iOS: Fleksy is an alternative keyboard with unprecedented predictive text skills. You can type a word completely wrong and it'll still figure out what you meant.
That's because Fleksy was designed with the blind in mind. The keyboard not only fixes your grievous typing errors, but speaks back the word to you so you know what it thinks you typed. The keyboard only consists of letters, however. To make a space you swipe right. To delete a word you swipe left. You can add punctuation by pressing and holding the keyboard to reveal a new row, or you can just make two spaces to create a period, then swipe down to change it to a question mark, exclamation point, or something else. While Fleksy takes a little getting used to at first, it's a very effective way to type because you can throw accuracy out the window pretty much entirely. The only thing it does require is that you know how to spell, otherwise it can't really figure out what you meant. If you're blind or just an awful mobile typer but have good spelling skills, this is the keyboard for you. Of course, it's an app an doesn't integrate full with the OS but you can use it to type out messages and copy/paste the text in elsewhere with all the extra time you'll save.
When Maxim Grew got bored, he decided to try building an instant camera out of a Polaroid film holder and a bunch of wooden popsicle sticks. He succeeded in building the thing—and it seems to work pretty well, too. More »
(Reuters) - Pfizer Inc on Tuesday reported better-than-expected quarterly results, helped by a rebound in sales in emerging markets.
The largest U.S. drugmaker said it earned $6.32 billion, or 86 cents per share, in the fourth quarter. That compared with $1.44 billion, or 19 cents per share, in the year-earlier quarter.
(Reporting by Ransdell Pierson; Editing by Jeffrey Benkoe)
You have a stomach. I have a stomach. It is one of our few universals. Humans, mate, sing, talk, and raise their children in many different ways, but we?ve all got stomachs. The question is why.
Stomachs help to digest food; they get the process rolling, boiling and grinding by coating our food in slime, enzymes and acid. This is the textbook explanation and no one is saying it is wrong, but in one of my treasured meanders through the library, I recently stumbled upon a paper suggesting this explanation is incomplete, perhaps woefully so. Just as important to our survival may be the stomach?s role in separating, sieving one might say, bacteria that are good for our guts from those that are bad. The study I found was led by Dr. Orla-Jensen, a retired professor from the Royal Danish Technical College. Orla-Jensen tested this new idea about the stomach by comparing the gut bacteria of young people, healthy older people and older people suffering from dementia. What Orla-Jensen found is potentially a major piece in the puzzle of the ecology of our bodies.
Image 1. A diagram of the human stomach. The stomach may act as a sieve, allowing only some kinds of microbes through to the small intestines.
Orla-Jensen and colleagues began by positing, or perhaps assuming is the better word, that a key function of the stomach is to kill bad bacteria with acid. The acid, they argue, serves as a sieve. It stops bad bacteria, particularly the most opportunistic of pathogens, but it does not stop all bacteria. It lets those beneficial bacteria that have adaptations for dealing with stomach acid?adaptations honed over many thousands of generations?on down the gastrointestinal road. In their model, if the stomach fails to kill bad bacteria, pathogens dominate the intestines. They do so in place of the beneficial microbes that help our bodies to digest food and produce nutrients. And when they do? death or at least the failure to thrive is nearly inevitable.
Orla-Jensen and colleagues knew from earlier work that the pH of the human stomach increases with age; the stomach becomes less acidic. This effect is most acute in individuals over seventy years of age. In these individuals Orla-Jensen predicted that the stomach?s effectiveness as a killer of bad microbes might be compromised. In turn, the intestines, recipients of everything that leaves the stomach, living or dead, might become dominated by pathogenic species such as the weedy and deadly Clostridium dificile or by oral species, that while beneficial in the mouth can become a pathogen in the gut. It was a simple enough prediction, but perhaps too simple. The biota of the gut is complex. It can contain thousands of species and is influenced by many, many factors which have proven in many ways intractable. Could the stomach?s pH really matter enough to make a measurable difference? As I read Orla-Jensen?s paper, I was skeptical, but I was curious enough to read through to the results. I sat down on the floor in the library and prepared to stay a while.
Image 2. Micrograph of Clostridium dificile. Image courtesy of CDC/ Lois S. Wiggs (PHIL #6260), 2004.
To test their hypothesis, Orla-Jensen and colleagues cultured bacteria they had collected from fecal samples of ninety human participants, one third of whom were between 30 and 40 years old and two thirds of whom were over seventy. They then compared the microbes found in the samples from these different age groups. Again, they would expect that in the older individuals that the bad bacteria and oral bacteria should be more common and, in their abundance, displace the good necessary bacteria, such as Bifidobacterium.
Remarkably, the authors? predictions from the sieve hypotheses held up. I have reproduced and slightly modified their main table below. Nine percent of the individuals over seventy had more than a million cells of the bad news?Clostridum bacteria per gram of feces; none of the thirty to forty-year-olds did. What was more, a third of the individuals over seventy had more than a billion cells per gram of feces of the oral bacteria, Streptococcus salivarius. Again, none of the thirty to forty-year-olds did. But were these pathogenic and oral bacteria doing well enough to actually compromise the success of good bacteria in the gut? Yes. While all of the thirty to forty year olds had at least a million cells of the good gut bacteria Bifidobacteriumper gram of sample, less than half of the individuals over seventy did.
Interestingly, the guts of those individuals over seventy years of age who had dementia were in the worst shape, by far. Nearly each and every one of their guts was dominated by Clostridium and oral bacteria. Other studies seem to lend support to these general findings, albeit from different angles. A study comparing healthy individuals and individuals with low stomach acidity found that those with low stomach acidity were less likely to have Bifidobacterium even though their total density of intestinal bacteria, particularly the pathogens, increased. Another study found that individuals with low stomach acidity tend to be more likely to suffer from diarrhea, as would be expected if their guts were being taken over by pathogens.
The ?differences seen here as a function of age are much more pronounced than those seen in another study, recently published in the journal Nature. The Nature article compares the gut microbes of more than ?five hundred individuals of different ages and ethnicities. In the Nature study the authors found little effect of age on gut microbes after the first few years of life (during which there was a large effect as newborns slowly acquired adult microbes). However, the Nature study only considered four individuals over seventy years of age (they also did not specifically look for shifts in beneficial versus problematic species, perhaps they will in the future). Orla-Jensen?s work suggests that it is precisely the very old individuals in whom the differences begin to be pronounced. ?Sometimes it takes the perspective of many studies and time to see the full picture.?This is probably where I should point out that the Orla-Jensen study I?m discussing was published in 1948. Interesting ideas can get lost in unread scientific articles; many, perhaps most, are. Orla-Jensen?s paper has only rarely been cited and never in the context of the discussion of the function of the stomach or even in the context of aging and the microbial wilderness of our bodies.
Table 1. Reproduced (with updates) from Orla-Jensen et al., 1948. Sample size for each group = 30 individuals. The author of this paper, Prof. Orla-Jensen was 77 at the time of the publication of this paper in 1948 and so had a personal interest in these results. One wonders if he sampled himself.
Percent of individuals with > than 1 billion cells of each bacteria per gram of feces, or, in parentheses, percent of individuals with > 1 million cells per gram.
Volunteers
Mutualist Bifidobacterium
Pathogen Clostridium
Oral bacteria, Streptococcus salivarius
Aged 30-40 (Healthy)
57? (100)
0
0
> 70 years (Healthy)
25 (44)
9
31
> 70 years (w/ Dementia)
7 (9)
48
35
More than sixty-five years later it is now up to us to figure out what other predictions the sieve hypothesis might make <sup>2/<sup>. Perhaps the most obvious prediction is that as one travels the body, from the skin to the mouth to the stomach and on into the intestines, that one should encounter, at each step, diminishing subsets of microbial lineages. Is this true? It seems hard to believe. After all, a huge number of studies have proudly announced the great diversity of microbes in the gut, a terrible diversity. Let?s look.
The best study I know of included samples from mouth and gut, and considered which taxa of microbes were found in the different habitats. The diversity of major lineages drops by half as you go from the mouth to the stomach AND the lineages present in the gut, particularly the colon, are a subset of those in the stomach which are a subset of those in the mouth (see Figure 2). Comparing the results of this studies with those of others suggests the mouth itself also serves as a kind of filter, winnowing the species that land on the skin and lips or in the mouth to the subset that are most beneficial. From this subset, the stomach further cleaves.
If the sieve hypothesis holds, there must be additional predictions. I have not thought this through terribly well, but I think I would probably expect differences in the stomachs of animals eating different foods. Animals that eat foods that are more likely to include pathogens ought to have filters that are more finely tuned to weeding out bad microbes; they ought, I think, to err on the side of killing too many. This does appear to be the case for some vultures. The stomach of the white-backed vulture has a pH of 1! Conversely it seems plausible to predict that animals that eat diets less likely to lead them to pathogens, fruit eaters for example, should be expected to relax the sieve, open it up a little to make sure that many good microbes make it through. ?I don?t know that it has been tested. There must be more predictions for the differences one expects among species. A broad survey of the evolution of the stomach seems in order.
Image 3. White backed vultures feeding on a wildebeest. These vultures need to very actively fight the pathogens in the dead meat on which they indulge. One way they do so is by having very, very, acidic stomachs. Photo by?Magnus Kjaergaard.
Modern living also presents us with another testable prediction about the stomach and its effects on microbes. Bariatric surgery is an ever more common medical intervention in which the size of a patient?s stomach is reduced so as to reduce the amount of food he or she can eat in one sitting. The surgery also has the consequence, however, of increasing the pH in the stomachs of those who have the surgery, making their stomachs less acidic. If the sieve hypothesis is right these individuals ought to have gut bacteria that look more like those of seventy years old than those of thirty year olds. They do. Recently a study has found that good Bifidobacterium species become more rare after bariatric surgery while oral bacteria (in this case Prevotella) and? E. coli, which can be a pathogen, become more common. These results seem to be what the sieve hypothesis would predict.
I am sure there are more predictions. I?ll leave you to them. The good news is that if there are more predictions now is a great time to look, to test them. The study of the microbes of our body is now hip, as sexy as a field of study that often involves the word fecal can be (see Image 4 or check out your own sexy fecal bugs at American Gut). New data are published every day. If we can develop good predictions they can be tested. We might finally figure out what the stomach does, or rather the complex mix of its roles, its churning melange of duties. No one denies that the stomach helps to break down proteins, it just might not be its most important job.
Image 4. Microbiologist Jonathan Eisen wearing his microbiome. Image courtesy of Jonathan Eisen.
Meanwhile, there is an interesting coda to this story. In addition to considering the difference between old and young individuals, Orla-Jensen, as you might remember, considered the difference between healthy individuals over seventy and individuals over seventy with dementia. The individuals with dementia had even more pathogens and oral microbes in their guts than did the healthy seventy-year-olds. This is interesting, but what is the cause and what is the effect here? Could a poorly functioning stomach lead to a pathogen heavy microbe community in the gut and could that gut community in turn lead to dementia??Could our minds really fail because our stomachs do? A few recent studies have begun to explore the possibility that dementia might result from infection, but it is WAY too soon to say anything conclusive. One is left to imagine the mechanism behind such a decline. I have some ideas, but I?ll need to think them over some more. Meanwhile, you can offer your hypotheses too, and I?ll go back to the library and see what other gems I can find, old studies that are as revolutionary as the new ones you read about in the press, studies that whether right or wrong confirm just how little we know and how slow and circular progress can be.
Footnotes (more to be added)
1- They did not sequence the genes of these microbes?now a common technique?and so their results represent just part of what was going on in the sampled guts, a few kinds of common trees in a diverse forest, and yet it was probably a reasonable measure of those trees.
2- Which, I will confess, I?ve named here. Orla-Jensen and colleagues thought the idea so obvious as to not even deserve a name.
Sight would dramatically alter a blind man's understanding of an elephant, according to the old story. Now, a look directly at a cell surface is changing our understanding of cell membrane organization.
Using a completely new approach to imaging cell membranes, a study by researchers from the University of Illinois, Lawrence Livermore National Laboratory and the National Institutes of Health revealed some surprising relationships among molecules within cell membranes.
Led by Mary Kraft, a U. of I. professor of chemical and biomolecular engineering, the team published its findings in the Proceedings of the National Academy of Sciences.
Cells are enveloped in semi-permeable membranes that act as a barrier between the inside and outside of the cell. The membrane is mainly composed of a class of molecules called lipids, studded with proteins that help regulate how the cell responds to its environment.
"Lipids have multiple functions serving as both membrane structure and signaling molecules, so they regulate other functions inside the cell," Kraft said. "Therefore, understanding how they're organized is important. You need to know where they are to figure out how they're doing these regulatory functions."
One widely held belief among cell biologists is that lipids in the membrane assemble into patches, called domains, that differ in composition. However, research into how lipids are organized in the membrane, and how that organization affects cell function, has been hampered by the lack of direct observation. Although the cell membrane is heavily studied, the imaging techniques used infer the locations of certain molecules based on assumed associations with other molecules.
In the new study, Kraft's team used an advanced, molecule-specific imaging method that allowed the researchers to look at the membrane itself and map a particular type of lipid on mouse cell membranes. The researchers fed lipids labeled with rare stable isotopes to the cells and then imaged the distribution of the isotopes with high-resolution imaging mass spectrometry.
Called sphingolipids (SFING-go-lih-pids), these molecules are thought to associate with cholesterol to form small domains about 200 nanometers across. The direct imaging method revealed that sphingolipids do indeed form domains, but not in the way the researchers expected.
The domains were much bigger than suggested by prior experiments. The 200-nanometer domains clustered together to form much larger, micrometer-sized patches of sphingolipids in the membrane.
"We were amazed when we saw the first images of the patches of sphingolipids across the cell surface," said Peter Weber, who directed the team at Lawrence Livermore National Laboratory. "We weren't sure if our imaging mass spectrometry method would be sensitive enough to detect the labeled lipids, let alone what we would see."
Furthermore, when the researchers looked at cells that were low on cholesterol ? thought to play a key role in lipid aggregation ? they were surprised to find that the lipids still formed domains. On the other hand, disruption to the cell's structural scaffold seemed to dissolve the lipid clusters.
"We found that the presence of domains was somewhat affected by cholesterol but was more affected by the cytoskeleton ? the protein network underneath the membrane," Kraft said. "The central issue is that the data are suggesting that the mechanism that's responsible for these domains is much more complicated than initially expected."
In addition, the new study found that sphingolipids domains were incompletely associated with a marker protein that researchers have long assumed dwelled where sphingolipids congregated. This means that data collected with imaging techniques that target this protein are not as accurate in representing sphingolipid distribution as previously thought.
"Our data are showing that if you want to know where sphingolipids are, look at the lipid, don't infer where it is based on other molecules, and now there's a way to directly image them," said Kraft, who also is affiliated with the department of chemistry at the U. of I.
Next, the researchers plan to use the direct-imaging method in conjunction with other more conventional methods, such as fluorescence, to further determine the organization of different kinds of molecules in the membrane, their interactions and how they affect the cell's function. They plan to begin by targeting cholesterol.
"Cholesterol abundance is important," Kraft said. "You change that, you tremendously change cell function. How is it organized? Is it also in domains? That's related to the question, what's the mechanism responsible for these structures and what are they doing?"
###
The paper, "Direct chemical evidence for sphingolipid domains in the plasma membranes of fibroblasts," is available from PNAS.
University of Illinois at Urbana-Champaign: http://www.uiuc.edu
Thanks to University of Illinois at Urbana-Champaign for this article.
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Click the arrow on the audio player to?hear Dean Young read this poem. You can also download?the recording or?subscribe?to?Slate's Poetry Podcast on iTunes.
Either that or the police blotter. Someone steals a bicycle because he wants to fly. Wants a new heart. A hive on the porch. There?s someone suspicious in the graveyard with a torch. What the librarian needs she cannot say but she?s listening to Bulgarian language tapes in her car anyway. Sure beats eating your own pancreas. The difference between surrealism and dada like the difference between first- and second-degree manslaughter hardly matters to most of us. What you get is a chalk outline of dust, bells for no reason, mouthfuls of starlight rusty as blood, gra gra gra gra grape stems stammering of summer and lots of dreams on paper like in analysis and graduate school. The difference between graduate school and analysis is approximately $20,000 although both occur mainly lying down. The white coats in the lab peer at the microscope slides and think it?s bad news that the blood is a wolf?s blood. Dear Oblivion, I love your old song. Let a spinning wheel be my fireplace, the lit-up nerves of jellyfish my universe. The greatest indication of truth is laughter and maybe now I?m ready to talk to my mother and father. This morning I have the distinct impression my house is about to crumble so let rubble be my crown. Release the hound! What a joke, she?s about a hundred years old and when you look into her almost-no-one-home eyes, you come to a river and when you come to that river, float.
Victoria Beckham might not be perfect in all facets of life, but she does know best when it comes to her fashion sense. The model and designer -- and, of course, former Spice Girl -- admits it hasn't been easy learning to rely on other people as her fashion empire grows.
While bucking one of the administration's few proposals on firearms that Republicans might actually accept, the National Rifle Association's Wayne LaPierre offered absolutely no new ideas ? indeed, old ideas ? during a speech that reveals the backwards thinking behind the gun lobby's future.
RELATED: Why This Time Was Different for Guns
In a speech late Tuesday at a Nevada hunting conference,?LaPierre attacked President Obama for a very subtle reference to gun control in his second inaugural address.?In fact, Obama's reference was so subtle that many gun-control advocates missed it ? "I was, personally, upset that Mr. Obama did not discuss gun control," The New York Times' Andrew Rosenthal wrote ??but LaPierre said that when Obama said, "We cannot mistake absolutism for principle," he was referring to gun advocates. Absolutism is okay when we're talking about the Second Amendment, LaPierre said. "Obama wants to turn the idea of absolutism into a dirty word," he said. The NRA executive vice president continued:
"I?ve got news for the president... Absolutes do exist. Words do have specific meaning in language and in law. It?s the basis of all civilization. Without those absolutes, without those protections, democracy decays into nothing more than two wolves and one lamb voting on, well, who to eat for lunch."
You know what that sounds a lot like? Barry Goldwater, who famously said in his 1964 presidential nomination acceptance speech, "I would remind you that extremism in the defense of liberty is no vice! And let me remind you also that moderation in the pursuit of justice is no virtue!"?Even though the NRA promised "meaningful contributions" after the Newtown shooting, all of its contributions are recycled slogans.
RELATED: Wayne LaPierre Only Said What Gun Nuts Have Been Posting on Facebook
The most quoted line from LaPierre's first press conference after the shooting ? "The only thing that stops a bad guy with a gun is a good guy with a gun" ? is so old that it had inspired Facebook memes long before the event. (Here's LaPierre saying it to USA Today in July 2010.?Here's a gun-rights advocate in South Dakota saying it in January 2008.?Here's LaPierre saying it in another article in USA Today?? this one from December 20, 2007?? after the Virginia Tech shooting.?"It has occurred to me that sitting next to a good guy with a gun is better than sitting next to abad guy with a gun," Don Galloway wrote in The New Hampshire Union Leader on July 30, 2004.)?Likewise, the NRA ad calling Obama a hypocrite for having Secret Service protection for his daughters but being "skeptical" of putting armed guards in elementary schools is another tired meme recycled on Facebook pages.
RELATED: The Executive Order the NRA Should Fear the Most
We should congratulate the NRA for recycling Barry Goldwater instead of its own talking points on Tuesday. Too bad the group doesn't really believe it. The NRA is in no way truly absolutist on the Bill of Rights; LaPierre called for a check on violence in video games?? which would put limits on the First Amendment. The NRA is on Team Wolf in that scenario.
RELATED: NRA Snubs Obama
LaPierre's speech served as an attack on the idea of universal background checks for gun purchases, one of the very few legislative ideas proposed by Obama that might have Republican support. Rep. Robert Goodlatte, chair of the House Judiciary Committee, said on C-SPAN, "[I]n terms of background checks, in terms of keeping weapons out of the hands of criminals and people who have serious mental health difficulties, we want to do that, and we would take a close look at that." About 40 percent of guns are currently sold without background checks. Republican support for changing that might be why the NRA has moved beyond quoting Facebook memes and onto cribbing from conservative classics.
Jan. 22, 2013 ? Stanford University School of Medicine investigators have found that for people harboring a genetic predisposition that is prevalent among Americans, beta carotene, which the body converts to a close cousin of vitamin A, may lower the risk for the most common form of diabetes, while gamma tocopherol, the major form of vitamin E in the American diet, may increase risk for the disease.
The scientists used a "big data" approach to hunt down interactions between gene variants previously associated with increased risk for type-2 diabetes and blood levels of substances previously implicated in type-2 diabetes risk. In people carrying a double dose of one such predisposing gene variant, the researchers pinpointed a highly statistically significant inverse association of beta carotene blood levels with type-2 diabetes risk, along with a suspiciously high positive association of gamma tocopherol with risk for the disease.
"Type-2 diabetes affects about 15 percent of the world's population, and the numbers are increasing," said Atul Butte, MD, PhD, associate professor of systems medicine in pediatrics. "Government health authorities estimate that one-third of all children born in the United States since the year 2000 will get this disease at some point in their lives, possibly knocking decades off their life expectancies."
Butte is the senior author of the new study, published online Jan. 22 in Human Genetics. The first author, Chirag Patel, PhD, is a former graduate student in Butte's lab and now a postdoctoral scholar at the Stanford Prevention Research Center.
The findings point the way to further experiments that could establish whether beta carotene and gamma tocopherol are, respectively, protective and harmful themselves, or merely "markers" whose blood levels dovetail with the presence or absence of some other substance, process or defect that is a true causal factor.
Moreover, the fact that both beta carotene and gamma tocopherol interact with the same gene variant to influence diabetes risk, albeit in opposite directions, suggests that the protein the gene called, SLC30A4, codes for may play a crucial role in the disease. Indeed, that protein is relatively abundant in insulin-producing islet cells of the pancreas, where it aids the transport of zinc into those cells. This, in turn, triggers the release of insulin, whose adequate secretion by the pancreas and efficient uptake in muscle, liver and fat tissue counters the dangerous buildup of glucose in the blood and, in the long run, the onset of type-2 diabetes.
The genomes of some 50 to 60 percent of the U.S. population carry two copies of that very gene variant, which previous studies have shown to confer a slightly increased risk of contracting type-2 diabetes. This variant was one of 18, each found by other researchers to have a mild association with type-2 diabetes risk, that the Butte team incorporated into its analysis.
These gene/disease connections had been identified via so-called "genome-wide association studies," or GWAS. In such analyses, the genomes of large numbers of people with a disease are compared with those of people without it to see if certain versions of any gene variants occur with substantially greater frequency in one group than in the other.
The most well-studied gene variations are substitutions of one type of chemical unit of DNA for another one at a single position along the genome. "It's like a single-letter spelling change," said Butte. "'Grey' versus 'gray' may not matter much, if at all. But when 'grey' turns into 'grew,' you might have some serious semantic issues." The genome contains millions of spots at which such differences occur, so advanced statistical techniques must be employed to screen out "frequency differences" between the "diseased" and "healthy" groups that are, at bottom, the mere results of blind chance.
"While plenty of genetic risk factors for type-2 diabetes have been found," said Butte, "none of them taken alone, and not even all of them taken together, comes close to accounting for the prevalence of type-2 diabetes." But genes don't act in a vacuum, he added. (If food is hard to find, nobody gets fat, obesity predisposition or not.)
A few years ago, Butte and his associates designed an approach analogous to the GWAS: the EWAS, or environment-wide association study. Unlike the genome, which is huge but finite (about 3 billion chemical units long), the environment contains an infinite number of substances, from dietary micronutrients to synthetic pollutants, to which a person might be exposed over a lifetime. But increasing numbers of exposures are being cataloged by investigators -- including, for example, scientists at the federal Centers for Disease Control and Prevention who conduct massive biennial screenings to collect data that can guide public-health policy decisions. This ongoing endeavor, called the National Health and Nutrition Examination Survey, involves a detailed analysis of substances in blood drawn from thousands of volunteers along with their heights, weights, blood pressures, fasting blood-glucose levels and other indicators of their medical status.
In 2010, Patel, Butte and their colleagues published the results of the first-ever EWAS, in which they combed large public databases to compare people with or without high blood-glucose levels -- a defining marker of type-2 diabetes -- in pursuit of differences between the two groups' exposures to myriad environmental substances. The analysis fingered five substances, including both beta carotene, found in carrots and many other vegetables, and gamma tocopherol, which is relatively abundant in vegetable fats such as soybean, corn and canola oils and margarine.
The Stanford investigators learned that the NHANES contained data on numerous individuals' environmental exposures and, for many of the same individuals, their genomic compositions. This enabled the researchers to perform a novel study pairing each of the 18 type-2-diabetes-implicated gene variants with each of the five suspect environmental substances to see how, for individuals carrying a particular gene variant, different blood levels of a given substance correlated with those individuals' blood-glucose levels.
None of the genetic factors studied in isolation had shown a particularly impressive impact on type-2 diabetes risk. But when they were paired off one by one with the environmental factors, a couple of statistically robust results jumped out. First, for those carrying two copies of the variant in SLC30A4, higher beta-carotene levels correlated with lower blood-glucose levels. "This vitamin was already known as being 'good' with respect to type-2 diabetes, so it was no surprise that we saw it, too," said Butte. "But it was reassuring, as it suggested we were doing things right, and interesting to find it paired with SLC30A4."
The second finding was at once novel and disconcerting. High blood levels of gamma tocopherol appeared to be associated with increased risk for the disease.
The Butte lab is now gearing up to perform studies in which purified beta carotene and gamma tocopherol will be fed to lab mice. This may show whether those substances themselves are critical to preventing or accelerating the onset of type-2 diabetes. It also may throw light on precisely how these substances affect the production or performance of the protein for which the implicated gene codes.
"We can't say, based on just this study, that 'vitamin E is bad for you,'" said Patel. He noted that blood levels of alpha tocopherol -- another form of vitamin E that predominates in most supplements -- showed no deleterious interaction with the predisposing gene variant in the new study.
But maybe it can't hurt to eat a few more carrots.
Other co-authors were John Ioannidis, MD, PhD, professor of medicine and of health research and policy; former staff bioinformatician Rong Chen, PhD; and research associate Keiichi Kodama, MD, PhD.
The Lucile Packard Foundation for Children's Health, National Library of Medicine, National Institute of General Medical Sciences and other National Institutes of Health agencies funded the study.
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The above story is reprinted from materials provided by Stanford University Medical Center.
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Journal Reference:
Chirag J. Patel, Rong Chen, Keiichi Kodama, John P. A. Ioannidis, Atul J. Butte. Systematic identification of interaction effects between genome- and environment-wide associations in type 2 diabetes mellitus. Human Genetics, 2013; DOI: 10.1007/s00439-012-1258-z
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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
Getting hacked is becoming an Internet rite of passage. Consider 2012 alone: First Zappos was hacked, its customers' passwords and other personal information exposed. Then LinkedIn announced that its users' passwords had been compromised. Then eHarmony. Then Yahoo. More than 30 million users' passwords were stolen. The growing, painful password problem is twofold: Hackers have gotten very good at what they do, with more capable tools than ever, and those tools can work so well because we are still really bad at choosing?and remembering?passwords.
Coming up with a password is a compromise between security and convenience. Very complex passwords are highly secure but difficult to remember. To make them work, users end up in a constant loop of resetting forgotten passwords or relying on writing them down on sticky notes. Simpler passwords are easier for us to remember but all too easy for others to discern. Even if you think your pet's name is rare and choose SenorFluffypants as a password, that information would be easy for an adversary to find on, say, Facebook. Because passwords are annoying and tedious to keep track of, most of us resist changing our obvious passwords, many of which can be found in leaked databases. The top passwords of 2012 remain what they have been for years: password, 123456, and 12345678.
Passwords like those are especially easy to crack, says Peter Theobald of KLG Computer Forensics. "Anyone with a password that can be found in the dictionary, even if it's a minor variation followed by a number, gets found quickly," he says.
It's possible that one or more of your passwords has already been stolen (you can check PwnedList, an online database with more than 966 million compromised passwords on file), but even if it hasn't, relying on weak passwords is a fool's game. Once hackers get into an account, they immediately start searching for any linked or related accounts. Before long, a complete stranger could be wreaking havoc on your social reputation, credit rating, and finances. If you suspect that one of your online accounts has been hacked, immediately change the passwords on any other important account you have; hackers have programs designed to try the cracked password at other sites. Even if you've been smart enough to maintain separate passwords for different accounts, hackers will leverage access to your email to reset passwords for other sites. ("Forgot your password? Have a new one sent to your email account.") But when you do reset passwords, don't repeat mistakes of the past. There are ways to make passwords both secure and memorable.
The Bad Guys
Before we examine what good passwords look like, it helps to know your adversary. Using a PC with inexpensive multicore graphics processing units (GPUs), a hacker can try about 8 billion password combinations in a second?thousands of times faster than just a few years ago, when the processing depended on just the CPU. Because they're designed for parallel computing, GPUs are much better at the large-scale mathematical operations needed for cracking passwords. Powerful password-cracking software is available for free, and hackers also have access to growing shared lists of millions of actual user passwords.
By analyzing these lists, professional password crackers know that when forced to pick a password with a mix of upper- and lowercase letters, a number, and a special character, users tend to choose a familiar word or a dictionary word, capitalize the first letter, and add the number and special character at the end (such as Fido1*). The geekiest among us may replace vowels with numbers (leetspeak), such as F1d01, or shift our hands on the keyboard to mask the actual password. But hackers know this, and a simple algorithm is all they need to get past it.
Even passwords that combine more than one strategy are vulnerable. Take, for example, the password MyS3cr3t!. It meets typical security guidelines, and online password-strength meters would call it strong. With faster processing, and programming rules that add characters and punctuation to a word list, a hacker could crack that password in just 12 hours.
Don't Be an Idiot: Make a Bad Password Good
It's not all that hard to turn a mediocre password into a great one. All it takes is the addition of some strategically placed numbers and symbols?and a good base word or phrase in the first place (which means saying goodbye to pet names and favorite sayings). Below, we chart a password's journey from weak to strong, showing how long it would take for a commonly used algorithm to crack each version.
Password: Aquarius Time to Crack: 9.08 Mintues
Password: Aquarius1 Time to Crack: 1.59 Days
Password: Aquar$ius1 Time to Crack: 19.24 Years
Password: Aqu57ar$iu3s Time to Crack: 17,400,000 Years
Global warming 'has had a role' in making 2012 the hottest ever recorded in the lower 48 states, says a US climatologist. The average temperature was 54.3 degrees F., a full degree higher than the previous annual record.
By Pete Spotts,?Staff writer / January 8, 2013
Alexander Merrill cools off in a cloud of mist at the Henry Doorly Zoo in Omaha, Neb., in this July 2012 file photo, taken when temperatures reached triple digits. Federal meteorologists say 2012 was the hottest year on record by far.
Nati Harnik / AP Photo / File
Enlarge
The year 2012 was the warmest on record for the continental United States, eclipsing 1998's record average temperature of 54.3 degrees by a full degree Fahrenheit.
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While one degree's difference may not seem like much, the spread between the record coldest year, 1917, and the previous record warm year, 1998, is just 4.2 degrees F. With 2012's record-high reading, the gap has grown by 25 percent, according to preliminary data from the National Climatic Data Center (NCDC) in Asheville, N.C.
Last year marked the 15th consecutive year of above-normal average annual temperatures for the continental US.
Global warming "has had a role in this," says Jake Crouch, a climatologist at the NCDC, during a briefing Tuesday on the year's data. Annual average temperatures for the lower 48 states have been increasing over the past century, although he noted that it's difficult to know how much of the warming in 2012 could be pegged to human-induced climate change versus natural variability.
Regionally, the Northeast, Southwest, South, and North West Central US posted record high annual temperatures, with the North West Central US coming in at 3.9 degrees F. above the long-term average, followed by the Northeast at 3.4 degrees F. above the long-term average.
Beyond temperatures, the continental US posted the second worst year, after 1998, for severe weather, as measured by the NCDC's US Climate Extremes Index.
The most pervasive severe conditions in 2012 centered on the ongoing drought in the US. At one point in July, moderate to exceptional drought, as measured by a gauge known as the Palmer Drought Severity index, covered 61 percent of the US. Other measures still put the drought coverage at 61 percent of the country, covering most of the western two-thirds of the US.
Toward the end of last year, a dearth of water flowing into the Mississippi River threatened to shut down barge traffic along a key section between St. Louis and Cairo, Ill. But the US Army Corps of Engineers released water from the Carlyle Lake Reservoir in Illinois, which fed water into the river. The Army Corps also used explosives to pulverize rocks on the river bottom that had become threats to navigation as the water level fell. These two actions, Corps officials say, are expected to keep the Mississippi open to barge traffic through the end of January.
Jan. 21, 2013 ? Ancient DNA has revealed that humans living some 40,000 years ago in the area near Beijing were likely related to many present-day Asians and Native Americans.
An international team of researchers including Svante P??bo and Qiaomei Fu of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, sequenced nuclear and mitochondrial DNA that had been extracted from the leg of an early modern human from Tianyuan Cave near Beijing, China. Analyses of this individual's DNA showed that the Tianyuan human shared a common origin with the ancestors of many present-day Asians and Native Americans. In addition, the researchers found that the proportion of Neanderthal and Denisovan-DNA in this early modern human is not higher than in people living in this region nowadays.
Humans with morphology similar to present-day humans appear in the fossil record across Eurasia between 40,000 and 50,000 years ago. The genetic relationships between these early modern humans and present-day human populations had not yet been established. Qiaomei Fu, Matthias Meyer and colleagues of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, extracted nuclear and mitochondrial DNA from a 40,000 year old leg bone found in 2003 at the Tianyuan Cave site located outside Beijing. For their study the researchers were using new techniques that can identify ancient genetic material from an archaeological find even when large quantities of DNA from soil bacteria are present.
The researchers then reconstructed a genetic profile of the leg's owner. "This individual lived during an important evolutionary transition when early modern humans, who shared certain features with earlier forms such as Neanderthals, were replacing Neanderthals and Denisovans, who later became extinct," says Svante P??bo of the Max Planck Institute for Evolutionary Anthropology, who led the study.
The genetic profile reveals that this early modern human was related to the ancestors of many present-day Asians and Native Americans but had already diverged genetically from the ancestors of present-day Europeans. In addition, the Tianyuan individual did not carry a larger proportion of Neanderthal or Denisovan DNA than present-day people in the region. "More analyses of additional early modern humans across Eurasia will further refine our understanding of when and how modern humans spread across Europe and Asia," says Svante P??bo.
Parts of the work were carried out in a new laboratory jointly run by the Max Planck Society and the Chinese Academy of Sciences in Beijing.
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JAIPUR, India (AP) ? Rahul Gandhi, the heir to India's Nehru-Gandhi political dynasty, said Sunday he would work to transform the country by decentralizing power after he was elevated to the governing Congress party's No. 2 post.
His career is the ultimate expression of Congress' reliance on the Gandhi family name, but the man widely expected to be the party's candidate for prime minister in next year's elections on Sunday condemned elitism as "the tragedy of India" and vowed to work to expand access to power for ordinary people.
"For me, the Congress party is my life. The people of India are my life and I will fight for them," Gandhi, a 42-year-old lawmaker, said in his acceptance speech Sunday in the western Indian city of Jaipur, a day after he was appointed the party vice president, a position behind his mother Sonia Gandhi, who is the Congress party president.
Reflecting on his eight years while working for the party organization, Rahul Ganhi said India's governmental system was struck in the past and the answer lay in completely transforming it.
"A handful of people control the entire political space. We don't respect knowledge, We respect position," he said to cheering party workers.
"If you don't have position, you have nothing. That's the tragedy of India," he said.
Rahul Gandhi also said many Indian youths are angry because they have been excluded from the political class.
"We only empower people at the top of the system. We don't believe in empowering all the way to the bottom," he said.
However, opposition parties are already seizing on the fast political rise of Rahul Gandhi ? the son, grandson and great-grandson of Indian prime ministers ? to brand Congress as nepotistic and elitist.
Arun Jaitley, a leader of the opposition Bharatiya Janata Party, said Rahul Gandhi's elevation in the Congress party was a move to convert the world's largest democracy into a dynastic one. Jaitley said the leader of his party was decided on the basis of ability, not lineage.
In 2004, Manmohan Singh, a technocrat, was chosen to fill the prime minister's seat in 2004 by Sonia Gandhi, the Congress leader and widow of assassinated Indian Prime Minister Rajiv Gandhi.
Singh has been widely seen as a regent, keeping the seat warm until Rahul Gandhi was ready to take what some see as his birthright.
But Gandhi has displayed little public sign that he is undergoing any sort of apprenticeship that would prepare him for running the country. He has never held a Cabinet-level position.
Party workers have been demanding Rahul Gandhi's elevation for years, but he had been shying away from holding a top position in the party.
His supporters argued he was rebuilding the party at the grassroots level and has taken a lead in the Congress' campaigns in state elections in Uttar Pradesh and in Bihar in recent years. The party performed poorly in both states' elections last year.
Rahul Gandhi entered politics in 2004 and became a lawmaker from Amethi seat in northern Uttar Pradesh state. The parliamentary seat was held by his mother until she shifted to a neighboring constituency.
Tonight was one of those nights.... icy cold outside .... nice and cozy inside.? And what better way to spend the evening, than with a hot chocolate in one hand, my keyboard in the other and my favorite blogs on my screen...
written by a Parisian called Lilly Rose.? I've just read her introduction and she sounds lovely and sweet and like all of us she is dreaming of a bigger brighter home!? Well Lilly Rose, here's to all our dreams come true...
On Planete Deco I found this post - about a beautiful family holiday home on the West Coast of South Africa, a couple of hours drive from Cape Town - located in a small see side town called 'Dwarskersbos'.?
I can now vaguely recall this project: while I was living in Cape Town a couple of years ago - I managed an interiors showroom called 'Cured Cement' and we worked with an amazing range of cement/ concrete finishing products by a well known manufacturer called Cemcrete.? One of our applicators at the time mentioned this project to me.? I'm just going to reconfirm it's definitely his work, so I can link him in.
I am still a very big fan of concrete finishes, especially when it's done with such perfection....?
a perfect imperfection as those in the know will say. ?I love the warmer tones they have used in this house against the crisp white walls and perfect blue skies.
My sister has a beautiful holiday home called 'C'est La Vie' in the same coastal town and I'm hoping to spend a good few days there in March with my family.? Sunshine, sea and sand and wide open spaces await.
And until then... I can just keep dreaming of my own retreat of a holiday home....
Starbucks causes jitters in artsy Parisian neighborhood
A new caf? set to open in one of Paris? biggest tourist draws is quickening pulses faster than a double espresso. A Starbucks is coming to the Place du Tertre in the bohemian Montmartre neighborhood of Paris, where Vincent van Gogh, Pablo Picasso and Ernest Hemingway once roamed the hilly streets.
We frequently speak about the importance of your crisis management team working in close connection with other departments for a reason ? it works. While crisis management covers a broad spectrum of responsibilities and is often managed by outside contractors, those in specific departments have not only focused their expertise, but also are intimately familiar with how to get things done within their organization.
It?s common to discuss tools to help you in handling external issues in crisis, but for the internal issues that inevitable arise look no further than the HR department for a pool of assistance. Here, a quote from a KBPJ.com artible by Dan Weedin explains exactly why:
When a crisis occurs, there is instantly fear and uncertainty. The human resources expert(s) in your business should be a calming and reassuring influence. Even if the honest answer to many questions is ?I don?t know,? at least there is a communications leader within the organization. Many times, the boss is busy putting out the fire. Someone needs to be available for the employees.
If the emergency results in notifying family members, the HR department is the best ?voice.? Because they are not dealing with the crisis directly, they can be a much more capable sounding board and empathetic communicator.
Human Resources knows the laws and regulations that could come into play with shutdowns, terminations, re-assignments, and other employee-related moves.
The Human Resources director has a direct line to the morale of the employees during and after the crisis. Most crises don?t just end quickly. The lingering effects can include uncertainty, fear, drama, lack of production, anger and depression. As the boss, you may be in the middle of dealing with your own feelings, stress, and responsibility, and need someone to be a leader for your team.
An inside source that knows the lay of the land and has files on all of the human resources you have at your disposal sounds like a key crisis management component to us.
How can you best prepare your HR department to handle its role when it comes to a crisis? Pretty much the same way you would any other group: assign crisis roles, create crisis plans that address the potential issues, as well as a few meant to blanket large areas of unpredictable ones, and then practice, practice, practice. If you have an in-house crisis management team, all the better! Set up a nice lunch and have everyone get chummy, then bring them back and get to work on those plans.
If you don?t, then (and you?d better believe we?re speaking from experience here) your contractors will be pleasantly surprised to hear they have a trained and prepared HR team ready to assist when they hit the scene, and that assistance will make it that much easier for them to jump into the situation and get to work.
This was a year of transitions. I like transitions one at a time?every few years?at least, if that ever happened, I think I would like it. This year, my oldest daughter went to college, my youngest daughter went to kindergarten, my tween son stopped kissing me back, and a year after my father?s death, my mother moved in with us. Oh, and I quit smoking because that seemed like a good idea while everything else in my life was in complete upheaval.
And the frosting on the cake will by my 40th birthday in two weeks. Although age really does feel like just a number to me, sometimes I look at that number and think, ?Really? 40?? Sure I?d like to have more accomplishments and less cellulite, but life really is good.
If you think I?m going to give great advice about how to deal with all these changes, sorry, I?m not.
Get a prescription for nerve pills, or get black market nerve pills from a friend who has a better doctor. My doctor actually said, ?Why don?t you have a glass of wine once in awhile??
They kind of frown on that at kids? sporting events, but thanks, Doc.
Don?t smoke.
Let?s just dive in: My daughter went to college. The thought that she will probably never live with me again full-time (until I?m old and move in with her, but then I guess technically I will live with her, see above) makes me sad. But what?s the alternative? Keep her at home? She has always had dreams bigger than our little community, so I had to release her to spread her wings and fly to reach them. We don?t skype as much as I?d envisioned. We text, tweet, fb, and instagram incessantly. She?s happy, and I?m happy she?s happy. My goal is to mold these young ones into kind, compassionate, considerate adults, and she is making a good start on her own.
I think after you move your firstborn out of the house and cry yourself into dehydration, other milestons are kind of anti-climactic for awhile. Baby girl going to Kindergarten wasn?t bad. I had kept her home for the ?Should I send her or not?? year, so I felt as if I had 365 days of bonus time with her. She was ready to go, and honestly I was ready for her to go. I did feel a little stab of pain watching her little blonde curls bounce onto the bus for the first time, but then I wrote all day. And no one asked me to make them food. Or turn on a show. Or get them another piece of paper to draw on.
And that was kind of awesome.
My boy might be the hardest transition to take, probably because I look at my husband?s relationship (or lack thereof) with his mother and really don?t want to end up there. He?s 12, and he?s still loving, just on his own terms. He thinks it?s cool that he can pick me up and sometimes hugs me and picks me up. Sometimes he still crawls into a chair with me, and usually he doesn?t move when I crawl into a chair with him. He ignores the fact that I sneak into his bed a full five minutes before he has to get up, just to snuggle him. He?s not my little boy anymore, but he?s growing into a really fine young man.
Yeah, yeah, yeah, kids grow up. The other thing that happens though, is we grow up, and our parents get old. Sometimes they die. Sometimes they have to go into a nursing home. Sometimes they move in with us. My dad died, and my mom moved in with us. She is in her early 80?s and still in pretty good health. She drives, cooks, visits friends, shops and so forth. I had all sorts of ideas of what things would be like when she moved in?I moved out at 20 because she drove me crazy?but mostly it has been good. There have been a few growing pains. We?re working on boundaries, my kids are making memories with their grandma, and I am making sure that when it?s time for her to go, there?s nothing left unsaid.
So that?s where I?ve been; what have you ladies been up to??
?If you enjoy this post, be sure to follow MomsGetReal on Twitter, Facebook, Pinterest, and Google+!
JCI early table of contents for Jan. 16, 2013Public release date: 16-Jan-2013 [ | E-mail | Share ]
Contact: Jillian Hurst press_releases@the-jci.org Journal of Clinical Investigation
Could probiotics help HIV patients?
Antiretroviral (ARV) drugs are the first line therapy for patients with HIV; however, ARV-treated, HIV-infected individuals still have a higher mortality rate than uninfected individuals. During the course of infection, HIV patients develop inflammation that damages the walls of the intestines, known as the gut mucosa, allowing intestinal microbes to escape and enter the blood stream to cause a life-threatening systemic infection. The health of the gut mucosa is significantly influenced by the complement of bacteria in the gut and there is mounting evidence that probiotic supplements benefit patients intestinal disorders, such as irritable bowel syndrome, C. difficile infection, and inflammatory bowel disease.
In this issue of the Journal of Clinical Investigation, researchers led by Jason Brenchley at the National Institute of Allergy and Infectious Disease, demonstrated that probiotic supplementation may also be beneficial for ARV-treated HIV patients. Brenchley and colleagues treated SIV-infected macaques (a model of human HIV-infection) with either ARV alone or ARV in combination with a mixture of probiotics. Macaques treated with probiotics had enhanced gastrointestinal immune function and decreased inflammation compared to macaques treated with ARV alone. In a companion article, Judith Aberg and colleagues at New York University School of Medicine discuss how these findings could benefit HIV patients.
TITLE:
Probiotic/prebiotic supplementation of antiretrovirals improves gastrointestinal immunity in SIV-infected macaques
AUTHOR CONTACT:
Jason M. Brenchley
NIAID NIH, Bethesda, MD, USA
Phone: 301-496-1498; E-mail: jbrenchl@mail.nih.gov
View this article at: http://www.jci.org/articles/view/66227?key=1cff041937d9040dfed7
ACCOMPANYING ARTICLE:
TITLE:
Clash of the microbes: let's bring back the good guys
AUTHOR CONTACT:
Judith Aberg
New York University School of Medicine, New York, NY, USA
Phone: 2122637300; E-mail: judith.aberg@nyumc.org
View this article at: http://www.jci.org/articles/view/66736?key=64b158b04e2a168811a3
Hepatitis B virus promotes oncogenesis through microRNA modulation
Viruses prompt oncogenic transformation by genetically altering infected cells. Several recent studies have demonstrated that viruses alter the expression of microRNAs, non-coding RNA molecules that can block the expression of target genes. In this issue of the Journal of Clinical Investigation, Xiaoje Xu and colleagues at the Beijing Institute of Biotechnology report that miR-148a is repressed by hepatitis B virus (HBV) X protein (HBx) to promote growth and metastasis of liver cancer. In normal liver cells, miR-148a represses the expression of the oncogenic protein HPIP, but the hepatitis B virus prevents expression of miR-148a, leading to increased levels of HPIP and subsequent oncogenic transformation. This study demonstrates that a cancer-associated virus promotes carcinogenesis through direct manipulation of a microRNA.
TITLE:
Hepatitis B virus X protein represses miRNA-148a to enhance tumorigenesis
AUTHOR CONTACT:
Qinong Ye
Beijing Institute of Biotechnology, Beijing, CHN
Phone: (8610)68180809; Fax: (8610)68248045; E-mail: yeqn66@yahoo.com
View this article at: http://www.jci.org/articles/view/64265?key=267b145ad442aacf5c02
ALSO IN THIS ISSUE
Osteoclast-specific cathepsin K deletion stimulates S1P-dependent bone formation
Dynamic visualization of RANKL and Th17-mediated osteoclast function
KDM2B promotes pancreatic cancer via Polycomb-dependent and -independent transcriptional programs
MiR-374a activates Wnt/ ?-catenin signaling to promote breast cancer metastasis
mTORC1 inhibition restricts inflammation-associated gastrointestinal tumorigenesis in mice
Loss of SPARC in bladder cancer enhances carcinogenesis and progression | Back to top
BONE BIOLOGY
TITLE:
Osteoclast-specific cathepsin K deletion stimulates S1P-dependent bone formation
AUTHOR CONTACT:
Roland Baron
Harvard School of Medicine and of Dental Medicine, Boston, MA, USA
Phone: 617.432.7320 or 7325; Fax: 617.432.1897; E-mail: roland_baron@hsdm.harvard.edu
View this article at: http://www.jci.org/articles/view/64840?key=c8170fcece15001cf8c0
TITLE:
Dynamic visualization of RANKL and Th17-mediated osteoclast function
AUTHOR CONTACT:
Masaru Ishii
WPI-Immunology Frontier Research Center, Osaka University, Osaka, JPN
Phone: 81668794268; Fax: 81668798296; E-mail: mishii@ifrec.osaka-u.ac.jp
View this article at: http://www.jci.org/articles/view/65054?key=63bed6989736b83be7fd
ONCOLOGY
TITLE:
KDM2B promotes pancreatic cancer via Polycomb-dependent and -independent transcriptional programs
AUTHOR CONTACT:
Nabeel Bardeesy
Massachusetts General Hospital, Boston, MA, USA
Phone: 617-643-2579; E-mail: bardeesy.Nabeel@mgh.harvard.edu
View this article at: http://www.jci.org/articles/view/64535?key=aecb23f1f9fae807216b
TITLE:
MicroRNA-374a activates Wnt/?-catenin signaling to promote breast cancer metastasis
AUTHOR CONTACT:
Mengfeng Li
Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, UNK, CHN
Phone: +86(20)87332748; Fax: +86(20)87331209; E-mail: limf@mail.sysu.edu.cn
View this article at: http://www.jci.org/articles/view/65871?key=3d080eabb1106f73d520
TITLE:
mTORC1 inhibition restricts inflammation-associated gastrointestinal tumorigenesis in mice
AUTHOR CONTACT:
Matthias Ernst
Ludwig Institute for Cancer Research Cancer Research, Melbourne, AUS
Phone: +61-3-9341-3155; Fax: +61-3-9341-3104; E-mail: matthias.ernst@ludwig.edu.au
View this article at: http://www.jci.org/articles/view/65086?key=30a0deb622897138b7bf
TITLE:
Loss of SPARC in bladder cancer enhances carcinogenesis and progression
AUTHOR CONTACT:
Dan Theodorescu
University of Colorado Denver, Aurora, CO, USA
Phone: 303-724-7135; E-mail: dan.theodorescu@ucdenver.edu
View this article at: http://www.jci.org/articles/view/64782?key=4dcefabf20a4259617c5
###
[ | E-mail | Share ]
?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
JCI early table of contents for Jan. 16, 2013Public release date: 16-Jan-2013 [ | E-mail | Share ]
Contact: Jillian Hurst press_releases@the-jci.org Journal of Clinical Investigation
Could probiotics help HIV patients?
Antiretroviral (ARV) drugs are the first line therapy for patients with HIV; however, ARV-treated, HIV-infected individuals still have a higher mortality rate than uninfected individuals. During the course of infection, HIV patients develop inflammation that damages the walls of the intestines, known as the gut mucosa, allowing intestinal microbes to escape and enter the blood stream to cause a life-threatening systemic infection. The health of the gut mucosa is significantly influenced by the complement of bacteria in the gut and there is mounting evidence that probiotic supplements benefit patients intestinal disorders, such as irritable bowel syndrome, C. difficile infection, and inflammatory bowel disease.
In this issue of the Journal of Clinical Investigation, researchers led by Jason Brenchley at the National Institute of Allergy and Infectious Disease, demonstrated that probiotic supplementation may also be beneficial for ARV-treated HIV patients. Brenchley and colleagues treated SIV-infected macaques (a model of human HIV-infection) with either ARV alone or ARV in combination with a mixture of probiotics. Macaques treated with probiotics had enhanced gastrointestinal immune function and decreased inflammation compared to macaques treated with ARV alone. In a companion article, Judith Aberg and colleagues at New York University School of Medicine discuss how these findings could benefit HIV patients.
TITLE:
Probiotic/prebiotic supplementation of antiretrovirals improves gastrointestinal immunity in SIV-infected macaques
AUTHOR CONTACT:
Jason M. Brenchley
NIAID NIH, Bethesda, MD, USA
Phone: 301-496-1498; E-mail: jbrenchl@mail.nih.gov
View this article at: http://www.jci.org/articles/view/66227?key=1cff041937d9040dfed7
ACCOMPANYING ARTICLE:
TITLE:
Clash of the microbes: let's bring back the good guys
AUTHOR CONTACT:
Judith Aberg
New York University School of Medicine, New York, NY, USA
Phone: 2122637300; E-mail: judith.aberg@nyumc.org
View this article at: http://www.jci.org/articles/view/66736?key=64b158b04e2a168811a3
Hepatitis B virus promotes oncogenesis through microRNA modulation
Viruses prompt oncogenic transformation by genetically altering infected cells. Several recent studies have demonstrated that viruses alter the expression of microRNAs, non-coding RNA molecules that can block the expression of target genes. In this issue of the Journal of Clinical Investigation, Xiaoje Xu and colleagues at the Beijing Institute of Biotechnology report that miR-148a is repressed by hepatitis B virus (HBV) X protein (HBx) to promote growth and metastasis of liver cancer. In normal liver cells, miR-148a represses the expression of the oncogenic protein HPIP, but the hepatitis B virus prevents expression of miR-148a, leading to increased levels of HPIP and subsequent oncogenic transformation. This study demonstrates that a cancer-associated virus promotes carcinogenesis through direct manipulation of a microRNA.
TITLE:
Hepatitis B virus X protein represses miRNA-148a to enhance tumorigenesis
AUTHOR CONTACT:
Qinong Ye
Beijing Institute of Biotechnology, Beijing, CHN
Phone: (8610)68180809; Fax: (8610)68248045; E-mail: yeqn66@yahoo.com
View this article at: http://www.jci.org/articles/view/64265?key=267b145ad442aacf5c02
ALSO IN THIS ISSUE
Osteoclast-specific cathepsin K deletion stimulates S1P-dependent bone formation
Dynamic visualization of RANKL and Th17-mediated osteoclast function
KDM2B promotes pancreatic cancer via Polycomb-dependent and -independent transcriptional programs
MiR-374a activates Wnt/ ?-catenin signaling to promote breast cancer metastasis
mTORC1 inhibition restricts inflammation-associated gastrointestinal tumorigenesis in mice
Loss of SPARC in bladder cancer enhances carcinogenesis and progression | Back to top
BONE BIOLOGY
TITLE:
Osteoclast-specific cathepsin K deletion stimulates S1P-dependent bone formation
AUTHOR CONTACT:
Roland Baron
Harvard School of Medicine and of Dental Medicine, Boston, MA, USA
Phone: 617.432.7320 or 7325; Fax: 617.432.1897; E-mail: roland_baron@hsdm.harvard.edu
View this article at: http://www.jci.org/articles/view/64840?key=c8170fcece15001cf8c0
TITLE:
Dynamic visualization of RANKL and Th17-mediated osteoclast function
AUTHOR CONTACT:
Masaru Ishii
WPI-Immunology Frontier Research Center, Osaka University, Osaka, JPN
Phone: 81668794268; Fax: 81668798296; E-mail: mishii@ifrec.osaka-u.ac.jp
View this article at: http://www.jci.org/articles/view/65054?key=63bed6989736b83be7fd
ONCOLOGY
TITLE:
KDM2B promotes pancreatic cancer via Polycomb-dependent and -independent transcriptional programs
AUTHOR CONTACT:
Nabeel Bardeesy
Massachusetts General Hospital, Boston, MA, USA
Phone: 617-643-2579; E-mail: bardeesy.Nabeel@mgh.harvard.edu
View this article at: http://www.jci.org/articles/view/64535?key=aecb23f1f9fae807216b
TITLE:
MicroRNA-374a activates Wnt/?-catenin signaling to promote breast cancer metastasis
AUTHOR CONTACT:
Mengfeng Li
Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, UNK, CHN
Phone: +86(20)87332748; Fax: +86(20)87331209; E-mail: limf@mail.sysu.edu.cn
View this article at: http://www.jci.org/articles/view/65871?key=3d080eabb1106f73d520
TITLE:
mTORC1 inhibition restricts inflammation-associated gastrointestinal tumorigenesis in mice
AUTHOR CONTACT:
Matthias Ernst
Ludwig Institute for Cancer Research Cancer Research, Melbourne, AUS
Phone: +61-3-9341-3155; Fax: +61-3-9341-3104; E-mail: matthias.ernst@ludwig.edu.au
View this article at: http://www.jci.org/articles/view/65086?key=30a0deb622897138b7bf
TITLE:
Loss of SPARC in bladder cancer enhances carcinogenesis and progression
AUTHOR CONTACT:
Dan Theodorescu
University of Colorado Denver, Aurora, CO, USA
Phone: 303-724-7135; E-mail: dan.theodorescu@ucdenver.edu
View this article at: http://www.jci.org/articles/view/64782?key=4dcefabf20a4259617c5
###
[ | E-mail | Share ]
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iOS: Fleksy is an alternative keyboard with unprecedented predictive text skills. You can type a word completely wrong and it'll still figure out what you meant. 
Let?s just dive in: My daughter went to college. The thought that she will probably never live with me again full-time (until I?m old and move in with her, but then I guess technically I will live with her, see above) makes me sad. But what?s the alternative? Keep her at home? She has always had dreams bigger than our little community, so I had to release her to spread her wings and fly to reach them. We don?t skype as much as I?d envisioned. We text, tweet, fb, and instagram incessantly. She?s happy, and I?m happy she?s happy. My goal is to mold these young ones into kind, compassionate, considerate adults, and she is making a good start on her own.![[ Back to EurekAlert! ]](http://www.eurekalert.org/images/back2e.gif){kind=small}
Public release date: 16-Jan-2013
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