Posts Tagged ‘science’

by Mike McCrae

Everything in our Universe is held together or pushed apart by four fundamental forces: gravity, electromagnetism, and two nuclear interactions. Physicists now think they’ve spotted the actions of a fifth physical force emerging from a helium atom.

It’s not the first time researchers claim to have caught a glimpse of it, either. A few years ago, they saw it in the decay of an isotope of beryllium. Now the same team has seen a second example of the mysterious force at play – and the particle they think is carrying it, which they’re calling X17.

If the discovery is confirmed, not only could learning more about X17 let us better understand the forces that govern our Universe, it could also help scientists solve the dark matter problem once and for all.

Attila Krasznahorkay and his colleagues from the Institute for Nuclear Research in Hungary suspected something weird was going on back in 2016, after analysing the way an excited beryllium-8 emits light as it decays.

If that light is energetic enough, it transforms into an electron and a positron, which push away from one another at a predictable angle before zooming off.

Based on the law of conservation of energy, as the energy of the light producing the two particles increases, the angle between them should decrease. Statistically speaking, at least.

Oddly, this isn’t quite what Krasznahorkay and his team saw. Among their tally of angles there was an unexpected rise in the number of electrons and positrons separating at an angle of 140 degrees.

The study seemed robust enough, and soon attracted the attention of other researchers around the globe who suggested that a whole new particle could be responsible for the anomaly.

Not just any old particle; its characteristics suggested it had to be a completely new kind of fundamental boson.

That’s no small claim. We currently know of four fundamental forces, and we know that three of them have bosons carrying their messages of attraction and repulsion.

The force of gravity is carried by a hypothetical particle known as a ‘graviton’, but sadly scientists have not yet detected it.

This new boson couldn’t possibly be one of the particles carrying the four known forces, thanks to its distinctive mass of (17 megaelectronvolts, or about 33 times that of an electron), and tiny life span (of about 10 to the minus 14 seconds … but hey, it’s long enough to smile for the camera).

So all signs point to the boson being the carrier of some new, fifth force. But physics isn’t keen on celebrating prematurely. Finding a new particle is always big news in physics, and warrants a lot of scrutiny. Not to mention repeated experiment.

Fortunately, Krasznahorkay’s team haven’t exactly been sitting on their laurels over the past few years. They’ve since changed focus from looking at the decay of beryllium-8 to a change in the state of an excited helium nucleus.

Similar to their previous discovery, the researchers found pairs of electrons and positrons separating at an angle that didn’t match currently accepted models. This time, the number was closer to 115 degrees.

Working backwards, the team calculated the helium’s nucleus could also have produced a short-lived boson with a mass just under 17 megaelectronvolts.

To keep it simple, they’re calling it X17. It’s a long way from being an official particle we can add to any models of matter.

While 2016’s experiment was accepted into the respectable journal, Physical Review Letters, this latest study is yet to be peer reviewed. You can read the findings yourself on arXiv, where they’ve been uploaded to be scrutinised by others in the field.

But if this strange boson isn’t just an illusion caused by some experimental blip, the fact it interacts with neutrons hints at a force that acts nothing like the traditional four.

With the ghostly pull of dark matter posing one of the biggest mysteries in physics today, a completely new fundamental particle could point to a solution we’re all craving, providing a way to connect the matter we can see with the matter we can’t.

In fact, a number of dark matter experiments have been keeping an eye out for a 17 megavolt oddball particle. So far they’ve found nothing, but with plenty of room left to explore, it’s too early to rule anything out.

Rearranging the Standard Model of known forces and their particles to make room for a new member of the family would be a massive shift, and not a change to make lightly.

Still, something like X17 could be just what we’re looking for.

This research is available on arXiv ahead of peer review: https://arxiv.org/abs/1910.10459

https://www.sciencealert.com/physicists-claim-a-they-ve-found-even-more-evidence-of-a-new-force-of-nature

Doctors have placed humans in suspended animation for the first time, as part of a trial in the US that aims to make it possible to fix traumatic injuries that would otherwise cause death.

Samuel Tisherman, at the University of Maryland School of Medicine, told New Scientist that his team of medics had placed at least one patient in suspended animation, calling it “a little surreal” when they first did it. He wouldn’t reveal how many people had survived as a result.

The technique, officially called emergency preservation and resuscitation (EPR), is being carried out on people who arrive at the University of Maryland Medical Centre in Baltimore with an acute trauma – such as a gunshot or stab wound – and have had a cardiac arrest. Their heart will have stopped beating and they will have lost more than half their blood. There are only minutes to operate, with a less than 5 per cent chance that they would normally survive.

EPR involves rapidly cooling a person to around 10 to 15°C by replacing all of their blood with ice-cold saline. The patient’s brain activity almost completely stops. They are then disconnected from the cooling system and their body – which would otherwise be classified as dead – is moved to the operating theatre.

A surgical team then has 2 hours to fix the person’s injuries before they are warmed up and their heart restarted. Tisherman says he hopes to be able to announce the full results of the trial by the end of 2020.

At normal body temperature – about 37°C – our cells need a constant supply of oxygen to produce energy. When our heart stops beating, blood no longer carries oxygen to cells. Without oxygen, our brain can only survive for about 5 minutes before irreversible damage occurs. However, lowering the temperature of the body and brain slows or stops all the chemical reactions in our cells, which need less oxygen as a consequence.

Tisherman’s plan for the trial was that 10 people who receive EPR will be compared with 10 people who would have been eligible for the treatment but for the fact that the correct team wasn’t in the hospital at the time of admittance.

The trial was given the go-ahead by the US Food and Drug Administration. The FDA made it exempt from needing patient consent as the participants’ injuries are likely to be fatal and there is no alternative treatment. The team had discussions with the local community and placed ads in newspapers describing the trial, pointing people to a website where they can opt out.

Tisherman’s interest in trauma research was ignited by an early incident in his career in which a young man was stabbed in the heart after an altercation over bowling shoes. “He was a healthy young man just minutes before, then suddenly he was dead. We could have saved him if we’d had enough time,” he says. This led him to start investigating ways in which cooling might allow surgeons more time to do their job.

Animal studies showed that pigs with acute trauma could be cooled for 3 hours, stitched up and resuscitated. “We felt it was time to take it to our patients,” says Tisherman. “Now we are doing it and we are learning a lot as we move forward with the trial. Once we can prove it works here, we can expand the utility of this technique to help patients survive that otherwise would not.”

“I want to make clear that we’re not trying to send people off to Saturn,” he says. “We’re trying to buy ourselves more time to save lives.”

In fact, how long you can extend the time in which someone is in suspended animation isn’t clear. When a person’s cells are warmed up, they can experience reperfusion injuries, in which a series of chemical reactions damage the cell – and the longer they are without oxygen, the more damage occurs.

It may be possible to give people a cocktail of drugs to help minimise these injuries and extend the time in which they are suspended, says Tisherman, “but we haven’t identified all the causes of reperfusion injuries yet”.

Tisherman described the team’s progress on Monday at a symposium at the New York Academy of Sciences. Ariane Lewis, director of the division of neuro-critical care at NYU Langone Health, said she thought it was important work, but that it was just first steps. “We have to see whether it works and then we can start to think about how and where we can use it.”

Read more: https://www.newscientist.com/article/2224004-exclusive-humans-placed-in-suspended-animation-for-the-first-time/#ixzz65qFgVd3X

By Rory Sullivan

Although hiccups seem a nuisance, scientists have discovered they may play a crucial role in our development — by helping babies to regulate their breathing.

In a study led by University College London (UCL), researchers monitoring 13 newborn babies found that hiccupping triggered a large wave of brain signals which could aid their development.

Lorenzo Fabrizi, the study’s senior author, said in a statement that this brain activity might help babies “to learn how to monitor the breathing muscles,” eventually leading to an ability to control breathing voluntarily.

He added: “When we are born, the circuits which process body sensations are not fully developed, so the establishment of such networks is a crucial developmental milestone for newborns.”

Since the babies involved in the study were pre-term and full-term, ranging from 30 to 42 weeks gestational age, the scientists believe this development could be typical of the final trimester of pregnancy.

According to the researchers, fetuses and newborn infants often hiccup.

The phenomenon is seen as early as nine weeks into pregnancy, and pre-term infants — those born at least three weeks premature — spend approximately 15 minutes hiccupping every day.

The pre-term and full-term newborns involved in the study had electrodes placed on their scalps and sensors on their torsos to monitor for hiccups.

Scientists found that contractions in the babies’ diaphragms produced three brainwaves, and believe that through the third brainwave babies may be able to link the ‘hic’ sound of the hiccup to the physical contraction they feel.

Kimberley Whitehead, the study’s lead author, told CNN: “The muscle contraction of a hiccup is quite big — it’s good for the developing brain because it suddenly gives a big boost of input, which helps the brain cells to all link together for representing that particular body part.”

She added that hiccups have no known advantage for adults, and suggested they could be an example of “a hangover from early periods of our life that persists into later life.”

The same researchers have previously theorized that a baby’s kicks in the womb may help it to create a mental map of its own body.

Their new findings may show the same process occurring internally.

https://www.cnn.com/2019/11/12/health/babies-hiccup-wellness-scli-intl-scn/index.html?utm_source=The+Good+Stuff&utm_campaign=2aa589d67e-EMAIL_CAMPAIGN_2019_11_14_08_33&utm_medium=email&utm_term=0_4cbecb3309-2aa589d67e-103653961

By Kristin Houser

Down syndrome is a cognitive disability that can affect a person’s memory or ability to learn — intellectual impairments researchers traditionally thought were untreatable and irreversible.

But now, researchers from the University of California San Francisco and Baylor College of Medicine say they’ve reversed the impairments in mouse models of Down syndrome — potentially foreshadowing an ethically-fraught future in which doctors can do the same for humans with the condition.

All people with Down syndrome share one thing in common: an extra copy of chromosome 21. For that reason, much of the research on Down syndrome has focused on genetics.

But for this new study, published Friday in the prestigious journal Science, researchers focused on the protein-producing cells in the brains of mice with Down syndrome. That led them to the discovery that the animals’ hippocampus regions produced 39 percent less protein than those of typical mice.

Further study led the researchers to conclude that the presence of an extra chromosome likely prompted the animals’ hippocampal cells to trigger the integrated stress response (ISR), which decreased protein production.

“The cell is constantly monitoring its own health,” researcher Peter Walter said in a press release. “When something goes wrong, the cell responds by making less protein, which is usually a sound response to cellular stress. But you need protein synthesis for higher cognitive functions, so when protein synthesis is reduced, you get a pathology of memory formation.”

By blocking the activity of PKR, the enzyme that prompted the ISR in the mouse model’s hippocampal cells, the researchers found they could not only reverse the decreased protein production but also improve the animals’ cognitive function.

Of course, just because something works in mice doesn’t mean it’ll work in humans.

However, when the researchers analyzed postmortem brain tissue samples of people with Down syndrome, they found evidence that the ISR had been activated. They also obtained a tissue sample from a person with Down syndrome who only had the extra copy of chromosome 21 in some of their cells — and those cells were the only ones with ISR activated.

“We started with a situation that looked hopeless,” Walter said. “Nobody thought anything could be done. But we may have struck gold.”

https://futurism.com/neoscope/scientists-reverse-cognitive-deficiets-of-down-syndrome-mice

Thanks to Kebmodee for bringing this to the It’s Interesting community.

Biology encodes information in DNA and RNA, which are complex molecules finely tuned to their functions. But are they the only way to store hereditary molecular information? Some scientists believe life as we know it could not have existed before there were nucleic acids, thus understanding how they came to exist on the primitive Earth is a fundamental goal of basic research. The central role of nucleic acids in biological information flow also makes them key targets for pharmaceutical research, and synthetic molecules mimicking nucleic acids form the basis of many treatments for viral diseases, including HIV. Other nucleic acid-like polymers are known, yet much remains unknown regarding possible alternatives for hereditary information storage. Using sophisticated computational methods, scientists from the Earth-Life Science Institute (ELSI) at the Tokyo Institute of Technology, the German Aerospace Center (DLR) and Emory University explored the “chemical neighbourhood” of nucleic acid analogues. Surprisingly, they found well over a million variants, suggesting a vast unexplored universe of chemistry relevant to pharmacology, biochemistry and efforts to understand the origins of life. The molecules revealed by this study could be further modified to gives hundreds of millions of potential pharmaceutical drug leads.

Nucleic acids were first identified in the 19th century, but their composition, biological role and function were not understood by scientists until the 20th century. The discovery of DNA’s double-helical structure by Watson and Crick in 1953 revealed a simple explanation for how biology and evolution function. All living things on Earth store information in DNA, which consists of two polymer strands wrapped around each other like a caduceus, with each strand being the complement of the other. When the strands are pulled apart, copying the complement on either template results in two copies of the original. The DNA polymer itself is composed of a sequence of “letters”, the bases adenine (A), guanine (G), cytosine (C) and thymine (T), and living organisms have evolved ways to make sure during DNA copying that the appropriate sequence of letters is almost always reproduced. The sequence of bases is copied into RNA by proteins, which then is read into a protein sequence. The proteins themselves then enable a wonderland of finely-tuned chemical processes which make life possible.

Small errors occasionally occur during DNA copying, and others are sometimes introduced by environmental mutagens. These small errors are the fodder for natural selection: some of these errors result in sequences which produce fitter organisms, though most have little effect, and many even prove lethal. The ability of new sequences to allow their hosts to better survive is the “ratchet” which allows biology to almost magically adapt to the constantly changing challenges the environment provides. This is the underlying reason for the kaleidoscope of biological forms we see around us, from humble bacteria to tigers, the information stored in nucleic acids allows for “memory” in biology. But are DNA and RNA the only way to store this information? Or are they perhaps just the best way, discovered only after millions of years of evolutionary tinkering?

“There are two kinds of nucleic acids in biology, and maybe 20 or 30 effective nucleic acid-binding nucleic acid analogues. We wanted to know if there is one more to be found or even a million more. The answer is, there seem to be many, many more than was expected,” says professor Jim Cleaves of ELSI.

Though biologists don’t consider them organisms, viruses also use nucleic acids to store their heritable information, though some viruses use a slight variant on DNA, RNA, as their molecular storage system. RNA differs from DNA in the presence of a single atom substitution, but overall RNA plays by very similar molecular rules as DNA. The remarkable thing is, among the incredible variety of organisms on Earth, these two molecules are essentially the only ones biology uses.

Biologists and chemists have long wondered why this should be. Are these the only molecules that could perform this function? If not, are they perhaps the best, that is to say, other molecules could play this role, and perhaps biology tried them out during evolution?

The central importance of nucleic acids in biology has also long made them drug targets for chemists. If a drug can inhibit the ability of an organism or virus to pass its knowledge of how to be infectious on to offspring, it effectively kills the organisms or virus. Mucking up the heredity of an organism or virus is a great way to knock it dead. Fortunately for chemists, and all of us, the cellular machinery which manages nucleic acid copying in each organism is slightly different, and in viruses often very different.

Organisms with large genomes, like humans, need to be very careful about copying their hereditary information and thus are very selective about not using the wrong precursors when copying their nucleic acids. Conversely, viruses, which generally have much smaller genomes, are much more tolerant of using similar, but slightly different molecules to copy themselves. This means chemicals that are similar to the building blocks of nucleic acids, known as nucleotides, can sometimes impair the biochemistry of one organism worse than another. Most of the important anti-viral drugs used today are nucleotide (or nucleoside, which are molecule differing by the removal of a phosphate group) analogues, including those used to treat HIV, herpes and viral hepatitis. Many important cancer drugs are also nucleotide or nucleoside analogues, as cancer cells sometimes have mutations that make them copy nucleic acids in unusual ways.

“Trying to understand the nature of heredity, and how else it might be embodied, is just about the most basic research one can do, but it also has some really important practical applications,” says co-author Chris Butch, formerly of ELSI and now a professor at Nanjing University.

Since most scientists believe the basis of biology is heritable information, without which natural selection would be impossible, evolutionary scientists studying the origins of life have also focused on ways of making DNA or RNA from simple chemicals that might have occurred spontaneously on primitive Earth. Once nucleic acids existed, many problems in the origins of life and early evolution would make sense. Most scientists think RNA evolved before DNA, and for subtle chemical reasons which make DNA much more stable than RNA, DNA became life’s hard disk. However, research in the 1960s soon split the theoretical origins field in two: those who saw RNA as the simple “Occam’s Razor” answer to the origins-of-biology problem and those who saw the many kinks in the armour of RNA’s abiological synthesis. RNA is still a complicated molecule, and it is possible structurally simpler molecules could have served in its place before it arose.

Co-author Dr. Jay Goodwin, a chemist with Emory University says “It is truly exciting to consider the potential for alternate genetic systems, based on these analogous nucleosides – that these might possibly have emerged and evolved in different environments, perhaps even on other planets or moons within our solar system. These alternate genetic systems might expand our conception of biology’s ‘central dogma’ into new evolutionary directions, in response and robust to increasingly challenging environments here on Earth.”

Examining all of these basic questions, which molecule came first, what is unique about RNA and DNA, all at once by physically making molecules in the laboratory, is difficult. On the other hand, computing molecules before making them could potentially save chemists a lot of time. “We were surprised by the outcome of this computation,” says co-author Dr. Markus Meringer, “it would be very difficult to estimate a priori that there are more than a million nucleic-acid like scaffolds. Now we know, and we can start looking into testing some of these in the lab.”

“It is absolutely fascinating to think that by using modern computational techniques we might stumble upon new drugs when searching for alternative molecules to DNA and RNA that can store hereditary information. It is cross-disciplinary studies such as this that make science challenging and fun yet impactful,” says co-author Dr. Pieter Burger, also of Emory University.

###

Reference:

Henderson James Cleaves, II*1,2,3, Christopher Butch1,3,4, Pieter Buys Burger4, Jay Goodwin4, and Markus Meringer5, One Among Millions: The Chemical Space of Nucleic Acid-Like Molecules, Journal of Chemical Information and Modeling, DOI: 10.1021/acs.jcim.9b00632

1. Earth-Life Science Institute, Tokyo Institute of Technology, 2-12-IE-1 Ookayama, Meguro-ku, Tokyo 152-8551, Japan
2. Institute for Advanced Study, Princeton, New Jersey 08540, United States

3. Blue Marble Space Institute for Science, 1515 Gallatin St. NW, Washington, DC 20011, United States

4. Department of Chemistry, Emory University, 1515 Dickey Dr., Atlanta, Georgia 30322, United States

5. German Aerospace Center (DLR), Earth Observation Center (EOC), Münchner Straße 20, 82234 Oberpfaffenhofen-Wessling, Germany

https://www.eurekalert.org/pub_releases/2019-11/tiot-dio103119.php


Francisco Lopera, a neurologist at the University of Antioquia in Medellin, Colombia, has been painstakingly collecting brains, birth and death records from one sprawling Colombian family to study Alzheimer’s.Credit…Federico Rios Escobar for The New York Times


A woman with lots of beta-amyloid buildup (red) in her brain remained cognitively healthy for decades.

by Kelly Servick

In 2016, a 73-year-old woman from Medellín, Colombia, flew to Boston so researchers could scan her brain, analyze her blood, and pore over her genome. She carried a genetic mutation that had caused many in her family to develop dementia in middle age. But for decades, she had avoided the disease. The researchers now report that another rare mutation—this one in the well-known Alzheimer’s disease risk gene APOE—may have protected her. They can’t prove this mutation alone staved off disease. But the study draws new attention to the possibility of preventing or treating Alzheimer’s by targeting APOE—an idea some researchers say has spent too long on the sidelines.

“This case is very special,” says Yadong Huang, a neuroscientist at the Gladstone Institutes in San Francisco, California, who was not involved with the research. “This may open up a very promising new avenue in both research and therapy.”

APOE, the strongest genetic risk factor for Alzheimer’s, has three common forms. A variant called APOE2 lowers risk of the disease. The most common variant, APOE3, doesn’t influence risk. APOE4 raises risk; roughly half of the people with the disease have at least one copy of this variant.

Researchers have long contemplated targeting APOE with therapies. A team at Cornell University will soon start a clinical trial that infuses the protective APOE2 gene into the cerebrospinal fluid of people with two copies of APOE4.

But mysteries about APOE have kept it from becoming a front-runner among drug targets. “It does so many things that it’s confusing,” says Eric Reiman, a neuroscientist at the Banner Alzheimer’s Institute in Phoenix and a co-author on the new paper. The APOE protein binds and transports fats and is abundant in the brain. And the APOE4 variant seems to encourage the formation of sticky plaques of the protein beta-amyloid, which clog the brain in Alzheimer’s. But powerful amyloid-busting drugs have repeatedly failed to benefit patients in clinical trials. Some researchers saw no reason to try an APOE-targeting therapy that seemed to be “just a poor man’s antiamyloid treatment,” Reiman says.

The Colombian woman’s case suggests other ways APOE could affect Alzheimer’s risk. The woman participated in a study led by researchers at the University of Antioquia in Medellín that has tracked roughly 6000 members of her extended family. About one-fifth of them carried an Alzheimer’s-causing mutation in a gene called presenilin 1; these carriers generally developed dementia in their late 40s. Yet the woman didn’t show the first signs of the disease until her 70s, even though she, too, carried the mutation. “She’s definitely an outlier,” says cell biologist Joseph Arboleda-Velasquez of Harvard Medical school in Boston. (The research team is keeping the woman’s name confidential to protect her privacy.)

In Boston, a positron emission tomography scan of the woman’s brain revealed more amyloid buildup than in any other family member who has been scanned. “It was very striking,” says Yakeel Quiroz, a clinical neuropsychologist at Massachusetts General Hospital and Harvard Medical School. But the team found no signs of major damage to neurons, and minimal buildup of another Alzheimer’s hallmark: the misfolded protein tau. Whatever protection this woman had didn’t depend on keeping the brain amyloid-free. Instead, her case supports the idea that tau has a “critical role … in the clinical manifestations of Alzheimer’s disease,” says Jennifer Yokoyama, a neurogeneticist at the University of California, San Francisco.

Genome sequencing revealed two copies of a rare mutation in the APOE gene, the researchers report this week in Nature Medicine. First discovered in 1987, the mutation, known as Christchurch, occurs in a region separate from those that determine a person’s APOE2, 3, or 4 status. (The woman has the neutral APOE3 variant.) Previous research found that the Christchurch mutation—like the more common protective APOE2 mutation—impairs APOE’s ability to bind to and clear away fats and sometimes leads to cardiovascular disease.

The researchers also found that the mutation prevents APOE from binding strongly to other molecules called heparan sulfate proteoglycans (HSPGs), which coat neurons and other cells “like a carpet,” says Guojun Bu, a neuroscientist at the Mayo Clinic in Jacksonville, Florida, who has studied the interaction between these molecules and APOE.

APOE2 may also impair the protein’s ability to bind HSPGs. But how that could protect against disease isn’t clear. One possible clue: Research by neuroscientist Marc Diamond of the University of Texas Southwestern Medical Center in Dallas and his colleagues suggest the toxic tau protein relies on HSPGs to help it spread between cells. Maybe the less APOE binds to HSPGs, the harder it is for tau to spread.

But, Diamond cautions, “It will require much more study to understand if this relationship exists.” The Christchurch mutation might have protective effects unrelated to HSPGs; it’s also possible that mutations other than Christchurch protected the woman.

If hampering APOE’s normal binding really staved off her Alzheimer’s, future treatments might aim to mimic that effect. An antibody or small molecule could latch onto the APOE protein to interfere with binding, gene editing could change the structure of APOE to imitate the Christchurch variant, or a “gene silencing” approach could reduce production of APOE altogether.

Reiman hopes the new study will rally researchers to pursue treatments related to APOE. He, Quiroz, Arboleda-Velasquez, and other collaborators also posted a preprint on the medRxiv server on 2 November showing that people with two copies of APOE2 have lower Alzheimer’s risk than previously thought—about 99% lower than people with two copies of APOE4. “When it comes to finding a treatment that could have a profound impact on the disease,” Reiman says, “APOE may be among the lowest hanging fruit.”

https://science.sciencemag.org/content/366/6466/674


With pressure to “publish or perish,” some scientists fake their research results. Elisabeth Bik spends her days correcting them.

by Gemma Milne

Elisabeth Bik spends her days trawling scientific papers, life sciences papers in particular, looking for signs of image manipulation. Put another way, she plays a backward game of “spot the difference” (backward because it’s more like “spot the similarity”) to seek out fraudulent work posing as science. She does this for free, week after week, along with other online science misconduct sleuths, in the pursuit of correcting the record upon which the world’s knowledge is based.

She is a self-appointed, image-manipulation detective — the Sherlock Holmes of science fraud.

It started with plagiarism before plagiarism became easy to catch. After reading about its prevalence in scientific papers, Bik, who had a 15-year career as a microbiology researcher, searched Google Scholar and found her own work had been copied. Then she set about finding other instances of this particular fraud. On one such investigation, she found a PhD thesis that not only had plagiarized text, but also an image that was reused throughout. The author had been trying to pass off the same image as a series of distinct results. “[The image] was mirrored, or turned around, but it had a very distinct little smear, which I recognized,” she says.

After reporting the fraudulent thesis to the university, resulting in its retraction, Bik realized she’d stumbled upon a new, strange hobby. “That was something I was good at, recognizing these patterns,” she says, “and so I started doing that more and more.” She soon found herself going through swaths of research papers during her evenings and weekends, and looking forward to getting home from her day job to continue.

It wasn’t long before Bik had amassed a huge collection of fraudulent papers. In 2016, she co-authored a paper revealing the fruits of her labor. Within her manual search of more than 20,000 pieces of biomedical research, 4% contained manipulated images. She reported those 800 papers, and she’s continued searching, sharing, and reporting ever since.

One of the initial 800 papers she reported was by Min-Jean Yin, who led the Pfizer California cancer lab at the time of the paper’s publication. It contained duplicated images of western blots, a common test used to detect specific protein molecules. The images produced from the test are the data, so editing them essentially amounts to chopping and changing results to fit whatever hypothesis the scientist is trying to prove.

After Bik reported the abnormalities both on popular research discussion forum PubPeer as well as on the science misconduct blog For Better Science, Pfizer not only fired Yin but also opened up a larger investigation into her years of work at their lab. This led them to retract many of her published papers focused on cancer therapeutics.


Image from the PubPeer listing questioning of one of Yin’s 2011 papers, with the red box annotating a copied crop. Credit: PubPeer

Bik is prolific on PubPeer and on Twitter, where she posts multicolored annotated graphics that point out how images have been manipulated to nearly 40,000 followers. “I’ve been a very quiet microbiologist until a few years ago when I joined Twitter,” she says with a laugh.

After earning a PhD in the Netherlands, 15 years at Stanford, and a few years in the science startup scene, this year, both Bik and her husband decided to take the leap into working on personal projects instead of for companies. Looking for fraud in research is more than just a fun hobby for Bik. “I’ve found this niche that I feel I can make a difference in,” she says. “I felt it was calling me.”

Bik often picks open-access journals, as they’re easier to flick through, or papers that are requested by other scientists who are tipping her off. “What I’m doing now is going into all the image manipulation cases I’ve already found and finding other papers by the same author, which could be in other journals.”

Living off savings, Bik reckons she has about a year’s leeway to work on her image manipulation sleuthing and hopes to find a way of monetizing her expertise as a science misconduct consultant to journals.

Published work in prestigious academic journals is the main currency of the science world, and career progression, respect, and compensation are often linked to publishing reputation. The most significant journals only publish research with big implications and strong evidence that represents a leap in knowledge, not just an incremental addition. Unfortunately, this can’t always be achieved through grit, hard work, and the right area of research, so some scientists succumb to “publish or perish” pressure by editing their images to show clearer results, re-using images to convey “desirable” scientific claims, or photoshopping their graphs to back up false, but exciting findings.

Other scientists may spend years of time and huge amounts of research funding trying to build upon false science. “My goal is not to have people disciplined; my goal is to correct the science,” Bik explains.

Despite Bik’s work finding these manipulations, she estimates that only 30% of those papers have been corrected or retracted. “By tweeting about it, I hope to accomplish two things,” she explains. “First, put pressure on journals to react, like those viral videos where people are mistreated on airplanes. And second, make them aware that fraud happens, so when they see a paper, they know what to look for.”

Journals are notoriously bad at handling scientific misconduct. Sometimes this failing is understandable: Correcting or retracting a published paper could mean getting in touch with a myriad of authors, who may have since changed universities, never reply, or be unable to produce the original data. It requires time and patience to hunt down either the rationale for an honest mistake or the admission of misconduct, and it reduces the bottom line of these profit-making enterprises.

But sometimes the lack of investigation is unjustified. Journals have been known to reject complaints that aren’t submitted correctly through their complex and out-of-date online systems, or — more worryingly — come from anonymous submissions. Ivan Oransky, co-founder of Retraction Watch, which keeps track of scientific retractions, says: “I would love for scientists, journals, and universities who refuse to take seriously anonymous complaints and allegations about papers to tell me how they feel about the anonymous whistle-blower [who brought forth concerns about President Donald Trump’s dealings with Ukraine].”

Because reputation is paramount in science, anonymity is often required.

Much of the sleuthing is done by active scientists who use pseudonyms for fear of being ousted by their university or ostracized by the affected researchers. One such sleuth is Smut Clyde who, like Bik, spends huge amounts of time finding irregularities, knowing that their anonymous posts may not be accepted by the journals. “There are an awful lot of scientists [committing fraud]. Just picking out one or two doesn’t really make much of a difference — it’s just a drop in the ocean,” they told OneZero. “The best we can hope for is to raise awareness that the ocean is rather full already and ultimately shift the incentives. It’s more long-term than identifying one particular person who is up to no good.”

Bik is well-known and well-respected within the science misconduct community, not only for the prolific nature of her work but also because she writes and reports under her own name. In some ways, then, Bik is a surrogate for so many. She posts and reports publicly, often after being tipped off to papers from those who aren’t able to do it themselves: “Every day I get a new request.”

“I hope more people join me in the image manipulation search, as I feel we need more people doing this. There’s so many papers and I feel we need to clean ship.”
It’s the volunteers, the puzzle aficionados, the ones who do it because they feel they must, that are holding science to account. Conan Doyle’s fictional Sherlock Holmes famously inspired changes in police reporting; maybe one day the tenacity and sharp eyes of Bik and the rest of the image manipulation sleuths might inspire the institutions of science to do the same.

https://onezero.medium.com/this-science-vigilante-calls-out-bogus-results-in-prestigious-journals-eb5a414c7f76