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Sensory feedback is important for amputees to be able to explore and interact with their environment. Now, researchers have developed a device that allows amputees to sense and respond to temperature by delivering thermal information from the prosthesis’ fingertip to the amputee’s residual limb. The “MiniTouch” device, presented February 9 in the journal Med, uses off-the-shelf electronics, can be integrated into commercially available prosthetic limbs, and does not require surgery. Using the thermally sensitive prosthetic hand, a 57-year-old transradial amputee was able to discriminate between and manually sort objects of different temperatures and sense bodily contact with other humans.
“This is a very simple idea that can be easily integrated into commercial prostheses,” says senior author Silvestro Micera of École Polytechnique Fédérale de Lausanne and Scuola Superiore Sant’Anna. “Temperature is one of the last frontiers to restoring sensation to robotic hands. For the first time, we’re really close to restoring the full palette of sensations to amputees.”
The team previously showed that their thermosensitive technology could restore passive thermosensation in 17/27 amputees. In the new study, they show that the MiniTouch can be easily integrated into commercial prosthetic limbs and that it enables active thermosensation during tasks that require feedback between sensory and motor neurons.
Beyond the functional importance of being able to sense hot and cold, thermal information could also improve amputees’ sense of embodiment and their ability to experience affective touch. “Adding temperature information makes the touch more human-like,” says senior author Solaiman Shokur of École Polytechnique Fédérale de Lausanne. “We think having the ability to sense temperature will improve amputees’ embodiment — the feeling that ‘this hand is mine.'”
To do this, they integrated the MiniTouch into the personal prosthesis of a 57-year-old male who had undergone a transradial amputation 37 years earlier by linking the device to a point on the participant’s residual limb that elicited thermal sensations in his phantom index finger. Then, they tested his ability to distinguish between objects of different temperatures and objects made of different materials.
Using the MiniTouch, the participant was able to discriminate between three visually indistinguishable bottles containing either cold (12°C), cool (24°C), or hot (40°C) water with 100% accuracy, whereas without the device, his accuracy was only 33%. The MiniTouch device also improved his ability to quickly and accurately sort metal cubes of different temperatures.
“When you reach a certain level of dexterity with robotic hands, you really need to have sensory feedback to be able to use the robotic hand to its full potential,” says Shokur.
Finally, the MiniTouch device improved the participant’s ability to differentiate between human and prosthetic arms while blindfolded — from 60% accuracy without the device to 80% with the device. However, his ability to sense human touch via his prosthesis was still limited compared to his uninjured arm, and the researchers speculate that this was due to limitations in other non-thermal sensory inputs such as skin softness and texture. Other technologies are available to enable these other sensory inputs, and the next step is to begin integrating those technologies into a single prosthetic limb.
“Our goal now is to develop a multimodal system that integrates touch, proprioception, and temperature sensations,” says Shokur. “With that type of system, people will be able to tell you ‘this is soft and hot,’ or ‘this is hard and cold.'”
The researchers say that their technology is ready for use from a technical point of view, but more safety tests are needed before it reaches the clinic, and they have plans to further improve the device so that it can be more easily fitted. Future models could also build upon the Minitouch to integrate thermal information from multiple points on an amputee’s phantom limb — for example, allowing people to differentiate thermal and tactile sensations on their finger and thumb might help them grasp a hot beverage, while enabling sensation in the back of the hand might improve the feeling of human connection by allowing amputees to sense when another person touches their hand.

A technique can determine for the first time how frequently, and exactly where, a molecular event called “backtracking” occurs throughout the genetic material (genome) of any species, a new study shows.
Published online February 9 in Molecular Cell, the study results support the theory that backtracking represents a widespread form of gene regulation, which influences thousands of human genes, including many involved in basic life processes like cell division and development in the womb.
Led by researchers from NYU Grossman School of Medicine, the work revolves around genes, the stretches of DNA molecular “letters” arranged in a certain order (sequence) to encode the blueprints for most organisms. In both humans and bacteria, the first step in a gene’s expression, transcription, proceeds as a protein “machine” called RNA polymerase II ticks down the DNA chain, reading genetic instructions in one direction.
In 1997, Evgeny Nudler, PhD and colleagues published a paper that showed RNA polymerase can sometimes slip backward along the chain it is reading, a phenomenon they named “backtracking.” Studies since then have shown that backtracking occasionally takes place in living cells soon after RNA polymerase begins RNA synthesis or when it encounters damaged DNA to make room for incoming repair enzymes. Subsequent work suggested that the backsliding and repair machinery had to work quickly and dissipate, or it might collide with DNA polymerase to cause cell-death-inducing breaks in DNA chains.
Now a new study led by Nudler’s team at NYU Langone Health reveals that their new technique, Long Range Cleavage sequencing (LORAX-seq), can directly detect where backtracking events begin and end. By complementing past approaches that were indirect or limited, the new method reveals that many such events move backward further than once thought, and in doing so, last longer. The results also suggest that persistent backtracking occurs frequently throughout genomes, happens more often near certain gene types, and has functions well beyond DNA repair.
“The surprising stability of backtracking at longer distances makes it likely that it represents a ubiquitous form of genetic regulation in species from bacteria to humans,” says Nudler, the study’s senior author, and the Julie Wilson Anderson Professor in the Department of Biochemistry and Molecular Pharmacology at NYU Langone. “If further work expands our findings to different developmental programs and pathological conditions, backtracking may be akin to epigenetics, the discovery of which revealed a surprising new layer of gene regulation without changing the DNA code.”
Central to Life?
RNA polymerase II translates DNA code into a related material called RNA, which then directs the building of the proteins. To do so, the complex moves down DNA chains in one direction, but backtracks in certain scenarios. Past studies have shown that as RNA polymerase II backtracks, it forces out (extrudes) from its interior channel the tip of the RNA chain it has been building based on the DNA code. As prolonged backtracking is prone to causing detrimental collisions, transcription is thought to be quickly restored by the transcription factor IIS (TFIIS), which promotes the cutting off (cleavage) of the extruded, “backtracked” RNA. This clears the way for RNA polymerase II to resume its forward code reading.

Other, earlier studies, however, had shown that when polymerase backtracks beyond a certain distance (e.g. 20 nucleobase DNA building blocks), the backtracked RNA can attach to the channel through which it is extruded, holding it in place longer. Locked, backtracked complexes are less likely to be rescued by TFIIS-driven cleavage, and more likely to delay transcription of the gene involved. This led to theory that backtracking, in addition to playing a key role in DNA repair pathways, may dial up or down the action of genes as a major regulatory mechanism.
According to the researchers, TFIIS likely occurs at low concentrations in living cells, and competes with hundreds of other proteins to get at and cut out backtracked RNA so transcription can continue. In the current study, the team instead used a high concentration of purified TFIIS (no competing proteins) to precisely cut out any piece of backtracked RNA anywhere it occurs in a cell’s genetic code. This made the cut-out snippets available to technologies that read code sequences and provide clues to their locations and functions.
The research team also found that the genes that control histones — protein “spools” that DNA chains wrap around within the chromatin that organizes gene expression — are highly prone to persistent backtracking. The authors theorize that the degree to which this happens, with related changes in the transcription of certain genes, may control the timing of large-scale histone accumulation needed during cell division to rebuild chromatin. They also suggest that persistent backtracking may influence the timely transcription of genes vital to tissue development.
“Along with its potentially useful functions, persistent backtracking could also result in DNA damage and other genetic malfunctions that contribute to disease,” says first study author Kevin Yang, a graduate student in Dr. Nudler’s lab. “We speculate that the measurement of backtracking in the context of aging or cancer, for instance, may help us understand why malfunctions occur in the cell stress response and cell replication, and to suggest new treatment approaches.”
Along with Yang and Nudler, study authors from the Department of Biochemistry and Molecular Pharmacology at NYU Langone Health were Aviram Rasouly, Vitaly Epshtein, Criseyda Martinez, Thao Nguyen, and Ilya Shamovsky. Nudler is also an Investigator with the Howard Hughes Medical Institute. The study is funded by the Blavatnik Family Foundation, Howard Hughes Medical Institute, and National Institutes of Health grants R01GM126891 and T32 AI007180.

Since 2018, the agency has mandated tracking the genetic signatures of viruses collected from people with H.I.V., a practice known as molecular surveillance.The Centers for Disease Control and Prevention on Friday revised its guidelines for tracking the genetic signatures of viruses collected from people newly diagnosed with H.I.V., a controversial practice used by state and local health departments to curb infections.The updated policy encouraged health officials to be more transparent with their communities about the tracking, one of many changes sought by H.I.V. advocacy organizations concerned about how so-called molecular surveillance could violate patients’ privacy and civil rights.But the agency stopped short of adopting more significant changes that some advocates had pushed for, such as allowing health agencies to opt out in states where people can be prosecuted for transmitting H.I.V.“We’re in a period in which health data is increasingly used in criminal prosecutions, as seen in prosecutions of people seeking abortion care or who have perhaps miscarried,” said Carmel Shachar, a professor at Harvard Law School who specializes in health care. The revised policy did not go far enough, she said, to protect people with H.I.V.Dr. Alexandra Oster, who leads the C.D.C.’s molecular surveillance team, said the benefits of the program far exceed the risks. “We need to do it well,” she said. “But we need to keep doing it.”H.I.V. has a distinctive genetic signature in each person that helps doctors decide which drugs are likely to thwart it. But the information can also be used to track its spread through a population — including identifying clusters of people who carry closely related viruses.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

Damian R. Murray, a psychologist at Tulane University, studies how various social circumstances and life events affect people’s political views. For instance, he found recently, becoming a parent makes a person grow more socially conservative. On the eve of the Super Bowl, he sat down for an interview with The New York Times to discuss another recent study, which examined how the political perspectives of sports fans can be altered by their teams’ wins and losses.This conversation has been edited and condensed for clarity.What inspired this work?These games are so emotionally potent, and people are so emotionally invested. The question is: What might be the downstream, real-world implications for things that have nothing to do with the sporting event itself? Are there consequences for political attitudes or voting patterns, or for our group affiliations?To be clear, we’re talking about fans, not people actually playing in the game.Right. As viewers, we’re experiencing the ups and downs of athletes that we otherwise have no relationship to. The material changes that we experience, whether the players win or lose, are essentially zero. But we still go along on this psychological ride.Can you describe the research?We did two different studies in two different populations. The first sample was of British people in England during the 2016 Euro Cup. a monthlong tournament held every four years to determine the best national soccer team in Europe.It’s huge over there, the closest thing to the Super Bowl, outside of the World Cup. So we sampled British people immediately after significant wins and losses in the tournament. We asked questions about their national in-group bias — which is, for example, how intelligent or charismatic they perceived a typical United Kingdom resident to be. We also asked them about what we call their financial egalitarianism.Which is?We asked them whether they agreed or disagreed that it’s the responsibility of better-off people to help those who are worse off, and things like that. It gets at how tolerant people are of financial inequality.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

Published4 minutes agoShareclose panelShare pageCopy linkAbout sharingImage source, PA MediaJunior doctors in England will strike on five days from 24 to 28 February, in an ongoing dispute with the government about pay.The British Medical Association (BMA), which represents junior doctors, wants a 35% pay increase, which was previously rejected by ministers.More on this storyGive us credible offer and we’ll end strikes – BMAPublished3 JanuaryRelated Internet LinksBritish Medical AssociationThe BBC is not responsible for the content of external sites.

The onset of psychosis can be predicted before it occurs, using a machine-learning tool which can classify MRI brain scans into those who are healthy and those at risk of a psychotic episode. An international consortium including researchers from the University of Tokyo, used the classifier to compare scans from over 2,000 people from 21 global locations. About half of the participants had been identified as being clinically at high risk of developing psychosis. Using training data, the classifier was 85% accurate at differentiating between people who were not at risk and those who later experienced overt psychotic symptoms. Using new data, it was 73% accurate. This tool could be helpful in future clinical settings, as while most people who experience psychosis make a full recovery, earlier intervention typically leads to better outcomes with less negative impact on people’s lives.
Anyone might experience a psychotic episode, which commonly involves delusions, hallucinations or disorganized thinking. There is no single cause, but it can be triggered by illness or injury, trauma, drug or alcohol use, medication, or a genetic predisposition. Although it can be scary or unsettling, psychosis is treatable and most people recover. As the most common age for a first episode is during adolescence or early adulthood, when the brain and body are undergoing a lot of change, it can be difficult to identify young people in need of help.
“At most only 30% of clinical high-risk individuals later have overt psychotic symptoms, while the remaining 70% do not,” explained Associate Professor Shinsuke Koike from the Graduate School of Arts and Sciences at the University of Tokyo. “Therefore, clinicians need help to identify those who will go on to have psychotic symptoms using not only subclinical signs, such as changes in thinking, behavior and emotions, but also some biological markers.”
The consortium of researchers have worked together to create a machine-learning tool which uses brain MRI scans to identify people at risk of psychosis before it starts. Previous studies using brain MRI have suggested that structural differences occur in the brain after the onset of psychosis. However, this is reportedly the first time that differences in the brains of those who are at very high risk but have not yet experienced psychosis have been identified.
The team from 21 different institutions in 15 different countries gathered a large and diverse group of adolescent and young adult participants. According to Koike, MRI research into psychotic disorders can be challenging because variations in brain development and in MRI machines make it difficult to get very accurate, comparable results. Also, with young people, it can be difficult to differentiate between changes that are taking place because of typical development and those due to mental illness.
“Different MRI models have different parameters which also influence the results,” explained Koike. “Just like with cameras, varied instruments and shooting specifications create different images of the same scene, in this case the participant’s brain. However, we were able to correct for these differences and create a classifier which is well tuned to predicting psychosis onset.”
The participants were divided into three groups of people at clinical high risk: those who later developed psychosis; those who didn’t develop psychosis; and people with uncertain follow-up status (1,165 people in total for all three groups), and a fourth group of healthy controls for comparison (1,029 people). Using the scans, the researchers trained a machine-learning algorithm to identify patterns in the brain anatomy of the participants. From these four groups, the researchers used the algorithm to classify participants into two main groups of interest: healthy controls and those at high risk who later developed overt psychotic symptoms.
In training, the tool was 85% accurate at classifying the results, while in the final test using new data it was 73% accurate at predicting which participants were at high risk of psychosis onset. Based on the results, the team considers that providing brain MRI scans for people identified as being at clinically high risk may be helpful for predicting future psychosis onset.
“We still have to test whether the classifier will work well for new sets of data. Since some of the software we used is best for a fixed data set, we need to build a classifier that can robustly classify MRIs from new sites and machines, a challenge which a national brain science project in Japan, called Brain/MINDS Beyond, is now taking on,” said Koike. “If we can do this successfully, we can create more robust classifiers for new data sets, which can then be applied to real-life and routine clinical settings.”

Lung tumors called adenocarcinomas sometimes respond to initially effective treatments by transforming into a much more aggressive small cell lung cancer (SCLC) that spreads rapidly and has few options for treatment. Researchers at Weill Cornell Medicine have developed a mouse model that illuminates this problematic process, known as histological transformation. The findings advance the understanding of how mutated genes can trigger cancer evolution and suggest targets for more effective treatments.
The researchers, whose results were published Feb. 8 in Science, discovered that during the transition from lung adenocarcinoma to small cell lung cancer (SCLC), the mutated cells appeared to undergo a change in cell identity through an intermediate, stem cell-like state, which facilitated the transformation.
“It is very difficult to study this process in human patients. So my aim was to uncover the mechanism underlying the transformation of lung adenocarcinoma to small cell lung cancer in a mouse model,” said study lead Dr. Eric Gardner, a postdoctoral fellow in the laboratory of Dr. Harold Varmus, the Lewis Thomas University Professor of Medicine and a member of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine. The complex mouse model took several years to develop and characterize but has allowed the researchers to crack this difficult problem.
This study was in collaboration with Dr. Ashley Laughney, assistant professor of physiology and biophysics and a member of the Meyer Cancer Center at Weill Cornell Medicine and Ethan Earlie, a graduate student in the Laughney lab and part of the Tri-Institutional Computational Biology and Medicine program.
“It is well known that cancer cells continue to evolve, especially to escape the pressure of effective treatments,” said Dr. Varmus. “This study shows how new technologies — including the detection of molecular features of single cancer cells, combined with computer-based analysis of the data — can portray dramatic, complex events in the evolution of lethal cancers, exposing new targets for therapeutic attack.”
Catching Transformation in the Act
SCLC most commonly occurs in heavy smokers, but this type of tumor also develops in a significant number of patients with lung adenocarcinomas, particularly after treatment with therapies that target a protein called Epidermal Growth Factor Receptor (EGFR), which promotes tumor growth. The new SCLC-type tumors are resistant to anti-EGFR therapy because their growth is fueled by a new cancer driver, high levels of Myc protein.

To unravel the interplay of these cancer pathways, the researchers engineered mice to develop a common form of lung adenocarcinoma, in which lung epithelial cells are driven by a mutated version of the EGFR gene. They then turned the adenocarcinoma tumors into SCLC-type tumors, which generally arise from neuroendocrine cells. They did this by shutting off EGFR in the presence of several other changes including losses of the tumor suppressor genes Rb1 and Trp53 as well as turning up the production of Myc,a known driver of SCLC.
Oncogenes, such as EGFR and Myc, are mutated forms of genes that normally control cell growth. They are known for their roles in driving the growth and spread of cancer. Tumor suppressor genes, on the other hand, normally inhibit cell proliferation and tumor development.
Context Matters
Surprisingly, this study showed that oncogenes act in a context-dependent manner. While most lung cells are resistant to becoming cancerous by Myc, neuroendocrine cells, are very sensitive to the oncogenic effects of Myc. Conversely, epithelial cells, which line the air sacs of the lungs and are the precursors to lung adenocarcinomas, grow excessively in response to mutated EGFR.
“This shows that an ‘oncogene’ in the wrong cell type doesn’t act like an oncogene anymore,” Dr. Laughney said. “So, it fundamentally changes how we think about oncogenes.”
The researchers also discovered a stem cell-like intermediate that was neither adenocarcinoma nor SCLC. Cells in this transitional state became neuroendocrine in nature only when mutations in the tumor suppressor genes RB1 and TP53 were present. They observed that loss of another tumor suppressor called Pten accelerated this process. At that stage, oncogenic Myc could drive these intermediate stem-like cells to form SCLC-type tumors.
This study further supports efforts seeking therapeutics that target Myc proteins, which are implicated in many types of cancers. The researchers now plan to use their new mouse model to further explore the adenocarcinoma-SCLC transition, detailing, for example, how the immune system normally responds to this transition.

Health care providers in developing countries know that oral rehydration salts (ORS) are a lifesaving and inexpensive treatment for diarrheal disease, a leading cause of death for children worldwide — yet few prescribe it.
A new study published in Science suggests that closing the knowledge gap between what treatments health care providers think patients want and what treatments patients really want could help save half a million lives a year and reduce unnecessary use of antibiotics.
“Even when children seek care from a health care provider for their diarrhea, as most do, they often do not receive ORS, which costs only a few cents and has been recommended by the World Health Organization for decades,” said Neeraj Sood, senior author of the study, senior fellow at the USC Schaeffer Center for Health Policy & Economics and a professor at the USC Price School of Public Policy.
“This issue has puzzled experts for decades, and we wanted to get to the bottom of it,” said Sood, who also holds joint appointments at the Keck School of Medicine of USC and the USC Marshall School of Business.
A closer look at childhood illness in India
There are several popular explanations for the underprescription of ORS in India, which accounts for the most cases of child diarrhea of any country in the world: Physicians assume their patients do not want oral rehydration salts, which come in a small packet and dissolve in water, because they taste bad or they aren’t “real” medicine like antibiotics. The salts are out of stock because they aren’t as profitable as other treatments. Physicians make more money prescribing antibiotics, even though they are ineffective against viral diarrhea.To test these three hypotheses, Sood and his colleagues enrolled over 2,000 health care providers across 253 medium-size towns in the Indian states of Karnataka and Bihar. The researchers selected states with vastly different socioeconomic demographics and varied access to health care to ensure the results were representative of a broad population. Bihar is one of the poorest states in India with below-average ORS use, while Karnataka has above-average per capita income and above-average ORS use.

The researchers then hired staff who were trained to act as patients or caretakers. These “standardized patients” were given scripts to use in unannounced visits to doctors’ offices where they would present a case of viral diarrhea — for which antibiotics are not appropriate — in their 2-year-old child. (For ethical considerations, children did not attend these visits.) The standardized patients made approximately 2,000 visits in total.
Providers were randomly assigned to patient visits where patients expressed a preference for ORS, a preference for antibiotics or no treatment preference. During the visits, patients indicated their preference by showing the health care provider a photo of an ORS packet or antibiotics. The set of patients with no treatment preference simply asked the physician for a recommendation.
To control for profit-motivated prescribing, some of the standardized patients assigned as having no treatment preference informed the provider that they would purchase medicine elsewhere. Additionally, to estimate the effect of stockouts, the researchers randomly assigned all providers in half of the 253 towns to receive a six-week supply of ORS.
Provider misperceptions matter most when it comes to ORS underprescribing
Researchers found that provider perceptions of patient preferences are the biggest barrier to ORS prescribing — not because caretakers do not want ORS, but rather because providers assume most patients do not want the treatment. Health care providers’ perception that patients do not want ORS accounted for roughly 42% of underprescribing, while stockouts and financial incentives explained only 6% and 5%, respectively.
Patients expressing a preference for ORS increased prescribing of the treatment by 27 percentage points — a more effective intervention than eliminating stockouts (which increased ORS prescribing by 7 percentage points) or removing financial incentives (which only increased ORS prescribing at pharmacies).

“Despite decades of widespread knowledge that ORS is a lifesaving intervention that can save lives of children suffering from diarrhea, the rates of ORS use remain stubbornly low in many countries such as India,” said Manoj Mohanan, co-author of the study and professor of public policy, economics, and global health at the Sanford School of Public Policy at Duke University. “Changing provider behavior about ORS prescription remains a huge challenge.”
Study authors said these results can be used to design interventions that encourage patients and caretakers to express an ORS preference when seeking care, as well as efforts to raise awareness among providers about patients’ preferences.
“We need to find ways to change providers’ perceptions of patient preferences to increase ORS use and combat antibiotic resistance, which is a huge problem globally,” said Zachary Wagner, the study’s corresponding author, an economist at RAND Corporation and professor of policy analysis at Pardee RAND Graduate School. “How to reduce overprescribing of antibiotics and address antimicrobial resistance is a major global health question, and our study shows that changing provider perceptions of patient preferences is one way to work toward a solution.”
This research was funded by the National Institute of Diabetes and Digestive and Kidney Diseases (Grant 5R01DK126049).

Researchers from The Australian National University (ANU) have discovered a previously unknown ability of a group of immune system cells, known as Atypical B cells (ABCs), to fight infectious diseases such as malaria.
The discovery provides new insight into how the immune system fights infections and brings scientists a step closer to harnessing the body’s natural defences to combat malaria.
The scientists say ABCs could also be key to developing new treatments for chronic autoimmune conditions such as lupus.
According to the researchers, ABCs have long been associated with malaria, as malaria patients have more of these cells in their system compared to the general population.
“In this study, we wanted to understand the mechanisms that drive the creation of ABCs in the immune system, but also find out whether these cells are good or bad for us when it comes to fighting infection,” lead author Dr Xin Gao, from ANU, said.
“Although ABCs are known to contribute to chronic inflammatory diseases and autoimmunity, we’ve discovered a previously unknown ability of these cells to fight disease. In this sense, ABCs are like a double-edged sword.
“Contrary to past belief, ABCs are not junk cells; they are more important than we thought.

“Our research found that ABCs are also instrumental in developing T follicular helper cells. These helper cells generate powerful antibodies that help the body fight malaria parasites.
“Antibodies can block parasites in the blood as they travel from the site of the infectious mosquito bite to the liver, where the infection is first established.”
In 2022, malaria killed more than 600,000 people worldwide. Although the disease is preventable and curable, scientists face an uphill battle to find long-lasting treatments as malaria parasites continue to find new ways to build resistance to current therapies.
Using gene-editing technology on mice, the ANU researchers discovered a gene called Zeb2 is crucial to the production of ABCs.
“We found that manipulating the Zeb2 gene disrupted the creation of ABCs in the immune system,” study co-author Professor Ian Cockburn, from The ANU John Curtin School of Medical Research, said.
“Importantly, we found that mice without the Zeb2 gene were unable to control malaria infection.

“Therefore, the findings show that ABCs play a crucial role in fighting malaria infections.”
The researchers say targeting ABCs could also pave the way for new treatments for certain autoimmune diseases such as lupus.
“ABCs also appear in large numbers in many autoimmune diseases, including lupus, which can be life-threating in severe cases,” Professor Cockburn said.
“By developing a better understanding of the role of ABCs in the immune system and the cells’ role in fighting disease, it could bring us a step closer to one day developing new and more effective therapies.”
The research is published in Science Immunology.

People with aphasia have more trouble coming up with words they want to use when they’re prompted by images and words that carry negative emotional meaning, new research suggests.
The study involved individuals whose language limitations resulted from damage to the brain caused by a stroke — the most common cause of aphasia, affecting at least one-third of stroke survivors. The disorder impairs the expression and understanding of language as well as reading and writing.
Researchers from The Ohio State University who led the study said the findings — suggesting that prompts with negative and even positive emotional context can disrupt word retrieval — have implications for clinical assessments and therapy, where the potential influence of emotion may not be taken into account. And because many patients already feel isolated by the condition, they said, insights from this study could help reduce interference with communication efforts by people with aphasia in multiple settings.
“Emotions are a big part of having aphasia — it impacts your quality of life drastically,” said first author Deena Schwen Blackett, who completed this work as a graduate student in speech and hearing science at Ohio State.
“The fact that an emotional reaction interferes with the ability of people with aphasia to come up with words — on top of how hard it already is — could validate their experience if they’re saying that a heightened emotional state makes it harder for them to communicate, so they might need to keep their environment mellow.”
The study was published recently in the journal Neuropsychologia.
Though previous research has found that emotional stimuli can improve performance by people with aphasia on auditory comprehension, reading and writing, and repetition tasks, this is one of the first such studies of emotions’ effects on word retrieval, said senior author Stacy Harnish, associate professor of speech and hearing science at Ohio State.

“This has practical implications but also theoretical significance,” Harnish said. “When we see behavior across people pointing to differences between emotional versus non-emotional words, that tells us something is going on in the brain to process these stimuli differently. So that warrants interrogating it more, figuring out why that is and building on it.”
The study involved 13 people with aphasia and 13 neurotypical people as controls who participated in four single-word naming tasks: two image-based tasks to name objects or actions represented by a picture, and two word-based tasks to name words that fit into a category or verbs that logically accompany the word used as a prompt.
The pictures and words used as stimuli had been previously validated as carrying either negative or positive emotional context or as neutral. Negative pictures included skull, garbage and kick and negative words included disaster, poison and mold. Positive pictures included images of bunnies and a waterfall, while positive words included food and pillow. In all, the tasks added up to 219 image and word prompts divided equally into negative, positive or neutral context categories.
Though there was some nuance and variation to the results, a pattern emerged in people with aphasia as a group. Emotional pictures and words, primarily those with negative meaning but also many with positive contexts, resulted in worse naming performance in terms of word accuracy and in the time it took to respond compared to results from neutral word and image prompts.
Results showed similar effects of emotional stimuli on neurotypical study participants’ performance on word retrieval tasks, though to a lesser degree — hinting that there could be some universality to how emotions place demands on the brain that compromise this specific type of language processing.
In fact, Schwen Blackett expected an earlier study she led in people who didn’t have aphasia to show that emotions surrounding stimuli would generate a strong performance in word retrieval — possibly by harnessing the right brain hemisphere to give a boost to language processing in the left hemisphere. But she found just the opposite to be true in a single word-retrieval task.

“So this new study using varied tasks was validating, and replicated those findings — we saw the same thing in people with mild to moderate aphasia but to a greater magnitude than what was seen in neurotypical people,” said Schwen Blackett, now a postdoctoral fellow at the Medical University of South Carolina.
Harnish and Schwen Blackett theorized that simultaneous emotional arousal and language processing led to fragmentation in the brain’s attention capabilities: Overlapping regions involved in both types of processing are triggered to tend to the physiological and memory components of an emotional response, which interferes with the focused attention on language required to perform well on word retrieval.
The team said more research is needed to fully understand the effect of emotional stimuli in people with aphasia, including in patients with differing aphasia origins.
“Deena’s work is at the forefront of emotional processing in word retrieval,” Harnish said. “We want to build on it now and see where it goes.”
This work was supported by grants from the National Institute on Deafness and Other Communication Disorders.
Additional co-authors were Shari Speer and Xueliang Pan of Ohio State and Joan Borod of Queens College.