How did the equatorial ridge on Saturn's moon Iapetus form?

by Brian Wallheimer.

ScienceDaily - A compound found in red wine, grapes and other fruits, and similar in structure to resveratrol, is able to block cellular processes that allow fat cells to develop, opening a door to a potential method to control obesity, according to a Purdue University study. Kee-Hong Kim, an assistant professor of food science, and Jung Yeon Kwon, a graduate student in Kim's laboratory, reported in this week's issue of the Journal of Biological Chemistry that the compound piceatannol blocks an immature fat cell's ability to develop and grow.

While similar in structure to resveratrol -- the compound found in red wine, grapes and peanuts that is thought to combat cancer, heart disease and neurodegenerative diseases -- piceatannol might be an important weapon against obesity. Resveratrol is converted to piceatannol in humans after consumption.

"Piceatannol actually alters the timing of gene expressions, gene functions and insulin action during adipogenesis, the process in which early stage fat cells become mature fat cells," Kim said. "In the presence of piceatannol, you can see delay or complete inhibition of adipogenesis."

Over a period of 10 days or more, immature fat cells, called preadipocytes, go through several stages to become mature fat cells, or adipocytes. "These precursor cells, even though they have not accumulated lipids, have the potential to become fat cells," Kim said. "We consider that adipogenesis is an important molecular target to delay or prevent fat cell accumulation and, hopefully, body fat mass gain."

Kim found that piceatannol binds to insulin receptors of immature fat cells in the first stage of adipogenesis, blocking insulin's ability to control cell cycles and activate genes that carry out further stages of fat cell formation. Piceatannol essentially blocks the pathways necessary for immature fat cells to mature and grow.

Piceatannol is one of several compounds being studied in Kim's laboratory for its health benefits, and it is also present in different amounts in red grape seeds and skin, blueberries, passion fruit, and other fruits.

Kim would like to confirm his current finding, which is based on a cell culture system, using an animal model of obesity. His future work would also include determining methods for protecting piceatannol from degrading so that concentrations large enough would be available in the bloodstream to stop adipogenesis or body fat gain. We need to work on improving the stability and solubility of piceatannol to create a biological effect," Kim said. The Purdue Research Foundation funded the work.

J. Y. Kwon, S. G. Seo, Y.-S. Heo, S. Yue, J.-X. Cheng, K. W. Lee, K.-H. Kim. Piceatannol, Natural Polyphenolic Stilbene, Inhibits Adipogenesis via Modulation of Mitotic Clonal Expansion and Insulin Receptor-dependent Insulin Signaling in Early Phase of Differentiation. Journal of Biological Chemistry, 2012; 287 (14): 11566 DOI: 10.1074/jbc.M111.259721

http://bit.ly/HogaXq

Feathers may have helped T. rex's relatives ride out a cold climate

Feathers are the defining feature of birds, but that wasn't always the case.

By John Timmer | Published 2 days ago

For millions of years, various species of dinosaurs sported feathers, some of which have left behind fossilized impressions. But for the most part, the feathers we've found have been attached to smaller dinosaurs, many of them along the lineage that gave rise to birds.

That situation was changed dramatically by a species that is described in today's issue of Nature. Three nearly complete skeletons have revealed a feathered dinosaur that its finders term "gigantic." At nearly 1,500kg and over forty times the weight of any previous feathered dinosaur, Yutyrannus huali was a beast—almost certainly an apex predator, and related to the ancestors of Tyrannosaurus Rex.

Feathers may have helped T. rex's relatives ride out a cold climate Photograph by Dr. Brian Choo

The relationship to its fellow Tyrannosaurids is implied by the genus name Yutyrannus; huali means "beautiful" in Mandarin. Fossils of three distinct individuals were discovered, largely intact. All of them share the feathers that are 10-15cm long filaments, and are present on the neck, back, and legs of the fossils. Other areas aren't as well preserved, but the authors suspect that this broad distribution indicates the feathers were pretty much everywhere. Yutyrannus also displays a second distinct feature: a crest that runs along the center of its snout, from its nostrils back to just in front of its eyes.

Beyond that, Yutyrannus is a mix of features common to the ancestors of T. rex and specializations. So, for example, its forelimbs have three fingers, a trait that's called "basal," since it was present at the base of this lineage. Other features are called "derived." Some of these are somewhere intermediate between Yutyrannus and its relatives from later in the Cretaceous. Others are distinct to this species.

Feathers are a basal trait that show up elsewhere in the Tyrannosaurids, so one of the key questions is why the giants of the late Cretaceous had lost them (and not why they appeared in Yutyrannus). Feathers probably got their start as a means of insulation, and the authors argue that T. rex et. al probably didn't need anything of the sort. For starters, the late Cretaceous was a hothouse, with temperatures well above anything like today's.

But, just as significantly, they note that many of the world's largest animals—think whales and elephants—have also lost most of their fur. That may be a consequence of the fact that, as an animal's size increases, there's relatively more volume of tissue generating metabolic heat than there is surface area to radiate it away. When an animal gets large enough, the insulation becomes superfluous, and could actually put a limit on the animal's activity.

Yutyrannus' skull, showing the ridge in the center of its head, feather impressions, and some serious looking teeth. Zang Hailong

There are exceptions to that. Large animals that live in cold climates, like the bison and mammoth, have retained their fur to deal with the chill. And that's exactly what the authors think is going on with Yutyrannus. At the time that the species was around, the area where it was found was about 10°C colder than it was during the late Cretaceous. In that climate, the feathers may have been necessary for even a giant Tyranosaurid to beat the chill. Nature, 2012. DOI: 10.1038/nature10906.

http://news.discovery.com/tech/seismic-wallpaper-120404.html

Seismic Wallpaper Stabilizes Walls in an Earthquake

During an earthquake, regular walls get shaken much like humans do. The side-to-side strain causes the masonry to crumble. This year, German materials scientists are producing seismic wallpaper that can hold a wall together.

Analysis by Alyssa Danigelis

Karlsruhe Institute of Technology's Institute of Solid Construction and Construction Material Technology has been simulating quake conditions to find better ways to shore up walls since the 1990s. Early attempts involved bonding thin carbon fiber slats to masonry, but that only made the crumbling worse.

Several years ago, they came up with another approach, one in which the surface of a whole wall could be reinforced using special wallpaper. In 2010, the institute's director, Lothar Stempniewski, and his colleagues began perfecting the material. They used stiff, high-strength glass fibers woven together to form a strong, elastic covering. The fibers run in four directions to distribute energy evenly when the walls are shaking, according to an article by Brigitte Osterath in Deutsche Welle.

Photo: The earthquake wallpaper is fixed to walls with a special adhesive. Credit: Bayer Material Science.

This special spun-glass covering alone isn't enough, though. Standard wallpaper glue can't hold up to an earthquake, so the KIT group collaborated with the polymer makers in the materials science division of the chemical company Bayer. They made a flexible, soft adhesive from water and a large amount of polyurethane beads. Once the adhesive penetrates grooves in the masonry, the water evaporates to anchor the substance in the wall. Similarly, when the wallpaper goes on, it gets completely surrounded by the beads. Together the whole setup won't tear during an earthquake.

To find out just how well it works, the seismic fabric was tested on a replica house in an earthquake simulator. "Because of the earthquake wallpaper, we were unable to make the building collapse," KIT researcher Mortiz Urban told Deutsche Welle. In a recent press video, Bayer indicated that the wallpaper will start going into commercial production this year through partner companies. It's expected to cost more than regular wallpaper, but the drastic difference for people living in earthquake-prone areas should be well worth the price.

http://blogs.scientificamerican.com/artful-amoeba/2012/04/04/can-diseases-cross-oceans-by-wind/

Can Diseases Cross Oceans By Wind?

Kawasaki Disease causes little kids to develop rash; fever; swollen hands, feet, and lymph nodes; red tongue and cracked lips and, develop coronary artery aneurysms that can kill right away or years later by heart attacks in otherwise totally healthy young adults

By Jennifer Frazer | April 4, 2012

That’s the question I examine in my first feature story for Nature, published today online and in the print magazine April 5. A bizarre disease of toddlers and infants called Kawasaki Disease — which only emerged in the 1960s in Japan — causes little kids to develop rash; fever; swollen hands, feet, and lymph nodes; red tongue and cracked lips; and, bizarrely, to develop coronary artery aneurysms that can kill them right away or years later by heart attacks in otherwise totally healthy young adults.

Here’s a story that didn’t make it into the final cut of the article that describes one such case:

In one case, a 42-year-old white triathelete keeled over of a massive heart attack 10 miles into a 100 mile bike ride. He had no classic risk factors: he was not a smoker, and he was an extremely fit elite athlete with inklings he might have heart disease.

When the cardiologist, who happened to be Burns’s husband, injected die into the man’s arteries, he saw the telltale Kawasaki aneurysms immediately. When the patient’s mother was consulted, it was discovered that when the man was five, he had been diagnosed with “atypical scarlet fever” in Florida. The man lived, but suffered ongoing cardiac disability as a result.

Aneurysms in the coronary arteries of a Kawasaki victim. Public domain

Despite decades of searching, no one has ever been able to figure out what causes it, even though some sort of infectious agent has long been suspected. And now, it seems that whatever is causing it — whether dead or alive — might be able to cross the Pacific Ocean and sicken children in Hawaii, North America, and beyond.

If this proves to be true, it will be the first time a human pathogen has ever been shown to do that. So head on over to Nature and check it out — and check out the podcast interview with me embedded in the story halfway through as well. You can hear what I sound like!

Dr. Jane Burns, who I interviewed for nearly two hours for the story and who graciously shared with me her lifetime of experience with the disease, was featured in the lead of the story about the infant from Wyoming. That baby was only 3 months old when she was airlifted to Colorado and died within 12 hours of arriving there.

Occasionally when you report a story you encounter amazing details that just don’t fit within the context of the story you want to write, but are nonetheless powerful. Burns told me this further story about that baby’s parents. It really pulled on my heartstrings, so I wanted to share it with you:

A month later the physicians invited the family back to go over the autopsy and interpret the results for them. Burns attended the meeting along with the pathologist. The family handed her a brown paper bag with $1,500 in small bills. They had gone door to door in their town in Wyoming to collect the money.

“[They] said, ‘We hope you’ll take this money and do research on Kawasaki Disease,’” Burns recalled. “That was obviously a very powerful moment for me.”

Dr. Burns went on to devote nearly her entire career to Kawasaki Disease.

On a personal note, can I just say what a thrill it was seeing the color proofs of a page from Nature with my name on the story? I kept looking at the bottom of the page “Nature, Vol. x, Issue x”, and then looking back up at my name. Surreal. Very surreal.

Thank you to my editor at Nature for all the hard work on the story and for encouraging me at every step of the way. Couldn’t have done it without you, Mitch!

http://www.eurekalert.org/pub_releases/2012-04/cp-tdb033012.php

Tackling dyslexia before kids learn to read

For children with dyslexia, the trouble begins even before they start reading and for reasons that don't necessarily reflect other language skills.

That's according to a report published online on April 5 in Current Biology, a Cell Press publication, that for the first time reveals a causal connection between early problems with visual attention and a later diagnosis of dyslexia. "Visual attention deficits are surprisingly way more predictive of future reading disorders than are language abilities at the prereading stage," said Andrea Facoetti of the University of Padua in Italy.

The researchers argue that the discovery not only closes a long-lasting debate on the causes of dyslexia but also opens the way to a new approach for early identification and interventions for the 10 percent of children for whom reading is extremely difficult.

The researchers studied Italian-speaking children for a period of three years, from the time they were prereading kindergarteners until they entered second grade. Facoetti's team, including Sandro Franceschini, Simone Gori, Milena Ruffino, and Katia Pedrolli, assessed prereaders for visual spatial attention—the ability to filter relevant versus irrelevant information - through tests that asked them to pick out specific symbols amid distractions. The children also took tests on syllable identification, verbal short-term memory, and rapid color naming, followed over the next two years by measures of reading. Those test results showed that kids who initially had trouble with visual attention were also the ones to later struggle in reading.

"This is a radical change to the theoretical framework explaining dyslexia," Facoetti said. "It forces us to rewrite what is known about the disorder and to change rehabilitation treatments in order to reduce its impact."

He says that simple visual-attention tasks should improve the early identification of children at risk for dyslexia. "Because recent studies show that specific prereading programs can improve reading abilities, children at risk for dyslexia could be treated with preventive remediation programs of visual spatial attention before they learn to read." Franceschini et al.: "A Causal Link between Visual Spatial Attention and Reading Acquisition."

http://www.eurekalert.org/pub_releases/2012-04/mgh-baa040512.php

Big advance against cystic fibrosis

Stem cell researchers create lung surface tissue in a dish

Harvard stem cell researchers at Massachusetts General Hospital (MGH) have taken a critical step in making possible the discovery in the relatively near future of a drug to control cystic fibrosis (CF), a fatal lung disease that claims about 500 lives each year, with 1,000 new cases diagnosed annually.

Beginning with the skin cells of patients with CF, Jayaraj Rajagopal, MD, and colleagues first created induced pluripotent stem (iPS) cells, and then used those cells to create human disease-specific functioning lung epithelium, the tissue that lines the airways and is the site of the most lethal aspect of CF, where the genes cause irreversible lung disease and inexorable respiratory failure.

That tissue, which researchers now can grow in unlimited quantities in the laboratory, contains the delta-508 mutation, the gene responsible for about 70 percent of all CF cases and 90 percent of the ones in the United States. The tissue also contains the G551D mutation, a gene that is involved in about 2 percent of CF cases and the one cause of the disease for which there is now a drug.

The work is featured on the cover of this month's Cell Stem Cell journal, which appeared online today. Postdoctoral fellow Hongmei Mou, PhD, is first author on the paper, and Rajagopal is the senior author.

Mou credits learning the underlying developmental biology in mice as the key to making tremendous progress in only two years. "I was able to apply these lessons to the iPS cell systems," she said. "I was pleasantly surprised the research went so fast, and it makes me excited to think important things are within reach. It opens up the door to identifying new small molecules [drugs] to treat lung disease."

Doug Melton, PhD, co-director of the Harvard Stem Cell Institute, said, "This work makes it possible to produce millions of cells for drug screening, and for the first time human patients' cells can be used as the target." Melton, who is also co-chair of Harvard's inter-School Department of Stem Cell and Regenerative Biology and is the Xander University Professor, added, "I would expect to see rapid progress in this area now that human cells, the very cells that are defective in the disease, can be used for screening."

Rajagopal said, "The key to our success was the ecosystem of the Harvard Stem Cell Institute and MGH. HSCI investigators pioneered the strategies we used, helped us at the bench, and gave us advice on how to combine our knowledge of lung development with their exciting new platforms. Indeed, we also enjoyed a wonderful collaboration with Darrell Kotton's lab at Boston University that was able to convert mouse cells into lung tissue. These interactions really helped fuel us ahead."

The epithelial tissue created by Rajagopal and his colleagues at the MGH Center for Regenerative Medicine (http://www.massgeneral.org/regenmed/) also provides researchers with the same cells that are involved in a number of common lung conditions, including asthma, lung cancer, and chronic bronchitis, and may hasten the development of new insights and treatments into those conditions as well.

"We're not talking about a cure for CF; we're talking about a drug that hits the major problem in the disease. This is the enabling technology that will allow that to happen in a matter of years," said Rajagopal, a Harvard Medical School assistant professor of Medicine. Also a physician trained as a pulmonologist, the specialty that treats CF patients, Rajagopal said, "When we talk about research and advances, donors and patients ask: 'When? How soon?' And we usually hesitate to answer. But we now have every single piece we need for the final push. So I have every hope that we'll have a therapy in a matter of years."

Cystic fibrosis, which used to claim its victims in infancy or early childhood, has evolved into a killer of those in their 30s because treatments of the infections that characterize the disease have improved. But despite those advances, there has been little progress in treating the underlying condition that affects the vast majority of patients: a defect in a single gene that interferes with the fluid balance in the surface layers of the airways and leads to a thickening of mucus, difficulty breathing and repeated infections and hospitalizations.

The discovery and recent FDA approval of the drug Ivacaftor, which corrects the G551D defect seen in about 2 percent of CF patients, has served as a proof of concept to demonstrate that the disease can be attacked with a conventional molecular treatment. In fact, Ivacaftor was found by screening thousands of drugs on a far less than ideal cell line. In the end, many drugs that functioned well on this cell line proved ineffective when used on genuine human airway tissue.

Genuine human airway tissue is the gold standard prior to drugs being tested clinically, but it has been extremely difficult to obtain the tissue from patients, and when it could be obtained, the tissue rarely survived long in the lab – all of which created a major bottleneck in screening for a therapy. But by creating iPS cells that contain the entire genome of a CF patient and directing those cells to develop into lung progenitor cells, which then develop into epithelium, the group appears to have solved this key problem.

Rajagopal, who did his own postdoctoral fellowship in Melton's laboratory during the first half of the past decade after completing his training in pulmonary medicine, said that having both the G551D and 508 genes in the epithelial tissue provides a way to prove that the tissue will be effective in testing drugs against CF.

"We've created the perfect cell line to show that the drug out there that works against G551D mutation works in this system, and then we're in business to screen for a drug against delta 508," he said. "We'll know soon that the cell line works. We know it makes bonafide airway epithelium, and we'll have the proof of principle that the tissue responds properly to the only known drug. We think this is the near-ideal tissue platform to find a drug for the majority of CF." Rajagopal's lab has created numerous other cell lines to further show that a CF drug that works in one patient should work in others and to see whether this will be an area that allows a more personalized approach to medicine.

"I'm most looking forward to working with the community of pulmonologists that concentrate in CF to generate therapies. This is occurring more than two decades after the remarkable work that identified the CF gene. Looking forward, I'm very excited that CF may lead the way in lung disease once more, by demonstrating that our iPS platform can be used to probe the diseases that are much less well understood. CF has more than two decades of great biology behind it. The reason we chose to attack this disease first was because of that pioneering work that lets us use our system with a very firm foundation," Rajagopal said.

http://www.eurekalert.org/pub_releases/2012-04/bmj-aas040412.php

Antibiotics a safe and viable alternative to surgery for uncomplicated appendicitis, say experts

Research: Safety and efficacy of antibiotic therapy with appendicectomy in the treatment of uncomplicated acute appendicitis: Meta-analysis

Giving antibiotics to patients with acute uncomplicated appendicitis is a safe and viable alternative to surgery, say experts in a study published on bmj.com today.

Surgery to remove an inflamed appendix (appendicectomy) has been the mainstay of treatment for acute appendicitis since 1889 and the general assumption is that, without surgery, the risk of complications, such as perforation or infection, is high. However, recent studies have reported fewer problems with antibiotic therapy than surgery in patients with uncomplicated appendicitis, but results have been inconclusive.

So a team of researchers at the Nottingham Digestive Diseases Centre NIHR Biomedical Research Unit set out to compare the safety and efficacy of antibiotic therapy as an initial treatment for uncomplicated acute appendicitis.

They analysed the results of four randomised controlled trials involving 900 adult patients diagnosed with uncomplicated acute appendicitis. A total of 470 patients received antibiotics and 430 underwent surgery.

Differences in study design and quality were taken into account to minimise bias.

Antibiotic therapy was associated with a 63% success rate at one year and a 31% relative reduction in complications compared with surgery. Even after excluding patients from one study who crossed over from the antibiotic group to the surgery group, a significant (39%) reduction in complications with antibiotic therapy compared with surgery remained.

Of 68 patients treated with antibiotics who were readmitted with recurrence of symptoms, four had normal appendix and 13 had complicated appendicitis. Three patients were treated successfully with another course of antibiotics. There were no significant differences in either length of hospital stay or risk of developing complicated appendicitis between the two groups of patients.

The authors argue that the role of antibiotics in acute uncomplicated appendicitis "has been overlooked based mainly on tradition rather than evidence" and they suggest that a careful 'wait, watch and treat' policy may be adopted in patients considered to have uncomplicated appendicitis or in whom the diagnosis is uncertain. However, they stress that for those with clear signs of perforation or peritonitis (inflammation of the abdominal wall) … early appendicectomy still remains the 'gold standard.' They conclude that antibiotic therapy "is a safe initial therapy for patients with uncomplicated acute appendicitis" and that it "merits consideration as a primary treatment option for early uncomplicated appendicitis."

In an accompanying editorial, Dr Olaf Bakker from the Department of Surgery at the University Medical Center Utrecht in the Netherlands argues that treating appendicitis conservatively has "major certain disadvantages" as the reoccurrence rate of appendicitis is up to 20% in the first year. He argues that until more convincing and longer term results are published, "appendectomy for uncomplicated appendicitis will probably continue."

http://www.realclimate.org/index.php/archives/2012/04/evaluating-a-1981-temperature-projection/