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Thanks for visiting the xenophilius blog. Normal posts of the world’s most ineresting strange news and science discoveries will resume in a few days. Happy new year!

Close-up photos of dying star show our sun’s fate

About 550 light-years from Earth, a star like our Sun is writhing in its death throes. Chi Cygni has swollen in size to become a red giant star so large that it would swallow every planet out to Mars in our solar system. Moreover, it has begun to pulse dramatically in and out, beating like a giant heart. New close-up photos of the surface of this distant star show its throbbing motions in unprecedented detail.

“This work opens a window onto the fate of our Sun five billion years from now, when it will near the end of its life,” said lead author Sylvestre Lacour of the Observatoire de Paris.

As a sunlike star ages, it begins to run out of hydrogen fuel at its core. Like a car running out of gas, its “engine” begins to splutter. On Chi Cygni, we see those splutterings as a brightening and dimming, caused by the star’s contraction and expansion. Stars at this life stage are known as Mira variables after the first such example, Mira “the Wonderful,” discovered by David Fabricius in 1596. As it pulses, the star is puffing off its outer layers, which in a few hundred thousand years will create a beautifully gleaming planetary nebula.

Chi Cygni pulses once every 408 days. At its smallest diameter of 300 million miles, it becomes mottled with brilliant spots as massive plumes of hot plasma roil its surface. (Those spots are like the granules on our Sun’s surface, but much larger.) As it expands, Chi Cygni cools and dims, growing to a diameter of 480 million miles — large enough to engulf and cook our solar system’s asteroid belt.

For the first time, astronomers have photographed these dramatic changes in detail. They reported their work in the December 10 issue of The Astrophysical Journal.

“We have essentially created an animation of a pulsating star using real images,” stated Lacour. “Our observations show that the pulsation is not only radial, but comes with inhomogeneities, like the giant hotspot that appeared at minimum radius.”

Imaging variable stars is extremely difficult, for two main reasons. The first reason is that such stars hide within a compact and dense shell of dust and molecules. To study the stellar surface within the shell, astronomers observe the stars at a specific wavelength of infrared light. Infrared allows astronomers to see through the shell of molecules and dust, like X-rays enable physicians to see bones within the human body.

The second reason is that these stars are very far away, and thus appear very small. Even though they are huge compared to the Sun, the distance makes them appear no larger than a small house on the moon as seen from Earth. Traditional telescopes lack the proper resolution. Consequently, the team turned to a technique called interferometry, which involves combining the light coming from several telescopes to yield resolution equivalent to a telescope as large as the distance between them.

They used the Smithsonian Astrophysical Observatory’s Infrared Optical Telescope Array, or IOTA, which was located at Whipple Observatory on Mount Hopkins, Arizona. …

via Close-up photos of dying star show our sun’s fate.

Calorie restriction: Scientists take important step toward ‘fountain of youth’

Going back for a second dessert after your holiday meal might not be the best strategy for living a long, cancer-free life say researchers from the University of Alabama at Birmingham. That’s because they’ve shown exactly how restricted calorie diets — specifically in the form of restricted glucose — help human cells live longer.

This discovery, published online in The FASEB Journal, could help lead to drugs and treatments that slow human aging and prevent cancer.

“Our hope is that the discovery that reduced calories extends the lifespan of normal human cells will lead to further discoveries of the causes for these effects in different cell types and facilitate the development of novel approaches to extend the lifespan of humans,” said Trygve Tollefsbol, Ph.D., a researcher involved in the work from the Center for Aging and Comprehensive Cancer Center at the University of Alabama at Birmingham. “We would also hope for these studies to lead to improved prevention of cancer as well as many other age-related diseases through controlling calorie intake of specific cell types.”

To make this discovery, Tollefsbol and colleagues used normal human lung cells and precancerous human lung cells that were at the beginning stages of cancer formation. Both sets of cells were grown in the laboratory and received either normal or reduced levels of glucose (sugar). As the cells grew over a period of a few weeks, the researchers monitored their ability to divide, and kept track of how many cells survived over this period.

They found that the normal cells lived longer, and many of the precancerous cells died, when given less glucose. Gene activity was also measured under these same conditions. The reduced glucose caused normal cells to have a higher activity of the gene that dictates the level of telomerase, an enzyme that extends their lifespan and lower activity of a gene (p16) that slows their growth. Epigenetic effects (effects not due to gene mutations) were found to be a major cause in changing the activity of these genes as they reacted to decreased glucose levels.

“Western science is on the cusp of developing a pharmaceutical fountain of youth” said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. “This study confirms that we are on the path to persuading human cells to let us to live longer, and perhaps cancer-free, lives.”

via Calorie restriction: Scientists take important step toward ‘fountain of youth’.

Amazing facts

Record Soccer Ball Juggling

The Greek Rocket War

Baby placenta facial treatments offered

Beauty conscious women in Dubai are being targeted by a controversial product claimed to make them look younger made from newborn baby placenta.

British therapist Mona Mirza says new customers walk through the doors of her Dubai clinic almost every day, as word spreads of the new procedure.

“The main reason why human placenta is effective is because it is bio-identical to our own physiology,” she said.

“Your own collagen starts to mimic the baby collagen and cells that are going in.”

And while adult skin will continue mimicking the placenta cells for about three months, the treatment is not cheap. A 60-minute session costs around £170 ($307).

Placenta treatments are not new, however. Some European clinics already use sheep or horse placenta in their treatments, but the placenta serum used in Mirza’s facials is made by a American manufacturer who claims the afterbirth is farmed from Russian babies and given voluntarily.

Simon Cowell, Victoria Beckham and Jennifer Lopez are among celebrities reported to use placenta treatments in their beauty regimes.

Ms Mirza advises women over the age of 35 to have their first three treatments in the space of a week, followed by one treatment a month.

But sceptics say there is no scientific evidence to support claims that the procedure works.

via Baby placenta facial treatments offered | News.com.au.

I guess placenta facials sound better than people eating placentas, which they do for similar reasons:

Dr. Peter Chew, a consultant OB/GYN at Gleneagles Hospital, Singapore, didn’t think that it worked, but also didn’t see any harm in eating human placenta:

A placenta is an organ rich in blood vessels that develops in female mammals during pregnancy. It lines the uterine wall and partially envelopes the foetus, to which it is attached by the umbilical cord. At full-term, it is about 18cm long and 5cm thick. It is expelled during child birth, forming part of the afterbirth.

Its function is to transfer oxygen and nutrients from the mother to the foetus. It also releases carbon dioxide and waste from the foetus through the umbilical cord to be disposed of by the mother.

Dr Peter Chew, a consultant obstetrician and gynaecologist at Gleneagles Hospital, says that though people have been talking about “frying, drying and eating placentas” for years, his patients rarely ask to keep theirs.

He says: “Placentas are full of hormones, so theoretically, they should improve the complexion, even though there’s no medical evidence to support this.”

As for the possibility of dangerous side effects from consuming it, he says “there’s no harm, seeing it’s your own body’s organ”. But to be on the safe side, he recommends cooking the placenta before consumption. – neatorama

Mobilizing the repair squad: Critical protein helps mend damaged DNA

In order to preserve our DNA, cells have developed an intricate system for monitoring and repairing DNA damage. Yet precisely how the initial damage signal is converted into a repair response remains unclear. Researchers at the Salk Institute for Biological Studies have now solved a crucial piece of the complex puzzle.

In a forthcoming article in the Dec. 24 issue of Molecular Cell, they show that a protein named CtIP plays an essential role in the DNA damage “signal-to-repair” conversion process. “Being able to repair damaged DNA is extremely important; the cell has to know when it has received this type of damage and respond appropriately,” explains Tony Hunter, Ph.D., American Cancer Society Professor in the Molecular and Cell Biology Laboratory and director of the Salk Institute Cancer Center, who led the study. “Failure to do so can have disastrous consequences.”

The DNA in our cells is under constant attack from reactive chemicals generated as byproducts of cellular metabolism. In addition, it is assaulted by x-rays, ultraviolet radiation from the sun, and environmental carcinogens such as tobacco smoke. As a result of this continuous bombardment, some studies have estimated that the DNA in a single human cell gets damaged over 10,000 times every day.

If not repaired properly, the damage leads to mutations, which over time can cause cancer. “As a result, individuals with an inherited impairment in DNA repair capability are often at increased risk of cancer,” notes first author Zhongsheng You, Ph.D., a former postdoctoral researcher at the Salk Institute and now an assistant professor at Washington University School of Medicine in St. Louis.

DNA consists of two intertwined strands so that when the DNA is broken, two ends are revealed, one from each strand. In order to repair the DNA break, one strand is trimmed away—or resected—like a loose thread, leaving only the second strand. This exposed strand then searches for a copy of itself (located on its sister chromosome), and “photocopies” past the broken region, repairing the DNA and zipping itself back up.

In yeast, CtIP is required for resection of the broken end, and since it is also recruited to sites of DNA damage in human cells, Hunter’s team wanted to know whether CtIP plays a similar role there. To find out, they depleted CtIP from human cells and caused DNA damage. Without the CtIP, they discovered, the cells could no longer trim back the damaged DNA strands, which brought the whole repair process to an abrupt halt.

“It looks like CtIP recruitment is a very important control point in the DNA repair process,” You observes. “Once CtIP is recruited, resection and repair begin, so regulating CtIP recruitment is one way to regulate DNA repair itself.”

In order to understand the process better, the researchers then asked which regions of the CtIP protein are involved in binding it to the broken DNA ends. By testing small portions of the protein, they found that a region in the central part of CtIP helps recruit the protein. They named this region the “damage recruitment” (DR) domain.

Further studies suggested that the DR domain within CtIP is normally hidden inside the folded protein. Only when the cell sends a DNA damage signal is CtIP’s DR domain exposed, and only then can CtIP bind to the broken DNA. In this way, CtIP is like a switchblade that cells open only in the presence of DNA damage.

The authors believe that exposure of CtIP ‘s DR domain and its recruitment to the site of DNA damage triggers a chain reaction that results in DNA repair, and they now want to understand exactly what CtIP does to start the DNA repair process.

You is also trying to understand the modifications in CtIP that cause the DR domain to be exposed, and is looking into the role of CtIP in cancer. “Mutations in CtIP have not been mapped extensively in human tumors, but from this data, we predict that mutations to the DR domain would lead to cancer,” he says.

In the long term, the team hopes that a better understanding of the DNA damage pathway may provide clues for cancer treatment in the future. “CtIP is another important player in the double-strand break response,” says Hunter. “We have added another piece to the complex puzzle of DNA repair.”

via Mobilizing the repair squad: Critical protein helps mend damaged DNA.

Citrus surprise: Vitamin C boosts the reprogramming of adult cells into stem cells

Famous for its antioxidant properties and role in tissue repair, vitamin C is touted as beneficial for illnesses ranging from the common cold to cancer and perhaps even for slowing the aging process. Now, a study published online on December 24th by Cell Press in the journal Cell Stem Cell uncovers an unexpected new role for this natural compound: facilitating the generation of embryonic-like stem cells from adult cells.

Over the past few years, we have learned that adult cells can be reprogrammed into cells with characteristics similar to embryonic stem cells by turning on a select set of genes. Although the reprogrammed cells, called induced pluripotent stem cells (iPSCs), have tremendous potential for regenerative medicine, the conversion is extremely inefficient.

“The low efficiency of the reprogramming process has hampered progress with this technology and is indicative of how little we understand it. Further, this process is most challenging in human cells, raising a significant barrier for producing iPSCs and serious concerns about the quality of the cells that are generated,” explains senior study author Dr. Duanqing Pei from the South China Institute for Stem Cell Biology and Regenerative Medicine at the Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences.

Dr. Pei and colleagues measured the production of reactive oxygen species or ROS during reprogramming and discovered a potential link between high ROS and low reprogramming efficiency. They became particularly interested in antioxidants, hypothesizing that they might suppress ROS and cell senescence, which seems to be a major roadblock for the generation of iPSCs.

The researchers found that adding vitamin C, an essential nutrient that is abundant in citrus fruits, enhanced iPSC generation from both mouse and human cells. Vitamin C accelerated gene expression changes and promoted a more efficient transition to the fully reprogrammed state. Somewhat to their surprise, they found that other antioxidants do not have the same effect, but vitamin C does seem to act at least in part through slowing cell senescence.

“Our results highlight a simple way to improve iPSC generation and provide additional insight into the mechanistic basis of reprogramming,” concludes Dr. Pei. “It is also of interest that a vitamin with long-suspected anti-aging effects has such a potent influence on reprogramming, which can be considered a reversal of the aging process at the cellular level. It is likely that our work may stimulate further research in this area as well.”

via Citrus surprise: Vitamin C boosts the reprogramming of adult cells into stem cells.