catastrophic

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there is a drastic need to use digital tools to preserve and grow India’s endangered languages

And that can be bad for the health of habitats.

This kind of uncertainty is an important part of any study.

Thinking about biomass can be especially useful when comparing species of different sizes.

Yet they are hardly unimportant.

The movie takes this idea and runs with it. If you learn a new language, your brain gets rewired, we are told.

Some supporters of linguistic relativity, which is another name for the Sapir-Whorf hypothesis, think that the cognitive benefits of language helped spur its evolution. This is relevant to the movie, as the fate of humanity, and possibly of the aliens, depends on us understanding their language

This is our introduction to the Sapir-Whorf hypothesis, which holds that a language shapes the way we think. In the 1940s, Edward Sapir and Benjamin Whorf proposed that the structure of a language determines, or at least influences, how we perceive and experience the world. The theory has been controversial, but there is now some support for it.

The Nicaraguan signers may well reveal more ways in which language fundamentally affects thought, for other aspects of the language besides spatial locations became more complex over time. These include ways of signifying mental states, and Pyers has already shown that as these became more sophisticated, so did the signers’ abilities to understand the fact that other people can hold false beliefs. Meanwhile, Ann Senghas and Molly Flaherty, who worked on the current study, are looking at how the emergence of a counting system in NSL affected the numerical skills of the signers.

This is a subtly different idea than the one espoused by the Sapir-Whorf hypothesis, which suggests that different languages influence how speakers think about their world. By contrast, Pyers’ results focus “on those aspects of human cognition that are dependent on acquiring a language, any language”. She says that the room tasks tap into a set of mental skills that “crucially depends on language and that this relationship between language and spatial cognition should hold true for speakers of all languages”.

This is a fascinating result, especially since the first group of adults were older and had been signing for a longer time. It’s clear evidence that our spatial reasoning skills depend, to an extent, on consistent spatial language. If we lack the right words, our mental abilities are limited in a way that extra life experience can’t fully compensate for.

Pyers explains, “The first-cohort signers find these tasks challenging because they do not have the language to encode the relevant aspects of the environment that would help them solve the spatial problem.” She added, “[They] did not have a consistent linguistic means to encode ‘left of’.”

The first group of NSL signers were very different. They were more accurate, suggesting that their experience and maturity does at least count for something. Their mistakes are evenly distributed around the three other corners, suggesting that they use neither the landmark nor the room’s geometry to help them. And they took a long time over the test and said that they found it very difficult. They were aware of their own uncertainty, as adults often are, but they simply didn’t have a reliable mental map of the room and its hidden token.

By comparing the first group of NSL signers to typical children, Pyers also learned something about what’s going on in their heads. Children find the task easy and answer quickly but they often make mistakes. They’ll orient themselves to the geometry of the room, using the long and short walls to tell them where the token is. But they tend to ignore the red wall landmark so when they make mistakes, they usually go for the corner diagonally opposite to the correct one.

In both tests, the second group of adults (who learned the more advanced form of NSL) outperformed the first group. Even though their memories and ability to understand the tasks were just as good, the expanded vocabulary of geographical gestures that they learned as children also gave them better spatial abilities well into adulthood.

Pyers compared the abilities of people from both groups, now fully grown adults, in two spatial tests. First, she led them into a small room with a single red wall. She hid a token in one corner of the room, blindfolded the children and spun them around until they lost their bearings. When she removed the blindfold, the children had to say where the token was. The second test, like the first, involved hiding a token in the corner of a room, but this time the room was a tabletop model that was rotated while the children were blindfolded.

But NSL hasn’t quite got to that stage yet. In the first version developed in the 1970s, the children hadn’t settled on a consistent way of indicating left and right, and the locations of objects in their conversations are fairly ambiguous. The second group of children to expand NSL in the 1980s had more specific conventions for position.

But NSL cuts through both of these problems. Here is a language that was learned by successive waves of children whose mental skills were relatively mature, who all came from the same culture, and who all learned the language at the same age.

By studying children who learned NSL at various stages of its development, Pyers has shown that the vocabulary they pick up affects the way they think. Specifically, those who learned NSL before it developed specific gestures for left and right perform more poorly on a spatial awareness test than children who grew up knowing how to sign those terms.

And in a new study led by Jennie Pyers from Wellesley College, it even tells us how language shapes our thought.

The mutation changes an amino acid in a protein that Zika instructs cells to make. That protein is called prM. It helps the virus mature within infected cells. It also helps them get out of those cells to infect others.

Brain cells from different people vary in their susceptibility to Zika infections, says Scott Weaver. He’s an infectious-disease researcher. Although he also works at the University of Texas Medical Branch, he was not part of Shi’s team. Weaver says scientists need to do more work. They should study cells from more people to see how the different versions of virus affect them. The scientists also should probe Zika’s effects in nonhuman primates. If they respond similarly, that might confirm that this mutation is really behind microcephaly.

The change in prM probably isn’t the whole reason Zika may cause smaller brains, Shi says. The Cambodian strain also led to the death of a few brain cells. But it may not kill enough to cause the birth defect. Shi and his colleagues believe other changes in the virus exaggerate its risks. In May, for instance, his team described another mutation seen in the epidemic strains. It makes Zika dangerous in a different way. It makes it easier for virus to infect mosquitoes.

“That’s pretty convincing evidence that [that mutation] at least plays some role in what we’re seeing now,” says Anthony Fauci.

A strain with one of the mutations seen in the epidemic version of the virus killed more brain cells in fetal mice than the earlier, Cambodian strain did. This mutant virus also attacked and killed human brain cells that were grown in lab dishes.

Researchers then made seven versions of the Cambodian virus. Each of these lab-made types contained one — and only one — of the different gene versions that had been seen in the epidemic strains. The team then infected the brains of fetal mice with these tweaked versions of the Cambodian strain.

The researchers compared a strain of Zika that came from a patient in Cambodia in 2010 to three other strains. Those others came from patients in 2015 or 2016 who had become infected in South America (Venezuela), on a South Pacific island (Samoa) and on a Caribbean island (Martinique). The team found each of these three strains from the recent epidemic shared seven genetic differences from the Cambodian virus.

Those scientists calculated that the mutation arose around May 2013.

The mutation changed just one amino acid in a protein that the gene instructs a cell to make. That altered protein helps the Zika virus kill brain cells more easily. It also may increase the risk of a birth defect called microcephaly (My-kroh-SEFF-uh-lee). Babies born with this condition have heads and brains that are abnormally small.

A single genetic change — or mutation — made the Zika virus far more dangerous, a new study suggests. That change upped the ability of the virus to kill nerve cells in the brain of a developing baby.

Amino-acid changes needed to protect the frogs from this toxin seem to have evolved three separate times in poison frogs, Tarvin says. Three different lines of the animals are immune to the poison. All of them got that immunity by flipping the same switch. But the extra changes that allowed them to still respond normally to acetylcholine differed in the three groups.

To see which change mattered most, they worked with the gene from humans that make that receptor. (Humans aren’t resistant to epibatidine.) They put those genes into frog eggs. Then they modified those genes. This involved replacing select amino acids in the human code with substitutions found in poison frogs. That let them home in on a single amino-acid change that protected the receptor from epibatidine.

It’s “cool”, Brodie says. “These other switches weren't identical,” he notes, yet achieved the same benefit.

The amino-acid recipe for the receptor protein differed elsewhere, too. And those extra changes appear to have compensated for any effects of the anti-toxin changes, the researchers found. The result is a protein that won’t let the toxin bind, yet still responds normally to acetylcholine.

Yet the frogs seemed fine.

The amino acid recipe of those receptors differed between poison frog species that are resistant to epibatidine and close relatives that aren’t.

To find out why, Tarvin and her colleagues focused on the amino acids that the frogs’ bodies used to build those brain proteins. Such proteins are known as acetylcholine receptors.

The frogs have managed to sidestep that potentially damaging side effect, however. It required evolving some additional genetic tweaks.

A new study shows that for some frogs, evolving a way to make and use this defensive weapon came with a price.

But it's simply not true that Eskimos have an extraordinary number of words for snow.

In other words, the influence of language isn't so much on what we can think about, or even what we do think about, but rather on how we break up reality into categories and label them. And in this, our language and our thoughts are probably both greatly influenced by our culture.

So our language doesn't force us to see only what it gives us words for, but it can affect how we put things into groups.

Yes.

Much of the time, yes. But not always.

But this doesn't necessarily mean that our language has forced a certain view of time on us; it could also be that our view of time is reflected in our language, or that the way we deal with time in our culture is reflected in both our language and our thoughts. It seems likely that language, thought, and culture form three strands of a braid, with each one affecting the others.

Whorf believed that because of this difference, Hopi speakers and English speakers think about events differently, with Hopi speakers focusing more on the source of the information and English speakers focusing more on the time of the event.

Most likely, the culture, the thought habits, and the language have all grown up together.

Part of the problem is that there is more involved than just language and thought; there is also culture.

What we have learned is that the answer to this question is complicated.

Whorf claimed that speakers of Hopi and speakers of English see the world differently because of differences in their language.

That cannot continue forever, and measures need to be explored to boost renewable energy through more efficient investment. The most efficient use possible of the transmission network’s capacity will be essential.

The issue highlights the need for more efficient use of the transmission network in order to expand the use of power from renewable sources.

To significantly boost the power supply from renewable sources — as the draft of the government’s new Basic Energy Plan advocates — both the government and the power industry need to maximize efficient use of the transmission network.

This should be reviewed.

The government and the power industry should keep exploring concrete steps to increase the use of renewable energy in Japan.

The obvious challenge for turning renewable energy into a major source of power supply will be to transform it into a competitive business even without the support of the FIT system.

To realize the idea of renewables as a major source of power, the basic plan should be followed up by more concrete programs to put this agenda into actual policy steps.

In fact, the new plan keeps much of the substance of the current plan intact — and fails to send a clear-cut message as to whether or how the government wants to change the nation’s energy supply structure. Still, it lays out the agenda for what’s needed to expand power generation through renewable sources — in which Japan still lags far behind many other industrialized economies.

But it falls short of setting new targets for boosting the share of renewable sources in the nation’s electricity generation — as the 2030 energy mix targets that accompanied the current energy plan set in 2014 are kept unchanged.

The new study is just “the beginning of the story,” Dunn says. He’s excited that researchers are finally taking notice of these microbes. In the past, scientists hadn’t seen archaea on people for a very simple reason: They weren’t looking. They’d go to hot springs or frozen lakes to search for them. As it turns out, they needn’t have looked farther than their own bodies.

Ecologist Rob Dunn, who was not involved in the study, is not too concerned. At North Carolina State University in Raleigh, he studies many species, from ants to microbes. Five years ago, he turned up archaea in human belly buttons. To him, “they're like the teddy bears of the single-celled world.”

One possible explanation is that the skin changes during puberty. That’s when many teens get zits. Those changes also may make the skin less inviting for archaea.

For their new study, the researchers examined samples from another 51 people, all in Germany. Again, all had archaea, but amounts varied. Those under age 12 had five to eight times more archaea on their skin than did teens and adults. So did people over age 60. In any age group, people with dry skin hosted more.

Some of these weird microbes “like [to eat] our sweat,” reports study author Hoi-Ying Holman.

New data now show that’s far from true. Researchers are finding them everywhere — even on skin. And the latest study shows that children and the elderly people host more of these unique tagalongs than do teens and adults.

Most importantly, the new estimate of how many bacteria live in and on people in no way reduces the size of the effect bacteria have on human health, scientists say. It doesn’t much matter what the real number is, most argue, as long as the number is right. Besides, “one-to-one is pretty impressive,” Rosner says. “There’s as much of them as there is of us.”

Other researchers also point out that the new paper’s calculations focused on bacteria. Yet the body can host other types of microbes as well. Those include viruses, fungi and archaea (Ar-KEE-uh). Viruses tend to vastly outnumber bacteria, so they could skew the microbe-to-human cell ratio upwards, says Julie Segre.

“Anytime people can add more precision, it’s good,” says Martin Blaser. He’s a microbiologist at the New York University School of Medicine. The Weizmann and Hospital for Sick Children team didn’t do any new experiments. Blaser says others should now begin measuring actual bacterial and human cell numbers to get a better gauge of the real numbers.

But already, microbiome scientists say they appreciate the team’s effort to look into the issue.

That means their bacteria-to-human cell ratio may be about 30 percent higher than that of men, the researchers found. Growing children probably have a ratio of bacteria-to-human cells similar to adult men. And being fat won’t change the ratio much, the team calculates.

But that bacterial estimate is not a solid number. It differs a bit, depending on who derived it, ranging anywhere from 30 trillion to 50 trillion cells. And among individual people, the new study finds, the number of resident bacteria could vary by up to 52 percent. “Indeed,” the researchers write, “the numbers are similar enough that each [poop] event may flip the ratio to favor human cells over bacteria.”

As expected, most of the bacteria in the body live in the colon. This tissue, which makes up most of the large intestine, is home to an estimated 39 trillion of the 40 trillion bacterial cells in the human body.

n terms of numbers, muscle and fat represent only about 0.2 percent of the total. Put all the types of cells together and the body of an average man — some guy weighing 70 kilograms (154 pounds) — may be built from about 30 trillion cells, the new study finds.

It probably wormed its way into research papers, he says, because it sounded good. “Everybody likes a nice, round number.

But that old number, a new study finds, appears to be highly inaccurate. Humans do host lots of germs, it found — but only about 30 percent more germs than human cells, not 9,000 percent more.

Behrens hopes the cells he developed can be used to predict how other sweeteners might interact. It might help scientists develop new, sweeter flavors. He has money to do this work from a large group of researchers and companies. Many of them will probably be very interested in any sweet results. And along the way, scientists may be able to resolve more taste mysteries of the past.

“This addresses a longstanding puzzle: why mixing two different sweeteners changes the aftertaste,” says Yuki Oka. “They are interrupting each other at the receptor level.” Oka studies the brain at the California Institute of Technology in Pasadena.

The researchers also tested whether the combo would boost activation of sweet receptors. Alas, no. In combination, saccharin and cyclamate stayed just as sweet.

The reverse is also true, somewhat. Saccharin blocks subtype 1. That’s one of the bitter receptors that cyclamate turns on. But saccharin doesn’t block the receptor very well. In fact, you would need so much saccharin to completely block cyclamate’s bitterness that the saccharin’s own bitterness would become overwhelming. So it’s probably cyclamate blocking saccharin’s bitter receptors that makes the duo a sweet combination.

But cyclamate doesn’t just activate the two bitter receptors, Behrens and his colleagues showed. It also blocks the bitter receptors that saccharin stimulates. Cyclamate slips into the space inside those bitter receptors and clogs it up. So with cyclamate around, saccharin can’t get at the bitter-taste receptors it normally triggers, Behrens explains. Bye-bye, bitter saccharin.

Human taste cells are difficult to work with in the lab. So the scientists inserted the taste genes into human kidney cells that were growing in dishes. Each gene came tagged with something called a reporter gene.

Behrens and his colleagues Kristina Blank and Wolfgang Meyerhof wanted to find out which bitter-taste receptors saccharin and cyclamate trigger.  To do that, the researchers examined the genes — or instructions for making molecules — for the 25 known subtypes of bitter receptors.

But scientists didn’t know why the combo was such a sweet deal. One reason: Scientists simply didn’t know a lot about how we taste. The receptors for bitter flavors were only discovered in 2000, explains Maik Behrens.

But when taken together, each sweetener blocks at least some of the other’s bitterness. The result could make your bitter soft drink better. And that could point scientists to the next super sweetener.

At last, scientists know why.

But there’s probably far more than just one molecule controlling the final hookup, Lee points out. Why does he say that? Even when the bitter or sweet taste cells had no semaphorins, the neurons still found their way to the proper taste receptor about half the time. This means that other molecules probably help the neurons find their way.

Among the five senses, taste is probably the least known or examined,” says Yuki Oka. He studies the brain at the California Institute of Technology in Pasadena. He was not involved in the Lee’s study but finds it “very elegant

To find out whether the semaphoring actually called out to bitter neurons, the scientists performed another experiment. They made the sweet- and umami-taste cells in other mice inappropriately produce semaphorin 3A. Now the bitter neurons came racing to hook up with sweet and umami cells.

Without semaphorin 3A, bitter neurons seemed to have lost their roadmap. Nearly half inappropriately hooked up with salty-, sweet- or umami-taste cells. Oops.

To find out if each type summoned different neurons to the taste cells, Lee and his colleagues created something called a knockout mouse. This mouse had a special gene that would make bitter-taste cells delete semaphorin 3A if the mouse received a certain drug. After this happened, the researchers watched as the new cells tried to hook up with the correct neurons.

Bitter-taste cells made a lot of one type of semaphorin, known as 3A. Sweet-taste cells made a lot of type 7A.

And soon they hit upon a group of molecules called semaphorins (Seh-mah-FOR-ins).

To find out what it was, he and his colleagues removed taste-receptor cells for sweet and bitter from mice. Then they looked at what genes — or sets of instructions — those cells had been using to function.

They send a specific, irresistible chemical summons, a new study shows.  

America's allies are nearly unanimous in urging Trump to stay in the deal.

But Trump, who talks tough but has generally avoided actions that would plunge us into war, may be dragged into the conflicts Israel and Saudi Arabia are already waging with Iran. If Israeli bombings of Iranians in Syria, or Saudi bombing of Iranian allies in Yemen, trigger an Iranian response, there is little doubt that these hot wars would erupt. Trump would be under great pressure to jump in.

Regime change, not agreements, is their prefered solution.

Worse, Trump's action pours gasoline on the fires already burning in the Middle East.

The nuclear arms race we had stopped in the region would be back on, but we would have fewer tools and fewer resources to stop it. The chance that Iran would agree to negotiate a "better deal" is a complete fantasy.

They understand what most serious experts believe: With the U.S. now in violation of the deal, the Iranians could easily decide to restart their nuclear program, even if this takes a few months.

It is hard to find a serious U.S. national security leader who agrees with Trump.

This is a crisis entirely of Trump's making. There was no need for him to do anything. The deal was working. Iran had ripped out almost 14,000 centrifuges, filled the core of its plutonium reactor with concrete, shipped out the tons of uranium gas it had stockpiled, then froze its now-shrunken program for a good 15 years.

In so doing, he has damaged American credibility around the world, broken faith with our closest allies and, most importantly, put us a path to a new war in the Middle East.

President Trump has just made the most destructive decision of his administration.

The idea that light at night matters to daytime pollinators is still a hypothesis at this point, says Darren Evans. He is an ecologist at Newcastle University in England. He also studies light pollution and pollination. The risk of light spillover at night is important, he notes, and scientists need to pay attention to it.

The researchers paid special attention to the cabbage thistle. But they also mapped which kinds of insects visited other plants by day or night.

To count insect visits, researchers walked a set path and caught any insects they saw wriggling on a flower. At dark sites, they tried to get data with as little light as possible. For half the walks, researchers wore small headlights. The other half were done — carefully — in full darkness. The team used night-vision goggles. Still, this didn’t give them a perfect view, Knop notes. The goggles give only a flat view of the world. There’s no sense of how near or far something is. With that kind of view, it’s “not that easy to catch insects,” she says.

So researchers painstakingly scouted sites near water-powered energy sources. They also used “really long cables,” she says.

The new study is the first to show how artificial light affects plants’ ability to make seeds, she says. The test is also unusual because it considers all kinds of insect pollinators instead of focusing only on, say, night-flying moths.

I hope people start to realize that it’s really something that changes the whole ecosystem,” Knop says.

o a lot of pollinators working the day and night shifts could be effected, Knop worries.

Light pollution might shrink a whole network of plants and their pollinators, Knop and her colleagues now suggest.

Overall, night-lit plants produced one-eighth fewer seeds than did plants that got full nights of darkness.

Researchers put up street lights in Swiss meadows, far from any real streets. It looked pretty odd, but it was all for science. The setup mimicked urban light pollution. (That is artificial light at night.) In these now-light-polluted fields, flowers had 62 percent fewer night visitors — insect pollinators — than did the flowers in dark meadows.

Too much light at night can cut the number of seeds a plant makes, a new study finds.

Why their sleep patterns don’t match expectations is unclear, Nunn says. However, he adds, neither monkey departs from its predicted sleep patterns as much as humans do.

People now spend an average of 1.56 hours of snooze time in REM, Nunn and Samson estimate. That’s about what they would predict. But that was accompanied by a hefty drop in non-REM sleep, they note. They calculated that people should actually spend an average of 8.42 hours daily in non-REM sleep. The actual figure: 5.41 hours.

Based on such traits, the researchers predicted humans should sleep an average of 9.55 hours each day. In fact, they sleep only around 7 hours daily. Some people slumber even less. The 36 percent shortfall between predicted and actual sleep is far greater than for any other species in this study.

For this, they looked at earlier studies of links between sleep patterns and various aspects of the species’ biology, behavior and environments. For instance, nocturnal animals tend to sleep longer than do those awake during the day. And species that travel in small groups or that inhabit open habitats along with predators tend to sleep less.

Nunn and Samson considered various traits about the animals and their environments in calculating how long they would expect each species to sleep. For 20 of those species, enough data existed to estimate how long the REM and non-REM portions of their sleep would last.

If the findings hold up, though, Capellini suspects that a change in sleeping patterns also may have lessened humans’ sleep time. People get most sleep in just one bout per day. Some other primates sleep in several bouts that vary in how long they last.

She says the new study does show that people may sleep for a surprisingly short time for primates. However, she cautions, their sample of 30 species is too small to reach any firm conclusions. There may be 300 or more primate species.

As sleep declined, rapid-eye movement — or REM — sleep took on an outsize role in humans, Nunn and Samson propose.

The researchers argue that two long-standing features of human life may play into our short sleep times. The first stems from when humans’ ancestors descended from the trees to sleep on the ground. At that point, people probably had to spend more time awake to guard against predators. The second may reflect the intense pressure humans face to learn and teach new skills and to make social connections. That has left less time for sleep.

Based on lifestyle and biological factors, however, people should get 9.55 hours, Nunn and Samson calculate. Most other primates in the study typically sleep as much as the scientists predicted they should.

In their new study, the two compared sleep patterns in 30 different species of primates, including humans. Most species slept between nine and 15 hours daily. Humans averaged just seven hours of shut-eye.

People have evolved to sleep much less than chimps, baboons or any other primate studied so far, a new study finds.

Mr. Bobley of the NEH says he has been impressed with the flu researchers’ "candid thoughts on how computational approaches like data mining are no magic bullet," even as they expand what humanists can do. The work is a reminder, he says, that "historical documents like newspapers are rich, messy, nuanced, and complex documents that defy easy computational analysis."

"We are very interested in working with any scholar, expert, or engineer who has access to interesting data sets and who has interesting questions to pose," Mr. Ramakrishnan says.

Getting the right blend of questions and algorithm "takes some practice," says Mr. Ramakrishnan. It’s a set of skills that can be applied to contemporary problems as well as historical ones. Mr. Ramakrishnan and his group at the Discovery Analytics Center ("a data-mining shop," he calls it) have dug through medical data in tandem with doctors, and worked with political scientists on election data.

"Our goal was to mimic it in an algorithm," Mr. Ramakrishnan says.

Mr. Ewing came armed with a set of "tone categories" to focus on: Were newspaper reports alarming, reassuring, factual?

Human beings recognize tone. Algorithms are better suited to sifting through data in search of keywords—like "influenza" and "kissing." But "when we see a word or something being highlighted with an algorithm, we don’t know what it means," says Mr. Ramakrishnan.

The researchers discovered traces of Copeland by identifying and then algorithmically searching for particular terms the health commissioner used ("influenza" and "kissing," for instance). Health officials in other locales, including St. Louis and Salt Lake City, transmitted Copeland’s antiflu advice to their citizens. By October, newspapers far from New York were sharing it. The Roanoke Times, for instance, ran an ad sharing Copeland’s assertion that theaters should be kept open as long as they were well ventilated and clean.

Using the Library of Congress’s Chronicling America database of historical newspapers, the HathiTrust Digital Library, and other sources, the Virginia Tech researchers sought out direct and indirect evidence of Copeland’s role: mentions and quotations, references to flu-containment strategies he promoted. "You can see his influence even if his name’s not used," Mr. Ewing says.

To understand Copeland’s influence, historians studying the Spanish flu usually turn to his public statements and comments made about him. That kind of primary-source analysis, the historian’s version of close reading, is a tried-and-true method of investigation. But large-scale digital databases, adroitly mined, can help historians pinpoint specific sources that are worth that kind of close look.

Copeland helped set the tone for how the nation reacted to a viral threat—and has been the subject of debate among historians ever since, with competing camps arguing about whether he did enough.

The team began with several questions: How did reporting on the Spanish flu spread in 1918? And how big a role did one influential person play in shaping how the outbreak was handled?

It’s also a historically minded project that speaks to the understandable contemporary obsession with fearsome diseases and how we respond to the threat they pose.

Now a team of humanists and computer scientists has combined early-20th-century primary sources and 21st-century big-data analysis to better understand how America responded to the viral threat in 1918. It’s a study in the possibilities as well as the pitfalls of interdisciplinary work, and a model-in-progress for how data-driven analysis and close reading can enhance each other.

Arts and humanities researchers still spend a great deal of time in libraries and archives; they still write excellent books; they still portray themselves as lone scholars. However, this approach is now only one component of an ecosystem that embraces technological change, collaborative and interdisciplinary engagement to address global challenges, and serious attention to how research can benefit society.

The impacts of arts and humanities research are as often global as they are local and national

What these changes point to is a widespread commitment to high quality research, innovation and impact.

Increasingly arts and humanities researchers operate in teams alongside other subject areas and deploy a combination of traditional scholarly techniques and practice-led research.

Humanities researchers have played a part in developing new technology too.

The potential for using large datasets to help us understand human society has been the subject of numerous digital humanities projects

Technology has enhanced the possibilities of humanities research in many ways.

But while research in arts and humanities disciplines has not been as visible, over the last decade or so, the methods, outputs and impact of this research have actually undergone dramatic changes.

But without native English speakers from the UK to police its linguist rules, Euro-English could develop a life of its own.

“With the British gone, no one will be there to carry on the work of defending the structural integrity of British English in the face of competition from not only American English, but also from [second language] users who increasingly utilise features indicative of discoursal nativisation which are in the processes of becoming systematic across continental Europe.”

Euro-English could help provide its users with a “sense of identity” among other benefits which were “both logical and welcome”.

He argued that English was likely to remain as the EU lingua franca despite suggestions it should be ditched with no member state having its as their official language. Ireland chose Irish and Malta chose Maltese despite widespread use of English in both countries.

Grammar is also changing.

Outside of Brussels, people are also developing their own English-language sayings.

Euro-English has already developed its own new definitions for some words based on the “Eurospeak” deployed in Brussels.

The Europeans might also decide to adopt American spellings

And this could eventually be codified in a dictionary and taught in schools in much the same way that American or Australian English is today if English is retained as the lingua franca of the European Union after the UK leaves.

Dr Marko Modiano, of Gavle University in Sweden, said there were already signs that “Euro-English” was developing its own distinct way of speaking.

Brexit could lead to the development of a new form of the English language, according to a new academic paper.

Rather than removing variables and regularizing something to make it conform to an established standard, the new normalize seems rather to shift the standard to make something considered an outlier “normal.”

But within a few decades, they didn’t just refer to a return to normalcy but also to the creation of normalcy by making something that had been variable conform to a given standard

In these and similar pieces, the meaning is clear; it's also clearly different from the definition you'll find in our dictionary.

Nancy Friedman has explored in detail the ways critics of Donald Trump have used the term normalization to describe the process of making something normal, as in the tweet above which describes "the normalization of hate."

It will sometimes happen that a word suddenly appears everywhere. In the wake of the 2016 presidential election, two such words are currently in the ether: the verb normalize and its related noun, normalization.

Until the Republican leadership pushes back against Trump, and until our allies abroad say "enough is enough," Trump will continue to endanger our national security. It is time for collective determination and action against Trump's dangerous policies and actions so as to ensure the safety of our country.

I do, however, resent his loud-mouthed bullying being represented as policy, and I resent his obstinate adherence to campaign tropes that are as dishonest today as they were on the stump.

I do not root against Trump on this issue, however much I disagree with him.

No longer, as Trump has recast our foreign policy as untrustworthy and erratic, very much in line with what he is doing domestically.

American credibility on the international stage is now shot to pieces.

now everyone faces a scary unknown future.

Almost no one argued that the Iranians were cheating on their JCPOA obligations, and international inspectors reported that Iran had fulfilled its commitments.

perhaps the simplest and most telling is that Trump gave up something tangible for an unknown and dangerous nothing.

Iran may not restart its entire nuclear program, but it has the "luxury" of choice. It can move incrementally while continuing to engage with the Europeans, the Russians and the Chinese. In so doing, it will continue and intensify the diplomatic isolation that Trump has constructed for the United States.

What's important now is what has been lost as a result of the U.S. withdrawal.

The same fate probably awaits him when he comes to regret leaving the JCPOA.

Having called it the worst deal ever negotiated, the President must have felt it incumbent to follow through on a campaign pledge.

It is hard to remember any other issue of this magnitude being decided for such a trivial reason.

So far, Lasley-Rasher and her group haven’t yet tested the copepods in the presence of predators. “It’s definitely a next step,” she says. But if the copepods really do get eaten more often after a meal of toxic algae, this could be one reason why they don’t eliminate algal blooms. “Predators are more likely to encounter the [copepods] eating the toxin,” she explains. That provides an explanation “for bloom persistence, if the ones that eat [the algae] get removed from the system.”

“It was kind of refreshing for [the scientists] to look past just ingestion and survival,” says Finiguerra. Normally, he explains, scientists might think that there’s one pathway: those algae make a toxin, which will kill whatever eats them. But, as Finiguerra notes, this study shows that “it’s much more complicated than that.”

Her group calculated that after eating toxic algae, the copepods could be 56 percent more likely to encounter a predator — such as a shrimp — that will snatch them up.

It’s not, however, just swimming straight that matters. By increasing their speed after eating harmful algae, the copepods make a slightly bigger wake as they plow through the water, Lasley-Rasher explains. This means predators that hunt by sensing the current produced by prey could find them easy pickings.

Unlike many other species of copepods, these didn’t die after dining on harmful algae. They produced as many eggs as those getting a healthy diet. The one big difference: They swam straighter and 25 percent faster than normal.

At this point, the scientists measured how many copepods had reproduced and died. They also studied the crustaceans’ behavior.

There her team divided the copepods into tanks. A share of the tanks got some A. fundyense to eat, mixed in with other, harmless algae. Copepods in other tanks were fed just the harmless algae. One tank of unfortunate copepods got no food at all. After two hours, the scientists moved all the copepods to tanks with normal algae, and let them feed for another 15 hours. This was to make sure that none of the tiny crustaceans were changing their behavior just because they were too hungry.

So her team packed the fresh-caught plankton in ice and shipped them south to her lab.

To find out, Lasley-Rasher and her colleagues collected many copepods from the Gulf of Maine in plankton nets. They looked for the species Temora Longicornis. “It co-occurs in the Gulf of Maine with the algae,” she explains.

But they don’t. And that puzzled Rachel Lasley-Rasher. “Why aren’t zooplankton removing this algae?” wondered the marine biologist, who now works at the University of Maine in Walpole. “Do they eat [the algae] and get sick? Do they eat it and die? How does it affect their behavior?”

But these algae don’t kill one species of copepod. Their toxin just changes the behavior of this tiny crustacean. It makes the critters swim faster and straighter, a new study shows.

The bad news: That just might send it straight into the jaws of a hungry fish.

But the concern is that some species might not be able to make that switch, Kohlbach says. “To determine the consequences on a species-level, we need to do more research.”

But they, too, will likely be affected, Kohlbach says. If falling summer sea ice affects life at the bottom of the food web, she says, eventually it also will affect those higher up.

Scientists have yet to look for markers of algae higher up in the food web — in bigger animals that may have dined on the zooplankton. So for now, the scientists can’t yet predict how the loss of sea ice algae might affect larger species, such as fish, seals or polar bears.

Animals that lived beneath the sea ice got a lot of their energy — sometimes described in terms of carbon (an ingredient in everything they eat) — from ice algae. Indeed, 60 to 90 percent of their meals had consisted of the algae,. But even pelagic species “showed a significant dependency” on ice algae, notes Kolbach. Those animals got 20 to 50 percent of their dietary energy from algae that had been embedded in sea ice.

For its new study, Kohlbach’s team looked at various species of zooplankton during late summer. Some of these tiny critters live near the sea ice. Others are pelagic. The researchers determined how much of their diet had come from sea-ice algae. To do that, they looked for markers of the algae. These were building blocks of the algae known as fatty acids. If they showed up in the zooplankton, it was sign these small animals had dined on the algae.

Climate change could therefore be a big problem for the Arctic ecosystem. That’s because a loss of ice there will affect more than just the organisms that have a close connection to the ice. It also will affect life in the open ocean, Kohlbach says

And they are an important source of food even for species that don’t live under the ice, her team now reports.

Disappearing sea ice is a symptom of a warming planet. It also poses risks to the life associated with that ice. That includes the algae that live in brine-filled channels within this ice.

A new study shows why this could be a big problem for life in and around the Arctic.