5 Bad Blogging Habits Stifling Your Audience Growth EContent (press release) Everyone has bad habits, and they're extraordinarily hard to break once they've manifested. The same is true in the blogging world, where habits can be especially damaging. Because the success of your strategy depends on the regularity of your …
FILE – Republican presidential candidate Donald Trump and his wife Melania meet with family members of Phyllis Schlafly before the start of a funeral Mass for Schlafly, Saturday, Sept. 10, 2016, in St. Louis. (Robert Cohen/St. Louis Post-Dispatch via AP, Pool))
The New York Times is in trouble, and they know it. The paper has lost all credibility, and even long-time readers comfortable with its editorial bias have been sickened by the all-out trashing of Donald Trump over the past several months.
When the publisher of the worlds most arrogant and all-knowing newspaper puts out a mea culpa promising to rededicate ourselves to the fundamental mission of Times journalism you can be pretty sure that something is awry. To pledge to report America and the world honestly, without fear or favor suggests they have been doing otherwise, and that is a fact.
That said, nothing seems to have changed at the Times. The reporting still is admiring of all-things Obama and derisive of all things Trump, to a laughable degree.
A case in point: an article in the Sunday Styles section last weekend about how fashion designers fret that their warm reception during the Obama years may be over. The thesis is this: that Hillary Clinton would likely have been more of a fashion icon and admirer while in the White House than Melania Trump, former model. Seriously.
This piece is worth reviewing because it is so outlandish, and buttresses the case that the Times editorial position overshadows reporting in all sections.
It is authored by authoritative fashion writer Vanessa Friedman, who knows better but who has adopted the political persuasion of her bosses, and undermined her own credibility in the process.
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Surely she knows that Melania could become one of our countrys great style icons and that Hillarys penchant for single-hue pants suit was a default mechanism, not a fashion statement.
A recent piece by Michael Cieply, who formerly worked at the single-hue Times for 12 years as a writer and editor, gives some insight into why the paper is such a Johnny-one-note. He says the New York Times has always or at least for many decades been a far more editor-driven, and self-conscious, publication than many of those with which it competes. Other papers, Cieply says, are reporter-driven (and) bottom-up, with editors asking reporters What are you hearing? What have you got? By contrast, the Times is strictly top-down. Even in the fashion section!
Ms. Friedman nearly waxes poetic about Hillarys Ralph Lauren pants suits, and especially the dark grey (with purple lapels) number she wore the morning of her concession speech. It underscored, writes Ms. Friedman, the way two colors/factions red and blue can unite to make something new.
Or, it might have underscored that Hillary had cycled through every other color in the Pantone universe as she barreled through each day of the campaign wearing the exact same garment. If a lot of women followed her lead, the fashion industry would promptly go under. But I digress.
Hillarys costume choice might also underscore, says Ms. Friedman, the end of fashions seat at the power table. The author explains that most fashion editors and designers were up to their necks in the Clinton quest, hosting fundraisers and publicly endorsing the Democrat candidate. They are, of course, disappointed.
But will that hamper their business or even their access to the White House? Friedman writes wistfully about how Michelle Obama delighted fashion people by elevating the industry beyond the superficial to the substantive. She framed clothing as a collection of values: diversity, creativity, entrepreneurship a trend that Ms. Friedman worries the Trumps will not carry forward.
The crime, apparently, is that the Trumps have ignored fashion designers. (Kind of like the press being outraged when the Trumps dump the press corps to have a family dinner. The nerve!) Even worse: Melanias wardrobe appears bought off the rack, as opposed to one that she had worked with the designer to create. Literally.
Friedman moans that the clothes worn by Mrs. Trump on the campaign trail evolved from a shopping spree, as opposed to a strategic plan which reflects her distance from the industry. Friedman is also offended that the incoming first lady sometimes has worn foreign designers like Fendi and Balmain.
Actually, maybe it reflects that Melania is not all-consumed with her appearance and has not had a lot of free time lately. Of course, Ms. Friedman is party to a long-standing double standard. Remember how Nancy Reagan was excoriated by the press for wearing expensive clothes designed for her by Adolfo and Carolina Herrera? But how Jacki O got a pass when she wore (foreign designers) Chanel and Dior?
Im only hitting the high points; the entire article is nonsensical. She quotes one designer saying the only unifying theme about the Trump wardrobes on election night was that they all had dressed in clothes that made them look rich. Well, thats often the case when you are rich.
Friedman tried and apparently failed to find a designer who would refuse to dress Mrs. Trump. What a shock. Designers actually want to make money; dressing one of the most beautiful women to ever occupy the White House would not only be a privilege, it could launch a career.
Ms. Friedman is, like so many other elites in the arts and publishing worlds, shocked that Hillary lost (in spite of her bold fashion statements!) Stefano Tonchi, editor of W, sums up the misery, saying it makes you realize how powerless we are.
Yes, Ms. Friedman, you couldnt overpower the voices of all those unkempt millions who need jobs and are fed up with the insufferable moral superiority of the Left. Maybe now you should go back to writing about fashion, and leave the political commentary to the editorial board.
Cowboys WR Allen Hurns chose opportunity over money Blogging The Boys (blog) Arguably the biggest free agent signing for the Dallas Cowboys to date is wide receiver Allen Hurns. He was seen as an immediate upgrade for the position group, and the recent reports of an offseason foot injury to Terrance Williams just makes him more …
One July afternoon last summer, Matt Wilsey distributed small plastic tubes to 60 people gathered in a Palo Alto, California, hotel. Most of them had traveled thousands of miles to be here; now, each popped the top off a barcoded tube, spat in about half a teaspoon of saliva, and closed the tube. Some massaged their cheeks to produce enough spit to fill the tubes. Others couldn’t spit, so a technician rolled individual cotton swabs along the insides of their cheeks, harvesting their skin cells—and the valuable DNA inside.
One of the donors was Asger Vigeholm, a Danish business developer who had traveled from Copenhagen to be here, in a nondescript lobby at the Palo Alto Hilton. Wilsey is not a doctor, and Vigeholm is not his patient. But they are united in a unique medical pursuit.
Wilsey’s daughter, Grace, was one of the first children ever diagnosed with NGLY1 deficiency. It’s a genetic illness defined by a huge range of physical and mental disabilities: muscle weakness, liver problems, speech deficiencies, seizures. In 2016, Vigeholm’s son, Bertram, became the first child known to die from complications of the disease. Early one morning, as Bertram, age four, slept nestled between his parents, a respiratory infection claimed his life, leaving Vigeholm and his wife, Henriette, to mourn with their first son, Viktor. He, too, has NGLY1 deficiency.
The night before the spit party, Vigeholm and Wilsey had gathered with members of 16 other families, eating pizza and drinking beer on the hotel patio as they got to know each other. All of them were related to one of the fewer than 50 children living in the world with NGLY1 deficiency. And all of them had been invited by the Wilseys—Matt and his wife Kristen, who in 2014 launched the Grace Science Foundation to study the disease.
These families had met through an online support group, but this was the first time they had all come together in real life. Over the next few days in California, every family member would contribute his or her DNA and other biological samples to scientists researching the disease. On Friday and Saturday, 15 of these scientists described their contributions to the foundation; some studied the NGLY1 gene in tiny worms or flies, while others were copying NGLY1 deficient patients’ cells to examine how they behaved in the lab. Nobody knows what makes a single genetic mutation morph into all the symptoms Grace experiences. But the families and scientists were there to find out—and maybe even find a treatment for the disease.
That search has been elusive. When scientists sequenced the first human genome in 2000, geneticist Francis Collins, a leader of the Human Genome Project that accomplished the feat, declared that it would lead to a “complete transformation in therapeutic medicine” by 2020. But the human genome turned out to be far more complex than scientists had anticipated. Most disorders, it’s now clear, are caused by a complicated mix of genetic faults and environmental factors.
And even when a disease is caused by a defect in just one gene, like NGLY1 deficiency, fixing that defect is anything but simple. Scientists have tried for 30 years to perfect gene therapy, a method for replacing defective copies of genes with corrected ones. The first attempts used modified viruses to insert corrected genes into patients’ genomes. The idea appeared elegant on paper, but the first US gene therapy to treat an inherited disease—for blindness—was approved just last year. Now scientists are testing methods such as Crispr, which offers a far more precise way to edit DNA, to replace flawed genes with error-free ones.
Certainly, the genetics revolution has made single-mutation diseases easier to identify; there are roughly 7,000, with dozens of new ones discovered each year. But if it’s hard to find a treatment for common genetic diseases, it’s all but impossible for the very rare ones. There’s no incentive for established companies to study them; the potential market is so small that a cure will never be profitable.
Which is where the Wilseys—and the rest of the NGLY1 families—come in. Like a growing number of groups affected by rare genetic diseases, they’re leapfrogging pharmaceutical companies’ incentive structures, funding and organizing their own research in search of a cure. And they’re trying many of the same approaches that Silicon Valley entrepreneurs have used for decades.
At 10:30 on a recent Monday morning, Grace is in Spanish class. The delicate 8-year-old with wavy brown hair twisted back into a ponytail sits in her activity chair—a maneuverable kid-sized wheelchair. Her teacher passes out rectangular pieces of paper, instructing the students to make name tags.
Grace grabs her paper and chews it. Her aide gently takes the paper from Grace’s mouth and puts it on Grace’s desk. The aide produces a plastic baggie of giant-sized crayons shaped like cylindrical blocks; they’re easier for Grace to hold than the standard Crayolas that her public school classmates are using.
The other kids have written their names and are now decorating their name tags.
“Are we allowed to draw zombies for the decorations?” one boy asks, as Grace mouths her crayons through the baggie.
Grace’s aide selects a blue crayon, puts it in Grace’s hand, and closes her hand over Grace’s. She guides Grace’s hand, drawing letters on the paper: “G-R-A-C-E.”
Grace lives with profound mental and physical disabilities. After she was born in 2009, her bewildering list of symptoms—weak muscles, difficulty eating, failure to thrive, liver damage, dry eyes, poor sleep—confounded every doctor she encountered. Grace didn’t toddle until she was three and still needs help using the toilet. She doesn’t speak and, like an infant, still grabs anything within arm’s reach and chews on it.
Her father wants to help her. The grandson of a prominent San Francisco philanthropist and a successful technology executive, Matt Wilsey graduated from Stanford, where he became friends with a fellow undergraduate who would one day be Grace’s godmother: Chelsea Clinton. Wilsey went on to work in the Clinton White House, on George W. Bush’s presidential campaign, and in the Pentagon.
But it was his return to Silicon Valley that really prepared Wilsey for the challenge of his life. He worked in business development for startups, where he built small companies into multimillion-dollar firms. He negotiated a key deal between online retailer Zazzle and Disney, and later cofounded the online payments company Cardspring, where he brokered a pivotal deal with First Data, the largest payment processor in the world. He was chief revenue officer at Cardspring when four-year-old Grace was diagnosed as one of the first patients with NGLY1 deficiency in 2013—and when he learned there was no cure.
At the time, scientists knew that the NGLY1 gene makes a protein called N-glycanase. But they had no idea how mistakes in the NGLY1 gene caused the bewildering array of symptoms seen in Grace and other kids with NGLY1 deficiency.
Wilsey’s experience solving technology problems spurred him to ask scientists, doctors, venture capitalists, and other families what he could do to help Grace. Most advised him to start a foundation—a place to collect money for research that might lead to a cure for NGLY1 deficiency.
As many as 30 percent of families who turn to genetic sequencing receive a diagnosis. But most rare diseases are new to science and medicine, and therefore largely untreatable. More than 250 small foundations are trying to fill this gap by sponsoring rare disease research. They’re funding scientists to make animals with the same genetic defects as their children so they can test potential cures. They’re getting patients’ genomes sequenced and sharing the results with hackers, crowdsourcing analysis of their data from global geeks. They’re making bespoke cancer treatments and starting for-profit businesses to work on finding cures for the diseases that affect them.
“Start a foundation for NGLY1 research, get it up and running, and then move on with your life,” a friend told Wilsey.
Wilsey heeded part of that advice but turned the rest of it on its head.
In 2014, Wilsey left Cardspring just before it was acquired by Twitter and started the Grace Science Foundation to fund research into NGLY1 deficiency. The foundation has committed $7 million to research since then, most of it raised from the Wilseys’ personal network.
Many other families with sick loved ones have started foundations, and some have succeeded. In 1991, for instance, a Texas boy named Ryan Dant was diagnosed with a fatal muscle-wasting disease called mucopolysaccharidosis type 1. His parents raised money to support an academic researcher who was working on a cure for MPS1; a company agreed to develop the drug, which became the first approved treatment for the disease in 2003.
But unlike Dant, Grace had a completely new disease. Nobody was researching it. So Wilsey began cold-calling dozens of scientists, hoping to convince them to take a look at NGLY1 deficiency; if they agreed to meet, Wilsey read up on how their research might help his daughter. Eventually he recruited more than 100 leading scientists, including Nobel Prize-winning biologist Shinya Yamanaka and Carolyn Bertozzi, to figure out what was so important about N-glycanase. He knew that science was unpredictable and so distributed Grace Science’s funding through about 30 grants worth an average of $135,000 apiece.
Two years later, one line of his massively parallel attack paid off.
Bertozzi, a world-leading chemist, studies enzymes that add and remove sugars from other proteins, fine-tuning their activity. N-glycanase does just that, ripping sugars off from other proteins. Our cells are not packed with the white, sweet stuff that you add to your coffee. But the tiny building blocks of molecules similar to table sugar can also attach themselves to proteins inside cells, acting like labels that tell the cell what to do with these proteins.
Scientists thought that N-glycanase’s main role was to help recycle defective proteins, but many other enzymes are also involved in this process. Nobody understood why the loss of N-glycanase had such drastic impacts on NGLY1 kids.
In 2016, Bertozzi had an idea. She thought N-glycanase might be more than just a bit player in the cell’s waste management system, so she decided to check whether it interacts with another protein that turns on the proteasomethe recycling machine within each of our cells.
This protein is nicknamed Nerf, after its abbreviation, Nrf1. But fresh-made Nerf comes with a sugar attached to its end, and as long as that sugar sticks, Nerf doesn’t work. Some other protein has to chop the sugar off to turn on Nerf and activate the cellular recycling service.
Think of Nerf’s sugar like the pin in a grenade: You have to remove the pin—or in this case, the sugar—to explode the grenade and break down faulty proteins.
But nobody knew what protein was pulling the pin out of Nerf. Bertozzi wondered if N-glycanase might be doing that job.
To find out, she first tested cells from mice and humans with and without working copies of the NGLY1 gene. The cells without NGLY1 weren’t able to remove Nerf’s sugar, but those with the enzyme did so easily. If Bertozzi added N-glycanase enzymes to cells without NGLY1, the cells began chopping off Nerf’s sugar just as they were supposed to: solid evidence, she thought, that N-glycanase and Nerf work together. N-glycanase pulls the pin (the sugar) out of the grenade (the Nerf protein) to trigger the explosion (boom).
The finding opened new doors for NGLY1 disease research. It gave scientists the first real clue about how NGLY1 deficiency affects patients’ bodies: by profoundly disabling their ability to degrade cellular junk via the proteasome.
As it turns out, the proteasome is also involved in a whole host of other diseases, such as cancer and brain disorders, that are far more common than NGLY1 deficiency. Wilsey immediately grasped the business implications: He had taken a moon shot, but he’d discovered something that could get him to Mars. Pharmaceutical companies had declined to work on NGLY1 deficiency because they couldn’t make money from a drug for such a rare disease. But Bertozzi had now linked NGLY1 deficiency to cancer and maladies such as Parkinson’s disease, through the proteasome—and cancer drugs are among the most profitable medicines.
Suddenly, Wilsey realized that he could invent a new business model for rare diseases. Work on rare diseases, he could argue, could also enable therapies for more common—and therefore profitable—conditions.
In early 2017, Wilsey put together a slide deck—the same kind he’d used to convince investors to fund his tech startups. Only this time, he wanted to start a biotechnology company focused on curing diseases linked to NGLY1. Others had done this before, such as John Crowley, who started a small biotechnology company that developed the first treatment for Pompe disease, which two of his children have. But few have been able to link their rare diseases to broader medical interests in the way that Wilsey hoped to.
He decided to build a company that makes treatments for both rare and common diseases involving NGLY1. Curing NGLY1 disease would be to this company as search is to Google—the big problem it was trying to solve, its reason for existence. Treating cancer would be like Google’s targeted advertising—the revenue stream that would help the company get there.
But his idea had its skeptics, Wilsey’s friends among them.
One, a biotechnology investor named Kush Parmar, told Wilsey about some major obstacles to developing a treatment for NGLY1 deficiency. Wilsey was thinking of using approaches such as gene therapy to deliver corrected NGLY1 genes into kids, or enzyme replacement therapy, to infuse kids with the N-glycanase enzyme they couldn’t make on their own.
But NGLY1 deficiency seems particularly damaging to cells in the brain and central nervous system, Parmar pointed out—places that are notoriously inaccessible to drugs. It’s hard to cure a disease if you can’t deliver the treatment to the right place.
Other friends warned Wilsey that most biotech startups fail. And even if his did succeed as a company, it might not achieve the goals that he wanted it to. Ken Drazan, president of the cancer diagnostics company Grail, is on the board of directors of Wilsey’s foundation. Drazan warned Wilsey that his company might be pulled away from NGLY1 deficiency. “If you take people’s capital, then you have to be open to wherever that product development takes you,” Drazan said.
But Wilsey did have some things going for him. Biotechnology companies have become interested of late in studying rare diseases—ones like the type of blindness for which the gene therapy was approved last year. If these treatments represent true cures, they can command a very high price.
Still, the newly approved gene therapy for blindness may be used in 6,000 people, 100 times more than could be helped by an NGLY1 deficiency cure. Wilsey asked dozens of biotechnology and pharmaceutical companies if they would work on NGLY1 deficiency. Only one, Takeda, Japan’s largest drug company, agreed to conduct substantial early-stage research on the illness. Others turned him down flat.
If no one else was going to develop a drug to treat NGLY1 deficiency, Wilsey, decided, he might as well try. “We have one shot at this,” he says. “Especially if your science is good enough, why not go for it?”
“Matt was showing classic entrepreneurial tendencies,” says Dan Levy, the vice president for small business at Facebook, who has known Wilsey since they rushed the same Stanford fraternity in the 1990s. “You have to suspend a little bit of disbelief, because everything is stacked against you.”
At 11 am, Grace sits in a classroom with a speech therapist. Though Grace doesn’t speak, she’s learning to use her “talker,” a tablet-sized device with icons that help her communicate. Grace grabs her talker and presses the icons for “play” and “music,” then presses a button to make her talker read the words out loud.
“OK, play music,” her therapist says, starting up a nearby iPad.
Grace watches an Elmo video on the iPad for a few moments, her forehead crinkled in concentration, her huge brown eyes a carbon copy of her dad’s. Then Grace stops the video and searches for another song.
Suddenly, her therapist slides the iPad out of Grace’s reach.
“You want ‘Slippery Fish,’” her therapist says. “I want you to tell me that.”
Grace turns to her talker: “Play music,” she types again.
The therapist attempts one more time to help Grace say more clearly which particular song she wants. Instead, Grace selects the symbols for two new words.
“Feel mad,” Grace’s talker declares.
There’s no denying how frustrating it can be for Grace to rely on other people to do everything for her, and how hard her family works to meet her constant needs.
Matt and Kristen can provide the therapy, equipment, medicines, and around-the-clock supervision that Grace needs to have a stable life. But that is not enough—not for Grace, who wants "Slippery Fish," nor for her parents, who want a cure.
So last summer, Wilsey raised money to bring the Vigeholms and the other NGLY1 families to Palo Alto, where they met with Grace’s doctors and the Grace Science Foundation researchers. One Japanese scientist, Takayuki Kamei, was overjoyed to meet two of the NGLY1 deficiency patients: “I say hello to their cells every morning,” he told their parents.
And because all of these families also want a cure, each also donated blood, skin, spit, stool, and urine to the world’s first NGLY1 deficiency biobank. In four days, scientists collected more NGLY1 deficiency data than had been collected in the entire five years since the disease was discovered. These patient samples, now stored at Stanford University and at Rutgers University, have been divvied up into more than 5,000 individual samples that will be distributed to academic and company researchers who wish to work on NGLY1 deficiency.
That same month, Wilsey closed a seed round of $7 million to start Grace Science LLC. His main backer, a veteran private equity investor, prefers not to be named. Like many in Silicon Valley, he’s recently become attracted to health care by the promise of a so-called “double bottom line”: the potential to both to make money and to do good by saving lives.
Wilsey is chief executive of the company and heavily involved in its scientific strategy. He’s looking for a head scientist with experience in gene therapy and in enzyme replacement therapy, which Mark Dant and John Crowley used to treat their sick children. Gene therapy now seems poised to take off after years of false starts; candidate cures for blood and nervous system disorders are speeding through clinical trials, and companies that use Crispr have raised more than $1 billion.
Wilsey doesn’t know which of these strategies, if any, will save Grace. But he hopes his company will find an NGLY1 deficiency cure within five years. The oldest known NGLY1 deficient patient is in her 20s, but since nobody has been looking for these patients until now, it’s impossible to know how many others—like Bertram—didn’t make it that long.
“We don’t know what Grace’s lifespan is,” Wilsey says. “We’re always waiting for the other shoe to drop.”
But at 3 pm on this one November day, that doesn’t seem to matter.
School’s out, and Grace is seated atop a light chestnut horse named Ned. Five staff members lead Grace through a session of equine therapy. Holding herself upright on Ned’s back helps Grace develop better core strength and coordination.
Grace and Ned walk under a canopy of oak trees. Her face is serene, her usually restless legs still as Ned paces through late-afternoon sunshine. But for a little grace, there may be a cure for her yet.
Crispr Gene Editing Explained
Maybe you've heard of Crispr, the gene editing tool that could forever change life. So what is it and how does it work? Let us explain.
President Donald Trump asked a federal judge to throw out a lawsuit filed by two attorneys general accusing him of profiting from his office, in violation of the U.S. Constitution.
The suit, filed by Maryland Attorney General Brian Frosh and his District of Columbia counterpart, Karl Racine, contends the president’s continued ownership of his global business empire — including the Trump International Hotel in Washington — enables him to make money from foreign and domestic governments, breaching two Constitutional clauses intended to prevent that.
"Plaintiffs’ broad-brush claims effectively assert that the Constitution disqualifies the President from serving as President while maintaining ownership interests in his commercial businesses," government lawyers argued in court papers Friday.
Justice Department lawyers argued the court can’t consider the case because Maryland and the District of Columbia lack legal standing — that they’re unable to claim injuries from Trump’s alleged Constitutional violation that would allow them to sue. The lawyers also said the Constitution doesn’t address presidents’ private business activities unrelated to their government service.
The filing at the federal courthouse in Greenbelt, Maryland — a Washington suburb — is the first formal response to the June lawsuit.
"By accepting benefits from foreign and domestic government actors, he is opening himself up to the type of divided loyalties and undue influence that the Constitution seeks to prevent," Racine said in a statement responding to the court filing. "President Trump must take the same kind of clear, transparent steps that all other presidents in recent history have taken and separate his personal business interests from the official business of the United States.”
The president’s bid for dismissal comes just a day after U.S. Supreme Court Justice Neil Gorsuch, whom Trump nominated earlier this year, delivered a speech to the Fund for American Studies in a crystal chandelier-bedecked conference room at the president’s D.C. hotel, which opened last year.
"Justice Gorsuch speaking to a conservative group in the Trump Hotel, where the president continues to hold a financial stake, is everything that was wrong with his nomination," U.S. Senate Minority Leader Chuck Schumer, a New York Democrat, said in a statement condemning the judge’s appearance.
The Frosh-Racine case is one of a flurry of such suits filed in the first six months of Trump’s presidency as lawmakers and watchdog groups grappled with the implications of a businessman moving directly into the White House without prior government experience and without cutting ties to those businesses.
The attorneys general allege the Constitution’s foreign and domestic emoluments clauses bar presidents from receiving compensation from foreign governments without congressional approval and ban payment from federal and state governments.
“Never before has a president acted with such disregard for this Constitutional prescription,” Racine and Frosh said in their complaint. They’re seeking an order forcing Trump to divest his businesses.
Trump also faces suits from about 200 Democratic members of Congress, led by U.S. Senator Richard Blumenthal of Connecticut and from Citizens for Responsibility and Ethics in Washington. His attorneys asked U.S. judges in Washington and New York to throw out both of those cases earlier this month.
The case is District of Columbia v. Trump, 17-cv-1596, U.S. District Court, District of Maryland (Greenbelt).
Fresh, funny and feminist, Jezebel blazed a trail when it launched in 2007. It forced others to follow but does it still have a place on the internet it helped to create?
Anna Holmes first realized that Jezebel, the online womens magazine she founded in 2007, had become culturally significant when it was parodied on the NBC sitcom 30 Rock.
In a 2011 episode, a blogpost on a fictional website called JoanOfSnark which is shown having a design similar to Jezebels original look charges Liz Lemon with hating women. Explaining JoanOfSnark, Liz Lemon says: Its this really cool feminist website where women talk about how far weve come and which celebrities have the worst beach bodies.
Holmes says she was less concerned with the implicit critique of her website than she was amazed that Jezebel was well-known enough to be fodder for a popular show. I wasnt offended, I was just flattered, she says, sitting at a Brooklyn coffee shop patio on a rainy Sunday.
Its hard to overstate the impact of Jezebel on feminisms modern resurgence, says Jill Filipovic, author of The H-Spot: The Feminist Pursuit of Happiness. By 2011, the website had captured the zeitgeist like no other womens publication of its time.
Perhaps the biggest sign of Jezebels impact is that it no longer stands out. It has been so successful in changing womens media that its once-signature blend of confessional essays, raunchy humor and outrage culture is no longer unique. Conversations that used to take place in Jezebels comments section now occur on Twitter. With the sites 10th anniversary this month, its clear that Jezebel changed our media landscape but its unclear if it still has a place on the internet it helped create.
The campaign involves simple banners promoting the streaming service’s original Twilight Zone-esque dystopian drama, Black Mirror, with a clever nod to its unnerving technology-run-amuck ethos.
“Hello ad block user,” their tagline reads. “You cannot see the ad. But the ad can see you. What’s on the other side of your black mirror?”
The ads seem to be running most frequently on tech-centric news sites (including Mashable), which users with ad blockers tend to favor.
Despite the name, ad blockers are becoming more porous than ever as ad blocking companies look for ways to make money off of their sizable user bases.
AdBlock Plus, the web’s largest such service, runs a whitelist of ads it deems acceptable and less intrusive. Heavily trafficked websites are charged a fee to be part of that list. The company even went so far as to start selling its own ads last month, further stoking tensions between ad blockers and the publishers that rely on ads for their livelihood.
It’s not clear whether these ads were placed through a network, individual contracts or through AdBlock Plus’ new program.
A Netflix spokesperson didn’t immediately return a request for comment.