New Study Shows This Common OTC Pain Reliever Has a Really Scary Side Effect

Ibuprofen, a common over-the-counter pain reliever, has a troubling side-effect that’s often overlooked, but new findings have proved it’s more important to know about this now than ever before. Recent evidence found that non-steroidal anti-inflammatory drugs (NSAIDs), like ibuprofen, can increase your chances of having a heart attack in as little as one week of continuous use.

In a recent study published in the British Medical Journal, data from almost 450,000 people, 61,460 of whom had suffered a heart attack, was analyzed looking for the effect over time of taking three common anti-inflammatory painkillers: ibuprofen, diclofenac and naproxen. The data revealed that compared with people who didn’t take the painkillers, those who did ingest them had a 20 percent to 50 percent increased risk of having a heart attack.

Additionally, the risk was found to be higher for people who ingested 1,200 mg a day of ibuprofen (about six tablets of Advil) and 750 mg a day for naproxen (about three and a half Aleves), Yahoo! reports. The study reported that it only took a week for a higher risk of heart attack to set in on a person, with the highest risk occurring at about a month of usage. After a month, researchers found that the risk didn’t increase further but rather stayed the same.

Typically, NSAIDs are safe when used correctly for mild pain relief, however, many people have begun relying on NSAIDs for prolonged periods of time at a higher dosage to treat their pain, which is why the risk of heart attack associated with the use of NSAIDs has begun to rise.

While this study certainly revealed a scary truth about the drug, it’s important to note that taking an NSAID for minor pain relief at the lowest effective dose and a minimal length of time isn’t likely to cause aheart attack. It’s the usage level over a longer time period at higher dosage that can be dangerous, so it’s best to limit your use as much as possible to avoid any unwanted negative side effects.





Experimental gene-silencing drug from Alnylam and Sanofi shows strong results in hemophilia

Alnylam CEO John Maraganore aims to compete with what is expected to be a blockbuster hemophilia drug from Roche.


n experimental hemophilia drug developed by Alnylam Pharmaceuticals continues to staunch bleeding in patients followed for almost one year in an ongoing, mid-stage clinical trial, the company reported Monday.

The promising results could intensify an already heated competition to develop novel treatments for the inherited bleeding disorder. The Alnylam drug, developed in partnership with Sanofi, uses a technology called RNAi to shut down dysfunctional genes. It’s a promising approach that’s attracted billions in research dollars, but hasn’t yet been used in an actual drug approved for sale.

The company says the new data support its recent decision to advance its RNAi hemophilia drug —  known as fitusiran —  into phase 3 clinical trials. If it succeeds, the drug could potentially compete against an expected blockbuster hemophilia drug from Roche.

In the current study, 33 patients have been injected once a month with fitusiran. The results so far: 48 percent have not bled after a median observation period of 11 months, according to data reported Monday at the International Society of Thrombosis and Haemostasis Congress in Berlin. Some patients in the study have been followed for up to 20 months.

Before starting the study, patients were reporting a median of 20 bleeding events per year. That number was reduced to 1 following the fitusarin injections.

The patients have two types of the disease, hemophilia A and B. Fourteen of the patients have inhibitors —  immune system antibodies that interfere with clotting factors commonly used to treat hemophilia. Patients with inhibitors are the hardest to treat effectively.

For this group, the median annualized bleed rate fell from 38 to zero, although the median observation period was shorter at six months.

Sixty-four percent of the inhibitor patients have not bled since starting treatment with fitusiran.

“These are really encouraging numbers,” said Alnylam Chief Medical Officer Pushtal Garg, in a phone interview from Berlin on Sunday. “To show annual bleed rates of one and zero is remarkable, particularly for a treatment that is administered once per month with a subcutaneous, low-volume injection.”

One third of the fitusiran-treated patients in the study reported elevated liver enzymes, a possible signal of liver toxicity, though all these patients also had hepatitis C, Alnylam said. One patient with increased liver enzymes stopped participating in the study; the rest had no symptoms and their liver enzyme issues were resolved.

There were no blood clots reported by patients in the fitusiran study. That could help the drug stand apart from Roche’s hemophilia drug emicizumab, which had a handful of serious blood clots reported in its phase 3 studies.

Roche intends to submit emicizumab for approval this year to treat hemophilia A patients with inhibitors to standard therapy. Sixty-three percent of patients receiving emicizumab reported zero treated bleeds compared with 6 percent of patients treated with bypassing agents, according to phase 3 study results previously announced. (Those results were also presented Monday at the Berlin meeting and published in the New England Journal of Medicine.)

Some analysts have projected emicizumab’s peak sales could hit $2 billion per year for patients with inhibitors, although that figure is hotly debated given the drug’s blood clotting safety issue. This leaves a potential opening for fitusiran, though its phase 3 trial won’t report data until 2019.

The Roche drug may eventually have other competition, too. Biomarin Pharmaceuticals, Spark Therapeutics, and Uniqure are all developing gene therapies to treat — and potentially cure — hemophilia.

Hemophilia drug franchises from Shire and Novo Nordisk are at risk of losing billions of dollars in sales if these new hemophilia drugs are approved. Though there are just 20,000 patients with hemophilia in the U.S., it’s a highly lucrative market.

On Sunday, Shire took the unusual step of fighting back with a preliminary injunction from a German court against Roche. Shire accused Roche of disseminating “inaccurate and misleading” information about the safety and serious adverse events that occurred in the phase 3 clinical trial of emicizumab, according to Reuters. In a statement, Roche said it stood behind the emicizumab data.

Alnylam, which is based in Cambridge, Mass., develops drugs that work through a process called RNA interference, or RNAi. All of its drugs, including fitusiran, are snippets of genetic code known as RNA that turn off genes producing disease-causing proteins. Fitusiran blocks the production of antithrombin, a protein made in the liver that prevents blood from clotting. Monthly injections of fitusiran reduce antithrombin in patients and increase corresponding levels of thrombin, another protein that promotes blood clotting.

Last October, Alnylam shares fell sharply after another of its RNAi drugs caused more deaths than a placebo in a phase 3 study. Work on that drug was halted.

But Alnylam shares have recovered this year, up 125 percent to date, on renewed investor optimism for its late-stage drug pipeline, including another RNAi drug, patisiran, targeting a rare nerve disease.

At Friday’s $84.08 close, Alnylam carries an almost $8 billion market valuation. It doesn’t yet have a drug on the market, which means investors are giving the company a lot of credit already for its late-stage RNAi pipeline, including fitusarin.


Google Maps now shows how hard it will be to park at your destination

google maps parking

Update 1/27/17: The feature is now available in the full version of the app. This article has been updated to reflect this news.

If you’ve ever taken longer to find a parking spot than you did driving somewhere, Google Maps might be able to help—or at least prepare you for a headache. Thanks to a new feature in the latest version of the app, you’ll now be able to tell how hard it will be to park once you arrive at your destination.

The new feature is easy to miss. The next time you pull up driving directions, you’ll see a small circular P icon to the right of your route overview, next to which will show three levels of parking difficulty: Easy, Medium, and Limited. (To make it easier to see at a glance, easy and medium are colored blue while limited is red.) While the feature doesn’t update to show the actual parking situation when you arrive (at least not yet), you can get a slightly longer description when you expand your directions.

The update is currently rolling out in the Google Play store, but if you’re not seeing it, you can sideload the Google-signed APK from APKMirror. Keep in mind that the feature is only available in 25 cities across the U.S: Atlanta, Boston, Charlotte, Chicago, Cleveland, Dallas/Fort Worth, Denver, Detroit, Houston, Los Angeles, Miami, Minneapolis/St. Paul, New York City, Orlando, Philadelphia, Phoenix, Pittsburgh, Portland, Sacramento, San Diego, San Francisco, Seattle, St. Louis, Tampa, and the Washington D.C. area.

Why this matters: Parking can be a major headache when driving somewhere new, so we’ll take any information we can get. And with the new Uber integration built right into the app, a red circle could mean the difference between driving or being driven somewhere.


Hacker shows how easy it is to take over a city’s public Wi-Fi network

A buffer overflow in a single router model could have endangered thousands of Wi-Fi users

151025 free wifi hotspot
A sign advertises free WiFi at Haneda Airport in Tokyo on Oct. 25, 2015. Credit: Martyn Williams
In a perfect example of how public wireless networks can be dangerous for privacy and security, an Israeli hacker showed that he could have taken over the free Wi-Fi network of an entire city.

On his way home from work one day, Amihai Neiderman, the head of research at Israeli cybersecurity firm Equus Technologies, spotted a wireless hotspot that he hadn’t seen before. What made it unusual was that it was in an area with no buildings.

It turned out that the hotspot he saw, advertised as “FREE_TLV,” was part of the citywide free Wi-Fi network set up by the local administration of Tel Aviv, Israel. This made Neiderman wonder: How secure is it?

For the next few weeks, finding a way to compromise this network became a side project to do in his free time. First he connected to the network through one of the access points spread around the city and checked what his new IP (Internet Protocol) address was. This is usually the public address assigned to the router through which all Wi-Fi clients access the internet.

He then disconnected and scanned that IP address from the internet for open ports. He found that the device was serving a web-based login interface over port 443 (HTTPS).

This interface displayed the manufacturer’s name — Peplink — but not other information about the device type or model. An analysis of the web interface didn’t reveal any basic vulnerabilities either, such as SQL injection, default or weak log-in credentials or authentication bypass flaws.

He realized that a more thorough analysis of the device’s actual firmware was required. Identifying the device and finding the exact firmware to download from the manufacturer’s website was not easy, because Peplink creates and sells many types of networking devices for various industries. However, he eventually pinned it down to firmware version 5 for Peplink’s Balance 380 high-end load balancing router.

The firmware used basic XOR-based encryption to make it harder for third-parties to reverse-engineer the firmware’s file system, but this was relatively easy to bypass. Once everything was unpacked and loaded into an emulator, Neiderman was able to access the CGI (Common Gateway Interface) scripts that made up the router’s web interface.

It didn’t take long until the researcher found a buffer overflow vulnerability in the CGI script that handled the log-out process. The flaw could be exploited by sending a very long session cookie to the script and successful exploitation resulted in arbitrary code execution and full control over the device.

Neiderman presented his findings and reverse-engineering efforts Thursday at the DefCamp security conference in Bucharest, Romania. He declined to say whether he actually tested his exploit on the live Peplink Balance routers used to operate Tel Aviv’s free Wi-Fi network, because that could land him in legal trouble.

However, when he reported the flaw to Peplink the company confirmed and patched it in a subsequent firmware update, so the firmware on FREE_TLV’s routers was certainly vulnerable when Neiderman found the flaw.

While finding vulnerabilities in routers is not uncommon, this case stands out because it shows that skilled hackers could potentially attack thousands or tens of thousands of users by compromising large public Wi-Fi networks like those run by municipalities.

By controlling a router, attackers can snoop on all unencrypted user traffic that passes through it and capture sensitive information. They can also launch active attacks, like redirecting users to rogue web servers when they’re trying to access legitimate websites or injecting malicious code into non-HTTPS web pages.

Large networks are typically standardized and use the same type of equipment throughout to allow for easier management. A vulnerability that allows a compromise of one of the network’s access points is likely to allow the compromise of all of them.

Attacks like these are why users are strongly encouraged to use a VPN (Virtual Private Network) service when they’re accessing the internet over public or untrusted Wi-Fi networks.

Neiderman said that he was impressed with how Peplink responded to his report and how the company handled the vulnerability. He stressed that this attack was also possible because of the insecure way in which the network’s routers had been deployed. Their administration interfaces shouldn’t have been exposed to the Internet.



In a ray of hope for preventing pre-term birth, researchers found that use of a drug in pregnant mice entirely stopped premature birth and reduced infant fatalities.

Pre-term birth (being born at less than 37 weeks’ gestation) is a major cause of death in children under five years of age.

“Our studies give us some encouragement that it may be possible to prevent many pre-term births, by using drugs that target the body’s inflammatory mechanisms, probably in combination with antibiotics as well,” said lead study author Sarah Robertson, Director of the Robinson Research Institute, University of Adelaide in Australia.

The study, published in the journal Scientific Reports, tested a drug known for its abilities to switch off pro-inflammatory pathways.

The main causes of pre-term birth are bacterial infection (in around 50 per cent of cases), physical injury or stress causing placental damage, carrying twins or triplets, or from environmental toxins such as air pollution.

Each of these is associated with what researchers describe as an “inflammatory cascade”, which can activate the mother’s immune response and ultimately lead to spontaneous pre-term birth.

This inflammatory cascade is triggered by an immune receptor known as Toll-Like receptor 4 (TLR4), responding to infection, physical injury or stress.

TLR4 is critical to the body’s immune response but it also produces a number of pro-inflammatory effects that are harmful to pregnancy.

“TLR4 is a trigger of spontaneous pre-term birth,” Robertson said.

“For this reason, we wanted to test a drug known for its ability to block the actions of TLR4, to see if that would also prevent pre-term birth,” Robertson noted.

The drug tested in this study is known as (+)-naloxone.

“We found that by treating pregnant mice with (+)-naloxone, it provided complete protection against pre-term birth triggered by bacteria. It also protected against stillbirth and infant death shortly after birth, and led to a correction in birth weight among infants that would otherwise be born at very low birth weight,” Robertson said.


Smoking a pack a day causes 150 mutations in every lung cell, research shows

Smoking a pack a day causes 150 mutations in every lung cell, research shows (Getty Images)Smoking a pack a day causes 150 mutations in every lung cell, research shows (Getty Images)
Scientists have found that smoking a pack a day of cigarettes can cause 150 damaging changes to a smoker’s lung cells each year.

The findings come from a study of the devastating genetic damage, or mutations, caused by smoking in various organs in the body.

Publishing in the journal Science on Thursday, the researchers said the findings show a direct link between the number of cigarettes smoked in a lifetime and the number of mutations in the DNA of cancerous tumors.

The highest mutation rates were seen in lung cancers, but tumors in other parts of the body – including the bladder, liver and throat – also had smoking-associated mutations, they said. This explains why smoking also causes many other types of cancer beside lung cancer.

Smoking kills six million people a year worldwide and, if current trends continue, the World Health Organization predicts more than 1 billion tobacco-related deaths this century.

Cancer is caused by mutations in the DNA of a cell. Smoking has been linked with at least 17 types of cancer, but until now scientists were not clear on the mechanisms behind many of them.

Ludmil Alexandrov of Los Alamos National Laboratory in the United States, one of those who carried out the research, explained that in particular, it had until now been difficult to explain how smoking increases the risk of cancer in parts of the body that don’t come into direct contact with smoke.

“Before now, we had a large body of epidemiological evidence linking smoking with cancer, but now we can actually observe and quantify the molecular changes in the DNA,” he said.

This study analyzed over 5,000 tumors, comparing cancers from smokers with those from people who had never smoked.

It found certain molecular fingerprints of DNA damage – called mutational signatures – in the smokers’ DNA, and the scientists counted how many of these were in different tumors.

In lung cells, they found that on average, smoking a pack of cigarettes a day led to 150 mutations in each cell every year. Each mutation is a potential start point for a “cascade of genetic damage” that can eventually lead to cancer, they said.

The results also showed that a smoking a pack of cigarettes a day led to an average 97 mutations in each cell in the larynx, 39 mutations for the pharynx, 23 for the mouth, 18 for the bladder, and six mutations in every cell of the liver each year.

Mike Stratton, who co-led the work at Britain’s Wellcome Trust Sanger Institute, said it was a bit like digging in to the archaeology of each tumor

“The genome of every cancer provides a kind of archaeological record, written in the DNA code itself, of the exposures that caused the mutations,” he said. “Looking in the DNA of cancers can provide provocative new clues to how (they) develop and thus, potentially, how they can be prevented.”


Leak shows Huawei Honor S1 smartwatch with a round e-paper display

A lot has been written about the upcoming Huawei Mate 9 but the company may have something up its sleeve (literally). An e-paper based smartwatch has leaked with a circular display with marginally smaller bezels than the Pebble Time Round (which was not upgraded in the last round of Pebbles).

Looking back at an teaser image from early last month, this seems to be the Huawei Honor S1 smartwatch (note the notches on the bezel).

Huawei Honor S1 smartwatch with an e-paper display Huawei Honor S1 smartwatch with an e-paper display
Huawei Honor S1 smartwatch with an e-paper display

For those unfamiliar, e-paper is a type of low-power display that has amazing sunlight legibility and can run for days on the tiny batteries found in smartwatches. It should not be confused with e-ink like Kindle e-readers), which uses less power but has very slow refresh rate and still doesn’t do color. Neither does the Huawei Fit, judging by these images.

The promo images provide answers to key questions – yes, there will be a heart rate sensor and yes, the watch will be waterproof. In fact, it can track your laps around the pool. No hardware buttons are visible, pointing to touchscreen only operation. It’s not clear what OS this is running, though – it may be neither Android Wear nor Tizen but instead a custom solution.


New Alcatel Idol 4S leak shows off packaging that transforms into VR headset

A T-Mobile training guide for the Windows 10-powered Alcatel Idol 4S has leaked online, suggesting an imminent launch. The leak not only confirms some of the device’s key specs, but also compares the phone with the iPhone 7 and Galaxy S7.

Aside from this, the leaked guide also reveals that the a free VR headset will be included with the handset – something we already know. In fact, the phone will have a VR-as-the-box kind of packaging, meaning the packaging for the Idol 4S will transform into VR goggles.

There is currently no information on exactly when the device will be made official and what price tag it would carry.

This week in games: EA gives away Dungeon Keeper, InXile shows off Wasteland 3

Wasteland 3

It’s October, so do me a favor: Curl up on a couch this weekend, drink some cider, andwatch a horror movie. You know, something cliché.

Or just play Gears of War 4. Whatever.

This week, we get our first look at Wasteland 3 and an extended look at Torment: Tides of Numenera, Ubisoft confirms Beyond Good & Evil 2 for like the tenth time, EA gives awayDungeon Keeper, and the Outlast 2 demo rustles some corn on Steam. This is gaming news for October 2 through 6.

My dungeon’s keeper

Remember when EA released that mobile follow-up to Dungeon Keeper a few years ago and completely ruined everything in the entire world? (Slight hyperbole, maybe.) Well, now you can head over to Origin and grab the unspoiled original Dungeon Keeper for the low, low price of free. Peter Molyneux’s 1997 classic is the latest in EA’s On the House program. Grab it while you can.

Band of brother heroes

Humble’s stepped up its game with some decent packages in recent months, including the latest Humble Company of Heroes 10th Anniversary Bundle: $1 for Company of Heroes, beat-the-average to add in Company of Heroes 2, and $10 gets you all theCompany of Heroes ever made. Not bad.


In case you missed it: The Fig campaign for Wasteland 3 started this week, and it’s doneokay—by which I mean they’ve already pretty much hit their goal, two days in. You’ve still got about a month to throw some money into the pot if you want, or you could just hang out and watch this gameplay trailer instead:


Speaking of InXile, Torment: Tides of Numenera is set to launch in early 2017 and that means it’s time to start ramping up the trailers. Here’s a brief look at the futuristic lunacy that is Numenera itself:

Meet the new boss

Fool me once Ubisoft, shame on you. Fool me…wait, how many times have they teased a new Beyond Good & Evil at this point? Who’s to blame if I’ve been fooled seven or eight different times?

Point is, Ubisoft is dangling Beyond Good & Evil again. Michel Ancel dropped some concept art last week in the lead-up, and now it’s been officially confirmed: “If you’ve been waiting for news about BG&E…well, here you go! We are delighted to confirm that Michel Ancel is currently working with the Ubisoft Montpellier Studio on a new Beyond Good & Evil game.”

I’d get excited, but uh…you can’t, uh, you can’t fool me again. Or something. (As a side note: The original Beyond Good & Evil will be the next free Uplay game starting October 12, as part of Ubisoft’s ongoing 30th anniversary celebration.)

Mortal Kombat X-ists

The “will-they-won’t-they” around Mortal Kombat XL has come to a close with a definitive “They did”—NetherRealm finally launched it on Steam this week after initially saying they weren’t going to and then, I guess, saying “Just kidding! It’s coming!”

Also, there’s a patch that supposedly fixes most of the problems with the lackluster PC port. Great. Now I guess we twiddle our thumbs and see if Injustice 2 makes it over.


In other patch news, the BioShock remasters got a long list of fixes. The bad news? Now people are reporting even more problems than before, including Windows 10 machines asking for players to install Windows 7 Service Pack 1. Oops.

Children of the corn

It’s October, the perfect month to try and find a horror game that’s a) Good and b) One you haven’t played yet. Well, here’s a candidate: The Outlast 2 demo, which is available for free until November 1. It’s the same short demo shown at PAX this year, and what it lacks in length it makes up for in corn-rustling and murderous religious fanatics. Hopefully it’ll tide you over until the full game’s release early next year.


Study Shows Health Improving Globally, But Progress Is Patchy

Study Shows Health Improving Globally, But Progress Is Patchy

Study Shows Health Improving Globally, But Progress Is Patchy

Study found world population had gained more than a decade of life expectancy since 1980

LONDON:  Globally, people’s health is improving and life expectancy is rising, but progress is far from universal with chronic diseases bringing long-term illness and causing seven out of 10 deaths, according to research published on Thursday.

The Global Burden of Disease study, which shows the key drivers of ill health, disability and death in individual countries, found that by 2015, the world population had gained more than a decade of life expectancy since 1980 – rising to 69.0 years in men and 74.8 years in women.

Among main contributors to this were large falls in death rates for many communicable or infectious diseases, including HIV/AIDS, malaria and diarrhoea. The rate of people dying from cardiovascular disease and cancers has also fallen, the study found, although at a slower pace.

The study analysed 249 causes of death, 315 diseases and injuries and 79 risk factors in 195 countries and territories between 1990 and 2015.

Christopher Murray, director of the Institute for Health Metrics and Evaluation at the University of Washington, which led the study, said its results painted a picture of patchy health gains across the world, driven in part by economic development.

“Development drives, but does not determine health,” he said in a statement as the findings were published in The Lancet medical journal.