancer treatment.
The complement system comprises a cascade of proteins that act as a fire alarm to alert the immune system to the presence of infection. In a bizarre twist, Lambris and colleagues show that tumour activation of one of the complement proteins – C5 – in fact leads to suppression of the anti-tumour immune response.
The surprising outcome is explained by the observation that the activated protein recruits ‘suppressor’ cells to the site. These act to disarm other immune cells and stop them from killing the tumour. Importantly, the authors show that blocking the activity of C5 slows tumour growth in mice and this treatment is as effective as taxol, a commonly used anti-cancer drug.
Author contact:
John Lambris (University of Pennsylvania, Philadelphia, PA, USA)
Tel: +1 215 746 5765; E-mail: lambris@mail.med.upenn.edu
Glacier acceleration through subsurface ocean warming
The sudden acceleration in 1997 of Jakobshavn Isbræ, one of Greenland’s largest outlet glaciers, was caused by subsurface ocean warming, according to research. The study suggests that ocean temperatures may be more important for glacier flow than previously thought. The prediction of future rapid dynamic responses of other outlet glaciers to climate change may therefore require detailed knowledge of regional ocean dynamics.
David Holland and colleagues present hydrographic data that show a sudden increase in subsurface ocean temperature in 1997 along the entire west coast of Greenland. The arrival of relatively warm water that originated from the Irminger Sea near Iceland could therefore have triggered the increase in the glacier speed. The authors trace these oceanic changes back to changes in the atmospheric circulation in the North Atlantic region.
Author contact:
David Holland (New York University, NY, USA)
Tel: +1 212 998 3245; E-mail: holland@cims.nyu.edu
The sudden acceleration in 1997 of Jakobshavn Isbræ, one of Greenland’s largest outlet glaciers, was caused by subsurface ocean warming, according to research. The study suggests that ocean temperatures may be more important for glacier flow than previously thought. The prediction of future rapid dynamic responses of other outlet glaciers to climate change may therefore require detailed knowledge of regional ocean dynamics.
David Holland and colleagues present hydrographic data that show a sudden increase in subsurface ocean temperature in 1997 along the entire west coast of Greenland. The arrival of relatively warm water that originated from the Irminger Sea near Iceland could therefore have triggered the increase in the glacier speed. The authors trace these oceanic changes back to changes in the atmospheric circulation in the North Atlantic region.
Author contact:
David Holland (New York University, NY, USA)
Tel: +1 212 998 3245; E-mail: holland@cims.nyu.edu
Thwarting tumour invasion
A mechanism used by metastasising tumour cells to invade lung tissue and establish secondary tumours. The research identifies a promising drug target to prevent the spread of cancer.
Primary tumours prepare the lung for invasion by inducing chemokines – chemical factors normally used to recruit immune cells during infection – which guide migration of tumour cells to the secondary site. Hiratsuka and colleagues show that primary tumours also induce lung cells to produce an additional factor, serum amyloid A3 (SAA3). SAA3 accelerates the recruitment of primary tumour cells by switching on genes involved in inflammation and boosting the production of chemokines. Importantly, the team show that blocking SAA3 or its receptor strikingly reduces lung metastasis in mice.
Metastasis is difficult to predict and even harder to treat. The new findings offer researchers vital clues for understanding how cancer cells can establish new tumours at sites quite distant from the original tumour.
Author contact:
Yoshiro Maru (Tokyo Women's Medical University School of Medicine, Japan)
Tel: +81 3 5269 7417; E-mail: ymaru@research.twmu.ac.jp
A mechanism used by metastasising tumour cells to invade lung tissue and establish secondary tumours. The research identifies a promising drug target to prevent the spread of cancer.
Primary tumours prepare the lung for invasion by inducing chemokines – chemical factors normally used to recruit immune cells during infection – which guide migration of tumour cells to the secondary site. Hiratsuka and colleagues show that primary tumours also induce lung cells to produce an additional factor, serum amyloid A3 (SAA3). SAA3 accelerates the recruitment of primary tumour cells by switching on genes involved in inflammation and boosting the production of chemokines. Importantly, the team show that blocking SAA3 or its receptor strikingly reduces lung metastasis in mice.
Metastasis is difficult to predict and even harder to treat. The new findings offer researchers vital clues for understanding how cancer cells can establish new tumours at sites quite distant from the original tumour.
Author contact:
Yoshiro Maru (Tokyo Women's Medical University School of Medicine, Japan)
Tel: +81 3 5269 7417; E-mail: ymaru@research.twmu.ac.jp
Risk factor for narcolepsy
A genetic variant that predisposes to narcolepsy has been identified, according to a study. Narcolepsy is characterized by excessive daytime sleepiness, impaired vision, and muscle weakness that may lead to collapse. It occurs in approximately 1 in 2,500 individuals in the United States and Europe, but is at least 4 times more frequent in Japanese.
Katsushi Tokunaga and colleagues carried out a genome-wide association of Japanese individuals, and found one variant to be significantly associated with risk of narcolepsy. They also found support for the association in Koreans, but not in individuals of European or African descent, probably because the frequency of the risk variant is much lower in the latter two populations.
The risk variant is located between the genes CPT1B and CHKB, each of which is a reasonable candidate to have a role in the disorder. The gene CPT1B encodes an enzyme involved in fatty acid oxidation, which has been implicated in sleep regulation. CHKB encodes an enzyme that catalyzes the production of one of the major components of cellular membranes, which is a precursor to a molecule that has been linked to the sleep-wake cycle.
Author contact:
Katsushi Tokunaga (University of Tokyo, Japan)
Tel: +81 3 5841 3692; E-mail: tokunaga@m.u-tokyo.ac.jp
A genetic variant that predisposes to narcolepsy has been identified, according to a study. Narcolepsy is characterized by excessive daytime sleepiness, impaired vision, and muscle weakness that may lead to collapse. It occurs in approximately 1 in 2,500 individuals in the United States and Europe, but is at least 4 times more frequent in Japanese.
Katsushi Tokunaga and colleagues carried out a genome-wide association of Japanese individuals, and found one variant to be significantly associated with risk of narcolepsy. They also found support for the association in Koreans, but not in individuals of European or African descent, probably because the frequency of the risk variant is much lower in the latter two populations.
The risk variant is located between the genes CPT1B and CHKB, each of which is a reasonable candidate to have a role in the disorder. The gene CPT1B encodes an enzyme involved in fatty acid oxidation, which has been implicated in sleep regulation. CHKB encodes an enzyme that catalyzes the production of one of the major components of cellular membranes, which is a precursor to a molecule that has been linked to the sleep-wake cycle.
Author contact:
Katsushi Tokunaga (University of Tokyo, Japan)
Tel: +81 3 5841 3692; E-mail: tokunaga@m.u-tokyo.ac.jp
Friday, September 26, 2008
Researchers Develop New Model for Cystic Fibrosis
In a first, researchers at the University of Iowa and the University of Missouri (MU) have developed a pig model for cystic fibrosis (CF) that appears to closely mimic the disease in human infants. The striking similarities between disease manifestations in the CF piglets and human newborns with CF suggest that this new model will help improve understanding of the disease and may also speed discovery of new treatments. The study is published in the Sept. 26 issue of Science.
CF is a common hereditary disease that affects multiple organ systems, including the intestines, pancreas, and lung. Mice with CF-causing mutations have helped researchers learn more about this disease, however, differences in physiology and biology mean that mice with CF mutations do not develop many of the typical symptoms that affect humans with CF.
"Lack of a better model has hampered our ability to answer long-standing questions in CF," explained Christopher Rogers, Ph.D., a former postdoctoral fellow in internal medicine at the UI Roy J. and Lucille A. Carver College of Medicine, and one of the study's lead authors. "The CF pig provides a unique opportunity to study one of the most common genetic diseases, and we hope to translate this new knowledge into better therapies and preventions."
In addition to Rogers, co-lead authors of the study were David Stoltz, M.D., Ph.D., UI assistant professor of internal medicine, and David Meyerholz, D.V.M., Ph.D., UI assistant professor of pathology.
The senior study author was Michael Welsh, M.D., UI professor of internal medicine and molecular physiology and biophysics, who holds the Roy J. Carver Chair of Internal Medicine and Physiology and Biophysics. Welsh also is a Howard Hughes Medical Institute investigator.
CF occurs when a person inherits two mutated copies of the CFTR gene leading to loss of ion channel function that adversely affects many organs. To create the CF pigs, the researchers used gene targeting to disrupt one copy of the normal gene in pig cells. They then cloned these altered cells to produce pigs with only one good copy of the gene. Like human CF-carriers, these animals did not show disease symptoms. The pigs were then bred naturally, and about one in four of the piglets were born with two disrupted copies of the gene.
The researchers established that piglets lacking CFTR have the abnormal ion channel activity that is a hallmark of CF disease. They also showed that the CF piglets develop the same disease characteristics that are commonly seen in newborn humans with CF, including a bowel obstruction known as meconium ileus, which often is the first sign of CF in humans. The pigs also have an abnormal pancreas, liver, and gall bladder, similar to CF patients.
"Thus far, the clinical, physiological and age-related appearance of disease in the pigs, as well as the organs involved, mimic CF seen in people," Stoltz said.
A primary cause of death and disability in patients with CF is lung disease. However, many questions remain about how infection and inflammation leads to lung damage. In the study, the lungs of the newborn CF pigs appeared similar to the lungs of their normal littermates and had no sign of infection or inflammation, possibly shedding some initial insight on the process. As the CF pigs mature and are exposed to airborne bacteria and viruses, the researchers hope to learn more about how and why lung disease develops in patients with CF.
"Researchers can now begin to study the disease progression as it is happening, something not possible in humans," Meyerholz said.
The research team included UI scientists from internal medicine, pediatrics, surgery and periodontics. In addition, Randall Prather, Ph.D., the distinguished professor of reproductive biology at MU College of Agriculture, Food and Natural Resources, and his colleagues were part of the research team.
The study was funded in part by grants from the National Heart, Lung, and Blood Institute and National Institute of Diabetes and Digestive and Kidney Disease of the National Institutes of Health, Food for the 21st Century and the Cystic Fibrosis Foundation.
In a first, researchers at the University of Iowa and the University of Missouri (MU) have developed a pig model for cystic fibrosis (CF) that appears to closely mimic the disease in human infants. The striking similarities between disease manifestations in the CF piglets and human newborns with CF suggest that this new model will help improve understanding of the disease and may also speed discovery of new treatments. The study is published in the Sept. 26 issue of Science.
CF is a common hereditary disease that affects multiple organ systems, including the intestines, pancreas, and lung. Mice with CF-causing mutations have helped researchers learn more about this disease, however, differences in physiology and biology mean that mice with CF mutations do not develop many of the typical symptoms that affect humans with CF.
"Lack of a better model has hampered our ability to answer long-standing questions in CF," explained Christopher Rogers, Ph.D., a former postdoctoral fellow in internal medicine at the UI Roy J. and Lucille A. Carver College of Medicine, and one of the study's lead authors. "The CF pig provides a unique opportunity to study one of the most common genetic diseases, and we hope to translate this new knowledge into better therapies and preventions."
In addition to Rogers, co-lead authors of the study were David Stoltz, M.D., Ph.D., UI assistant professor of internal medicine, and David Meyerholz, D.V.M., Ph.D., UI assistant professor of pathology.
The senior study author was Michael Welsh, M.D., UI professor of internal medicine and molecular physiology and biophysics, who holds the Roy J. Carver Chair of Internal Medicine and Physiology and Biophysics. Welsh also is a Howard Hughes Medical Institute investigator.
CF occurs when a person inherits two mutated copies of the CFTR gene leading to loss of ion channel function that adversely affects many organs. To create the CF pigs, the researchers used gene targeting to disrupt one copy of the normal gene in pig cells. They then cloned these altered cells to produce pigs with only one good copy of the gene. Like human CF-carriers, these animals did not show disease symptoms. The pigs were then bred naturally, and about one in four of the piglets were born with two disrupted copies of the gene.
The researchers established that piglets lacking CFTR have the abnormal ion channel activity that is a hallmark of CF disease. They also showed that the CF piglets develop the same disease characteristics that are commonly seen in newborn humans with CF, including a bowel obstruction known as meconium ileus, which often is the first sign of CF in humans. The pigs also have an abnormal pancreas, liver, and gall bladder, similar to CF patients.
"Thus far, the clinical, physiological and age-related appearance of disease in the pigs, as well as the organs involved, mimic CF seen in people," Stoltz said.
A primary cause of death and disability in patients with CF is lung disease. However, many questions remain about how infection and inflammation leads to lung damage. In the study, the lungs of the newborn CF pigs appeared similar to the lungs of their normal littermates and had no sign of infection or inflammation, possibly shedding some initial insight on the process. As the CF pigs mature and are exposed to airborne bacteria and viruses, the researchers hope to learn more about how and why lung disease develops in patients with CF.
"Researchers can now begin to study the disease progression as it is happening, something not possible in humans," Meyerholz said.
The research team included UI scientists from internal medicine, pediatrics, surgery and periodontics. In addition, Randall Prather, Ph.D., the distinguished professor of reproductive biology at MU College of Agriculture, Food and Natural Resources, and his colleagues were part of the research team.
The study was funded in part by grants from the National Heart, Lung, and Blood Institute and National Institute of Diabetes and Digestive and Kidney Disease of the National Institutes of Health, Food for the 21st Century and the Cystic Fibrosis Foundation.
Gene Variant Boosts Risk of Fatty Liver Disease
Researchers at UT Southwestern Medical Center have found that individuals who carry a specific form of the gene PNPLA3 have more fat in their livers and a greater risk of developing liver inflammation.
They also found that Hispanics are more likely to carry the gene variant responsible for higher liver-fat content than African-Americans and Caucasians.
The new findings, published online today in the journal Nature Genetics, provide a gene-based explanation for the results of a 2004 UT Southwestern-led study that determined that the propensity to develop nonalcoholic fatty liver disease differs among ethnic groups, with a higher percentage of Hispanics developing the disorder than African-Americans or Caucasians.
“A single variation in the PNPLA3 gene was strongly associated with hepatic fat content, even after adjusting for other factors, such as obesity, diabetes status and alcohol intake,” said senior study author Dr. Helen Hobbs, director of the Eugene McDermott Center for Human Growth and Development and an investigator for the Howard Hughes Medical Institute at UT Southwestern.
“Sequence variations in this gene explain much of the increased propensity of Hispanics to accumulate excess liver fat,” she said.
Nonalcoholic fatty liver disease (NAFLD) is the most common form of liver disease in Western countries, and its incidence is growing. Previous UT Southwestern research has shown that it may affect as many as one-third of adults in America.
“The gene variations we have identified might provide a way to predict who is most at risk for developing fatty liver disease and liver injury in response to environmental stresses such as obesity or infection,” said Dr. Jonathan Cohen, professor of internal medicine in the McDermott Center and one of the authors of the study.
NAFLD results from the accumulation of triglycerides in the liver and is associated with metabolic disorders such as insulin resistance, obesity, diabetes and high cholesterol – many of the conditions that contribute to heart disease. It can also lead to liver inflammation, cirrhosis and liver cancer. Approximately 10 percent of liver transplants performed in the U.S. are for cirrhosis related to NAFLD, according to the researchers.
Treatments for NAFLD include weight loss, exercise, reducing alcohol intake and improved diabetes control.
“Knowing who is at increased risk of developing liver disease could aid physicians in encouraging their patients to make lifestyle changes or take other preventive measures to help mitigate their underlying genetic risk for the disorder,” said Dr. Cohen, holder of the C. Vincent Prothro Distinguished Chair in Human Nutrition Research.
The new findings come out of the Dallas Heart Study, an 8-year-old groundbreaking investigation of cardiovascular disease that involves a large multiethnic group of participants. The $12 million study investigates the links between genetics, lifestyle and the risks for heart disease.
As part of the Dallas Heart Study, more than 3,500 individuals from Dallas County provided blood samples in 2000 for DNA isolation and other tests. Each participant also underwent multiple body scans with magnetic resonance imaging and computed tomography to examine the heart and other organs. Along with discovering new genetic ties to differences in blood levels of cholesterol and triglycerides, the researchers have used this information to identify new drug targets for the prevention and treatment of heart disease.
Data-gathering for the new study on fatty liver disease took advantage of a unique aspect of the Dallas Heart Study. Researchers with the study were the first to analyze hepatic fat in a large population using a technique called proton magnetic resonance spectroscopy – the most sensitive and quantitative noninvasive imaging technique available to measure the amount of fat in the liver. With this technique, they screened more than 2,100 individuals across multiple ethnicities. They then correlated that data with DNA tests from the same people and found the link to the PNPLA3 gene.
The next step in the research is to investigate how the various forms of the PNPLA3 gene affect lipid metabolism.
Other researchers from the McDermott Center involved with the study were lead author Dr. Stefano Romeo, a postdoctoral research fellow; Dr. Alexander Pertsemlidis, assistant professor; Dr. Chao Xing, assistant professor of clinical sciences; and Julia Kozlitina, a graduate student participating in a joint program between Southern Methodist University and UT Southwestern. Researchers from Perlegen Sciences, Lawrence Berkeley National Laboratory and the UT Health Science Center at Houston also were involved.
The research was funded by the Donald W. Reynolds Foundation, the National Institutes of Health and the Department of Energy.
Researchers at UT Southwestern Medical Center have found that individuals who carry a specific form of the gene PNPLA3 have more fat in their livers and a greater risk of developing liver inflammation.
They also found that Hispanics are more likely to carry the gene variant responsible for higher liver-fat content than African-Americans and Caucasians.
The new findings, published online today in the journal Nature Genetics, provide a gene-based explanation for the results of a 2004 UT Southwestern-led study that determined that the propensity to develop nonalcoholic fatty liver disease differs among ethnic groups, with a higher percentage of Hispanics developing the disorder than African-Americans or Caucasians.
“A single variation in the PNPLA3 gene was strongly associated with hepatic fat content, even after adjusting for other factors, such as obesity, diabetes status and alcohol intake,” said senior study author Dr. Helen Hobbs, director of the Eugene McDermott Center for Human Growth and Development and an investigator for the Howard Hughes Medical Institute at UT Southwestern.
“Sequence variations in this gene explain much of the increased propensity of Hispanics to accumulate excess liver fat,” she said.
Nonalcoholic fatty liver disease (NAFLD) is the most common form of liver disease in Western countries, and its incidence is growing. Previous UT Southwestern research has shown that it may affect as many as one-third of adults in America.
“The gene variations we have identified might provide a way to predict who is most at risk for developing fatty liver disease and liver injury in response to environmental stresses such as obesity or infection,” said Dr. Jonathan Cohen, professor of internal medicine in the McDermott Center and one of the authors of the study.
NAFLD results from the accumulation of triglycerides in the liver and is associated with metabolic disorders such as insulin resistance, obesity, diabetes and high cholesterol – many of the conditions that contribute to heart disease. It can also lead to liver inflammation, cirrhosis and liver cancer. Approximately 10 percent of liver transplants performed in the U.S. are for cirrhosis related to NAFLD, according to the researchers.
Treatments for NAFLD include weight loss, exercise, reducing alcohol intake and improved diabetes control.
“Knowing who is at increased risk of developing liver disease could aid physicians in encouraging their patients to make lifestyle changes or take other preventive measures to help mitigate their underlying genetic risk for the disorder,” said Dr. Cohen, holder of the C. Vincent Prothro Distinguished Chair in Human Nutrition Research.
The new findings come out of the Dallas Heart Study, an 8-year-old groundbreaking investigation of cardiovascular disease that involves a large multiethnic group of participants. The $12 million study investigates the links between genetics, lifestyle and the risks for heart disease.
As part of the Dallas Heart Study, more than 3,500 individuals from Dallas County provided blood samples in 2000 for DNA isolation and other tests. Each participant also underwent multiple body scans with magnetic resonance imaging and computed tomography to examine the heart and other organs. Along with discovering new genetic ties to differences in blood levels of cholesterol and triglycerides, the researchers have used this information to identify new drug targets for the prevention and treatment of heart disease.
Data-gathering for the new study on fatty liver disease took advantage of a unique aspect of the Dallas Heart Study. Researchers with the study were the first to analyze hepatic fat in a large population using a technique called proton magnetic resonance spectroscopy – the most sensitive and quantitative noninvasive imaging technique available to measure the amount of fat in the liver. With this technique, they screened more than 2,100 individuals across multiple ethnicities. They then correlated that data with DNA tests from the same people and found the link to the PNPLA3 gene.
The next step in the research is to investigate how the various forms of the PNPLA3 gene affect lipid metabolism.
Other researchers from the McDermott Center involved with the study were lead author Dr. Stefano Romeo, a postdoctoral research fellow; Dr. Alexander Pertsemlidis, assistant professor; Dr. Chao Xing, assistant professor of clinical sciences; and Julia Kozlitina, a graduate student participating in a joint program between Southern Methodist University and UT Southwestern. Researchers from Perlegen Sciences, Lawrence Berkeley National Laboratory and the UT Health Science Center at Houston also were involved.
The research was funded by the Donald W. Reynolds Foundation, the National Institutes of Health and the Department of Energy.
Monday, May 12, 2008
Modeling psychiatric disorders in mice
One of the molecular causes of the behavioral and cognitive deficits observed in mice with a small chromosomal deletion has been identified, according to a study published online this week in Nature Genetics. The corresponding deletion in the human genome gives rise to a range of psychiatric disorders, and accounts for approximately 1–2% of cases of schizophrenia in the general population.
Deletion of a small region on chromosome 22 is associated with anxiety, depression, attention-deficit hyperactivity disorder, autism, and deficits in working memory. Approximately 30% of the individuals carrying such a deletion eventually develop schizophrenia.
Maria Karayiorgou, Joseph Gogos and colleagues generated a model in which the corresponding region was deleted in the mouse genome. Mice carrying a single deletion show a range of behavioral and cognitive deficits that mimic some aspects of the human syndrome. Of particular interest is the increased expression of precursors of the small regulatory RNAs known as microRNAs in the brains of the mutant mice. The authors went on to show that loss of one of genes in the deleted region, Dgcr8, is responsible for this increased abundance of precursors, as the normal role of Dgcr8 is to process them into mature microRNAs. By generating mice that have only one copy of Dgcr8, the authors showed that this mutation by itself results in at least some of the deficits observed in mice with the deletion of the surrounding region.
Although the specific downstream targets of altered microRNA expression in the brain are not yet known, the authors suggest these findings could have general implications for understanding the genetic basis of psychiatric disorders.
Author contacts:
Maria Karayiorgou (Columbia University Medical Center, New York, NY, USA)
Tel: +1 212 568 4189; E-mail: mk2758@columbia.edu
Joseph Gogos (Columbia University Medical Center, New York, NY, USA)
Tel: +1 212 305 0744; E-mail: jag90@columbia.edu
One of the molecular causes of the behavioral and cognitive deficits observed in mice with a small chromosomal deletion has been identified, according to a study published online this week in Nature Genetics. The corresponding deletion in the human genome gives rise to a range of psychiatric disorders, and accounts for approximately 1–2% of cases of schizophrenia in the general population.
Deletion of a small region on chromosome 22 is associated with anxiety, depression, attention-deficit hyperactivity disorder, autism, and deficits in working memory. Approximately 30% of the individuals carrying such a deletion eventually develop schizophrenia.
Maria Karayiorgou, Joseph Gogos and colleagues generated a model in which the corresponding region was deleted in the mouse genome. Mice carrying a single deletion show a range of behavioral and cognitive deficits that mimic some aspects of the human syndrome. Of particular interest is the increased expression of precursors of the small regulatory RNAs known as microRNAs in the brains of the mutant mice. The authors went on to show that loss of one of genes in the deleted region, Dgcr8, is responsible for this increased abundance of precursors, as the normal role of Dgcr8 is to process them into mature microRNAs. By generating mice that have only one copy of Dgcr8, the authors showed that this mutation by itself results in at least some of the deficits observed in mice with the deletion of the surrounding region.
Although the specific downstream targets of altered microRNA expression in the brain are not yet known, the authors suggest these findings could have general implications for understanding the genetic basis of psychiatric disorders.
Author contacts:
Maria Karayiorgou (Columbia University Medical Center, New York, NY, USA)
Tel: +1 212 568 4189; E-mail: mk2758@columbia.edu
Joseph Gogos (Columbia University Medical Center, New York, NY, USA)
Tel: +1 212 305 0744; E-mail: jag90@columbia.edu
Stem-cell regeneration of the breast relies on adhesion
Interaction of basal stem cells in the breast with their cellular environment is crucial for their function, and helps towards the regeneration of the mammary glands during pregnancy, reports a paper online this week in Nature Cell Biology.
The basal stem cells of the breast are enriched in proteins called integrins that mediate contact with the extracellular matrix surrounding the cells. Marina Glukhova and colleagues show that expression of beta 1 integrin in the basal cells is essential for the regenerative potential of these stem cells and for proper development of the mammary gland during pregnancy.
Deletion of the beta 1 integrin gene from the basal layer of mouse mammary tissue led to an abnormal ductal branching pattern in the mammary gland during pregnancy, which results in the regenerative potential of the mammary tissue stem cells being abolished, leading to a dysfunctional gland. In basal stem cells lacking beta 1 integrin, cells divide abnormally and this results in the altered branching pattern.
The environment that surrounds most stem cells, the stem cell niche, is known to be important for a number of stem cells. However, our understanding of stem cell niches remains patchy. These findings establish a central role of direct interaction between basal stem cells and their extracellular matrix in the maintenance of the mammary stem-cell population.
Author contact:
Marina Glukhova (CNRS-Institut Curie Research, Paris, France)
Tel: +33 1 42 34 63 33; E-mail: Marina.Glukhova@curie.fr
Interaction of basal stem cells in the breast with their cellular environment is crucial for their function, and helps towards the regeneration of the mammary glands during pregnancy, reports a paper online this week in Nature Cell Biology.
The basal stem cells of the breast are enriched in proteins called integrins that mediate contact with the extracellular matrix surrounding the cells. Marina Glukhova and colleagues show that expression of beta 1 integrin in the basal cells is essential for the regenerative potential of these stem cells and for proper development of the mammary gland during pregnancy.
Deletion of the beta 1 integrin gene from the basal layer of mouse mammary tissue led to an abnormal ductal branching pattern in the mammary gland during pregnancy, which results in the regenerative potential of the mammary tissue stem cells being abolished, leading to a dysfunctional gland. In basal stem cells lacking beta 1 integrin, cells divide abnormally and this results in the altered branching pattern.
The environment that surrounds most stem cells, the stem cell niche, is known to be important for a number of stem cells. However, our understanding of stem cell niches remains patchy. These findings establish a central role of direct interaction between basal stem cells and their extracellular matrix in the maintenance of the mammary stem-cell population.
Author contact:
Marina Glukhova (CNRS-Institut Curie Research, Paris, France)
Tel: +33 1 42 34 63 33; E-mail: Marina.Glukhova@curie.fr
The origins of the modern tomato
Scientists have identified a genetic mutation that acts as a major contributor to the extreme fruit size associated with the modern tomato, according to a study.
Modern cultivated tomatoes produce fruit as much as 1,000 times larger than their wild progenitors. One clear reason for the increase in tomato size during its domestication is the increased number of carpels – organs – which determines the final number of compartments in the fruit.
Steven Tanksley and colleagues crossed lines of tomatoes with either high or low compartment number, and carried out genetic mapping studies to identify the gene or genes responsible for the variation in carpel number. They identified an insertion of 6–8 kilobases in a gene they call fas only in the tomatoes with high compartment number. Expression of the gene is reduced in the developing flower buds in tomatoes carrying the insertion. A survey of 30 different lines of cerasiforme, the wild form of tomato thought to be related to the smaller progenitors, showed that none carried the insertion.
As the insertion is found exclusively in modern cultivated tomatoes, the authors suggest that the mutation occurred recently in tomato domestication, and then spread rapidly as a result of selection for larger fruit.
Author contact:
Steven Tanksley (Cornell University, Ithaca, NY, USA)
Tel: +1 607 255 1673; E-mail: sdt4@cornell.edu
Scientists have identified a genetic mutation that acts as a major contributor to the extreme fruit size associated with the modern tomato, according to a study.
Modern cultivated tomatoes produce fruit as much as 1,000 times larger than their wild progenitors. One clear reason for the increase in tomato size during its domestication is the increased number of carpels – organs – which determines the final number of compartments in the fruit.
Steven Tanksley and colleagues crossed lines of tomatoes with either high or low compartment number, and carried out genetic mapping studies to identify the gene or genes responsible for the variation in carpel number. They identified an insertion of 6–8 kilobases in a gene they call fas only in the tomatoes with high compartment number. Expression of the gene is reduced in the developing flower buds in tomatoes carrying the insertion. A survey of 30 different lines of cerasiforme, the wild form of tomato thought to be related to the smaller progenitors, showed that none carried the insertion.
As the insertion is found exclusively in modern cultivated tomatoes, the authors suggest that the mutation occurred recently in tomato domestication, and then spread rapidly as a result of selection for larger fruit.
Author contact:
Steven Tanksley (Cornell University, Ithaca, NY, USA)
Tel: +1 607 255 1673; E-mail: sdt4@cornell.edu
Friday, May 09, 2008
The planets: Mysteries surrounding the ‘butterscotch’ planet’s equator
Saturn, the second largest planet in the Solar System, is easily spotted because of the brightness of the rings around its equator. Two companion papers in this week’s Nature report on features of its atmosphere, one using data collected by the Cassini mission and the other from over two decades of ground-based observations.
The equatorial stratospheres of Earth and Jupiter oscillate more or less periodically on timescales of about two and four years, respectively. By analysing infrared observations from the Cassini probe, Thierry Fouchet and colleagues discovered that Saturn has an equatorial oscillation like Earth's and Jupiter's, as well as a mid-latitude subsidence that may be associated with the equatorial motion. Glenn Orton and co-workers’ ground-based observations of Saturn's stratospheric emission reveal a similar oscillation.
The period of the oscillation is approximately 15 terrestrial years, which is roughly half of Saturn's year, suggesting the influence of seasonal forcing —rather like the Earth's semi-annual oscillation.
CONTACT
Glenn Orton (Jet Propulsion Laboratory, Pasadena, CA, USA) Author paper [3]
Tel: +1 818 354 2460; E-mail: Glenn.Orton@jpl.nasa.gov
Thierry Fouchet (Observatoire de Paris, Meudon, France) Author paper [4]
Tel: +33 1 45 07 71 11; E-mail: Thierry.Fouchet@obspm.fr
Timothy Dowling (University of Louisville, KY, USA) N&V author
Tel: +1 502 852 3927; E-mail: dowling@louisville.ed
Saturn, the second largest planet in the Solar System, is easily spotted because of the brightness of the rings around its equator. Two companion papers in this week’s Nature report on features of its atmosphere, one using data collected by the Cassini mission and the other from over two decades of ground-based observations.
The equatorial stratospheres of Earth and Jupiter oscillate more or less periodically on timescales of about two and four years, respectively. By analysing infrared observations from the Cassini probe, Thierry Fouchet and colleagues discovered that Saturn has an equatorial oscillation like Earth's and Jupiter's, as well as a mid-latitude subsidence that may be associated with the equatorial motion. Glenn Orton and co-workers’ ground-based observations of Saturn's stratospheric emission reveal a similar oscillation.
The period of the oscillation is approximately 15 terrestrial years, which is roughly half of Saturn's year, suggesting the influence of seasonal forcing —rather like the Earth's semi-annual oscillation.
CONTACT
Glenn Orton (Jet Propulsion Laboratory, Pasadena, CA, USA) Author paper [3]
Tel: +1 818 354 2460; E-mail: Glenn.Orton@jpl.nasa.gov
Thierry Fouchet (Observatoire de Paris, Meudon, France) Author paper [4]
Tel: +33 1 45 07 71 11; E-mail: Thierry.Fouchet@obspm.fr
Timothy Dowling (University of Louisville, KY, USA) N&V author
Tel: +1 502 852 3927; E-mail: dowling@louisville.ed
Genomes: Is it a bird, is it a mammal…?
The duck-billed platypus (Ornithorhynchus anatinus) is a truly unique animal, and its fascinating genome. Platypuses are monotremes with almost no close relatives alive on earth. Scientists just had to take a look at that genome, and now an international collaboration of researchers report its sequencing and analysis.
Famously considered a hoax when sent from Australia to European researchers in the nineteenth century, the platypus is an amalgam of reptilian, mammalian and unique characteristics that provide clues to the function and evolution of all mammalian genomes. Sequencing of the platypus genome has helped to uncover the following: the origins of genomic imprinting in vertebrates; platypus venom proteins were co-opted independently from the same gene families that provided reptile venom; milk protein genes are conserved; and immune gene family expansions are directly related to platypus biology. As well as providing an invaluable resource for comparative genomics, the sequence will be important for monotreme conservation.
CONTACT
Wesley Warren (Washington University School of Medicine, St Louis, MO, USA)
Tel: +1 314 286 1899; E-mail: wwarren@wustl.edu
Jennifer Marshall Graves (Australian National University, Canberra, Australia)
Tel: +61 261 252 492; E-mail: jenny.graves@anu.edu.au
Ewan Birney (The European Bioinformatics Institute, Cambridge, UK)
E-mail: birney@ebi.ac.uk
The duck-billed platypus (Ornithorhynchus anatinus) is a truly unique animal, and its fascinating genome. Platypuses are monotremes with almost no close relatives alive on earth. Scientists just had to take a look at that genome, and now an international collaboration of researchers report its sequencing and analysis.
Famously considered a hoax when sent from Australia to European researchers in the nineteenth century, the platypus is an amalgam of reptilian, mammalian and unique characteristics that provide clues to the function and evolution of all mammalian genomes. Sequencing of the platypus genome has helped to uncover the following: the origins of genomic imprinting in vertebrates; platypus venom proteins were co-opted independently from the same gene families that provided reptile venom; milk protein genes are conserved; and immune gene family expansions are directly related to platypus biology. As well as providing an invaluable resource for comparative genomics, the sequence will be important for monotreme conservation.
CONTACT
Wesley Warren (Washington University School of Medicine, St Louis, MO, USA)
Tel: +1 314 286 1899; E-mail: wwarren@wustl.edu
Jennifer Marshall Graves (Australian National University, Canberra, Australia)
Tel: +61 261 252 492; E-mail: jenny.graves@anu.edu.au
Ewan Birney (The European Bioinformatics Institute, Cambridge, UK)
E-mail: birney@ebi.ac.uk
Monday, May 05, 2008
Developmental genetics: Starting out on the road to maleness
Growing up male is a genetic lifestyle decision — early in embryonic development, genes on the Y chromosome activate the development of specialized cells that ultimately become the testes. Without this ‘on switch’ for maleness, the developing gonads become ovaries by default and the embryo develops as a female.A study of mice now shows how the developing gonads start out on this road to maleness. In a paper geneticists Robin Lovell-Badge and Ryohei Sekido describe how a gene called Sry, carried on the Y chromosome, boosts another gene elsewhere in the genome that in turn governs the development of sperm-producing cells called Sertoli cells — a crucial component of the testes.By studying gene expression patterns in developing mouse embryos, the researchers deduced that Sry produces a protein that combines with another protein, steroidogenic factor 1 (SF1). This complex then binds to a DNA region that boosts the expression of another gene, Sox9, which controls a host of genes involved in sperm development.Elucidating this pathway not only reveals how maleness develops from the ‘default’ female developmental pathway; defects in this process may also explain how people who are genetically ‘male’ or ‘female’ end up developing the ‘wrong’ sexual anatomy.
contact:
Robin Lovell-Badge (National Institute for Medical Research, London, UK)Tel: +44 20 8816 2126;
Genetic susceptibility to obesity
Scientists have discovered genetic variants that increase the risk of obesity and insulin resistance in the general population, according to two studies published online this week in Nature Genetics. Until now only one locus (FTO) has been associated convincingly with increased risk of obesity.A consortium of investigators led by Mark McCarthy, Ines Barroso and Nicholas Wareham analyzed the genomes of more than 90,000 individuals and found that a variant near MC4R, encoding the melanocortin-4 receptor, increases susceptibility to obesity. Previous studies had shown that the melanocortin-4 receptor is expressed in neurons in the hypothalamus and is a key regulator of food intake and energy expenditure. Although it is unclear how this variant affects MC4R expression or function, the fact that mutations in the gene are known to cause rare cases of severe childhood obesity lends confidence to the association.In a separate study, Jaspal Kooner and colleagues carried out a genome-wide scan of several thousand individuals of Indian Asian or European ancestry, and identified a variant near MC4R as increasing risk of obesity and insulin resistance. The risk variant was more frequent in individuals of Indian Asian ancestry, which the authors suggest may account for the increased burden of obesity in Indian Asians.Author contacts:Mark McCarthy (University of Oxford, UK) Author paper [7]Tel: +44 1865 857 298; E-mail: mark.mccarthy@drl.ox.ac.ukInês Barroso (Wellcome Trust Sanger Institute, Hinxton, UK) Co-author paper [7]Tel: +44 1223 495 341; E-mail: ib1@sanger.ac.ukNicholas Wareham (Addenbrooke’s Hospital, Cambridge, UK) Co-author paper [7]Tel: +44 1223 330 315; E-mail: nick.wareham@mrc-epid.cam.ac.ukJaspal Kooner (Imperial College London, UK) Author paper [8]Tel: +44 20 8383 4751; E-mail: j.kooner@imperial.ac.uk
Growing up male is a genetic lifestyle decision — early in embryonic development, genes on the Y chromosome activate the development of specialized cells that ultimately become the testes. Without this ‘on switch’ for maleness, the developing gonads become ovaries by default and the embryo develops as a female.A study of mice now shows how the developing gonads start out on this road to maleness. In a paper geneticists Robin Lovell-Badge and Ryohei Sekido describe how a gene called Sry, carried on the Y chromosome, boosts another gene elsewhere in the genome that in turn governs the development of sperm-producing cells called Sertoli cells — a crucial component of the testes.By studying gene expression patterns in developing mouse embryos, the researchers deduced that Sry produces a protein that combines with another protein, steroidogenic factor 1 (SF1). This complex then binds to a DNA region that boosts the expression of another gene, Sox9, which controls a host of genes involved in sperm development.Elucidating this pathway not only reveals how maleness develops from the ‘default’ female developmental pathway; defects in this process may also explain how people who are genetically ‘male’ or ‘female’ end up developing the ‘wrong’ sexual anatomy.
contact:
Robin Lovell-Badge (National Institute for Medical Research, London, UK)Tel: +44 20 8816 2126;
Genetic susceptibility to obesity
Scientists have discovered genetic variants that increase the risk of obesity and insulin resistance in the general population, according to two studies published online this week in Nature Genetics. Until now only one locus (FTO) has been associated convincingly with increased risk of obesity.A consortium of investigators led by Mark McCarthy, Ines Barroso and Nicholas Wareham analyzed the genomes of more than 90,000 individuals and found that a variant near MC4R, encoding the melanocortin-4 receptor, increases susceptibility to obesity. Previous studies had shown that the melanocortin-4 receptor is expressed in neurons in the hypothalamus and is a key regulator of food intake and energy expenditure. Although it is unclear how this variant affects MC4R expression or function, the fact that mutations in the gene are known to cause rare cases of severe childhood obesity lends confidence to the association.In a separate study, Jaspal Kooner and colleagues carried out a genome-wide scan of several thousand individuals of Indian Asian or European ancestry, and identified a variant near MC4R as increasing risk of obesity and insulin resistance. The risk variant was more frequent in individuals of Indian Asian ancestry, which the authors suggest may account for the increased burden of obesity in Indian Asians.Author contacts:Mark McCarthy (University of Oxford, UK) Author paper [7]Tel: +44 1865 857 298; E-mail: mark.mccarthy@drl.ox.ac.ukInês Barroso (Wellcome Trust Sanger Institute, Hinxton, UK) Co-author paper [7]Tel: +44 1223 495 341; E-mail: ib1@sanger.ac.ukNicholas Wareham (Addenbrooke’s Hospital, Cambridge, UK) Co-author paper [7]Tel: +44 1223 330 315; E-mail: nick.wareham@mrc-epid.cam.ac.ukJaspal Kooner (Imperial College London, UK) Author paper [8]Tel: +44 20 8383 4751; E-mail: j.kooner@imperial.ac.uk
Obesity: Your number of fat cells stays constant in adulthood
number of fat cells, or adipocytes, in your body remains more or less constant throughout adulthood, a new study finds। The discovery suggests that the difference in the number of fat cells between lean and obese people is established in childhood, and then persists for life।The number of fat cells remains constant even in formerly obese adults who have lost significant amounts of weight, report researchers led by Kirsty Spalding, who studied fat samples from liposuction and abdominal reconstruction surgery in lean and obese volunteers। This reflects the fact that the level of obesity is determined by a combination of the number and size of fat cells, which can grow or shrink as fat from food is deposited in them।Although fat cell numbers remain constant during adulthood, this is a dynamic process of death and replenishment, Spalding and her colleagues report. Fat cells are replaced at the same rate that they die — roughly 10% every year. The researchers made their discovery by studying levels of radioactive isotopes in fat cells from people who had lived through the brief period of Cold War nuclear bomb testing from 1955 to 1963. People whose fat cells were deposited before the onset of testing nevertheless incorporated radioactive matter after, showing that their fat cells were being replenished.The fact that fat cells are constantly dying and being replaced could potentially offer an opportunity to develop new anti-obesity therapies, the researchers suggest.
Author contact:
Kirsty Spalding (Karolinska Institute, Stockholm, Sweden)Tel: +46 70 437 1542; E-mail:
kirsty.spalding@cmb.ki.se
number of fat cells, or adipocytes, in your body remains more or less constant throughout adulthood, a new study finds। The discovery suggests that the difference in the number of fat cells between lean and obese people is established in childhood, and then persists for life।The number of fat cells remains constant even in formerly obese adults who have lost significant amounts of weight, report researchers led by Kirsty Spalding, who studied fat samples from liposuction and abdominal reconstruction surgery in lean and obese volunteers। This reflects the fact that the level of obesity is determined by a combination of the number and size of fat cells, which can grow or shrink as fat from food is deposited in them।Although fat cell numbers remain constant during adulthood, this is a dynamic process of death and replenishment, Spalding and her colleagues report. Fat cells are replaced at the same rate that they die — roughly 10% every year. The researchers made their discovery by studying levels of radioactive isotopes in fat cells from people who had lived through the brief period of Cold War nuclear bomb testing from 1955 to 1963. People whose fat cells were deposited before the onset of testing nevertheless incorporated radioactive matter after, showing that their fat cells were being replenished.The fact that fat cells are constantly dying and being replaced could potentially offer an opportunity to develop new anti-obesity therapies, the researchers suggest.
Author contact:
Kirsty Spalding (Karolinska Institute, Stockholm, Sweden)Tel: +46 70 437 1542; E-mail:
kirsty.spalding@cmb.ki.se
Thursday, May 01, 2008
The Hunt for the Kill Switch
The U.S. Department of Defense wants to know if chip makers are building remotely accessible kill switches into high-end microprocessors. These days, the U.S. military consumes only about 1 percent of the world's integrated circuits, and offshoring has begun to raise some alarms about the safety of the chips in the military's most mission-critical electronics.
Recognizing an enormous vulnerability, the DOD recently launched an extremely ambitious program to verify the integrity of the electronics that will underpin future additions to its arsenal. In December, the DOD's advanced-research wing released details about a three-year initiative it calls the Trust in Integrated Circuits program. The findings from the program could give the military--and defense contractors who make sensitive microelectronics like the weapons systems for the F-35--a guaranteed method of determining whether their chips have been compromised with a kill switch.
But how exactly would you kill an integrated switch, and for what purpose? In "The Hunt for the Kill Switch," IEEE Spectrum's Sally Adee reports on the methods that could kill a chip, the possible consequences, and the methods being devised to verify the Pentagon's most important microchips.(NewsWise)
The U.S. Department of Defense wants to know if chip makers are building remotely accessible kill switches into high-end microprocessors. These days, the U.S. military consumes only about 1 percent of the world's integrated circuits, and offshoring has begun to raise some alarms about the safety of the chips in the military's most mission-critical electronics.
Recognizing an enormous vulnerability, the DOD recently launched an extremely ambitious program to verify the integrity of the electronics that will underpin future additions to its arsenal. In December, the DOD's advanced-research wing released details about a three-year initiative it calls the Trust in Integrated Circuits program. The findings from the program could give the military--and defense contractors who make sensitive microelectronics like the weapons systems for the F-35--a guaranteed method of determining whether their chips have been compromised with a kill switch.
But how exactly would you kill an integrated switch, and for what purpose? In "The Hunt for the Kill Switch," IEEE Spectrum's Sally Adee reports on the methods that could kill a chip, the possible consequences, and the methods being devised to verify the Pentagon's most important microchips.(NewsWise)
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