Month: October 2016

As more of our work, purchases, and interactions take place online, the state of digital privacy becomes a growing concern. Web users worried about how their personal data is being used will soon be able to rest a little easier, thanks to new rules passed by the Federal Communications Commission (FCC) on October 27. As The Washington Post reports, the FCC imposed unprecedented regulations on internet providers this Thursday in a three-to-two vote.

The new rules forbid providers from using or sharing personal user data with third parties like advertisers unless explicit consent is given. This covers location data, search histories, and information mined from emails. If users agree to being tracked online, providers will be required to tell them what information is being collected and for what purpose. Users can expect to see updated privacy policies from websites, as well as possible incentives like discounts to persuade users to hand over the rights to their data.

The decision is troubling news for big companies like Verizon and AT&T, who might push back against regulations with legal action. But in a time when more and more web giants are relaxing their privacy standards, many are hailing the move as a victory for web users. FCC Chairman Tom Wheeler, the commissioner who led the initiative, told The Washington Post, “It’s the consumers’ information. How it is used should be the consumers’ choice, not the choice of some corporate algorithm.”

The new laws will only affect internet service providers (ISPs): Individual companies like Facebook and Google, which have both come under fire for their handling of user data, are free to proceed as usual. This discrepancy has been one of the major criticisms from the law’s opponents, but Wheeler hasn’t expressed interest in tackling that part of the web anytime soon.

[h/t The Washington Post]

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The body has a tendency to sprout hair in many strange places: Ears, noses, knuckles. For those afflicted with a rare type of tumor dubbed a limbal dermoid, it can even grow out of an eyeball.

But few follicles cause as much stress as a synophrys, the medical term for the unibrow—hair in the center of the forehead that creates the impression of a single, unified, stern-looking eyebrow.

Waxing, laser treatments, or just old-fashioned shaving can alleviate symptoms. But if you’re curious what actually causes it, you’ll need to turn to your DNA. According to a recent study published in Nature Communications, an investigation of more than 6000 subjects yielded specific genes that were associated with hair density, greying, curling, and brow fusion. Unibrows were found in people (specifically, men) with the gene dubbed PAX3. The paper’s authors theorized that once a feature has been isolated to a specific gene, the cosmetics industry may one day come up with a product that can inhibit or alter its behavior.

That assumes you would want to. While unibrows aren’t the style of choice in the United States, the Asian nation of Tajikistan considers it to be a trademark of beauty. Women lacking in PAX3 use a green herb called usma to fake it, creating a solid line of brow.   

Most research centers don’t allow smoking in the lab, but the Wyss Institute at Harvard University is a little different. There, researchers have built a device that can smoke 10 cigarettes at a time, as STAT reports.

The smoking machine, described in a recent paper in Cell Systems, is helping advance research on the ways in which smoking and vaping affect lung cells, with a focus on chronic obstructive pulmonary disease, which is most often caused by smoking. The machine can “breathe” in and out with a respirator, mimicking the way people take in air and smoke at the same time. It’s lined with a chip containing the cells from the lung’s smallest passageways, bronchioles, with mucus and cilia (hair-like projections that move liquids and particles), as found in a real lung.

In this study, the researchers lined the “smoking airway-on-a-chip” with diseased lung cells and healthy lung cells. They were able to identify 147 genes whose expression differed based on their disease status. In another test, they used vapor from e-cigarettes in the machine, showing that vaping changed the way the cilia moved in healthy lung cells.

The smoking machine likely won’t replace animal lung studies entirely, but does provide a convenient way to test smoking’s effects on human lung cells. 

[h/t STAT] 

All images courtesy Benam et al., Cell Systems (2016)

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Some of the most powerful human experiences are universal. Love. Heartbreak. Elation. Hating acne. The microscopic jerk known as Propionibacterium acnes wreaks havoc on our skin, makes middle school harder, and can cause pain and scarring. Now scientists say we’re one step closer to understanding what makes acne so devious—and how we might conquer it. They published their findings in the journal Science Immunology.

Acne breakouts are the result of a perfect storm of disgusting conditions near the surface of your skin. Natural oils and dead cells build up around your hair follicles, creating the ideal environment for bacteria to breed. The resulting infection sets off your immune system, which leads to inflammation, redness, and those oh-so-delightful pustules on your face, neck, chest, back, or shoulders.

We knew all this already. What we didn’t know was how P. acnes, which ordinarily lives harmlessly on the skin, could multiply out of control—or how its little fortresses in your follicles send your immune system into such a panic.

Previous studies on the bacteria in the human gut have found that certain bacteria produce chemicals called short-chain fatty acids (SCFAs). These acids then block the action of an immune compound called histone deacetylase (HDAC). Suppressed HDAC can then lead to immune trouble and, from there, inflammation.

Dermatology and biochemists at the University of California, San Diego were curious to see if the same patterns would play out on and inside our skin. First, they simulated the greasy skin experience by culturing acne bacteria in Petri dishes full of blood cells or oil-producing skin cells. They ensured that the environment in the dish was smothering, starved of oxygen like the inside of a clogged follicle. Then they let it fester.

Once they had a good SCFA stew going, they ran the cultures through an RNA sequencer to see how the bacteria and cells were performing. They also applied SCFAs both on and just under the skin of lab mice to see how skin layers might react.

The team found that, as with gut cells, the skin cells could be goaded into inflammation by acne’s SCFA bullies. The same pattern bore out for the mice—but only on the topmost layer of keratinocytes, the most common type of epidermal cells. Exposing lower skin layers to acne and SCFA actually activated those cells’ immune systems, making it easier for them to fight off infection.

Adam Friedman teaches and researches dermatology at the George Washington University School of Medicine. He was unaffiliated with the study but praised the findings, telling mental_floss that they “unveil a new understanding of how P. acnes contributes to the pathogenesis of acne, but also give us more insight (and also much more work to do) with respect to the way the bacteria on our skin can change how skin works at the genetic level.”

The research goes well beyond skin problems, he says, and has “huge implications for microbiome research,” because it highlights how “our many tiny friends who live on our skin have the ability to modify how we work, which has broader implications for other inflammatory diseases.”
 
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