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Google's Laszlo Bock on Strategies for Hiring and Managing Employees

Google's Laszlo Bock, head of what the company refers to as "people operations," argues that companies ought to invest more science and rigor into how they hire and deal with their employees. He joins us to share insights from his book "Work Rules!" including the best interview questions to ask and how a "nudge," or small signal, can result in large behavioral changes.

PBS NewsHour

Why we’re drawn to fizzy drinks

Gin and tonic. Photo by Nathan Blaney/ Getty Images

Gin and tonic. Photo by Nathan Blaney/ Getty Images

Snap-click, ahh, gulp. It’s a familiar sound at a barbecue, an ingredient in summertime nostalgia. Who doesn’t crave a fizzy drink on a hot summer day?

Indeed, sales of carbonated water have seen a sharp incline over the past half decade, increasing by 56.4 percent from 2009 to 2014, according to the market research firm, Euromonitor International. Sales of La Croix alone, the trendy carbonated water in a can, have tripled to $179 million since 2009, the Washington Post reports.

But why? What’s happening in our mouth when we guzzle fizzy drinks? Why are we drawn to carbonation?

“The main component of carbonation sensation is the pain,” said Paul Wise, a scientist at Monell Chemical Senses Center in Philadelphia. Scientists like Wise have studied the interplay of gas and bubbles on the human taste system.

science-wednesday

The slightly painful quality of the drink — its bite — is thanks to a receptor found on our tongues. This receptor, called TRPA1, detects sour tastes, among other things.

Sour receptors protect us from hazardous chemicals like the hydrogen peroxide found in cleaning supplies — our tongues are designed to taste danger. They also give seltzer its bite. It’s the carbon dioxide in carbonated drinks that triggers these sour receptors.

Carbon dioxide – the bubbles in our beverage – enters the mouth and dissolves into oral tissue. A protein in the mouth, called carbonic anhydrase, converts carbon dioxide into acid. The TRPA1 receptor detects the acid and sends a message to the brain.

The degree to which this receptor is stimulated may determine whether the signal is interpreted as pleasure or pain. Such a theory could explain our varying response to the cinnamon flavor, which also excites TRPA1. We happily chew Big Red gum, but consuming large amounts of cinnamon — known in pop culture as the cinnamon challenge — is painful, and extremely dangerous.

In fact, the body mounts a defense response when many TRPA1 receptors are activated, Wise said.

“At higher levels [of stimulation], in addition to sensation, you’ll get physiological defense responses designed to dilute and clear – so that is increased saliva, coughing, sneezing, tearing and also respiratory reactions.”

Pain sensors that detect harmful gases are also found in your nose. But the skin of the tongue and the mucous in the nose are different as they relate to carbon dioxide, said Bruce Bryant, a scientist also at the Monell Chemical Senses Center.

In the case of the tongue, carbon dioxide has a thick layer of cells to get through before it reaches the receptor. But in the nose, that layer is thin. This is why a belch can burn in our noses — the nasal cavities are more sensitive to the carbon dioxide that gurgles back up.

Which brings us back to the bubbles. What role do the bubbles play in the bite? Researchers tested this by asking people to drink carbonated drinks in a hyperbaric chamber, where controlled atmospheric pressure removes the bubbles, but not the carbon dioxide, from the drink. Without the bubbles, they found, participants still taste the bite.

Not true for mountain climbers who take carbonic anhydrase inhibitors to avoid altitude sickness, which keeps the bubbles, but removes the bite. Such medicine prevents carbon dioxide from becoming an acid and stimulating TRPA1. The adventurers described their victory beverages as dishwater-y, according to a researcher interviewed in this NPR segment. (This taste could be due to more than just the lack of acid, Bryant adds. The medicine “plays havoc with your taste system.)

A close up look at sparkling water. Photo by Foodcollection RF/ Getty Images

A close up look at sparkling water. Photo by Foodcollection RF/ Getty Images

Scientists have also found that bubbles increase the perception of sourness. Bryant and colleagues collected evidence showing that bubbles can enhance the pungency of carbonation. Even when paired with sugary drinks, bubbles can actually decrease a drinker’s perception of sweetness. A study published on July 10 in Neuropsychologia showed that foods with rougher textures are rated as more sour.

But Bryant thinks that seltzer’s success may be thanks to it’s “refreshing” taste, which he defines as “some combination of cooling and clean mouth feel.” Mucins are proteins in the mouth that reduce friction between oral surfaces, like your tongue and teeth. Astringent drinks, like lemonade or tannin-heavy wine, wash out mucins and give that clean-mouth feeling.

And just like all cold beverages, chilled seltzer stimulates nerves that detect cooler temperatures. “The cooling may interact to reduce or change the quality of the pungency that you get out of carbon dioxide,” Bryant said. From personal experience, we probably all agree that seltzer cans left in the sun are less refreshing on a hot day than the chilled version.

By the way, only a small amount of the fizz released from a bottled beverage makes it into the stomach. Despite concerns that have been raised, research shows that carbon dioxide doesn’t cause gastroesophageal reflux disease, gastrointestinal cancer or bone disease. And while sugars and other acids found in sodas can contribute to tooth decay, carbon dioxide alone doesn’t have a significant impact on oral health.

Seltzer scientists agree that our love for carbonation and other pain-inducing foods like chili peppers is learned.

“A lot of kids take a while to develop a taste; I saw it with my own kids,” Wise said.

And interestingly, animals in the lab reject carbonated drinks, Bryant said.

Children develop strong flavor associations. Consider spicy desserts: Habanero jam, kiwi salsa, or ghost pepper brownies. Pair the spice of a hot chili with a pleasurable carbohydrate like sugar, and over time you develop a preference for the painful taste.

This may be true for seltzer and soda too. Today’s carbonated soda does pack a lot of sugar — just over ten sugar cubes. And many of us start with soda and graduate to seltzer water.

But would we love seltzer if we’d never loved soda?

As yesterday’s soda drinkers enter today’s low-sugar diet, they are increasingly turning to seltzer – a calorie-free drink with a sensation that reminds them of the sugar. Some food for thought: if our passion for bubbles comes from a previous love for sodas, then will new, health-conscious generations avoid soda and never learn to love seltzer?

The post Why we’re drawn to fizzy drinks appeared first on PBS NewsHour.

What makes this monkey red in the face?

Red Uakari (Cacajao calvus ucayalii) sleeping showing pale eyelids. Photo by Mark Bowler/via Getty Images

Red Uakari (Cacajao calvus ucayalii) sleeping showing pale eyelids. Photo by Mark Bowler/via Getty Images

Why the red face, bald uakari monkey? Are you hot? Are you embarrassed that your Amazonian treemate isn’t wearing any clothes? Or are you sick?

A new study in Royal Society Open Science opts for choice #3. By scanning the skin architecture of bald uakari monkeys, the scientists argue that the primates’ red faces serve as an indicator of health status.

There are a couple of ways to change skin color. The first involves melanin, a natural colored pigment made by the body. This pigment sits in microscopic pouches in the skin, called granules, and helps protect against damaging UV rays. Mild sun exposure causes the skin to produce more of these melanin granules as a defensive shield. The result is a tan.

Blood flow is a second route for darkening skin. When extra blood cells course into the skin, it turns red. Such is the case when people get sunburns. Excessive exposure to the sun’s UV rays causes damage and inflammation in the skin, which widens vessels and ups the blood flow. The same happens when you blush after being embarrassed, though the trigger in that case is a hormone — adrenaline — rather than sun rays. The intensity of the redness depends on how much oxygen is carried by the blood.

To explore which option accounts for red faces in Amazonian primates, an international group of veterinarians and scientists collected skin specimens from deceased monkeys in the jungles of Peru. The primates had either died of natural of causes or been hunted for food by the local indigenous people. “No animals were killed specifically for the research, and hunters were never paid to collect samples,” the scientists write.

In the end, the team compared skin specimens from two red uakari monkeys (Cacajao calvus ucayalii) against two Poeppig’s woolly monkeys (Lagothrix poepigii), two monk sakis (Pithecia monachus), two brown capuchin monkeys (Sapajus macrocephalus) and one howler monkey (Alouatta seniculus).

Facial regions studied in the bald uakari monkey and other Peruvian neotropical primates: (a) frontal (forehead) region,
         (b) parietal region, (c) temporal region, (d) zygomatic (cheek) region and (e) mandible (mouth) region. Skin samples were
         dissected from monkeys that either died of natural causes or were collected by subsistence hunters. Courtesy of Mayor P et
         al., R. Soc. open sci., 2015.

Facial regions studied in the bald uakari monkey and other Peruvian neotropical primates: (a) frontal (forehead) region, (b) parietal region, (c) temporal region, (d) zygomatic (cheek) region and (e) mandible (mouth) region. Skin samples were dissected from monkeys that either died of natural causes or were collected by subsistence hunters. Courtesy of Mayor P et al., R. Soc. open sci., 2015.

The researchers found that the red faces of uakari monkeys are caused by a higher density of blood vessels located just underneath the surface of the skin. This trait is especially true for the uakari monkey’s cheeks and forehead, which have four times as many blood vessels per square millimeter as primates without red faces. The facial skin of uakari monkeys is also 60 to 70 percent thinner than other monkeys, meaning when their blood vessels are full, the redness seems more pronounced versus regular primates.

With regards to melanin, there is none. The researchers didn’t spot any melanin granules in the facial skin of red uakari monkeys.

The team argues that if facial hue is tied to blood flow, then it might serve as a beacon for when a monkey is sick with blood parasites. As evidence, they reference a study that showed uakari faces turn white when they’re infected with the South American germ Trypanosoma cruzi. Another theory suggests that the red faces help the monkeys choose a mate, as blushing in mammals is tied to sexual hormones like estrogen and testosterone.

It will take more research to explain why these faces are red and if subtle changes in hue are cues for certain behaviors. But for now, we know the how.

The post What makes this monkey red in the face? appeared first on PBS NewsHour.

How do ants synchronize to move really big stuff?

A foraging longhorn crazy ant often encounters food items that are considerably larger than herself (a Cheerio in this
         case). A new study explains how the ant groups keep direction while moving "giant" things. Photo by Asaf Gal and
         Ofer Feinerman of the Weizmann Institute of Science

A foraging longhorn crazy ant often encounters food items that are considerably larger than herself (a Cheerio in this case). A new study explains how the ant groups keep direction while moving “giant” things. Photo by Asaf Gal and Ofer Feinerman of the Weizmann Institute of Science

Two weeks ago, Brooke Borel witnessed a modern wonder in Brooklyn. She gaped, transfixed as a group of ants hauled a piece of dog food up a vertical wall. How did they not only have the brute strength to accomplish this feat, but also coordinate their movements to carry their prize?

Today, a new study in Nature Communications offers an answer. By videotaping longhorn crazy ants (Paratrechina longicornis) as the buggers carry large food, like Cheerios, a team of physicists outlines the precise behaviors needed to haul large objects to the nest.

Ants tug a piece a dog food up a vertical wall in science writer Brooke Borel's apartment in Brooklyn. Photo by Brooke
         Borel

Ants tug a piece a dog food up a vertical wall in science writer Brooke Borel‘s apartment in Brooklyn. Photo by Brooke Borel

From an evolutionary perspective, group carrying has advantages and disadvantages. On the one hand, the ants can move bigger pieces of food as a team, but then an individual can’t react as quickly to danger, such as an approaching predator.

That tradeoff might explain why group carrying is fairly rare in nature. Outside of a few social spiders, dung beetles and baby rats, humans and ants are the only animals known to do it. But when you and your pals move really big furniture, you have the luxury of being able to swivel your head and talk to each other in order to work together. In contrast, an ant’s jaws are locked onto whatever it’s carrying and its antennae, which it uses to “see and smell”, are blocked too. Plus, due to how their bodies are built, ants can only pull and lift objects; they can’t push.

As physicist Ofer Feinerman and his colleagues at Weizmann Institute of Science in Israel explained in their study, there are a few ways for ants to carry a Cheerio or artificial large object over a flat, 3-foot journey to their nest without getting stuck in a tug of war. (Artificial objects were dipped overnight in plastic bags of cat food to lure the ants).

First, a majority of the ants could collect along the leading edge and pull, while a couple of stragglers lift on the other side. The second option is the group could appoint a captain. This leader would be attached to the cereal for the whole trip and lead the pack home.

A group of longhorn crazy ants cooperate to transfer an item much too heavy for each of them to move alone. Photo by
         Ehud Fonio and Ofer Feinerman

A group of longhorn crazy ants cooperate to transfer an item much too heavy for each of them to move alone. Photo by Ehud Fonio and Ofer Feinerman

The team’s video didn’t observe either of these scenarios, however. For small objects, ants might congregate along the leading edge and do some dragging, but for the larger food, the bugs were evenly distributed around the load. Their “captain ant” hypothesis went out the window, too. For most of the 98 journeys that the team recorded, they did spot one ant that clung to the object for the whole journey, but its orientation rarely matched the direction of team’s movement.

“We therefore conclude that the collective movement does not arise neither from a wisdom-of-the-crowds type averaging over all opinions nor by the continuous leadership of any single individual,”Feinerman and his colleagues wrote.

Instead, the scientists learned that the newest members of the group guide the mission. Whenever a new ant joins the group, it bites onto the object and gives a little tug, typically in the direction of the nest. This behavior repeats — new ant, fresh tug — and as this happens, the ants still attached to the load seem to relent and move in the direction of the fresh tug. That makes sense because the newest members should have a fresh, informed perspective on where the group needs to go, the team surmised. Informed ants lead the bunch.

There should be an embedded item here. Please visit the original post to view it.

A group of longhorn crazy ants are cooperatively transporting a food item to their nest. The movie was automatically analyzed to track the object, the carrying ants (yellow numbers), and the free ants (white numbers). Video by Ehud Fonio, Aviram Gelblum and Ofer Feinerman

By making a computer model of the movements and the forces applied in this collective behavior, the team learned that ants were more likely to relent as their load grew in size. In other words, bigger objects required more ants and greater conformity.

The scientists also resolved that the ideal size for a load is 1 centimeter in diameter or about four times the ant’s body length. However, the team also tested if 100 ants could carry objects as large as 8 centimeters in diameter, which is must larger than anything they carry in nature. The scientist observed that the ants struggled to guide objects around obstacles once they were bigger than 4 centimeters wide. This result means that the advantages of groupthink have their limits.

A group of longhorn crazy ants cooperate to transfer an item much too heavy for each of them to move alone. Here, the
         ants (about 120 of them) have been tricked into transferring an object that is much larger than anything they would naturally
         carry. Photo by Ehud Fonio and Ofer Feinerman

A group of longhorn crazy ants cooperate to transfer an item much too heavy for each of them to move alone. Here, the ants (about 120 of them) have been tricked into transferring an object that is much larger than anything they would naturally carry. Photo by Ehud Fonio and Ofer Feinerman

There should be an embedded item here. Please visit the original post to view it.

A group of longhorn crazy ants cooperate to transfer an item much too heavy for each of them to move alone. Here, the ants have been tricked into transferring an object that is much larger than anything they would naturally carry. Video by Ehud Fonio and Ofer Feinerman

The post How do ants synchronize to move really big stuff? appeared first on PBS NewsHour.

This chicken vaccine makes its virus more dangerous

Marek's disease virus is severely lethal for chickens, especially baby chicks. A new study shows the vaccines for
         the disease give the virus a boost. Photo by Christopher Kimmel/Getty Images.

Marek’s disease virus is fatal for industrialized chickens, especially baby chicks. A new study shows the vaccines for Marek’s disease give the virus an evolutionary boost. Photo by Christopher Kimmel/Getty Images

The deadliest strains of viruses often take care of themselves — they flare up and then die out. This is because they are so good at destroying cells and causing illness that they ultimately kill their host before they have time to spread.

But a chicken virus that represents one of the deadliest germs in history breaks from this conventional wisdom, thanks to an inadvertent effect from a vaccine. Chickens vaccinated against Marek’s disease rarely get sick. But the vaccine does not prevent them from spreading Marek’s to unvaccinated birds.

“With the hottest strains, every unvaccinated bird dies within 10 days. There is no human virus that is that hot. Ebola, for example, doesn’t kill everything in 10 days.”

In fact, rather than stop fowl from spreading the virus, the vaccine allows the disease to spread faster and longer than it normally would, a new study finds. The scientists now believe that this vaccine has helped this chicken virus become uniquely virulent. (Note: it only harms fowl). The study was published on Monday in the journal PLOS Biology.

This is the first time that this virus-boosting phenomenon, known as the imperfect vaccine hypothesis, has been observed experimentally.

The reason this is a problem for Marek’s disease is because the vaccine is “leaky.” A leaky vaccine is one that keeps a microbe from doing serious harm to its host, but doesn’t stop the disease from replicating and spreading to another individual. On the other hand, a “perfect” vaccine is one that sets up lifelong immunity that never wanes and blocks both infection and transmission.

It’s important to note childhood vaccines for polio, measles, mumps, rubella and smallpox aren’t leaky; they are considered “perfect” vaccines. As such, they are in no way in danger of falling prey to this phenomenon.

But the results do raise the questions for some human vaccines that are leaky – such as malaria, and other agricultural vaccines, such as the one being used against avian influenza, or bird flu.

Marek’s disease has plagued the chicken industry, it causes $2 billion in losses annually for fowl farmers across the globe. The virus attacks the brain, spawns tumors in the birds and comes in different varieties or “strains”, which are classified as “hot” or “cold” based on their brutality.

Andrew Read, who co-led the study, had heard about the severe effects of the hottest Marek’s strains before his lab started studying the disease about a decade ago, but even he was surprised when he finally saw the virus in action.

“With the hottest strains, every unvaccinated bird dies within 10 days. There is no human virus that is that hot. Ebola, for example, doesn’t kill everything in 10 days,” said Read, who is an evolutionary biologist at Penn State University.

Clip from the New York Times announcing the a vaccine for Marek's disease, February 30, 1970. Photo by

Clip from the New York Times announcing the a vaccine for Marek’s disease, February 30, 1970. Photo by The New York Times.

In recent years, experts have wondered if leaky vaccines were to blame for the emergence of these hot strains. The 1970s introduction of the Marek’s disease immunizations for baby chicks kept the poultry industry from collapse, but people soon learned that vaccinated birds were catching “the bug” without subsequently dying. Then, over the last half century, symptoms for Marek’s worsened. Paralysis was more permanent; brains more quickly turned to mush.

“People suspected the vaccine, but the problem was that it was never shown before experimentally,” said virologist Klaus Osterrieder of the Free University of Berlin, who wasn’t involved in the study. “The field has talked about these types of experiments for a very long time, and I’m really glad to see the work finally done.”

Read’s group started their investigation by exposing vaccinated and unvaccinated Rhode Island Red chickens to one of five Marek’s disease strains that ranged from hot to cold. The hottest strains killed every unvaccinated bird within 10 days, and the team noticed that barely any virus was shed from the feathers of the chickens during that time. (The virus spreads via contaminated dust in chicken coops). In contrast, vaccination extended the lifespan of birds exposed to the hottest strains, with 80 percent living longer than two months. But the vaccinated chickens were transmitting the virus, shedding 10,000 times more virus than an unvaccinated bird.

“Previously, a hot strain was so nasty, it wiped itself out. Now, you keep its host alive with a vaccine, then it can transmit and spread in the world,” Read said. “So it’s got an evolutionary future, which it didn’t have before.”

But does this evolutionary future breed more dangerous viruses?

The close quarters of industrialized chicken farms are breeding grounds for Marek's disease. Vaccines keep the disease
         in check, but don't stop infections or transmission. Photo by Edwin Remsberg/via Getty Images.

The close quarters of industrialized chicken farms are breeding grounds for Marek’s disease. Vaccines keep the disease in check, but don’t stop infections or transmission. Photo by Edwin Remsberg/via Getty Images

This study argues yes. In a second experiment, unvaccinated and vaccinated chickens were infected with one of the five Marek’s disease strains, and then put into a second arena with a second set of unimmunized birds, known as sentinels. In particular, the team was interested in a middle-of-the-road strain called “595” and whether it would become hotter.

It did. The virus spread to sentinel birds nine days faster if it came from a vaccinated chicken versus an unvaccinated one. In addition, sentinels died faster when exposed to vaccinated chickens versus unvaccinated chickens.

“One way to look at that experiment is that shows vaccinating birds kills unvaccinated birds. The vaccination of one group of birds leads to the transmission of a virus so hot that it kills the other birds, said Read said. “If you vaccinate the mothers, the same thing happens. The offspring are protected by the maternal antibodies of the mother and that allows the virus in the chicks to transmit before they kill the host. So they transmit and kill the other individuals.”

This trend persisted when the team tried the experiment in a setting meant to simulate a commercial chicken farm.

“At the moment, the vaccines are working well enough, and you can vaccinate every bird,” Read said. “There are 20 billion birds on the planet at any time; the vast majority are Marek’s vaccinated.”

However, both Read and Osterrieder worry about what might happen if Marek’s continues to change or if its vaccines were to fail.

“If the virus continues to evolve, then it could be pretty devastating for the chicken industry, which is suffering quite a bit right now in the U.S. with the influenza virus,” Osterrieder said.

Like Marek’s vaccines, vaccines for avian influenza are leaky. For this reason, they’re banned from agricultural use in the U.S. and Europe. When bird flu breaks out in these western chicken populations, farmers must cull their herds. However, Southeast Asia uses these leaky vaccines, raising the possibility for virus evolution akin to what’s happened with Marek’s disease.

“In those situations, they’re creating the conditions where super hot avian influenza could emerge,” Read said. “Then the issues become what does that mean when it spills over into other flocks, into wildlife or into humans. Avian flu is the setting to watch for evolutionary problems down the line.”

Bird flu isn’t alone. The world’s first vaccine for malaria, which was recently approved by European Medicines Agency, is also leaky. Vaccines for HPV and whooping cough can leak too; however it is unknown if this scenario creates more dangerous viruses for each of these diseases.

“Our concern here, primarily and foremost, is whether this is going to happen with any of the vaccines that we give to people,” said molecular biology James Bull of the University of Texas Austin, who specializes in the evolution of viruses and bacteria. “But there is a lot we don’t know about how the scenario with Marek’s could apply to newer human vaccines.”

To test the imperfect vaccine hypothesis in humans, you would need monitor the vaccine response for either a large or isolated population for a long time. Doing this would allow a researcher to gauge how the vaccine interacts with the virus and if that relationship is evolving. Does the vaccine merely reduce symptoms, or does it also keep patients from getting infected and transmitting the virus?

Clinical trials for Ebola might be an arena for keeping an eye on this trend.

“It’s important that we pay close attention to the Ebola vaccine in the ongoing trials. We want to know if a person who has been vaccinated and comes in contact with Ebola, whether there is any virus replication in that person and whether that means there could be onward transmission,” Read said. “If those are leaky in humans, it would be potentially very disadvantageous as it could help establish an endemic.”

However, in the end, Read said, leakiness isn’t a strike against these vaccines, but more motivation to conduct surveillance of their effects after they exit clinical trials and enter the broader population. Take Marek’s disease for example.

“Even if this evolution happens, you don’t want to be an unvaccinated chicken,” Read said. “Food chain security and everything rests on vaccines. They are the most successful and cheapest public health interventions that we’ve ever had. We just need to consider the evolutionary consequences of these ones with leaky transmission.”

The post This chicken vaccine makes its virus more dangerous appeared first on PBS NewsHour.