Astronomy

A star shredded by a black hole may have spit out an extremely energetic neutrino

A neutrino that plowed into the
Antarctic ice offers up a cautionary message: Don’t stray too close to the edge
of an abyss.

The subatomic particle may have been blasted
outward when a star was ripped to pieces during a close encounter with a
black hole, physicists report May 11 at arXiv.org. If it holds up, the result
would be the first direct evidence that such star-shredding events can
accelerate subatomic particles to extreme energies. And it would mark only the
second time that a high-energy neutrino has been traced back to its cosmic
origins.

With no electric charge and very
little mass, neutrinos are known to blast across the cosmos at high energies.
But scientists have yet to fully track down how the particles get so juiced up.

One potential source of energetic
neutrinos is what’s called a tidal disruption event. When a star gets too close
to a supermassive black hole, gravitational forces pull the star
apart
(SN: 10/11/19). Some of the star’s guts
spiral toward the black hole, forming a hot pancake of gas called an accretion
disk before the black hole gobbles the gas up. Other bits of the doomed star
are spewed outward. Scientists had predicted that such violent events might
beget energetic neutrinos like the one detected.

Spotted on October 1, 2019, the little neutrino packed a punch: an energy of 200 trillion electron volts. That’s about 30 times the energy of the protons in the most powerful human-made particle accelerator, the Large Hadron Collider. The neutrino’s signature was picked up by IceCube, a detector frozen deep in the Antarctic ice. That detector senses light produced when neutrinos interact with the ice.

When IceCube finds a high-energy
neutrino, astronomers scour the sky for anything unusual in the direction from
which the particle came, such as a short-lived flash of light, or transient, in
the sky. This time, astronomers with the Zwicky Transient Facility came up with
a possible match: a tidal disruption event called AT2019dsg.

First observed in April 2019, that event
had been spied emitting light of various wavelengths: visible, ultraviolet,
radio and X-rays. And the maelstrom was still raging when IceCube detected the
neutrino, according to a team of physicists including Marek
Kowalski
of the Deutsches Elektronen-Synchrotron, or DESY, in Zeuthen,
Germany.

While intriguing, the association
between the neutrino and the shredded star is not certain, says IceCube physicist
Francis Halzen of the University of Wisconsin–Madison, who was not involved with the new study. “I
don’t know if I have to bet my wallet, but I probably would,” Halzen says. “But
it doesn’t have much money in it.”

The probability that a neutrino and a similar
tidal disruption event would overlap by chance is only 0.2 percent, the
researchers report. But that doesn’t meet physicists’ stringent burden of proof.
“Just one event is difficult to convince [us] this source is really a neutrino
emitter,” says astrophysicist Kohta Murase of Penn
State University. “I am waiting for more data.”

Kowalski declined to comment for this
article, as the paper has not yet been accepted for publication in a scientific
journal.

To have birthed such an energetic
neutrino, the star-shredding event must have first accelerated protons to high
energies. Those protons must then have crashed into other protons or photons (particles
of light). That process produces other particles, called pions, that emit
neutrinos as they decay.

Now, scientists are aiming to pin down
exactly how that acceleration happened. The protons might have been launched
within a wind of debris that flowed outward in all directions. Or they could
have been accelerated in a powerful, geyserlike jet of matter and radiation.

AT2019dsg shows some unusual features
that any explanation should be able to account for. X-rays produced in the event,
for example, appeared to drop off rapidly. So physicists WalterWinter of
DESY and Cecilia Lunardini of Arizona State
University in Tempe suggest May 13 at arXiv.org that the event did produce a
jet, but that a cocoon of material gradually shrouded
the
region, hiding the X-rays from view while still allowing the neutrino to escape. Lunardini declined to comment
because the paper is not yet published in a journal.

But Murase argues that for the jet to be
hidden, that means it can’t be that powerful of an outflow, making it hard to
explain the energetic neutrino this way. “If it injects a lot of energy, this
energy gets out,” he says. In a third study posted May 18 at arXiv.org, Murase
and colleagues favor the idea that the protons get accelerated in an outward
flowing wind or in a corona
, a superhot
region near the black hole’s accretion disk.

Determining where these particles come
from can help scientists better understand some of the most extreme
environments in the cosmos. Previously, astronomers had matched up a different energetic neutrino with a blazar experiencing a flare-up (SN:7/12/18). A blazar is a bright source of light powered by a
supermassive black hole at the center of a galaxy. Both a blazar flare and a
tidal disruption event “are very special activities, which is when a lot of
energy is released in a small amount of time,” says astrophysicist Ke Fang of Stanford University, who was not involved
with the study.

Making more observations of high-energy neutrinos
is crucial, Fang says. “This is the only way we can clearly understand how the
universe is operating at this extreme energy.”

Is the coronavirus mutating? Yes. But here’s why you don’t need to panic

In novels and movies,
infectious pathogens mutate and inevitably become more dangerous. In the blockbuster
movie Contagion, for instance, a deadly virus acquires a mutation in
Africa that causes the global death toll to spike in mere days.

Reality, however, is far less
theatrical.

Over the past few months, a
few research groups have claimed to identify new strains of the coronavirus,
called SARS-CoV-2, that’s infecting people around the globe. That sounds scary.
But not only is it sometimes difficult to determine whether a change amounts to
a “new strain,” none of the reported changes to the virus have been shown to
make it more dangerous.

This has led to great
confusion for the general public. Each time such studies surface, fears arise,
and virus experts rush to explain that changes in a virus’s genetic blueprint,
or genome, happen all the time. The coronavirus is no exception.

“In fact, it really just
means that it’s normal,” says Kari Debbink, a virologist at Bowie State
University in Maryland. “We expect viruses to evolve. But not all of those
mutations are meaningful.”

Here’s what it means to find mutations
in the novel coronavirus, and what evidence is needed to actually raise a red
flag.

First, a mutation is just a change

Most of the time, mutations
don’t do anything to a virus at all.

Viruses are simply protein shells that contain either DNA or RNA as their genetic material. In the case of SARS-CoV-2, it’s RNA. The building blocks of RNA, called nucleotides, are arranged in triplets, called codons. These nucleotide trios provide the code for building amino acids, which make up the virus’s proteins. A mutation is a change to one of these nucleotides in the virus’s genetic material — in SARS-CoV-2’s case, one of around 30,000 nucleotides.

Sometimes a mutation in a
triplet is silent, meaning the codon still codes for the same amino acid. But
even when an amino acid does change, the virus might not behave in a way that’s
obviously different. Some mutations could also spawn dysfunctional viruses that
quickly disappear as a result.

And in fact, these changes can
actually be helpful when it comes to tracing the virus’s path around the globe, something researchers have been doing ever
since experts from China released the first coronavirus genetic sequence in
January (SN: 2/13/20). Scientists can
decipher, or sequence, the virus’s RNA to track changes as it infects more people.
They can then track where and how the coronavirus is spreading in a population,
and monitor for further changes in its genetics.

Epidemiologists are interested
in tracking mutations even if they don’t alter the protein, says Emma Hodcroft,
a molecular epidemiologist at the University of Basel in Switzerland. “But that
doesn’t mean that it’s a new strain or that it’s a virus that behaves
differently.”

A new ‘strain’ of virus doesn’t mean much

The term “strain” is “used
very, very loosely by most scientists,” Hodcroft says. “There isn’t really a
strict definition of the word ‘strain,’” particularly when talking about
viruses. Experts might simply be referring to viruses that aren’t genetically identical
— almost like discussing different people.  

Viruses are always changing.
When a virus infects a cell, it begins making copies of its genetic
instructions. Most viruses don’t have the necessary tools to proofread each
string of RNA for mistakes, so the process is error-prone and differences build up over time.

Coronaviruses like
SARS-CoV-2, on the other hand, do have a proofreading enzyme — a rarity for RNA viruses. But that doesn’t mean their genomes don’t have
errors. Changes still accumulate, just more slowly than in other RNA viruses such
as influenza. “Strains,” “variants” or “lineages” are all terms researchers
might use to describe viruses that have identical or closely related strings of
RNA.

But for the general public, a
word like “strain” is often interpreted to mean a whole new scourge. “I think
the use of the term ‘strain’ does little more than cause panic,” says Jeremy
Luban, a virologist at the University of Massachusetts Medical School in
Worcester. “It doesn’t really get at what the important issues are.”

SARS-CoV-2 coronavirus and single-stranded RNA
The genetic material for coronaviruses is made up of single-stranded RNA (pictured in yellow). Changes, or mutations, to single nucleic acids (protruding lines in this illustration) in that RNA can either be silent — meaning nothing changes — or alter a small portion of one of the virus’s proteins.Vchal/iStock / Getty Images Plus

Most mutations aren’t dangerous

A mutation can affect a virus
in a number of ways, but only certain kinds of mutations might make the virus
more dangerous to people. Perhaps the change shields the virus from the immune
system, or makes it
resistant to treatments. Mutations could also alter how easily the virus
spreads among people or cause shifts in disease severity.

Luckily,
such mutations are rare. Unfortunately, they can be hard to identify.

A preliminary study published
May 5 at bioRxiv.org, for instance, found a mutation in the SARS-CoV-2 spike, a
protein on the outside of the coronavirus that allows it to break into cells. This
new variant is now found more often in places like Europe and the United States
than the original form of the coronavirus. That may mean the change makes the virus more transmissible, the authors concluded. But the study lacked
laboratory experiments to support the claim.

Other explanations could also
explain the pattern. The SARS-CoV-2 variant with the mutation could have ended
up in certain regions thanks to random chance — a person infected with a virus that had the new
mutation just happened to hop on a plane — and might have nothing to do with the
virus itself. The study didn’t provide enough evidence to distinguish among the
possibilities.

“What I think has been
potentially confusing to people is that we’re watching this very normal process
of [viral] transmission and mutation happen in real time,” says Louise Moncla,
an evolutionary epidemiologist at the Fred Hutchinson Cancer Research Center in
Seattle. “And there’s this real desire to understand whether these mutations
have any functional difference.”

‘Take a deep breath,’ experts say, and expect mutations

To understand whether a
single mutation changes how the virus works, “it’s not just going to be one
experiment,” Bowie State virologist Debbink says. “It takes a lot of research.”

In addition to examining
genetic sequences of viruses from coronavirus patients all over the world,
researchers will also rely on studies in lab-grown cells or animals. Such studies
could help pinpoint whether viruses with particular mutations behave
differently. Competition experiments —
where two different viruses are mixed in cells in a dish or used to infect an
animal — can help scientists figure out which variant is more successful at
making copies of itself, that is, which one “wins.”

Other types of tests could
reveal if mutations in the coronavirus’ spike protein alter how strongly it
attaches to the protein on human cells that allows it to get inside the cells, virologist
Luban says (SN: 2/3/20), or whether changes
modify how easily the virus gets into a cell after binding.

But lab results might not provide
the full picture either. “Just because something’s different in a cell doesn’t
necessarily mean that it’s different when you scale that up to the whole human
body,” Hodcroft says. “At the end of the day, you’re going to need some animal
studies or some really good human data.”

These studies take time. Meanwhile,
more coronavirus mutations are guaranteed to pop up over the coming months — and experts will continue to track
them.   

“The data will tell us whether we need to worry, and in what way we need to worry,” Moncla says. “Everyone should take a deep breath and realize that this is exactly what we’ve always expected to happen, and we don’t necessarily need to be concerned.”

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New species of scaly, deep-sea worms named after Elvis have been found

A new
look at the critters known as “Elvis worms” has the scale worm family all shook
up.

These
deep-sea dwellers flaunt glittery, iridescent scales reminiscent of the sequins
on Elvis’ iconic jumpsuits (SN: 1/23/20).
“For a while, we thought there was just one kind of Elvis worm,” says Greg
Rouse, a marine biologist at the Scripps Institution of Oceanography in La
Jolla, Calif. But analysis of the creatures’ genetic makeup shows that Elvis worms comprise four species
of scale worm
,
Rouse and colleagues report May 12 in ZooKeys.

Rouse’s
team compared the genetic material of different Elvis worms with each other,
and with DNA from other scale worm species. This analysis places Elvis worms in
the Peinaleopolynoe genus of scale worms, which includes two other known
species — one found off the coast of Spain, the other off California.

A new genetic analysis of the deep-sea creatures nicknamed “Elvis worms” reveals that that these iridescent creatures include four separate species. The Elvis worms seen in this video belong to the species Peinaleopolynoe orphanae, which mostly sport glittery blue scales, but also come in other colors, like black and red. These worms may look dainty, but they fight dirty, chomping at each other’s scales when they get into skirmishes.

The four
newly identified Elvis worm species are scattered across the Pacific, from P.
elvisi
and P. goffrediae in Monterey Canyon off California to P.
orphanae
in the Gulf of California by Mexico and P. mineoi near
Costa Rica.

These
deep-sea Elvis impersonators share some common traits, such as nine pairs of scales.
But each species has its own distinct flare. P. elvisi’s gold and pink iridescent
color scheme earned it the honor of keeping the worms’ namesake in its official
title. P. orphanae, on the other hand, mostly sports rainbow-sparkled
scales of a bluish hue. 

The researchers don’t know why Elvis worms have evolved such eye-catching scales, since the animals live in the dark, deep sea. It could just be a side effect of developing thicker scales over time, which happen to refract more light, Rouse says. Thicker scales could come in handy in a fight, since Elvis worms are apparently biters, a behavior discovered while watching a worm skirmish. “Suddenly, they started doing this amazing jitterbugging — wiggling, and then fighting and biting each other” on their scales, Rouse says. “No one’s ever seen any behavior like this in scale worms.”

How coronavirus stress may scramble our brains

I’m on deadline, but
instead of focusing, my mind buzzes with unrelated tidbits. My first-grader’s
tablet needs an update before her online school session tomorrow. Heartbreaking
deaths from COVID-19 in New York City make me tear up again. Was that a kid’s
scream from upstairs? Do I need to run up there, or will my husband take care
of it?

These
hornets of thoughts drive out the clear thinking my job demands. Try as I might
to conjure up a coherent story, the relevant wisps float away.

I’m
scattered, worried and tired. And even though we’re all socially isolated, I’m
not alone. The pandemic — and its social and economic upheavals — has left
people around the world feeling like they can’t string two thoughts together.
Stress has really done a number on us.

That’s
no surprise to scientists who study stress. Our brains are not built to do
complex thinking, planning and remembering in times of massive upheaval. Feeling
impaired is “a natural biological response,” says Amy Arnsten, a neuroscientist
at Yale School of Medicine. “This is how our brains are wired.”

Decades
of research have chronicled the ways stress can disrupt business as usual in
our brains. Recent studies have made even more clear how stress saps our
ability to plan ahead and have pointed to one way that stress changes how
certain brain cells operate.

Scientists recognize the pandemic as an opportunity for a massive, real-time experiment on stress. COVID-19 foisted on us a heavy mix of health, economic and social stressors. And the end date is nowhere in sight. Scientists have begun collecting data to answer a range of questions. But one thing is clear: This  pandemic has thrown all of us into uncharted territory.

Short-circuited

The human brain’s
astonishing abilities rely on a web of nerve cell connections. One hub of
activity is the prefrontal cortex, which is important for some of our fanciest
forms of thinking. These “executive functions” include abstract thinking,
planning, focusing, juggling multiple bits of information and even practicing
patience. Stress can muffle that hub’s signals, studies of lab animals and
humans have shown.

“Even
relatively mild stress can impair the prefrontal cortex,” says Elizabeth
Phelps, a psychologist and neuroscientist at Harvard University. “That’s one of
the most robust effects of stress on the brain.”

That impairment has been described in lots of studies. One memorable example comes from 20 panicky medical students facing licensing exams. After a month of high-stress test prep, the students performed worse on an attention test than they did after exams were over. Functional MRI scans showed that under stress, the students’ prefrontal connections to other brain areas were diminished, scientists reported in Proceedings of the National Academy of Sciences in 2009.

experiment diagram of brains
Normally, an alert person’s brain has moderate amounts of chemical messengers that lead the prefrontal cortex to take charge and perform high-level thinking (left). But with stress, those chemical signals can flood the brain, activating amygdala-linked brain networks involved in sensing and responding to threats (right).A. Arnsten
experiment diagram of brains
Normally, an alert person’s brain has moderate amounts of chemical messengers that lead the prefrontal cortex to take charge and perform high-level thinking (left). But with stress, those chemical signals can flood the brain, activating amygdala-linked brain networks involved in sensing and responding to threats (right).A. Arnsten

When
the prefrontal cortex goes quiet, more reactionary brain networks take over.
Some of these “primitive” circuits, as Arnsten calls them, center on the
amygdalae, two almond-shaped structures buried deep inside the brain that help
us sense and respond to threats. Those fast, instinctual reactions “are helpful
if you’re being faced with a snake,” Arnsten says, “but not helpful if you’re
being faced with a complex medical decision.”

A more recent experiment, published online April 2 in Current Biology, illustrates how stress can shift people away from thoughtful planning. When people were threatened with electric shocks, their abilities to plan ahead flew out the window. Anthony Wagner, a cognitive neuroscientist at Stanford University, and colleagues asked 38 people to learn a familiar route through virtual towns. With practice, people learned these routes, as well as the locations of recognizable objects, such as a zebra, an apple, a stapler or Taylor Swift’s face, along the way.

“Our
question was, ‘What are the effects of stress?’ ” Wagner says. To find out, the
researchers used “moderately painful” electric zaps to induce stress in some
participants, who returned to familiar virtual towns and were asked to find
their way to the zebra, for instance. Subjects didn’t know when they would be
shocked, and they couldn’t control any aspect of it.

After
the training, the participants — some under stress from the expectation of
further shocks and some not — were sent back into the virtual town and asked to
find their way to a specific item.

But
there was a trick: Participants could reach the stapler, for example, faster
and more efficiently by taking a shortcut. The shortcut, however, required more
planning, more initiative and a heavier reliance on previously learned
relationships among streets.

Stressed
people were less inclined to take the shortcut, the researchers found. People
who were stressed by the possibility of a shock took the shortcut 31 percent of
the time, compared with 47 percent for those who weren’t stressed. The stressed
people still reached the object they were after, but in a roundabout way.

Functional
MRI brain scans hinted at what the added stress did to the volunteers’
thinking. The objects planted around town evoked recognizable patterns of brain
activity when a person was seeing one of the previously seen objects, or even
just thinking about it. By spotting these neural signposts, researchers could
tell when people were thinking of a particular path — or of no path at all.

Participants
were given eight seconds to plan their approach to reach the target object.
Unstressed people generally had a plan; their brain activity contained patterns
that signaled these volunteers were thinking about the objects along the
shortcut route. Neural signals of a plan even showed up among those who chose
to take the familiar route.

Those
awaiting a shock appeared to use little foresight. “The stressed people didn’t
seem to be thinking about the familiar route when they took it,” says study
coauthor Thackery Brown, a cognitive neuroscientist at Georgia Tech in Atlanta.
“They were on this fight-or-flight autopilot type behavior.”

What’s
more, stress quieted the activity of brain areas needed to make a good plan,
including a part of the prefrontal cortex and the hippocampus, a structure
important for memory. Those findings suggest that under stress, we are less
able to call up our previously learned knowledge and memories. We are working
with a deficit.

“In
some sense, we’re privileged when we’re not stressed, able to fully harness our
cognitive machinery,” Wagner says. “That allows us to behave in more strategic,
more efficient, more goal-directed ways.”

Brown
sees parallels between these lab-based stressors and the complex and
longer-lasting stresses of real life. The participants were attempting to do
something complicated while worrying about something else. The stressor is
“operating in the background while you’re trying to plan your daily life,”
Brown says. “There’s a connection there with the type of thing people are
experiencing right now in the context of the pandemic.”

Shrunken cells

Zooming in to individual
cells provides a view of stress’s physical destruction in the brain. Stress can
shrink nerve cells and cull their connections, and the prefrontal cortex is
particularly vulnerable, studies in both humans and other animals suggest.
Other kinds of brain cells are affected too, new research on mice shows.

Big, arboreal cells called astrocytes have many jobs in the brain. Specialized astrocytes called Bergmann glia extend into synapses, the space between nerve cells where chemical messages flow, and slurp up extra chemical signals. This helps keep nerve cells communicating clearly with one another (SN Online: 8/4/15).

But in a test of mice stressed by the ominous smell of a predatory fox, these astrocytes retracted from synapses, neuroscientist Siqiong June Liu of Louisiana State University School of Medicine in New Orleans and colleagues found. That pulling away occurred with a single exposure to that stressful fox odor, and the cells were still retracted 24 hours later, the researchers reported in the April 22 Journal of Neuroscience.

Stress
sends a “shrink” message to these astrocytes by reducing the levels of a
protein called GluA1. It’s not known whether a similar process, and the
resulting changes in how brain cells communicate under stress, happens in the
brains of people.

Some stress signals may travel certain neural highways. Physiologist Kazuhiro Nakamura of Nagoya University Graduate School of Medicine in Japan and colleagues studied rats that had just been through the stressful experience of losing a fight, a defeat that is meant to mimic human social stress. A somewhat mysterious region inside the rat’s prefrontal cortex, called the DPC/DTT for dorsal peduncular cortex and dorsal tenia tecta, is important for sending stressed-out signals, the researchers reported in the March 6 Science.

From
there, the signals shoot to the hypothalamus, a brain structure that can spark
some of stress’s most obvious effects in the body, including a racing heart and
sweating. It’s possible that similar brain areas in humans might have roles in
sparking stress signals.

These
clues are giving scientists a more precise understanding of how stress moves
through and affects the brain. But lab studies on stress, by design, have to be
somewhat short-lived, with relatively mild stress. Applying lab findings to
people’s experiences in life comes with caveats. Huge questions remain about
how the crushing and varied stresses of a pandemic might influence people.

A natural experiment

Psychologists and brain scientists are on it. As of mid-May, a database tracking COVID-19 social science projects had 294 research projects related to the current pandemic.

These kinds of natural experiments — studying people who had experienced uncontrollable, intense stress in their lives — have happened before. Phelps and colleagues studied how people remember the events of 9/11. People who were in downtown Manhattan at the time of the attacks seemed to rely more heavily on their amygdalae to call up memories of the shocking event than people who were farther away, the researchers reported in 2007 in Proceedings of the National Academy of Sciences. Other researchers have identified thinking problems in people who lived through Hurricane Katrina and other natural disasters.

Stress
from the COVID-19 pandemic might influence decision making, Phelps suspects.
How do you respond to positive and negative feedback when you’re stressed? Does
your desire to do hard work change? She and colleagues are hoping to get
answers by surveying people across the United States. Participants will
describe their stress reactions and complete online tasks that test decision
making and memory.

Other
long-term studies will examine how autobiographical memories of the pandemic
change over time, how the pandemic affects stress during pregnancy and how
mind-set might influence how people cope.

As
this chaotic period rolls on, stressors will change and accumulate. Sustained
crisis, scientists suspect, can change our brains and their capabilities in
even more profound ways than temporary stress. 

For
now, each of us is left to manage our own personalized stress cocktails. Mine
grows more potent with an expanding backlog of tasks, both domestic and
job-related, the cumulative sorrow of seeing my kids isolated from their
friends and a steady drip of small losses. And I worry for the many people who
are worse off, facing illness and financial strain. It’s a lot.

As we all grapple with this reality, scientists have a message for us, one that I find comforting: “Forgive yourself,” Phelps says. “If you’re finding it challenging right now to focus, forgive yourself.”

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Scientists sometimes conceal a lack of knowledge with vague words

You can’t
kill a virus, common wisdom contends, because viruses aren’t alive to begin
with.

Yet some viruses
sure act like they’re alive. And in fact, you can find biologists and
philosophers who will insist that viruses do deserve a branch on the tree of
life. Still, many oth­er experts refuse to confer viruses with life status.

Debates
about viruses as life-forms (or not) have raged for decades. But as more and
more data on viral vitality accumulate, the disagreements do not diminish. Perhaps
that’s because the argument is not really about the nature of viruses. Rather
it’s about the definition of life. Scientists can’t agree on that,
either.

Science’s
inability to define life reveals not merely a lack of lexicographic
dexterity, but also signifies a broader issue — the peculiar way that science’s
relationship with reality is connected to science’s relationship with words.

Words are
obviously indispensable for scientists, both to communicate among themselves
and to report their findings to the rest of civilization. Even in the most
mathematical of sciences, words must be attached to symbols in order to relate
mathematical relationships to real-world phenomena. Words like energy or
force or stress tensor describe a physical entity corresponding
to a symbol in an equation.

But many
scientific ideas do not reduce to a neat mathematical expression, so the words
are on their own. And sometimes the ideas originate with the words. Throughout
history, scientists have often coined a word before fully formulating the underlying
idea. As Johann Wolfgang von Goethe wrote in his poetic play Faust, in
the absence of ideas, words can come to the rescue. “With words, the mind does
its conceiving,” reads one translation. (Or, in another version, “If your
meaning’s threatened with stagnation, then words come in, to save the
situation.”)

So sometimes
scientists adopt a term, and use it widely, even though no precise definition
of that term is universally accepted. Life is an obvious example. It’s a
word that most people instinctively understand yet nobody can define to everybody
else’s satisfaction.

“We all think we can recognize a living organism when we see one,” biochemists Athel Cornish-Bowden and María Luz Cárdenas wrote in the February issue of the journal BioSystems, “but it is not so easy to give a definition of ‘living’ that includes all the entities we consider to be alive, and excludes the ones we do not.”

Some
proposed definitions of life, for instance, include the capacity to reproduce,
note Cornish-Bowden and Cárdenas, of Aix-Marseille University in France. Sounds
good, but what about mules? They can’t reproduce, but most people would agree
that mules are alive, the biochemists point out. “Taking the minority view that
mules cannot be regarded as alive does not solve the problem, because many
people, including many distinguished biologists, have passed the age when they
can reproduce, but would dispute any claim that they are not alive.”

Life is one of many common scientific
words that elude precise definition. And scientists have often used much vaguer
terms, typically as stand-ins for primitive, imprecise ideas — some that turned
out to be in essence correct, others totally wrong.

Ancient
Greeks, for instance, invented the word atom to describe the tiniest,
“uncuttable” pieces of matter. But no Greek had any real knowledge of what an
atom actually was like (and of course, they had no proof that atoms even
existed, as atom denier Aristotle vigorously argued). But the concept turned
out to be roughly right. Chemists in the 18th century, on the other hand,
insisted that fire depended on a substance called phlogiston. But phlogiston
was just a word, linked to an idea that turned out to be completely erroneous.
Similarly impetus, a term popular in medieval times for discussing
Aristotle’s views on how objects in motion kept moving, lost its momentum once
Galileo and Newton debunked Aristotle.

In more
modern times, the word gene, like atom, initially described a
primitive idea, not yet fully formed. (Gene, referring to an element of
heredity, was coined by the Danish botanist Wilhelm Johannsen in 1909, decades
before anybody knew how DNA worked.) Over the last century the definition of
gene has evolved, though it’s still not as rigorously defined as all scientists would like.

Part of science’s
problem in linking words to meanings is (as experts in language repeatedly
remind us) that there’s always a gap between a word and the reality it
represents. “The word is not the thing,” the semanticist S.I. Hayakawa emphasized
in his famous book Language in Thought and Action, just as a map is not
identical to the territory it depicts. Some scientific terms serve as pretty
reliable maps of reality, while others turn out to be decoys leading to dead
ends. A major part of scientific progress is narrowing the gap between word and
thing — transforming vague labels into more specific symbols.

It’s easy
to find many current examples of scientific terms that mimic knowledge while
actually disguising a lack of understanding. “Dark matter” and “dark energy”
must exist, physicists insist, while admitting nobody yet can say what they
actually are. Other deep mysteries baffling today’s best scientific detectives
also reflect an inability to bring words closer to things. Consciousness
is a prime example, referring to mental processes that have eluded anything
approaching a coherent physical description. Intelligence comes a little
closer to intelligible meaning, but not sufficiently to avoid all sorts of
arguments about reproducing it artificially.

Another
favorite problem word for physicists, time, poses a plethora of puzzles.
For one thing, it has multiple meanings — time of day is not the same
thing as period of time is not the same thing as time travel. Physicists
still squabble over why time’s arrow points only to the future and whether the flow of time is an
objective physical fact or an illusion in a “block universe” where all events are already
sitting there, just waiting for a conscious observer to witness them. Of
course, it may turn out that time’s mysteries are problems more of language
than of physics. “We run into puzzles about the concept of time and then
we say, oh, what a terrible thing,” the physicist John Archibald
Wheeler once said. “We don’t realize we’re the source of the
puzzle because we invented the word.”

Only time
(another meaning) will tell whether words like time and consciousness
express ideas of greater depth than scientific understanding has yet reached. Maybe
consciousness and time will turn out to be prophetic terms, like atom,
that foreshadow the emergence of reliable scientific concepts. Or maybe time
and consciousness (and who know what other words) will go poof! like phlogiston.

In any
case, it’s remarkable how often words masquerading as ideas can eventually lead
to successful scientific endeavors. Entire fields of scientific research have grown
from word-seeds invented in the absence of substantiated ideas — atom
and gene being the best examples. As Goethe went on to note in Faust:

“With
words fine arguments can be weighted, with words whole systems can be created.”

But it
might be a good idea to remember that the character speaking those lines was
Mephistopheles, Goethe’s representative of the devil himself.