everyone has their own issue they hold as important, weed, wages, guns.
I was just chosing one I thought was important to you, I'm not trying to pigeon hole you. So lets just say it's wages, and that's what is most important to you. Obviously the person that caters to the same issues that are important to you are going to be the ones you side with.
That said, It doesn't mean that that group isn't going to try and restrict other freedoms that are less important to you but very important to someone else.
Both groups are equally guilty of trying to over reach the boundaries of controling our personal lives, it's just a matter of which issues you stand on.
Both equally guilty and both equally hypoctitical.
Saying one is any worse than the other is purely speculative and based on matters of personal perception .
why are wages more important than the second amendment, or vice versa? personal perception . They are both important,but one side is going to emphasize one over the other, whether it's a for or against.
I see what you are saying and believe it.
Both sides suck ass but what are we to do? Thing is no one is going to take guns from people while there s an ongoing war on unions every second of the day. Even Biden said, and I agree with it, that a shotgun can protect your house and family and no one is trying to take anyone's shotguns away.
But that's the thing. Combined with all the rest of the stupidity republicans are the worst of the two evils. Look at how our republicans are acting with Obama. It's like they're playing payback for all the crap Bush took while in office. I thought they would be above that but they've gone beyond the bashing Bush took.
And then it's not about any one or two issues with me but a combined fuck pit of hypocrisy that blows my mind. For 8 years I watch republicans complain about liberals giving Bush shit, all the while sayin the Office of the President should be respect regardless. Yeah, now it's all of a sudden patriotic to dissent.
Really though, republicans love guns and have this unnatural desire to kill people. Going to the range, blowing shit up preparing for the momentous occasion when they can finally blow someone's face off. Add to that the pure hatred for anyone that is down on their luck, laid off, collecting unemployment or having to get food stamps because their jobs got sent to China. Republican love that shit too. They sit there and complain that auto workers are overpaid and that their jobs should be shipped offshore just out of pure spite and hatred for an American that would take the best possible opportunity to raise a family. Combined, all the issues republicans are behind will destroy America and American families.
And then again, look at all the shit get for trying to better myself, all from right wingers while leftys actually encourage me along.
It blows my fucking mind but I'll be laughing my ass off when Hillary becomes President in 2016. People are sick of republicans, sick of the constant attack on other people's way of life and the way republicans are tolerant of no one or nothing that is out of line with their way of thinking.
GOP will die and I will dance on their grave while pissing all over it.
__________________
"And I will lubricate myself with my arrogance, and continue to ass fuck people's stupidity." ~ MrsShrodingersBox
Oxfam International?invites applications??from qualified and talented applicants for the vacancy of?Global Communications Intern to work with?Global Communications Department to help deliver high quality, reliable and user friendly brand and communications products and platforms.?The location of this internship will be based in ?Oxfam International Secretariat office in Oxford, UK.
Key Competencies?
Excellent written and oral communication skills.
Relevant university degree
Accuracy, consistency and attention to detail.
Strong command of Microsoft Office (Word, Excel, PowerPoint).
Knowledge and strong interest in development and humanitarian work.
Excellent organizational and administrative skills, experience in minute taking is desirable
Effective team player with the ability to work and think independently
Resourceful and proactive.
Proven organizational and time management skills.
Experience of working with teams based remotely.
Fluent English essential, additional languages (French, Spanish) would be highly desirable.
Previous communications experience is highly desirable.
Experience of working within a multicultural environment desirable.
Multimedia and website management skills are highly desirable
How to Apply
Online
Please note: applications that do not have a Covering Letter and CV will not be considered.
A new study shows how important it is for men to carefully consider treatments for early-stage prostate cancer. Fifteen years after surgery or radiation treatment, nearly all of the older men in the study had some problems having sex.
About one-fifth had bladder or bowel trouble, researchers found.
The study doesn't compare these men ? who were 70 to 89 at the end of the study ? to others who did not treat their cancers or to older men without the disease. At least one study suggests that half that age group has sexual problems even when healthy.
The study isn't a rigorous test of surgery and radiation, but it is the longest follow-up of some men who chose those treatments.
Since early prostate cancers usually don't prove fatal but there are no good ways to tell which ones really need treatment, men must be realistic about side effects they might suffer, said one study leader, Dr. David Penson of Vanderbilt University.
"They need to look at these findings and say, 'Oh my gosh, no matter what I choose, I'm going to have some quality-of-life effect and it's probably greater than my doctor is telling me,'" he said.
The study appears in Thursday's New England Journal of Medicine.
Prostate cancer is the most common cancer in American men. In the United States alone, there were about 240,000 new cases and 28,000 deaths from the disease last year. Radiation or surgery to remove the prostate are common treatments when the disease is confined to the gland.
Men usually live a long time after treatment ? 14 years on average ? so it's important to see how they fare, said another study leader, Vanderbilt's Dr. Matthew Resnick.
The study involved 1,655 men diagnosed in 1994 or 1995, when they were ages 55 to 74. About two-thirds of them had surgery and the rest, radiation. They were surveyed two, five and 15 years later. By that time, 569 had died.
Men who had surgery had more problems in the first few years after their treatments than those given radiation, but by the end of the study, there was no big difference.
After 15 years, 18 percent of the surgery group and 9 percent of the radiation group reported urinary incontinence, and 5 percent of the surgery group and 16 percent of the radiation group said they were bothered by bowel problems. But the differences between the two groups could have occurred by chance alone once researchers took other factors such as age and the size of the men's tumors into account.
Impotence was "near universal" at 15 years, the authors write ? 94 percent of the radiation group and 87 percent of the surgery group. But the difference between the groups also was considered possibly due to chance. Also, less than half of men said they were bothered by their sexual problems.
"These men do get some help from pills like Viagra, Cialis, Levitra," but it may not be as much as they would like and most men would rather not need those pills, Penson said.
The National Cancer Institute paid for the study. Two authors have consulted for several makers of prostate cancer treatment drugs.
No study is perfect and this one has many limitations, said Dr. Timothy Wilson, urology chief at City of Hope, a cancer center in Duarte, Calif. Men who are having problems are more likely to complete follow-up surveys because they're angry, so that could skew results, he noted.
Still, "it's a high percentage" with side effects, said Wilson, who has been a paid speaker for two makers of surgery equipment.
"There's no question we overtreat" many cases of early prostate cancer, yet the disease is still the second-leading cause of cancer deaths in men. "We need to better sort out who really needs treatment," he said.
___
Online:
New England Journal: http://www.nejm.org
___
Marilynn Marchione can be followed at http://twitter.com/MMarchioneAP
Jan. 29, 2013 ? Coral reefs build their structures by both producing and accumulating calcium carbonate, and this is essential for the maintenance and continued vertical growth capacity of reefs. An international research team has discovered that the amount of new carbonate being added by Caribbean coral reefs is now significantly below rates measured over recent geological timescales, and in some habitats is as much as 70% lower.
Coral reefs form some of the planet's most biologically diverse ecosystems, and provide valuable services to humans and wildlife. However, their ability to maintain their structures and continue to grow depends on the balance between the addition of new carbonate, which is mostly produced by corals themselves, set against the loss of carbonate through various erosional processes. Scientists have long known that reef ecosystems are in decline and that the amount of live coral on reefs is dwindling. But the paper, published on DATE TBC in Nature Communications, is the first evidence that these ecological changes are now also impacting on the growth potential of reefs themselves.
Professor Chris Perry of the University of Exeter, who led the research, said: "Our estimates of current rates of reef growth in the Caribbean are extremely alarming. Our study goes beyond only examining how much coral there is, to also look at the delicate balance of biological factors which determine whether coral reefs will continue to grow or will erode. Our findings clearly show that recent ecological declines are now suppressing the growth potential of reefs in the region, and that this will have major implications for their ability to respond positively to future sea level rises.
"It is most concerning that many coral reefs across the Caribbean have seemingly lost their capacity to produce enough carbonate to continue growing vertically, whilst others are already at a threshold where they may start to erode. At the moment there is limited evidence of large-scale erosion or loss of actual reef structure, but clearly if these trends continue, reef erosion looks far more likely. Urgent action to improve management of reef habitats and to limit global temperature increases is likely to be critical to reduce further deterioration of reef habitat."
The team was funded by the Leverhulme Trust (UK), through an International Network Grant. It included scientists from James Cook University and The University of Queensland in Australia, from The University of Auckland in New Zealand, Memorial University in Canada, and the University of Maine in the USA. They examined rates of carbonate production across 19 reefs in the four Caribbean countries of the Bahamas, Belize, Bonaire and Grand Cayman.
They discovered that declines in rates of carbonate production were especially evident in shallow water habitats, where many fast growing branching coral species have been lost. The study compared modern day rates with those measured in the region over approximately the last 7,000 years. In key habitats around the Caribbean, the findings suggested that in waters of around five metres in depth, reef growth rates are now reduced by 60-70% compared to the regional averages taken from historical records. In waters of around 10 metres in depth, the rates are reduced by 25%.
The study also suggests that these key habitats must have a minimum of around 10% living coral cover to maintain their current structures. The amount of cover varies between sites, but some are already below this threshold and are therefore at risk of starting to erode. Given that previous studies have shown that coral cover on reefs in the Caribbean has declined by an average of 80 per cent since the 1970s, this raises alarm bells for the future state of reefs in the region. These changes have been driven by human disturbance, disease and rising sea temperatures, and are only expected to intensify as a result of future climate change.
Share this story on Facebook, Twitter, and Google:
Other social bookmarking and sharing tools:
Story Source:
The above story is reprinted from materials provided by University of Exeter, via EurekAlert!, a service of AAAS.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
Chris T. Perry, Gary N. Murphy, Paul S. Kench, Scott G. Smithers, Evan N. Edinger, Robert S. Steneck, Peter J. Mumby. Caribbean-wide decline in carbonate production threatens coral reef growth. Nature Communications, 2013; 4: 1402 DOI: 10.1038/ncomms2409
Note: If no author is given, the source is cited instead.
Disclaimer: Views expressed in this article do not necessarily reflect those of ScienceDaily or its staff.
While most businesses are hit hard by the economic crisis, the claims market actually thrives during a financial downturn. Although many experts grumble about the compensation culture, statistics show that economic booms correlate with fewer personal injury claims. So why are people calling up their lawyers so readily during a recession?
Redundancies
With more than 1.3 million people losing their jobs by 2010, due to the economic downturn, and employment opportunities few and far between, those who?d been made redundant seemed more likely to file a claim. Why?
While under employment, staff can be concerned about losing their job, if they make a personal injury claim. Even though this rarely happens ? and if it did, you could take your employers to court over unfair dismissal ? employees seem to be hesitant about collecting compensation. However, when made redundant, there?s no loyalty left to the business, and people seem to be more comfortable about making a claim.
There?s also a large window of opportunity to contact a solicitor, as you can make your claim up to three years after the incident occurred. With increasing numbers of people fired or made redundant, the personal injury claim figures have likewise grown.
Business Negligence
Homes and corporations alike are suffering from severe expenditure cutbacks. Businesses are having to make-do with spartan levels of staff and resources.
With employees rushed off their feet, quality of service can be jeopardised, such as in the NHS, where nurses are thin on the ground due to ?reforms? ? medical negligence can then occur, purely because the staff-to-patient ratio is inequitable, leading to an increased amount of complaints.
Health and safety, as well as training, can be affected, and stress levels can go through the roof, leading to medical problems.
Rise Of the ?No Win No Fee?
From personal injury claims in Liverpool to medical negligence complaints in London, ?no win no fee? solicitors are making it easier than ever to file a personal injury claim. With court fees being what they are, the claimant now has the security of knowing that they?ll only have to pay-up, if they win their case. Equally, solicitors are likely to give it their all, as the only way that their company makes a profit is if they win!
Poor Financial Situation
Thanks to the recession, most UK citizens are in a worse financial position than before. When your bank balance is in dire straits, making a claim will be more attractive, if that means you can lift your family above the bread line or afford a much-needed holiday. In a pinch, the possibility of money is a compelling incentive to contact a solicitor.
Also, a drop in disposable income will mean that individuals will choose cheaper services, such as home improvements that could go awry. Although low-end contracting doesn?t necessarily mean substandard work, you may find yourself injured after an inexpensive workman does a poor quality job on your house.
Composed by Hughes Carlisle personal injury solicitors in Liverpool who are reflecting on economy changes and the role we as a nation have helping improve the claiming situation.
Personal Injury Claims Blawg is a personal injury law blog. Register today via the get started button above to join us as a guest personal injury law blogger.
No related posts.
Tagged as: Injury claims in the recession, Injury lawyers, No win no fee personal injury claims
Despite the seemingly rushed nature of Sony Pictures? reboot of the Spider-Man franchise after dropping Sam Raimi?s problematic Spider-Man 4, The Amazing Spider-Man ? despite its flaws ? successfully reintroduced Peter Parker in large part due to its roster of talent onscreen. For?The Amazing Spider-Man 2, Marc Webb looks to keep that magic flowing with inspired casting that already includes Jamie Foxx as the villainous Electro, Shailene Woodley (The Descendants) as Mary Jane?and Dane DeHaan (Chronicle) as Harry Osborn.
Today we?ve learned that Sony is looking to bolster the cast led by Andrew Garfield and Emma Stone even more by adding?Paul Giamatti and Felicity Jones.
The scoop comes from?THR?who have it on good authority that Oscar-nominated Paul Giamatti is in?negotiations?to join The Amazing Spider-Man 2 as the villainous Rhino, while Brit actress?Felicity Jones (Like Crazy) is also in talks for another, unknown role. Could she play one-time love interests?Betty Brant or Liz Allan, or is Webb pulling out all the stops and introducing?Felicia Hardy AKA Black Cat?
Felicity Jones in Like Crazy
The report confirms Sony?s attempt at distancing itself from the Sam Raimi trilogy of?Spider-Man films by taking advantage of a different set of villains. Both Electro and Rhino were mentioned among fan wishlists for inclusion in Raimi?s ill-fated?Spider-Man 4 and will finally get their chance in the Marc Webb universe.
Every character Giamatti touches is gold and to see him play the physically-dominant Rhino will be something unique for the superhero genre, especially given the track record of the franchise to successfully adapt the more ?out there? characters like Sandman and The Lizard. So, expect to see a super-powered and gigantic Rhino on screen battling Spider-Man.
Paul Giamatti in Shoot ?Em Up
In Marvel Comics, Rhino (real name:?Aleksei Sytsevich) was a member of the Russian mafia who, after?undergoing?a lengthy process genetic manipulation with chemicals and radiation, was given his superhuman abilities, but unfortunately no superhuman level of intelligence. His powers are further enhanced by a suit he wears on top of his thick armored skin.
As our own Kofi Outlaw brought up in chatting with Marc Webb last summer, it looks as if the end credits sequence of?The Amazing Spider-Man and the plans for the sequel could be leading to the formation of the Sinister Six?(read Webb?s curious response here), where multiple Spidey villains (The Lizard, Electro and Rhino included in various incarnations) form together. Such a large-scale threat certainly boosts the blockbuster appeal of the franchise in a post-Avengers genre.
For fans of?The Amazing Spider-Man video game, I met with the producers behind it who spent many hours working with Sony to ensure the game fits within the plans for the film universe where Oscorp and their biological?experimentation?were the central point for all of the super-powered characters we know from years of Marvel Comics. Rhino (pictured up top) was?re-imagined?for the game.
Fun fact: The Oscorp tower from The Amazing Spider-Man almost made its way into The Avengers but digital effects on the New York skyline were already near completion.
Does Sanjay Gupta have a clone? That’s what I wrote jokingly on Twitter as I was preparing to interview the multiple Emmy Award-winning chief medical correspondent for CNN who is still a practicing neurosurgeon and who managed to also find time to write three best-selling books. Oh yes, the 43-year-old’s also a father of three who runs triathlons!!! One of his colleagues at CNN joked in a Twitter reply that Sanjay has “Seacrest-like energy” referring to the omnipresent Ryan Seacrest.
Jan. 28, 2013 ? More powerful gene-sequencing tools have increasingly been uncovering disease secrets in DNA within the cell nucleus. Now a research team is expanding those rapid next-generation sequencing tests to analyze a separate source of DNA -- within the genes inside mitochondria, cellular power plants that, when abnormal, contribute to complex, multisystem diseases.
The study team, headed by a specialist in mitochondrial medicine at The Children's Hospital of Philadelphia (CHOP), adapted next-generation sequencing to simultaneously analyze the whole exome (all the protein-coding DNA) of nuclear genes and the mitochondrial genome. "A first step in developing treatments for a disease is to understand its precise cause," said Marni J. Falk, M.D., the director and attending physician in the Mitochondrial-Genetic Disease Clinic at Children's Hospital. "We have developed a one-step, off-the-shelf tool that analyzes both nuclear and mitochondrial DNA to help evaluate the genetic cause of suspected mitochondrial disease."
Falk and colleagues describe their customized, comprehensive test, which they call the "1:1000 Mito-Plus Whole-Exome" kit, in the journal Discovery Medicine, published Dec. 26, 2012. Her co-corresponding author, biostatistician Xiaowu Gai, Ph.D., now of the Loyola University Stritch School of Medicine, collaborated on developing the test while at Children's Hospital.
While each mitochondrial disease is very rare in the population, hundreds of causes of mitochondrial diseases are known. Some originate in mutations in DNA specific to the mitochondria, tiny structures located outside the cell nucleus, while many other mitochondrial diseases are based in nuclear DNA genes that affect mitochondrial function. The role of mitochondria in human disease has been recognized only since the 1980s, based on pioneering research by Douglas C. Wallace, Ph.D., now at Children's Hospital, and a co-author of the current study.
Many mitochondrial diseases remain poorly understood. One complicating factor is heteroplasmy -- a mixture of mutated and normal mitochondrial genomes within the same cells or tissues. In contrast to conventional gene sequencing, which can detect only heteroplasmic mutations that reach levels of at least 30 to 50 percent, the customized kit has the sensitivity to detect mitochondrial genome mutations present at levels as low as 8 percent. To achieve their results, the study team adapted an existing whole-exome sequencing kit from Agilent Technologies, expanding it to encompass the mitochondrial genome.
The availability of the new kit, said Falk, if used for either clinical or research purposes, may shorten the "diagnostic odyssey" experienced by many patients and families seeking the cause of debilitating and puzzling symptoms. "Many families travel from one specialist to another for years, searching for the cause of their rare disease," she says. Specific treatments are not always available, but identifying their disease cause may be the first step toward discovering treatments.
A second recent study by Falk and colleagues reviews progress in diagnosing mitochondrial disease, through their experience at a single center over a rapidly changing three-year period before whole-exome sequencing was generally available. The retrospective review in Neurotherapeutics, published Dec. 27, 2012, covers 152 child and adult patients evaluated at CHOP's Mitochondrial-Genetics Diagnostic Clinic from 2008 to 2011.
"Before 2005, very few individuals could receive definitive molecular diagnoses for mitochondrial diseases, because of limitations in both knowledge and technology," said Falk. "Since that time, the clinical ability to sequence whole mitochondrial DNA genomes has significantly improved the diagnosis of many mitochondrial disorders."
During the study period covered in the review article, the clinic at CHOP confirmed definite mitochondrial disease in 16 percent of patients and excluded primary mitochondrial disease in 9 percent. While many diagnostic challenges clearly remain, Falk says the advent of massively parallel nuclear exome sequencing is revealing increasingly more of the genes in nuclear DNA that affect mitochondrial function, and the precise genetic disorder in a given patient, even if it is novel or uncommon. She added that molecular genetics is yielding a more nuanced understanding of the cellular pathways underlying symptoms in many mitochondrial disorders. "Those pathways offer potential new targets for treating these disorders," said Falk.
Funding for both studies came from the National Institutes of Health, grant DK082446. The Discovery Medicine study also was funded through a Foerderer Award for Excellence from The Children's Hospital of Philadelphia Research Institute. Co-authors of the Discovery Medicine study included Eric A. Pierce, M.D., Ph.D., and Mark Consugar, M.S., of the Massachusetts Eye and Ear Infirmary; research and development staff from Agilent under the guidance of Emily LeProust, Ph.D.; and other collaborators from CHOP.
Share this story on Facebook, Twitter, and Google:
Other social bookmarking and sharing tools:
Story Source:
The above story is reprinted from materials provided by Children's Hospital of Philadelphia, via Newswise.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal References:
Elizabeth McCormick, Emily Place, Marni J. Falk. Molecular Genetic Testing for Mitochondrial Disease: From One Generation to the Next. Neurotherapeutics, 2012; DOI: 10.1007/s13311-012-0174-1
Marni J Falk et al. Mitochondrial Disease Genetic Diagnostics: Optimized Whole-Exome Analysis for All MitoCarta Nuclear Genes and the Mitochondrial Genome. Discovery Medicine, 2013
Note: If no author is given, the source is cited instead.
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.
Welcome to IRL, an ongoing feature where we talk about the gadgets, apps and toys we're using in real life and take a second look at products that already got the formal review treatment.
We swear we didn't plan it this way, but it looks like we've got a little trifecta this week, with write-ups pertaining to Apple, Google and, last but not least, Microsoft. On the pessimistic end of the spectrum, Dana would rather have the third-generation iPod shuffle than the model she's using. Terrence is hooked on Google Now and Jon likes the HTC 8X -- just not as much as the Lumia 920.
HTC 8X
What's this? Another Windows Phone 8 test? Yes, while I was trying the Lumia 920 and before I reviewed the ATIV S, I felt it was only fair to give the third flagship of the platform, HTC's Windows Phone 8X, a proper shakedown. I spent a few weeks with one to gauge the differences and came back with the impression that HTC has a worthy flagship -- but not necessarily the one I'd choose for myself.
If you talk solely about ergonomics, the 8X is undoubtedly my first pick. It's much lighter and grippier than the Lumia 920, and the smaller screen makes it easier to reach every corner with one hand than the ATIV S. About the only reservations I have are that hard-to-press power button and the relatively sharp edges. The stand-out appearance can't help but sway me, too. If you get the phone in one of the bolder colors (read: not black), it's simply iconic. No one will mistake an 8X for another phone, while both the ATIV S and Lumia 920 have familiar-looking peers.
Yet there are a few ingredients missing that make it hard to call HTC's creation my perfect Windows Phone 8 device. Simply speaking, the camera just isn't as good as it needs to be in early 2013. While the 8X is sometimes a better pick for up-close photography than the Lumia 920, it falls apart in low-light situations where the Lumia is a champ. Apps matter, as well. Nokia Drive and Nokia Maps aren't vital, but I missed their navigation when I switched devices. And I'll have to admit that being Canadian skews my preferences towards the Nokia phone's glove-friendly screen: it's great to avoid the binary choice of making a phone call versus preserving my fingers. While I'd be inclined to choose the 8X over the ATIV S as long as storage wasn't a priority, I would still give Nokia the ultimate nod as the most relevant to real-world use.
-- Jon Fingas
Google Now
Pretty much from the moment I first launched Google Now it changed the way I interacted with my phone. I've used Siri and toyed with S Voice, but Now is the only virtual assistant that seems like more than an occasionally useful gimmick. Truth is, at this point I unlock directly into it almost as often as I go to the home screen. Sure, in the early days its functionality was fairly limited (and still is), but there was enough information presented by default to keep me coming back. When Gmail was added to its repository of information, the app became a true game-changer for me. While other "assistant" apps are little more than voice commands with personality, Now actually helps track information for you and presents it at valuable times. I don't have to ask what the weather is like or how long it'll take me to get to my next appointment -- it just tells me without prompting.
Of course, things aren't perfect. Now still has a lot of rough edges to work out. For one, the mobile boarding pass feature has yet to work as advertised for me, though, its flight tracking feature turns out to be quicker and more accurate than United's own app. It also stumbles a bit on tracking packages. I like that it recognizes tracking numbers and presents them to me with a quick link, but Now doesn't actually do any tracking itself. Instead it simply shows the card to you for a predetermined amount of time. That's fine if you're enjoying free two-day shipping thanks to Amazon Prime, but if your delivery takes more than a couple of days the card disappears before the box hits your doorstep. It also has an unfortunate habit of presenting me directions to a "new place" almost any time I perform a web search. Oh, and some higher-res icons for the sports score cards would be greatly appreciated.
None of that is enough to ruin the experience, however. If I need to know when my bus is coming, what the temperature is, if my flight is on time or even how many steps I took this month I simply swipe up on my Nexus lock screen and let Google do the work for me. What's more, things can only get better as the company improves its algorithms, opens up new sources of data and, hopefully, develops an API to let other apps tap into the power of Now.
-- Terrence O'Brien
iPod shuffle (fourth generation)
We runners are a superstitious bunch. In my training group, "Nothing new on race day" is our mantra, and it's one to which I've adhered earnestly. It goes without saying that new shoes, running shorts and Snozberry-flavored energy gels are out of the question, but I even get antsy about wearing my Spibelt around my waist instead of my hips. Yeah, I'm neurotic, but running 26.2 miles is scary, yo.
So I was none too pleased when I had a gadget emergency the week before the 2011 New York City Marathon. I'd been training with the Sansa Clip Zip for two months when it abruptly began having mood swings. It started repeating songs, even when I had set my library to shuffle. Sometimes, if it encountered a song it didn't like, it just froze. On a good day, I could side-step the issue by selecting a different artist or song. At its worst, the only way to revive it was to perform a hard reset.
Obviously, that wasn't going to cut it for my epic run, so I did what any desperate person would do: I went to Best Buy and spent $50 on an iPod shuffle. Truly, I would have preferred something like the nano, which would have let me choose specific songs, but I wasn't about to drop $149 on what was essentially an impulse buy. Fifty bucks was about as much as I was willing to spend without having had the opportunity to hem and haw over my purchase.
So I used it. And it was okay. The clip doesn't feel as strong as on the third-generation model. Also, it came with regular headphones (i.e., ones without inline controls), which meant I had to press the player on the device to pause the music and skip tracks. To this day, I find the keys a bit too small, and I often hit the wrong one, mistaking pause for fast-forward, etc. Fortunately, I've since subbed in a pair with an inline remote, which means I barely have to touch the device anymore (except, perhaps, to reposition it in a place where the clip will stay put). Battery life was initially awesome -- I got through that nearly six-hour marathon (oof) with plenty of juice to spare. It's since seen better days, though, to the point where I now have to recharge it several times a week. Faint praise, if ever you've heard it, but at least it doesn't force me to listen to the same Madonna song over and over. That would just be cruel.
By Jonathan Allen NEW YORK, Jan 26 (Reuters) - The carcass of a dolphin that died after becoming mired in a notoriously toxic New York City canal has been removed and will be sent for a necropsy, a marine research group said on Saturday. The animal, a common dolphin, was first spotted in Brooklyn's Gowanus Canal on Friday morning, where it was described as looking disoriented and unwell as it struggled to avoid getting bogged down in the canal's muddy floor. Biologists from the Riverhead Foundation for Marine Research and Preservation, who monitored the dolphin with police and a crowd of onlookers, hoped the animal might be able to free itself and head back out to the harbor as waters rose. It died Friday evening before high tide. "The option that gave the animal the best chance for a positive outcome was waiting," Robert DiGiovanni, Riverhead's executive director and senior biologist, said on Saturday. "If an animal wasn't going to be able to survive through the next tide cycle then it was an animal that was compromised and wouldn't make it." Approaching the dolphin by boat would have been difficult in the shallow, polluted canal and may have achieved little besides adding to the animal's distress, he said. A necropsy will be performed on the adult dolphin, estimated to weigh about 200 pounds, on Sunday at Riverhead's laboratory on Long Island, he said. The findings and tissue samples will be shared with the National Oceanic and Atmospheric Administration. Common dolphins are social animals that travel in groups known as pods. To see a solitary common dolphin, especially so far inland, is unusual, and is a sign that the animal is sick or dying, biologists and other marine officials said. The dolphin's unusual trek into Brooklyn - DiGiovanni could not recall a dolphin coming so far into New York City in at least two decades - brought wide attention to one of the city's dirtier and most malodorous corners. The Environmental Protection Agency declared the Gowanus Canal a Superfund site in 2010, calling it one of the country's "most extensively contaminated water bodies." Mayor Michael Bloomberg had opposed the designation, arguing the city's own plan would have cleaned the canal in less time. The canal is laced with heavy metals, coal tar wastes and other pollutants from the factories and tanneries that have lined its banks, the EPA says. The EPA is still working on its plan, which is currently open to public comment, to spend an estimated $300 million to $400 million of federal money to clean up the canal. (Editing by Paul Thomasch and Doina Chiacu)
PORT SAID, Egypt (AP) ? Egyptian health officials say three people have been killed and more than 400 injured in renewed clashes between protesters and police in the Mediterranean city of Port Said.
They said Sunday's casualties occurred during a funeral procession for most of 37 people killed in clashes in the previous day and when gunmen exchanged gunfire with police at two police stations and the city's main prison.
They spoke on condition of anonymity because they were not authorized to speak to the media.
The Port Said violence broke out after a court on Saturday sentenced 21 defendants to death for their roles in a mass soccer riot in the city's stadium nearly a year ago. The Feb. 1, 2012 riot left 74 people dead. Most of those sentenced were local soccer fans.
With Facebook deciding to hide monthly and daily active users, we have lost the one game platform that could give us reasonably objective data about game performance. We are back to the Dark Ages of vanity metrics as a result. This is something that needs to change.
New research reveals a potential way for how parents' experiences could be passed to their offspring's genes. The research was published today, 25 January, in the journalScience.
Epigenetics is a system that turns our genes on and off. The process works by chemical tags, known as epigenetic marks, attaching to DNA and telling a cell to either use or ignore a particular gene.
The most common epigenetic mark is a methyl group. When these groups fasten to DNA through a process called methylation they block the attachment of proteins which normally turn the genes on. As a result, the gene is turned off.
Scientists have witnessed epigenetic inheritance, the observation that offspring may inherit altered traits due to their parents' past experiences. For example, historical incidences of famine have resulted in health effects on the children and grandchildren of individuals who had restricted diets, possibly because of inheritance of altered epigenetic marks caused by a restricted diet.
However, it is thought that between each generation the epigenetic marks are erased in cells called primordial gene cells (PGC), the precursors to sperm and eggs. This 'reprogramming' allows all genes to be read afresh for each new person - leaving scientists to question how epigenetic inheritance could occur.
The new Cambridge study initially discovered how the DNA methylation marks are erased in PGCs, a question that has been under intense investigation over the past 10 years. The methylation marks are converted to hydroxymethylation which is then progressively diluted out as the cells divide. This process turns out to be remarkably efficient and seems to reset the genes for each new generation. Understanding the mechanism of epigenetic resetting could be exploited to deal with adult diseases linked with an accumulation of aberrant epigenetic marks, such as cancers, or in 'rejuvenating' aged cells.
However, the researchers, who were funded by the Wellcome Trust, also found that some rare methylation can 'escape' the reprogramming process and can thus be passed on to offspring ? revealing how epigenetic inheritance could occur. This is important because aberrant methylation could accumulate at genes during a lifetime in response to environmental factors, such as chemical exposure or nutrition, and can cause abnormal use of genes, leading to disease. If these marks are then inherited by offspring, their genes could also be affected.
Dr Jamie Hackett from the University of Cambridge, who led the research, said: "Our research demonstrates how genes could retain some memory of their past experiences, revealing that one of the big barriers to the theory of epigenetic inheritance - that epigenetic information is erased between generations - should be reassessed."
"It seems that while the precursors to sperm and eggs are very effective in erasing most methylation marks, they are fallible and at a low frequency may allow some epigenetic information to be transmitted to subsequent generations. The inheritance of differential epigenetic information could potentially contribute to altered traits or disease susceptibility in offspring and future descendants."
"However, it is not yet clear what consequences, if any, epigenetic inheritance might have in humans. Further studies should give us a clearer understanding of the extent to which heritable traits can be derived from epigenetic inheritance, and not just from genes. That could have profound consequences for future generations."
Professor Azim Surani from the University of Cambridge, principal investigator of the research, said: "The new study has the potential to be exploited in two distinct ways. First, the work could provide information on how to erase aberrant epigenetic marks that may underlie some diseases in adults. Second, the study provides opportunities to address whether germ cells can acquire new epigenetic marks through environmental or dietary influences on parents that may evade erasure and be transmitted to subsequent generations, with potentially undesirable consequences."
###
University of Cambridge: http://www.cam.ac.uk
Thanks to University of Cambridge for this article.
This press release was posted to serve as a topic for discussion. Please comment below. We try our best to only post press releases that are associated with peer reviewed scientific literature. Critical discussions of the research are appreciated. If you need help finding a link to the original article, please contact us on twitter or via e-mail.
Have you been asking yourself when to begin with using anti aging cream lately? If you have, you are probably in your 20s or 30s and are thinking if you should begin safety actions before those first experience lines appear. It might also be that you are not sure what anti aging items you should use, too.
If that's the situation, let me discuss some of my healthy epidermis care guidance and perhaps we can get some of those concerns eliminated.
First let's get one factor clear: there is no particular age or time frame you should definitely begin using anti aging items. It all relies on your genetics, way of life, choices and also on your kind of epidermis. Some individuals have excellent genetics and look like youngsters into their 40s, the relax of us must manage what we eat strategy, work out program and remain non-smokers to arrive at the same impact (and even then there's no guarantee). Those who greasy epidermis or a few excess weight usually look young for more time, but slimmer individuals and dry-skinned individuals need to begin actions against the ravages of time previously.
So when do you individually need to begin with using anti aging cream? My healthy epidermis care guidance is to begin with when the first experience lines begin to appear, usually around the sight or oral cavity. Based on the aspects detailed above, this could be when you are 21, or it could be when you are 31 or even mature. Keep an eye on your experience and take activity as soon as you see the first wrinkles-in-the-making.
Some individuals suggest getting safety actions before any ravages of time are noticeable, but in my perspective this is not necessary.
But what anti aging items should I use, you ask. Again, you need to look at yourself and your epidermis to choose. Most individuals can begin with an anti aging day cream and a experience clean with some anti aging advantages. But if you have dry epidermis, you might want to use an anti aging evening cream right away. Using covers every few several weeks is also a wise decision - at first you can use any (all-natural) covers and later on shift to ones with more juvenating substances.
ST. CATHARINES ? At least 14 people have fallen victim to a ?paving scam? in St. Catharines, Niagara Regional Police say.
According to investigators, a male going door-to-door approaches victims offering to pave their driveway at a much reduced cost.
Once the suspect receives the cash up front, he claims he will return with his equipment.
In some cases, the suspect has even asked the victim to drive him to a location to pick up his equipment.
The male then disappears with the cash and never returns.
While legitimate businesses seek customers through door-to-door sales, there are others that use the opportunity to defraud unsuspecting victims who are quick to respond to a great offer.
The Niagara Regional Police Service cautions the public that before paying cash for a service, or agreeing to a contract, ensure you know who you are doing business with.
Information on crimes can be submitted anonymously using Crime Stoppers of Niagara.
To leave an anonymous tip, please contact Crime Stoppers via: Telephone: 1-800-222-8477 (TIPS) Online: www.niagaratips.com Text: 274637 (CRIMES), keyword ?Niagara,? then your tip.
Crime Stoppers guarantees that you will remain anonymous through any of the methods offered to provide tips.
You may also be eligible to receive a cash reward of up to $2,000 if the information leads to an arrest.
Jan. 25, 2013 ? At least one in five people in countries for which data are available were infected with influenza during the first year of the 2009 H1N1 pandemic, according to a new study.
The highest rates of infection were in children, with 47 per cent of those aged five to 19 showing signs of having caught the virus. Older people were affected less, with only 11 per cent of people aged 65 or older becoming infected.
The findings come from an international collaboration led by the World Health Organization and Imperial College London, which analysed data from 19 countries, including the UK, US, China and India, to assess the global impact of the 2009 influenza pandemic.
The results, published in the journal Influenza and Other Respiratory Viruses, showed that 20-27 per cent of people studied were infected in the pandemic during the first year of circulation. The researchers believe the incidence of influenza is likely to have been similar in countries where data were not available, meaning that as many as a quarter of the world's population may have been infected.
The study collated results from more than two dozen research studies involving more than 90,000 blood samples collected before, during and after the pandemic. The samples were tested for antibodies produced by the body in response to the specific flu strain that caused the pandemic.
While this study did not set out to look at mortality, the authors also used previously published estimates of pandemic influenza mortality together with mortality estimates that are still in progress, to estimate the proportion of people infected who died from the pandemic virus. Based on an estimate of approximately 200,000 deaths, they suggest that the case fatality ratio was less than 0.02 per cent.
Multiple exposures to previously circulating influenza viruses may have given older people some protection against the strain that emerged in 2009. Blood samples from before the pandemic showed that 14 per cent of people aged 65 or over already had antibodies that reacted to the 2009 strain.
Dr Maria Van Kerkhove, from the Medical Research Council Centre for Outbreak Analysis and Modelling at Imperial College London, one of the lead authors of the study, said: "This study is the result of a combined effort by more than 27 research groups worldwide, who all shared their data and experience with us to help improve our understanding of the impact the pandemic had globally."
Dr Anthony Mounts of the World Health Organization, the senior author, said: "Knowing the proportion of the population infected in different age groups and the proportion of those infected who died will help public health decision-makers plan for and respond to pandemics. This information will be used to quantify severity and develop mathematical models to predict how flu outbreaks spread and what effect different interventions may have."
The study was funded by the Medical Research Council.
Share this story on Facebook, Twitter, and Google:
Other social bookmarking and sharing tools:
Story Source:
The above story is reprinted from materials provided by Imperial College London.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
Maria D. Van Kerkhove, Siddhivinayak Hirve, Artemis Koukounari, Anthony W. Mounts. Estimating age-specific cumulative incidence for the 2009 influenza pandemic: a meta-analysis of A(H1N1)pdm09 serological studies from 19 countries. Influenza and Other Respiratory Viruses, 2013; DOI: 10.1111/irv.12074
Note: If no author is given, the source is cited instead.
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.
Researchers discover new mutations driving malignant melanoma Public release date: 24-Jan-2013 [ | E-mail | Share ]
Contact: Bill Schaller william_schaller@dfci.harvard.edu 617-632-5357 Dana-Farber Cancer Institute
BOSTONTwo new mutations that collectively occur in 71 percent of malignant melanoma tumors have been discovered in what scientists call the "dark matter" of the cancer genome, where cancer-related mutations haven't been previously found.
Reporting their findings in the Jan. 24 issue of Science Express, the researchers from Dana-Farber Cancer Institute and the Broad Institute said the highly "recurrent" mutations occurring in the tumors of many people may be the most common mutations in melanoma cells found to date.
The researchers said these cancer-associated mutations are the first to be discovered in the vast regions of DNA in cancer cells that do not contain genetic instructions for making proteins. The mutations are located in non-protein-coding DNA that regulates the activity of genes.
This non-coding DNA, much of which was previously dismissed as "junk," accounts for 99 percent of a cell's genome. A large number of oncogenic mutations in cancer have been identified in the past several decades, but all have been found within the actual genetic blueprints for proteins.
"This new finding represents an initial foray into the 'dark matter' of the cancer genome," said Levi Garraway, MD, PhD, of Dana-Farber and the Broad and the article's senior author.
"In addition, this represents the discovery of two of the most prevalent melanoma gene mutations. Considered as a whole, these two TERT promoter mutations are even more common than BRAF mutations in melanoma. Altogether, this discovery could cause us to think more creatively about the possible benefits of targeting TERT in cancer treatment or prevention."
The mutations affect a promoter region a stretch of DNA code that regulates the expression of a gene adjacent to the TERT gene. TERT contains the recipe for making telomerase reverse transcriptase, an enzyme that can make cells virtually immortal, and is often found overexpressed in cancer cells. A promoter region of DNA controls the rate of a gene's transcription the copying of its DNA recipe into a message used by the cell to manufacture a protein.
"We think these mutations in the promoter region are potentially one way the TERT gene can be activated," said Franklin Huang, MD, PhD, co-first author of the report along with Harvard MD-PhD student Eran Hodis, of Dana-Farber and the Broad Institute.
To investigate the mutation's effect, the researchers hooked the mutant TERT promoter to a gene that makes luciferase a light-emitting protein. They observed that the mutant promoter increased the production of luciferase in laboratory cell lines. In the same way, the scientists presume, the mutant promoter in human pigmented skin cells can send the TERT gene into overdrive, potentially contributing to the development of melanoma.
The mutations were discovered when the scientists sifted through data from whole-genome sequencing of malignant melanoma tumors. Unlike "whole-exome" searches that examine only the protein-coding DNA of a cell's genome, whole-genome searches scan all of the DNA, including the non-coding regions.
In analyzing whole-genome data, the investigators discovered the two somatic, or not-inherited, mutations in 17 of 19 (89 percent) of the tumors. Next, they sequenced a larger number of melanoma tumors and found that the two mutations were present in 71 percent of tumors in total.
The researchers said the same mutations are present in cell lines from some other malignancies, and that preliminary evidence showed they might be unusually common in bladder and liver cancers. They also noted that the discovery of these important mutations in DNA previously not linked to cancer-causing alterations highlights the value of whole-genome searches of tumor DNA.
###
Other authors include Mary Jue Xu, a student at Harvard Medical School; Gregory V. Kryukov, PhD, of the Broad; and Lynda Chin, MD, of M.D. Anderson Cancer Center.
The research was supported in part by the National Institutes of Health (T32 CA009172, T32GM07753, DP2OD002750, and R33CA126674), the Mittelman Family Fellowship, the American Cancer Society, the Novartis Institutes for Biomedical Research, the Melanoma Research Alliance, and the Starr Cancer Consortium.
About Dana-Farber Cancer Institute
Dana-Farber Cancer Institute is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer research and care centers in the United States. It is a founding member of the Dana-Farber/Harvard Cancer Center (DF/HCC), designated a comprehensive cancer center by the National Cancer Institute. It provides adult cancer care with Brigham and Women's Hospital as Dana-Farber/Brigham and Women's Cancer Center and it provides pediatric care with Boston Children's Hospital as Dana-Farber/Children's Hospital Cancer Center. Dana-Farber is the top ranked cancer center in New England, according to U.S. News & World Report, and one of the largest recipients among independent hospitals of National Cancer Institute and National Institutes of Health grant funding. Follow Dana-Farber on Twitter: @danafarber or Facebook.
About the Broad Institute of MIT and Harvard
The Eli and Edythe L. Broad Institute of MIT and Harvard was founded in 2003 to empower this generation of creative scientists to transform medicine with new genome-based knowledge. The Broad Institute seeks to describe all the molecular components of life and their connections; discover the molecular basis of major human diseases; develop effective new approaches to diagnostics and therapeutics; and disseminate discoveries, tools, methods and data openly to the entire scientific community.
Founded by MIT, Harvard and its affiliated hospitals, and the visionary Los Angeles philanthropists Eli and Edythe L. Broad, the Broad Institute includes faculty, professional staff and students from throughout the MIT and Harvard biomedical research communities and beyond, with collaborations spanning over a hundred private and public institutions in more than 40 countries worldwide. For further information about the Broad Institute, go to www.broadinstitute.org.
[ | 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.
Researchers discover new mutations driving malignant melanoma Public release date: 24-Jan-2013 [ | E-mail | Share ]
Contact: Bill Schaller william_schaller@dfci.harvard.edu 617-632-5357 Dana-Farber Cancer Institute
BOSTONTwo new mutations that collectively occur in 71 percent of malignant melanoma tumors have been discovered in what scientists call the "dark matter" of the cancer genome, where cancer-related mutations haven't been previously found.
Reporting their findings in the Jan. 24 issue of Science Express, the researchers from Dana-Farber Cancer Institute and the Broad Institute said the highly "recurrent" mutations occurring in the tumors of many people may be the most common mutations in melanoma cells found to date.
The researchers said these cancer-associated mutations are the first to be discovered in the vast regions of DNA in cancer cells that do not contain genetic instructions for making proteins. The mutations are located in non-protein-coding DNA that regulates the activity of genes.
This non-coding DNA, much of which was previously dismissed as "junk," accounts for 99 percent of a cell's genome. A large number of oncogenic mutations in cancer have been identified in the past several decades, but all have been found within the actual genetic blueprints for proteins.
"This new finding represents an initial foray into the 'dark matter' of the cancer genome," said Levi Garraway, MD, PhD, of Dana-Farber and the Broad and the article's senior author.
"In addition, this represents the discovery of two of the most prevalent melanoma gene mutations. Considered as a whole, these two TERT promoter mutations are even more common than BRAF mutations in melanoma. Altogether, this discovery could cause us to think more creatively about the possible benefits of targeting TERT in cancer treatment or prevention."
The mutations affect a promoter region a stretch of DNA code that regulates the expression of a gene adjacent to the TERT gene. TERT contains the recipe for making telomerase reverse transcriptase, an enzyme that can make cells virtually immortal, and is often found overexpressed in cancer cells. A promoter region of DNA controls the rate of a gene's transcription the copying of its DNA recipe into a message used by the cell to manufacture a protein.
"We think these mutations in the promoter region are potentially one way the TERT gene can be activated," said Franklin Huang, MD, PhD, co-first author of the report along with Harvard MD-PhD student Eran Hodis, of Dana-Farber and the Broad Institute.
To investigate the mutation's effect, the researchers hooked the mutant TERT promoter to a gene that makes luciferase a light-emitting protein. They observed that the mutant promoter increased the production of luciferase in laboratory cell lines. In the same way, the scientists presume, the mutant promoter in human pigmented skin cells can send the TERT gene into overdrive, potentially contributing to the development of melanoma.
The mutations were discovered when the scientists sifted through data from whole-genome sequencing of malignant melanoma tumors. Unlike "whole-exome" searches that examine only the protein-coding DNA of a cell's genome, whole-genome searches scan all of the DNA, including the non-coding regions.
In analyzing whole-genome data, the investigators discovered the two somatic, or not-inherited, mutations in 17 of 19 (89 percent) of the tumors. Next, they sequenced a larger number of melanoma tumors and found that the two mutations were present in 71 percent of tumors in total.
The researchers said the same mutations are present in cell lines from some other malignancies, and that preliminary evidence showed they might be unusually common in bladder and liver cancers. They also noted that the discovery of these important mutations in DNA previously not linked to cancer-causing alterations highlights the value of whole-genome searches of tumor DNA.
###
Other authors include Mary Jue Xu, a student at Harvard Medical School; Gregory V. Kryukov, PhD, of the Broad; and Lynda Chin, MD, of M.D. Anderson Cancer Center.
The research was supported in part by the National Institutes of Health (T32 CA009172, T32GM07753, DP2OD002750, and R33CA126674), the Mittelman Family Fellowship, the American Cancer Society, the Novartis Institutes for Biomedical Research, the Melanoma Research Alliance, and the Starr Cancer Consortium.
About Dana-Farber Cancer Institute
Dana-Farber Cancer Institute is a principal teaching affiliate of the Harvard Medical School and is among the leading cancer research and care centers in the United States. It is a founding member of the Dana-Farber/Harvard Cancer Center (DF/HCC), designated a comprehensive cancer center by the National Cancer Institute. It provides adult cancer care with Brigham and Women's Hospital as Dana-Farber/Brigham and Women's Cancer Center and it provides pediatric care with Boston Children's Hospital as Dana-Farber/Children's Hospital Cancer Center. Dana-Farber is the top ranked cancer center in New England, according to U.S. News & World Report, and one of the largest recipients among independent hospitals of National Cancer Institute and National Institutes of Health grant funding. Follow Dana-Farber on Twitter: @danafarber or Facebook.
About the Broad Institute of MIT and Harvard
The Eli and Edythe L. Broad Institute of MIT and Harvard was founded in 2003 to empower this generation of creative scientists to transform medicine with new genome-based knowledge. The Broad Institute seeks to describe all the molecular components of life and their connections; discover the molecular basis of major human diseases; develop effective new approaches to diagnostics and therapeutics; and disseminate discoveries, tools, methods and data openly to the entire scientific community.
Founded by MIT, Harvard and its affiliated hospitals, and the visionary Los Angeles philanthropists Eli and Edythe L. Broad, the Broad Institute includes faculty, professional staff and students from throughout the MIT and Harvard biomedical research communities and beyond, with collaborations spanning over a hundred private and public institutions in more than 40 countries worldwide. For further information about the Broad Institute, go to www.broadinstitute.org.
[ | 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.
What's this? Another 
Pretty much from the moment I first launched 
We runners are a superstitious bunch. In my training group, "Nothing new on race day" is our mantra, and it's one to which I've adhered earnestly. It goes without saying that new shoes, running shorts and Snozberry-flavored energy gels are out of the question, but I even get antsy about wearing my Spibelt around my waist instead of my hips. Yeah, I'm neurotic, but running 26.2 miles is scary, yo.
With Facebook deciding to hide monthly and daily active users, we have lost the one game platform that could give us reasonably objective data about game performance. We are back to the Dark Ages of vanity metrics as a result. This is something that needs to change.
Bullet News![[ Back to EurekAlert! ]](http://www.eurekalert.org/images/back2e.gif){kind=small}
Public release date: 24-Jan-2013
Share ]