A new study has claimed that sugar intake is not directly associated with nonalcoholic fatty liver disease, as it was earlier believed.

Rather, high-calorie diets promote the progression of this serious form of liver disease.

Researchers conducted a double-blind study of healthy, but centrally overweight men to compare the effects of high intakes of two types of sugar, glucose and fructose, in two conditions — weight-maintaining (moderate-calorie diet) and weight-gaining (high-calorie diet).

In the weight-maintaining period, men on neither diet developed any significant changes to the liver.

However, in the weight-gaining period, both diets produced equivalent features of nonalcoholic fatty liver disease, including steatosis (fatty liver) and elevated serum transaminase and triglycerides.

These findings indicate that fructose and glucose have comparable effects on one’s liver, and calorie intake is the factor responsible for the progression of liver disease.

“Based on the results of our study, recommending a low-fructose or low-glycemic diet to prevent nonalcoholic fatty liver disease is unjustified,” Professor Ian A. Macdonald, study author and faculty of medicine and health sciences, University of Nottingham, UK, said.

“The best advice to give a patient is to maintain a healthy lifestyle with diet and exercise. Our study serves as a warning that even short changes in lifestyle can have profound impacts on your liver,” he said.

The study is published in Gastroenterology, the official journal of the American Gastroenterological Association.

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Max Kelmon, 13, has his own little version of a man cave in Palo Alto, Calif. Behind the family kitchen in a converted garage, he has an Xbox, a big-screen TV, headphones and a microphone. There’s an old couch covered in a sheet. And that couch where he parks himself, surrounded by boxes and Christmas lights, is one of Max’s favorite places on the planet.

From that couch, he connects to friends all over the globe — and he spends hours, pretty much every day, honing his skills in Call of Duty.

The first commercially successfully video game, Pong, invaded Americans’ living rooms 38 years ago. Since then, the industry has evolved from a simple bouncing ball in the Atari original to games with astounding graphics and sound, most of them connected to the Internet.

That means that kids like Max can play with people spread across the globe. It also means that gaming companies can analyze how gamers play — each and every decision they make.

So when kids sit down with a game, they are actually sitting across a screen from adults who are studying them — and, in some cases, trying to influence their behavior in powerful ways.

Researchers in game companies tweak games to get players to stay on longer, or to encourage them to spend money on digital goods. They study gamers’ reactions. It’s become a science.

And parents like Max’s mom, Vanessa Kelmon, often feel outgunned.

“I hate it. I really do,” she says. “He could play Xbox for 12 straight hours. [He has] friends in Mexico City and friends in England.”

Vanessa says Max is addicted to video games. “When I took it away, he started to cry,” she says. “My God, I am offering you to go play tennis or go play golf … and I am making you shut this down, and you’re crying about it.”

Tracking Clicks And Purchases

In millions of families, video games are a source of intense love and intense hate because they can be so incredibly compelling. You might not believe that if you don’t play them, but you can get lost in a great game. They make you feel good.

And it’s no accident, says Ramin Shokrizade, the game economist for Wargaming America.

“The technology for this has gotten quite sophisticated,” says Shokrizade, who began his career in neuroscience and behavioral economics. “At this point, every major gaming company worldwide either has in place a fully developed business intelligence unit, or they’re in the process of building one.”

Today’s game design is dominated by research, he says. As we play games, game developers are tracking every click, running tests and analyzing data.

They are trying to find out: What can they tweak to make us play just a bit longer? What would make the game more fun? What can get us to spend some money inside a game and buy something?

So as millions of people play, designers introduce little changes and get answers to all of these questions in real time. And games evolve.

For example, most games today sell virtual goods right inside the game — like a new gun in Call of Duty or a cow in FarmVille. Shokrizade’s job is to get people to buy them.

One of the tricks of the trade is something developers at Zynga — which created FarmVille — used to call “fun pain” or “the pinch.” The idea is to make gamers uncomfortable, frustrate them, take away their powers, crush their forts — and then, at the last second, offer them a way out for a price.

John Davison, who works at video game company Red Robot Labs, says free-to-play smartphone games like Candy Crush Saga and Puzzle & Dragons have become brilliant at using these tests to figure out how to get people to spend money.

And the research is working. Davison says those games are making millions of dollars — every day.

Kids Who Cash In

When adults play games, they consent to share that personal information about how they play. But Shokrizade worries about the millions of kids who play. “If it’s a child, how do you even get consent for something like that?” he says.

Many of the people spending cash are kids, including Davison’s children. Game consoles sell gift cards at convenience stores that allow kids to make purchases on video games, even if they don’t have a credit card.

Davison’s kids started playing Clash of Clans this year. In the game, developed by Supercell, you get to run your own little Viking village and team up with friends. To protect your clan, you can spend money on forts and weapons.

It’s free to download — but because of these virtual goods, it’s one of the highest-grossing apps in Apple’s store.

Davison’s two boys loved it. “They were clearly getting a lot of enjoyment out of it,” he says. “But it did get to the point where my wife and I were like, ‘Do you really want to be spending everything on this?’ ”

And this is coming from a man who has devoted his life to video games.

“I was trying to sort of total up in my head how much the kids had spent on this game,” he says. “But there was also a degree of admiration for the team at Supercell, that they had managed to get under my 10-year-old’s skin to this degree.”

Apple recently settled a class-action lawsuit about kids making in-app purchases like this without their parents’ permission, and the European Union is considering new regulations on games.

Some regulations are taking place on a smaller scale. In Menlo Park, Calif., Michelle DeWolf banned her 10-year-old son, Austin Newman, from playing games during the school week.

Originally, she gave him 30 minutes a day, but that didn’t work.

“He couldn’t think about doing his homework. He couldn’t think about walking the dog or helping in any other way, because he couldn’t get his mind off the idea that he had 30 minutes coming,” she says.

“Once he knew there was nothing, he didn’t think about it during the week, and he almost — maybe I’m not objective — but he almost seemed relieved.”

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Researchers report that wood-biochar supercapacitors can produce as much power as today’s activated-carbon supercapacitors at a fraction of the cost – and with environmentally friendly byproducts.

The report appears in the journal Electrochimica Acta.

“Supercapacitors are power devices very similar to our batteries,” said study leader Junhua Jiang, a senior research engineer at the Illinois Sustainable Technology Center at the University of Illinois. While batteries rely on chemical reactions to produce sustained electrical energy, supercapacitors collect charged ions on their electrodes (in this case, the biochar), and quickly release those ions during discharge. This allows them to supply energy in short, powerful bursts– during a camera flash, for example, or in response to peak demand on the energy grid, Jiang said.

“Supercapacitors are ideal for applications needing instant power and can even provide constant power– like batteries, but at lower cost,” he said. They are useful in transportation, electronics and solar- and wind-power energy storage and distribution.

Many of today’s supercapacitors use activated carbon – usually from a fossil-fuel source, Jiang said.

“Costly and complicated procedures are normally used to develop the microstructures of the carbon – to increase the number of pores and optimize the pore network,” he said. “This increases the surface area of the electrode and the pores’ ability to rapidly capture and release the ions.”

In wood-biochar supercapacitors, the wood’s natural pore structure serves as the electrode surface, eliminating the need for advanced techniques to fabricate an elaborate pore structure. Wood biochar is produced by heating wood in low oxygen.

The pore sizes and configurations in some woods are ideal for fast ion transport, Jiang said. The new study used red cedar, but several other woods such as maple and cherry also work well.

Expensive and corrosive chemicals are often used to prepare the activated carbon used in supercapacitors, giving the electrodes the physical and chemical properties they need to function well, Jiang said.

“The use of those chemicals will probably impose some environmental impacts,” he said. “This should be avoided or at least substantially reduced.”

Jiang and his team activated their biochar with mild nitric acid, which washed away the ash (calcium carbonate, potassium carbonate and other impurities) in the biochar. The byproduct of this process has a beneficial use, Jiang said: The resulting solution of nitrate compounds can be used as fertilizer.

These simple approaches dramatically cut the material and environmental costs of assembling supercapacitors.

“The material costs of producing wood-biochar supercapacitors are five to 10 times lower than those associated with activated carbon,” Jiang said. And when a biochar supercapacitor has reached the end of its useful life, the electrodes can be crushed and used as an organic soil amendment that increases fertility.

“The performance of our biochar materials is comparable to the performance of today’s advanced carbon materials, including carbon nanotubes and graphenes,” Jiang said. “We can achieve comparable performance with much less cost and probably much lower environmental costs.”

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The human face is as unique as a finger print, no one else looks exactly like you. But what is it that makes facial morphology so distinct? Certainly genetics play a major role as evident in the similarities between parents and their children, but what is it in our DNA that fine-tunes the genetics so that siblings – especially identical twins – resemble one another but look different from unrelated individuals? A new study by researchers at the U.S. Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab) has now shown that gene enhancers – regulatory sequences of DNA that act to turn-on or amplify the expression of a specific gene – are major players in craniofacial development.

“Our results suggest it is likely there are thousands of enhancers in the human genome that are somehow involved in craniofacial,” says Axel Visel, a geneticist with Berkeley Lab’s Genomics Division who led this study. “We don’t know yet what all of these enhancers do, but we do know that they are out there and they are important for craniofacial development.”

Visel is the corresponding author of a paper in the journal Science that describes this research. The paper is titled “Fine Tuning of Craniofacial Morphology by Distant-Acting Enhancers.”

While some genetic defects responsible for craniofacial pathologies such as clefts of the lip or palate have been identified, the genetic drivers of normal craniofacial variation have been poorly understood. Previous work by Visel and his collaborators, in which they mapped gene enhancers in the heart, the brain and other organ systems, demonstrated that gene enhancers can regulate their targets from across distances of hundreds of thousands of base pairs. To learn whether gene enhancers can also have the same long-distance impact on craniofacial development, Visel and a multinational team of collaborators studied transgenic mice.

“We used a combination of epigenomic profiling, in vivo characterization of candidate enhancer sequences, and targeted deletion experiments to examine the role of distant-acting enhancers in the craniofacial development of our mice,” says Catia Attanasio, the lead author on the Science paper. “This enabled us to identify complex regulatory landscapes, consisting of enhancers that drive spatially complex developmental expression patterns. Analysis of mouse lines in which individual craniofacial enhancers had been deleted revealed significant alterations of craniofacial shape, demonstrating the functional importance of enhancers in defining face and skull morphology.”

In all, Visel, Attanasio and their colleagues identified more than 4,000 candidate enhancer sequences predicted to be active in fine-tuning the expression of genes involved in craniofacial development, and created genome-wide maps of these enhancers by pin-pointing their location in the mouse genome. The researchers also characterized in detail the activity of some 200 of these gene enhancers and deleted three of them. A majority of the enhancer sequences identified and mapped are at least partially conserved between humans and mice, and many are located in human chromosomal regions associated with normal facial morphology or craniofacial birth defects.

Knowing about the existence of these enhancers, which are inherited from parents to their children just like genes, knowing their exact location in the human genome, and knowing their general activity pattern in craniofacial development should facilitate a better understanding of the connection between genetics and human craniofacial morphology,” Visel says. “Our results also offer an opportunity for human geneticists to look for mutations specifically in enhancers that may play a role in birth defects, which in turn may help to develop better diagnostic and therapeutic approaches.”

Visel says he and his collaborators are now in the process of refining their genome-wide maps to gain additional information about the activity patterns of these enhancer sequences. They are also working with human geneticists to perform targeted searches for mutations of these enhancer sequences in human patients who have craniofacial birth defects.

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A new study is providing insights into the interaction between bacteria and mucus building mucins – proteins that have sugars associated with them – and how the specificity of these interactions affects health.

Dr Nathalie Juge and her team at the IFR have shown that the ability to use mucins in the human gut varies between different gut bacteria strains.

The IFR researchers looked at Ruminococcus gnavus. This is a common species of gut bacteria found in over 90 percent of people, including infants just a few days old. It has also been implicated in gut-related health conditions.

A number of studies have shown that patients suffering from Inflammatory Bowel Diseases have a disproportionate representation of R. gnavus.

This study looked at two different R. gnavus strains. Although both R. gnavus strains can use mucins, only one had the ability to survive when mucins were the sole source of food.

Comparing the genomes of the R. gnavus strains identified gene clusters used to breakdown mucins. Differences in these genes explain the different abilities of the strains to use mucins.

The mucin sugar structures change in different parts of the gut and over time, suggesting the strains may be adapted for different environments or to colonize us at different times.

A better understanding of which strains use mucins and exactly how they do this will give us new insights into what makes a healthy gut bacteria population, and how fluctuations from this might link to gut diseases like Crohn’s disease and ulcerative colitis.

The study has been published in the journal PLOS ONE

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A type of HIV medicine that stops the AIDS virus from entering immune system cells could in future be put to work against cancer in new combination therapies being developed by drug companies.

Interest in using so-called CCR5 inhibitors to fight tumors was fuelled last year when U.S. researchers, testing the drugs on mice, reported a marked reduction in aggressive breast cancer cells spreading to the animals’ lungs.

Researchers from the Thomas Jefferson University Kimmel Cancer Center described the results as “dramatic” after they were published in the Journal of Cancer Research.

Now industry analysts at Citi believe Merck & Co Inc is set to take things to the next stage by testing its CCR5 drug vicriviroc in cancer patients. The product was abandoned as a treatment for HIV in 2010 following an unsuccessful study.

Pfizer Inc and Bristol-Myers Squibb – which also have similar drugs in their portfolios – could follow suit, Citi said in a note on Friday.

Asked to comment on the suggestion that it would start testing vicriviroc in patients in 2014 as part of a combination therapy for cancer, a spokesman for Merck said: “We have not disclosed any such plans.”

Citi said it expected vicriviroc to re-enter clinical testing in combination with cancer immunotherapy as Merck explores its potential across multiple tumor types, including melanoma, colorectal, breast, prostate and liver cancer.

Immunotherapy, which harnesses the body’s immune system to fight cancer, is a hot new area for cancer research, with some experts predicting the approach will in future form the backbone of many cancer treatments.

However, drug combinations are expected to be critical to its success as oncologists will need to block cancer cells on several fronts at once.

One option is to combine two immunotherapies, while another approach, also being pursued by other companies like Roche Holding AG and AstraZeneca Plc, is to combine immunotherapy medicines with different drug types.

CCR5 inhibitors are one such option, given the encouraging signals from pre-clinical research. As these drugs have already been studied in HIV, their development could be relatively rapid.

Pfizer could also start clinical trials in cancer with its approved CCR5 drug Selzentry, which is currently marketed for HIV via the ViiV Healthcare alliance with GlaxoSmithKline Plc and Shionogi & Co Ltd.

Bristol, meanwhile, has a dual CCR2/5 inhibitor in mid-stage Phase II development, which is being tested for diabetes and kidney disease.

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