Monday, November 27, 2023

Ukraine takes delivery of 3D printed Titan Falcon drones

Three drones were provided by an American-Ukrainian NGO, Germany's Donaustahl GmbH, and Titan Dynamics Inc.

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In addition to all the other noteworthy implications 3D printing technology is having on different industries, it is also revolutionizing the defense sector – offering innovative solutions for military applications. This transformative impact is evident in various projects, including the development of advanced drones like the Titan Falcon, which has been provided to Ukrainian troops through the collaboration of an American-Ukrainian NGO, Germany’s Donaustahl GmbH, and Titan Dynamics Inc.

So far, three Titan Falcon drones, produced through 3D printing techniques, have been delivered to the Armed Forces of Ukraine. These drones are undergoing intensive testing in the country – demonstrating their versatility and durability in various environments. The Titan Falcon stands out for its impressive flight endurance of up to 6 hours and a range of 400 kilometers. It features a first-person view (FPV) camera for real-time surveillance and can be equipped with a 2.5-inch lens camera – boosting its reconnaissance capabilities.

Ukraine takes delivery of 3D printed Titan Falcon drones thanks to Germany's Donaustahl GmbH and Titan Dynamics Inc.
Source: German Aid to Ukraine on X.

Titan Dynamics Inc. is leading this initiative. The company specializes in creating fixed-wing and Vertical Take-Off and Landing (VTOL) aircraft. They focus on enhancing efficiency, maximizing utility, and increasing the range of unmanned aerial vehicles (UAVs) – all while reducing manufacturing costs.

Beyond the Titan Falcon project, 3D printing technology is being utilized in other defense areas including the production of lightweight yet durable components for military vehicles, the creation of custom parts for weaponry, and the manufacturing of protective gear and equipment. The technology’s ability to produce complex designs quickly and cost-effectively is proving to be a game-changer in this field – offering new possibilities for rapid innovation and deployment.

Recently, London Defense R&D, a leading British defense enterprise, created a 3D printed Anti-Drone System – the LD-80 – to counteract the increasing number of drones. Built using MJF, this development signified a substantial transition in the international arms market – introducing a new paradigm in the defense industry where individuals and institutions can manufacture their own tactical products, rather than buy the completed product.

 

Mind the gap: Caution needed when assessing land emissions in the COP28 Global Stocktake


Peer-Reviewed Publication

INTERNATIONAL INSTITUTE FOR APPLIED SYSTEMS ANALYSIS

Figure 1 

IMAGE: 

FIG 1: ALIGNING CONVENTIONAL SCIENTIFIC MODELS WITH NATIONAL GREENHOUSE GAS INVENTORY DEFINITIONS OF LAND USE, LAND USE CHANGE, AND FORESTRY FLUXES. THE VARIATIONS ARE A RESULT FROM DIFFERENCES IN WHAT LAND IS CONSIDERED MANAGED AND WHETHER FLUXES RELATED TO ENVIRONMENTAL AND CLIMATIC CHANGES ARE INCLUDED.  

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CREDIT: GIDDEN, ET AL.





Effective management of land, whether for agriculture, forests, or settlements, plays a crucial role in addressing climate change and achieving future climate targets. Land use strategies to mitigate climate change include stopping deforestation, along with enhancing forest management efforts. Countries have recognized the importance of the land use, land-use change, and forestry (LULUCF) sector, with 118 of 143 countries including land-based emissions reductions and removals in their Nationally Determined Contributions (NDCs), which are at the heart of the Paris Agreement and the achievement of its long-term goals.

A new study, published in Nature, demonstrates that estimates of current land-based emissions vary between scientific models and national greenhouse gas inventories due to differing definitions of what qualifies as "managed" land and human-induced, or anthropogenic, removals on that land, and shows how global mitigation benchmarks change when accounting for LULUCF fluxes in scientific models from the national inventory perspective. The research team underscores the necessity to compare like for like when assessing progress towards the Paris Agreement with countries needing to achieve more ambitious climate action when comparing their national starting points with global models.

“Countries estimate their LULUCF fluxes (emissions and removals) differently. Direct fluxes are a result of direct human intervention, such as agriculture and forest harvest. The models in the Assessment Reports by the Intergovernmental Panel on Climate Change (IPCC) use this accounting approach to determine the remaining carbon budget and the timing for achieving net-zero emissions. Indirect fluxes are the response of land to indirect human-induced environmental changes, such as increase in atmospheric CO2 or nitrogen deposition that both enhance carbon removal,” explains Giacomo Grassi, a study coauthor and researcher with the Joint Research Centre at the European Commission.

Grassi points out that it is practically not possible to separate direct and indirect fluxes through observations such as national forest inventories or remote sensing. Therefore, national greenhouse gas inventory methods follow reporting conventions that define anthropogenic fluxes using an area-based approach, whereby all fluxes occurring on managed land are considered anthropogenic. In contrast, greenhouse gas fluxes on unmanaged land are not included in the reporting.

Globally, this results in a difference between bookkeeping models and country inventories of around 4-7 gigatons of CO2, or around 10% of today’s greenhouse gas emissions, but this difference varies from country to country.

The research team assessed key mitigation benchmarks using the inventory-based LULUCF accounting approach. They found that, in pathways achieving the 1.5 °C long-term temperature goal of the Paris Agreement, net-zero CO2 emissions is achieved one to five years earlier, emission reductions by 2030 need to be 3.5-6% stronger, and cumulative CO2 emissions are between 55-95 Gt CO2 less. The research team emphasizes that results do not conflict with the benchmarks assessed by the IPCC, but rather assesses the same kinds of benchmarks using an inventory-based approach.

“The IPCC Assessment Reports use direct, land-based emissions as input and include the indirect emissions due to climate and environmental responses in their physical climate emulation to calculate the global temperature response to anthropogenic emissions. In our analysis, we make it clear that we’re looking at these two kinds of emissions separately. The climate outcome of each scenario we assess remains the same, but the benchmark – when viewed through the lens of national greenhouse gas inventory accounting conventions – shifts. Without making adjustments, countries could appear in a better position than they actually are,” explains Thomas Gasser, a study coauthor and senior researcher associated with both the IIASA Advancing Systems Analysis and Energy, Climate, and Environment programs.

“Our findings show the danger of comparing apples to oranges: To achieve the Paris Agreement, it’s critical that countries aim for the correct target. If countries achieve model-based benchmarks using inventory-based accounting, they will miss the mark,” says Matthew Gidden, study author and senior researcher in the IIASA Energy, Climate, and Environment Program.

Ahead of the COP28 summit and its first Global Stocktake – a process that will enable countries and other stakeholders to see where they’re collectively making progress toward meeting the goals of the Paris Agreement and where they’re not – the researchers are urging for more detailed national climate goals. They recommend distinct targets for land-based mitigation separate from actions in other sectors.

“Countries can bring clarity to their climate ambition by communicating their planned use of the LULUCF sector separately from emissions reductions elsewhere. While modelers and practitioner communities can come together to improve comparability between global pathways and national inventories, it is vital that the message that significant mitigation effort is needed this decade, is not lost in the details of reporting technicalities,” concludes Gidden.

Reference:

Gidden, M., Gasser, T., Grassi, G., Forsell, N., Janssens, I., Lamb, W., Minx, J., Nicholls Z., Steinhauser, J., Riahi, K. (2023). Aligning climate scenarios to emissions inventories shifts global benchmarks. Nature DOI: 10.1038/s41586-023-06724-y


About IIASA:

The International Institute for Applied Systems Analysis (IIASA) is an international scientific institute that conducts research into the critical issues of global environmental, economic, technological, and social change that we face in the twenty-first century. Our findings provide valuable options to policymakers to shape the future of our changing world. IIASA is independent and funded by prestigious research funding agencies in Africa, the Americas, Asia, and Europe. www.iiasa.ac.at

 

Revolutionary breakthrough in the manufacture of photovoltaic cells at the University of Ottawa


Another step towards miniaturization of electronic devices


Peer-Reviewed Publication

UNIVERSITY OF OTTAWA

Revolutionary breakthrough in the manufacture of photovoltaic cells at the University of Ottawa 

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“THESE MICROMETRIC PHOTOVOLTAIC CELLS HAVE REMARKABLE CHARACTERISTICS, INCLUDING AN EXTREMELY SMALL SIZE AND SIGNIFICANTLY REDUCED SHADOWING”. KARIN HINZER — VICE-DEAN, RESEARCH, AND UNIVERSITY RESEARCH CHAIR IN PHOTONIC DEVICES FOR ENERGY

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CREDIT: THE UNIVERSITY OF OTTAWA





The University of Ottawa, together with national and international partners, has achieved a world first by manufacturing the first back-contact micrometric photovoltaic cells.

The cells, with a size twice the thickness of a strand of hair, have significant advantages over conventional solar technologies, reducing electrode-induced shadowing by 95% and potentially lowering energy production costs by up to three times.

The technological breakthrough—led by Mathieu de Lafontaine, a postdoctoral researcher at the University of Ottawa and a part-time physics professor; and Karin Hinzer, vice-dean, research, and University Research Chair in Photonic Devices for Energy at the Faculty of Engineering—paves the way for a new era of miniaturization in the field of electronic devices.

The micrometric photovoltaic cell manufacturing process involved a partnership between the University of Ottawa, the Université de Sherbrooke in Quebec and the Laboratoire des Technologies de la Microélectronique in Grenoble, France.

“These micrometric photovoltaic cells have remarkable characteristics, including an extremely small size and significantly reduced shadowing. Those properties lend themselves to various applications, from densification of electronic devices to areas such as solar cells, lightweight nuclear batteries for space exploration and miniaturization of devices for telecommunications and the internet of things,” Hinzer says.

A breakthrough with huge potential

“This technological breakthrough promises significant benefits for society. Less expensive, more powerful solar cells will help accelerate the energy shift. Lightweight nuclear batteries will facilitate space exploration, and miniaturization of devices will contribute to the growth of the internet of things and lead to more powerful computers and smartphones,” de Lafontaine says.

“The development of these first back-contact micrometric photovoltaic cells is a crucial step in the miniaturization of electronic devices,” he adds.

“Semiconductors are vital in the shift to a carbon-neutral economy. This project is one of many research initiatives that we’re undertaking at the Faculty of Engineering to achieve our societal goals,” says Hinzer. Semiconductors are included in three of the five research areas at the Faculty of Engineering, namely, information technologies, photonics and emerging materials, and two of the four strategic areas of research at the University of Ottawa, namely, creating a sustainable environment and shaping the digital world.  

This international partnership between Canada and France illustrates the importance of innovation and research in micromanufacturing, leading the way to a future in which technology will become more powerful and accessible than ever. It also marks an historic step in the evolution of the global scientific and technology scene.

This initiative was funded by the Natural Sciences and Engineering Research Council of Canada, the Fonds de recherche du Québec Nature et technologies, the Horizon Europe Framework program, Prompt Québec and STACE Inc.

This innovative achievement is described in more detail in the article titled “3D Interconnects for III-V Semiconductor Heterostructures for Miniaturized Power Devices” in Cell Reports Physical Science.

 

 

From the first bite, our sense of taste helps pace our eating


Brainstem recording shows that our tastebuds are the first line of defense against eating too fast. Understanding how may lead to new avenues for weight loss. 


Peer-Reviewed Publication

UNIVERSITY OF CALIFORNIA - SAN FRANCISCO






When you eagerly dig into a long-awaited dinner, signals from your stomach to your brain keep you from eating so much you’ll regret it – or so it’s been thought. That theory had never really been directly tested until a team of scientists at UC San Francisco recently took up the question.  
 
The picture, it turns out, is a little different. 
 
The team, led by Zachary Knight, PhD, a UCSF professor of physiology in the Kavli Institute for Fundamental Neuroscience, discovered that it’s our sense of taste that pulls us back from the brink of food inhalation on a hungry day. Stimulated by the perception of flavor, a set of neurons – a type of brain cell – leaps to attention almost immediately to curtail our food intake.  
 
“We’ve uncovered a logic the brainstem uses to control how fast and how much we eat, using two different kinds of signals, one coming from the mouth, and one coming much later from the gut,” said Knight, who is also an investigator with the Howard Hughes Medical Institute and a member of the UCSF Weill Institute for Neurosciences. “This discovery gives us a new framework to understand how we control our eating.” 
 
The study, which appears Nov. 22, 2023 in Nature, could help reveal exactly how weight-loss drugs like Ozempic work, and how to make them more effective. 
 
New views into the brainstem 
 
Pavlov proposed over a century ago that the sight, smell and taste of food are important for regulating digestion. More recent studies in the 1970s and 1980s have also suggested that the taste of food may restrain how fast we eat, but it’s been impossible to study the relevant brain activity during eating because the brain cells that control this process are located deep in the brainstem, making them hard to access or record in an animal that’s awake. 
 
Over the years, the idea had been forgotten, Knight said.  
 
New techniques developed by lead author Truong Ly, PhD, a graduate student in Knight’s lab, allowed for the first-ever imaging and recording of a brainstem structure critical for feeling full, called the nucleus of the solitary tract, or NTS, in an awake, active mouse. He used those techniques to look at two types of neurons that have been known for decades to have a role in food intake. 
 
The team found that when they put food directly into the mouse’s stomach, brain cells called PRLH (for prolactin-releasing hormone) were activated by nutrient signals sent from the GI tract, in line with traditional thinking and the results of prior studies. 
 
However, when they allowed the mice to eat the food as they normally would, those signals from the gut didn’t show up. Instead, the PRLH brain cells switched to a new activity pattern that was entirely controlled by signals from the mouth.  
 
“It was a total surprise that these cells were activated by the perception of taste,” said Ly. “It shows that there are other components of the appetite-control system that we should be thinking about.” 
 
While it may seem counterintuitive for our brains to slow eating when we’re hungry, the brain is actually using the taste of food in two different ways at the same time. One part is saying, “This tastes good, eat more,” and another part is watching how fast you’re eating and saying, “Slow down or you’re going to be sick.” 
 
“The balance between those is how fast you eat,” said Knight. 
 
The activity of the PRLH neurons seems to affect how palatable the mice found the food, Ly said. That meshes with our human experience that food is less appetizing once you’ve had your fill of it.  
 
Brain cells that inspire weight-loss drugs 
 
The PRLH-neuron-induced slowdown also makes sense in terms of timing. The taste of food triggers these neurons to switch their activity in seconds, from keeping tabs on the gut to responding to signals from the mouth.  
 
Meanwhile, it takes many minutes for a different group of brain cells, called CGC neurons, to begin responding to signals from the stomach and intestines. These cells act over much slower time scales – tens of minutes – and can hold back hunger for a much longer period of time. 
 
“Together, these two sets of neurons create a feed-forward, feed-back loop,” said Knight. “One is using taste to slow things down and anticipate what’s coming. The other is using a gut signal to say, ‘This is how much I really ate. Ok, I’m full now!’”  
 
The CGC brain cells’ response to stretch signals from the gut is to release GLP-1, the hormone mimicked by Ozempic, Wegovy and other new weight-loss drugs.  
 
These drugs act on the same region of the brainstem that Ly’s technology has finally allowed researchers to study. “Now we have a way of teasing apart what’s happening in the brain that makes these drugs work,” he said.  
 
A deeper understanding of how signals from different parts of the body control appetite would open doors to designing weight-loss regimens designed for the individual ways people eat by optimizing how the signals from the two sets of brain cells interact, the researchers said. 
 
The team plans to investigate those interactions, seeking to better understand how taste signals from food interact with feedback from the gut to suppress our appetite during a meal. 
 
 
Co-authors: Nilla Sivakumar, Zhengya Liu, Naz Dundar, Brooke C. Jarvie, Anagh Ravi, Olivia K. Barnhill and Heeun Jang of UCSF and Jun Y. Oh, Sarah Shehata, Naymalis La Santa Medina, Heidi Huang, Wendy Fang, Chris Barnes, Chelsea Li, Grace R. Lee and Jaewon Choi of HHMI. 
 
Funding: This work was supported by NIH grants (R01-DK106399, F31DK137586). 

 

About UCSF: The University of California, San Francisco (UCSF) is exclusively focused on the health sciences and is dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care. UCSF Health, which serves as UCSF's primary academic medical center, includes top-ranked specialty hospitals and other clinical programs, and has affiliations throughout the Bay Area. UCSF School of Medicine also has a regional campus in Fresno. Learn more at https://ucsf.edu, or see our Fact Sheet.

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7 in 8 homicide victims in South Africa are male


Peer-Reviewed Publication

PLOS





7 in 8 homicide victims in South Africa are male, with homicide rates peaking on weekends and holidays, and firearms and sharp items being the most common murder weapons, in analysis of almost 20,000 2017 post-mortems.

Segregated patterns of hospital care delivery and health outcomes

JAMA Health Forum

Peer-Reviewed Publication

JAMA NETWORK




About The Study: This study of Medicare claims data for 4,386 hospitals found that higher segregation of hospital care was associated with poorer health outcomes for both Black and white patients, with significantly greater negative health outcomes for Black populations, supporting racial segregation as a root cause of health disparities. Policymakers and clinical leaders could address this important public health issue through payment reform efforts and expansion of health insurance coverage, in addition to supporting upstream efforts to reduce racial segregation in hospital care and residential settings. 

Authors: Sunny C. Lin, Ph.D., M.S., of the Washington University School of Medicine in St. Louis, is the corresponding author.

To access the embargoed study: Visit our For The Media website at this link https://media.jamanetwork.com/

(doi:10.1001/jamahealthforum.2023.4172)

Editor’s Note: Please see the article for additional information, including other authors, author contributions and affiliations, conflict of interest and financial disclosures, and funding and support.

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Embed this link to provide your readers free access to the full-text article This link will be live at the embargo time https://jamanetwork.com/journals/jama-health-forum/fullarticle/10.1001/jamahealthforum.2023.4172?utm_source=For_The_Media&utm_medium=referral&utm_campaign=ftm_links&utm_term=112223

About JAMA Health Forum: JAMA Health Forum is an international, peer-reviewed, online, open access journal that addresses health policy and strategies affecting medicine, health and health care. The journal publishes original research, evidence-based reports and opinion about national and global health policy; innovative approaches to health care delivery; and health care economics, access, quality, safety, equity and reform. Its distribution will be solely digital and all content will be freely available for anyone to read.

 

New clues into the head-scratching mystery of itch


Researchers identify common microbe as a previously unknown culprit behind itch


Peer-Reviewed Publication

HARVARD MEDICAL SCHOOL

A New Clue into the Mystery of Itch 

VIDEO: 


SCIENTISTS AT HARVARD MEDICAL SCHOOL HAVE SHOWN FOR THE FIRST TIME THAT A COMMON SKIN BACTERIUM — STAPHYLOCOCCUS AUREUS — CAN CAUSE ITCH BY ACTING DIRECTLY ON NERVE CELLS. THE RESEARCH ADDS AN IMPORTANT PIECE TO THE LONG-STANDING PUZZLE OF ITCH AND HELPS EXPLAIN WHY COMMON SKIN CONDITIONS LIKE ECZEMA AND ATOPIC DERMATITIS ARE OFTEN ACCOMPANIED BY PERSISTENT ITCH.

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CREDIT: HARVARD MEDICAL SCHOOL

 



Scientists at Harvard Medical School have shown for the first time that a common skin bacterium — Staphylococcus aureus — can cause itch by acting directly on nerve cells. 

The findings, based on research in mice and in human cells, are reported Nov. 22 in Cell. The research adds an important piece to the long-standing puzzle of itch and helps explain why common skin conditions like eczema and atopic dermatitis are often accompanied by persistent itch.

In such conditions, the equilibrium of microorganisms that keep our skin healthy is often thrown off balance, allowing S. aureus to flourish, the researchers said. Up until now, the itch that occurs with eczema and atopic dermatitis was believed to arise from the accompanying inflammation of the skin. But the new findings show that S. aureus single-handedly causes itch by instigating a molecular chain reaction that culminates in the urge to scratch.

“We’ve identified an entirely novel mechanism behind itch — the bacterium Staph aureus, which is found on almost every patient with the chronic condition atopic dermatitis. We show that itch can be caused by the microbe itself,” said senior author Isaac Chiu, associate professor of immunology in the Blavatnik Institute at HMS.

The study experiments showed that S. aureus releases a chemical that activates a protein on the nerve fibers that transmit signals from the skin to the brain. Treating animals with an FDA-approved anti-clotting medicine successfully blocked the activation of the protein to interrupt this key step in the itch-scratch cycle. The treatment relieved symptoms and minimized skin damage.

The findings can inform the design of oral medicines and topical creams to treat persistent itch that occurs with various conditions linked to an imbalance in the skin microbiome, such as atopic dermatitis, prurigo nodularis, and psoriasis.

The repeated scratching that is a hallmark of these conditions can cause skin damage and amplify inflammation.

“Itch can be quite debilitating in patients who suffer from chronic skin conditions. Many of these patients carry on their skin the very microbe we’ve now shown for the first time can induce itch,” said study first author Liwen Deng, a postdoctoral research fellow in the Chiu Lab.

Identifying the molecular spark plug that ignites itch 

Researchers exposed the skin of mice to S. aureus. The animals developed intensifying itch over several days, and the repeated scratching caused worsening skin damage that spread beyond the original site of exposure.

Moreover, mice exposed to S. aureus became hypersensitive to innocuous stimuli that would not typically cause itch. The exposed mice were more likely than unexposed mice to develop abnormal itching in response to a light touch.

This hyperactive response, a condition called alloknesis, is common in patients with chronic conditions of the skin characterized by persistent itch. But it can also happen in people without any underlying conditions — think of that scratchy feeling you might get from a wool sweater.

To determine how the bacterium triggered itch, the researchers tested multiple modified versions of the S. aureus microbe that were engineered to lack specific pieces of the bug’s molecular makeup. The team focused on 10 enzymes known to be released by this microbe upon skin contact. One after another, the researchers eliminated nine suspects — showing that a bacterial enzyme called protease V8 was single-handedly responsible for initiating itch in mice. Human skin samples from patients with atopic dermatitis also had more S. aureus and higher V8 levels than healthy skin samples.

The analyses showed that V8 triggers itch by activating a protein called PAR1, which is found on skin neurons that originate in the spinal cord and carry various signals —touch, heat, pain, itch — from the skin to the brain. Normally, PAR1 lies dormant but upon contact with certain enzymes, including V8, it gets activated. The research showed that V8 snips one end of the PAR1 protein and awakens it. Experiments in mice showed that once activated, PAR1 initiates a signal that the brain eventually perceives as itch. When researchers repeated the experiments in lab dishes containing human neurons, they also responded to V8.

Interestingly, various immune cells implicated in skin allergies and classically known to cause itch — mast cells and basophils — did not drive itch after bacterial exposure, the experiments showed. Nor did inflammatory chemicals called interleukins, or white cells, which are activated during allergic reactions and are also known to be elevated in skin diseases and even in certain neurologic disorders.

“When we started the study, it was unclear whether the itch was a result of inflammation or not,” Deng said. “We show that these things can be decoupled, that you don’t necessarily have to have inflammation for the microbe to cause itch, but that the itch exacerbates inflammation on the skin.”

Interrupting the itch-scratch cycle

Because PAR1 — the protein activated by S. aureus — is involved in blood-clotting, researchers wanted to see whether an already approved anticlotting drug that blocks PAR1 would stop itch. It did.

The itchy mice whose skin was exposed to S. aureus experienced rapid improvement when treated with the drug. Their desire to scratch diminished dramatically, as did the skin damage caused by scratching.

Moreover, once treated with PAR1 blockers, the mice no longer experienced abnormal itch in response to innocuous stimuli.

The PAR1 blocker is already used in humans to prevent blood clots and could be repurposed as anti-itch medication. For example, the researchers noted, the active ingredient in the medicine could become the basis for anti-itch topical creams.

One immediate question that the researchers plan to explore in future work is whether other microbes besides S. aureus can trigger itch.

“We know that many microbes, including fungi, viruses, and bacteria, are accompanied by itch but how they cause itch is not clear,” Chiu said.

Beyond that, the findings raise a broader question: Why would a microbe cause itch? Evolutionarily speaking, what’s in it for the bacterium?

One possibility, the researchers said, is that pathogens may hijack itch and other neural reflexes to their advantage. For example, previous research has shown that the TB bacterium directly activates vagal neurons to cause cough, which might enable it to spread more easily from one host to another. 

“It’s a speculation at this point, but the itch-scratch cycle could benefit the microbes and enable their spread to distant body sites and to uninfected hosts,” Deng said. “Why do we itch and scratch? Does it help us, or does it help the microbe? That’s something that we could follow up on in the future.”

Authorship, funding, disclosures

Additional authors included Flavia Costa, Kimbria J. Blake, Samantha Choi, Arundhasa Chandrabalan, Muhammad Saad Yousuf, Stephanie Shiers, Daniel Dubreuil, Daniela Vega-Mendoza, Corinne Rolland, Celine Deraison, Tiphaine Voisin, Michelle D. Bagood, Lucia Wesemann, Abigail M. Frey, Joseph S. Palumbo, Brian J. Wainger, Richard L. Gallo, Juan-Manuel Leyva-Castillo, Nathalie Vergnolle, Theodore J. Price, Rithwik Ramachandran, and Alexander R. Horswill.

The work was funded by the National Institutes of Health (grants R01AI168005, R01AI153185, R01NS065926, R01NS102161, R01NS111929, R37AI052453, R01AR076082, U01AI152038, UM1AI151958, R01AI153185, R01JL160582, F32AI172080, T32AI049928, 1R21AG075419), Food Allergy Science Initiative (FASI), Burroughs Wellcome Fund, Drako Family Fund, Jackson-Wijaya Research Fund, Canadian Institutes of Health Research (CIHR) (grants 376560 and 469411), and ANR-PARCURE (PRCE-CE18, 2020).

Chiu serves on the scientific advisory board of GSK Pharmaceuticals. Provisional patent application Serial No. 63/438,668, in which some coauthors are listed as inventors, was filed based on these findings.