Tag Archives: university research

Image of Viral Coat

image of exterior of virus - made up of 5 million atoms

High-energy X-ray diffraction was used to pinpoint some 5 million atoms in the protective protein coat of the PsV-F virus. The coat’s symmetrical features are shared by hundreds of viruses. The red and yellow sections illustrate how building blocks of four proteins come together to form the spherical shell.

The image reveals the structure of a type of protein coat shared by hundreds of known viruses containing double-stranded RNA genomes. The image was painstakingly created from hundreds of high-energy X-ray diffraction images and paints the clearest picture yet of the viruses’ genome-encasing shell called a “capsid.”

Viruses can reproduce themselves only by invading a host cell and highjacking its biochemical machinery. But when they invade, viruses need to seal off their genetic payload to prevent it from being destroyed by the cell’s protective mechanisms. Though there are more than 5,000 known viruses, including whole families that are marked by wide variations in genetic payload and other characteristics, most of them use either a helical or a spherical capsid.

“Spherical viruses like this have symmetry like a soccer ball or geodesic dome,” Pan said. “The whole capsid contains exactly 120 copies of a single protein.” Previous studies had shown that spherical capsids contain dozens of copies of the capsid protein, or CP, in an interlocking arrangement. The new research identified the sphere’s basic building block, a four-piece arrangement of CP molecules called a tetramer, which could also be building blocks for other viruses’ protein coats.

Full press release

Why People Often Get Sicker When They’re Stressed

Researchers at UT Southwestern Medical Center identified a receptor, known as QseE, which resides in a diarrhea-causing strain of E coli. The receptor senses stress cues from the bacterium’s host and helps the pathogen make the host ill. A receptor is a molecule on the surface of a cell that docks with other molecules, often signaling the cell to carry out a specific function.

Dr. Vanessa Sperandio, associate professor of microbiology at UT Southwestern and the study’’ senior author, said QseE is an important player in disease development because the stress cues it senses from a host, chiefly epinephrine and phosphate, are generally associated with blood poisoning, or sepsis.

“Patients with high levels of phosphate in the intestine have a much higher probability of developing sepsis due to systemic infection by intestinal bacteria,” Dr. Sperandio said. “If we can find out how bacteria sense these cues, then we can try to interfere in the process and prevent infection.”

Millions of potentially harmful bacteria exist in the human body, awaiting a signal from their host that it’s time to release their toxins. Without those signals, the bacteria pass through the digestive tract without infecting cells. What hasn’t been identified is how to prevent the release of those toxins.

“There’s obviously a lot of chemical signaling between host and bacteria going on, and we have very little information about which bacteria receptors recognize the host and vice versa,” Dr. Sperandio said. “We’re scratching at the tip of the iceberg on our knowledge of this.”

“When people are stressed they have more epinephrine and norepinephrine being released. Both of these human hormones activate the receptors QseC and QseE, which in turn trigger virulence. Hence, if you are stressed, you activate bacterial virulence.” Dr. Sperandio said the findings also suggest that there may be more going on at the genetic level in stress-induced illness than previously thought.

“The problem may not only be that the stress signals are weakening your immune system, but that you’re also priming some pathogens at the same time,” she said. “Then it’s a double-edged sword. You have a weakened immune system and pathogens exploiting it.”

Previous research by Dr. Sperandio found that phentolamine, an alpha blocker drug used to treat hypertension, and a new drug called LED209 prevent QseC from expressing its virulence genes in cells. Next she will test whether phentolamine has the same effect on QseE.

Full press release: Researchers probe mechanisms of infection

Very Cool Wearable Computing Gadget from MIT

Pattie Maes presentation at TED shows a very cool prototype for wearable, useful computing spearheaded by Pranav Mistry (who received a standing ovation at TED). It’s a wearable device with a projector that paves the way for profound interaction with our environment.

The prototype of the system cost only $350. The software, created by them, obviously is the key, but how amazing is that, $350 for the hardware used in the prototype! There is a useful web site on the Sixth Sense project.

The SixthSense prototype is comprised of a pocket projector, a mirror and a camera. The hardware components are coupled in a pendant like mobile wearable device. Both the projector and the camera are connected to the mobile computing device in the user’s pocket. The projector projects visual information enabling surfaces, walls and physical objects around us to be used as interfaces; while the camera recognizes and tracks user’s hand gestures and physical objects using computer-vision based techniques.

The software program processes the video stream data captured by the camera and tracks the locations of the colored markers (visual tracking fiducials) at the tip of the user’s fingers using simple computer-vision techniques. The movements and arrangements of these fiducials are interpreted into gestures that act as interaction instructions for the projected application interfaces. The maximum number of tracked fingers is only constrained by the number of unique fiducials, thus SixthSense also supports multi-touch and multi-user interaction.

Resurrection of the Human IRGM Gene

Interesting open access paper on Death and Resurrection of the Human IRGM Gene. Author summary:

The IRG gene family plays an important role in defense against intracellular bacteria, and genome-wide association studies have implicated structural variants of the single-copy human IRGM locus as a risk factor for Crohn’s disease. We reconstruct the evolutionary history of this region among primates and show that the ancestral tandem gene family contracted to a single pseudogene within the ancestral lineage of apes and monkeys.

Phylogenetic analyses support a model where the gene has been “dead” for at least 25 million years of human primate evolution but whose ORF became restored in all human and great ape lineages. We suggest that the rebirth or restoration of the gene coincided with the insertion of an endogenous retrovirus, which now serves as the functional promoter driving human gene expression. We suggest that either the gene is not functional in humans or this represents one of the first documented examples of gene death and rebirth.

Open Science: Explaining Spontaneous Knotting

Shedding light on why long strands tend to become knotted

Anyone who has ever put up Christmas lights knows the problem: Holiday strands so carefully packed away last year are now more knotty than nice. In fact, they have become an inextricable, inexplicable, seemingly inevitable mess. It happens every year, like some sort of universal law of physics.

Which, it turns out, it basically is. In October, two UCSD researchers published the first physical explanation of why knots seem to form magically, not just in strands of Christmas lights, but in pretty much anything stringy, from garden hoses to iPod earbud cords to DNA.
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“We’re not mathematicians,” Smith said. “We’re physicists. Physicists do experiments.”

UCSD researchers constructed a knot probability machine that involved placing a single length of string in a plastic box, sealing it, then rotating the box at a set speed for a brief period of time.
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The experiment involved placing a single length of floppy string into a plastic box, sealing it, then rotating the box at a set speed for a brief time. The researchers did this 3,415 times, sometimes changing variables such as box size and string length.

Open access research paper: Spontaneous knotting of an agitated string by Dorian M. Raymer and Douglas E. Smith.

Above a critical string length, the probability P of knotting at first increased sharply with length but then saturated below 100%. This behavior differs from that of mathematical self-avoiding random walks, where P has been proven to approach 100%. Finite agitation time and jamming of the string due to its stiffness result in lower probability, but P approaches 100% with long, flexible strings.
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As L [length] was increased from 0.46 to 1.5 m, P increased sharply. However, as L was increased from 1.5 to 6 m, P saturated at 50%.
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Tripling the agitation time caused a substantial increase in P, indicating that the knotting is kinetically limited. Decreasing the rotation rate by 3-fold while keeping the same number of rotations caused little change in P.
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We also did measurements with a stiffer string and observed a probability of finding a knot would approach 100% with an substantial drop in P.

Yet another interesting case of scientists explaining the world around us (and the value of open science).

John Conyers Against Open Science

Lawrence Lessig once again has written a good blog post: John Conyers and Open Access

Open access journals, such as, for example, those created by the Public Library of Science, have adopted a different publishing model, to guarantee that all all research is freely accessible online (under the freest Creative Commons license) immediately, to anyone around the world. This guarantee of access, however, is not purchased by any compromise in academic standards. There is still a peer-review process. There is still even a paper-based publication.

Pushed by scientists everywhere, the NIH and other government agencies were increasingly exploring this obviously better model for spreading knowledge. Proprietary publishers, however, didn’t like it. And so rather than competing in the traditional way, they’ve adopted the increasingly Washington way of competition — they’ve gone to Congress to get a law to ban the business model they don’t like. If H.R. 801 is passed, the government can’t even experiment with supporting publishing models that assure that the people who have paid for the research can actually access it. Instead, if Conyers has his way, we’ll pay for the research twice.
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The insanity in this proposal is brilliantly described by Jamie Boyle in this piece in the FT. But after you read his peace, you’ll be even more puzzled by this. For what possible reason could Conyers have for supporting a bill that 33 Nobel Prize Winners, and the current and former heads of the NIH say will actually hurt scientific research in America? More pointedly, what possible reason would a man from a district that insists on the government “Buying American” have for supporting a bill that basically subsidizes foreign publishers (for the biggest players in this publishing market are non-American firms, making HR 801 a kind of “Foreign Publishers Protection Act”)?
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the co-sponsors of this bill who sit on the Judiciary Committee received on average two-times the amount of money from publishing interests as those who haven’t co-sponsored the bill.

The damage done to science by dinosaurs fighting progress and corrupt or inept politicians is very disheartening. Thankfully we have been able to achieve great things in spite of politicians trying to favor their donors and harm the scientific community.

Study Shows Weight Loss From Calorie Reduction Not Low Fat or Low Carb

A Randomized Trial Comparing Low-Fat and Low-Carbohydrate Diets Matched for Energy and Protein

The preliminary results presented in this paper are for the first four of six postmenopausal overweight or obese participants who followed, in random order, both a VLC [very-low-carbohydrate] and an LF [low-fat] diet for 6 weeks. Other outcome measures were serum lipids, glucose, and insulin, as well as dietary compliance and side effects. Our results showed no significant weight loss, lipid, serum insulin, or glucose differences between the two diets. Lipids were dramatically reduced on both diets, with a trend for greater triglyceride reduction on the VLC diet. Glucose levels were also reduced on both diets, with a trend for insulin reduction on the VLC diet. Compliance was excellent with both diets, and side effects were mild

Essentially the study showed that the calories had an impact on weight loss but the makeup of those calories did not. Don’t forget this is just one study. Listen to interview with the Author, Frank Sacks, on Science Friday on NPR.

Problems Using Corn as Biofuel

The pluses and (mostly) minuses of biofuels by Robert Sanders

one ripple effect from the stampede to create more ethanol from corn in the United States. As corn prices skyrocketed several years ago, soybean fields were converted to corn, and the price of soy rose. As a result, farmers in Brazil, one of the main countries with the soil, climate and infrastructure to make up the difference, began to bulldoze rainforest to grow more soybeans.

“If reduced U.S. soybean production results in a parallel increase in Brazilian soybean production, a potential net release of 1,800 to 9,100 Tg (trillion grams) of CO2-equivalents of greenhouse gas emissions due to land-use change is possible,” Coe wrote in a summary of his talk. That is equivalent to more than 9 billion metric tons of carbon dioxide.

Scientists Say Biotechnology Seed Companies Prevent Research

Crop Scientists Say Biotechnology Seed Companies Are Thwarting Research

Biotechnology companies are keeping university scientists from fully researching the effectiveness and environmental impact of the industry’s genetically modified crops, according to an unusual complaint issued by a group of those scientists.
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The researchers, 26 corn-insect specialists, withheld their names because they feared being cut off from research by the companies. But several of them agreed in interviews to have their names used.

The problem, the scientists say, is that farmers and other buyers of genetically engineered seeds have to sign an agreement meant to ensure that growers honor company patent rights and environmental regulations. But the agreements also prohibit growing the crops for research purposes.

So while university scientists can freely buy pesticides or conventional seeds for their research, they cannot do that with genetically engineered seeds. Instead, they must seek permission from the seed companies. And sometimes that permission is denied or the company insists on reviewing any findings before they can be published, they say.

Such agreements have long been a problem, the scientists said, but they are going public now because frustration has been building.

This is not acceptable. Regulators need to put safety above politically connected powerful groups. The bigger problem is we keep electing people more interested in who gives than money than the public interest. But part of the dynamic is embarrassing those that subvert the public good to reward those providing the politicians money. By shining light on what is being done the abuses are often reduced a bit.

Gene Duplication and Evolution

Roughly 10 million years ago, a major genetic change occurred in a common ancestor of gorillas, chimpanzees, and humans. Segments of DNA in its genome began to form duplicate copies at a greater rate than in the past, creating an instability that persists in the genome of modern humans and contributes to diseases like autism and schizophrenia. But that gene duplication also may be responsible for a genetic flexibility that has resulted in some uniquely human characteristics.

“Because of the architecture of the human genome, genetic material is constantly being added and deleted in certain regions,” says Howard Hughes Medical Institute investigator and University of Washington geneticist Evan Eichler, who led the project that uncovered the new findings. “These are really like volcanoes in the genome, blowing out pieces of DNA.”

Eichler and his colleagues focused on the genomes of four different species: macaques, orangutans, chimpanzees, and humans. All are descended from a single ancestral species that lived about 25 million years ago. The line leading to macaques broke off first, so that macaques are the most distantly related to humans in evolutionary terms. Orangutans, chimpanzees, and humans share a common ancestor that lived 12-16 million years ago. Chimps and humans are descended from a common ancestral species that lived about 6 million years ago.

By comparing the DNA sequences of the four species, Eichler and his colleagues identified gene duplications in the lineages leading to these species since they shared a common ancestor. They also were able to estimate when a duplication occurred from the number of species sharing that duplication. For example, a duplication observed in orangutan, chimpanzees, and humans but not in macaques must have occurred sometime after 25 million years ago but before the orangutan lineage branched off.

Eichler’s research team found an especially high rate of duplications in the ancestral species leading to chimps and humans, even though other mutational processes, such as changes in single DNA letters, were slowing down during this period.