Medical News

Indiana University School of Medicine researchers have successfully developed a blood test for anxiety. The test looks for biomarkers that can help them determine an individual’s risk of developing anxiety, the severity of their current anxiety, and which therapies are likely to treat their anxiety the best.

MindX Sciences is developing the test for wider use by physicians now that it has been validated by researchers.

“Many people are suffering from anxiety, which can be very disabling and interfere with daily life,” said professor of psychiatry Alexander Niculescu, MD, PhD. “The current approach is to talk to people about how they feel to see if they could be on medications, but some medications can be addictive and create more problems. We wanted to see if our approach to identify blood biomarkers could help us match people to existing medications that will work better and could be a non-addictive choice.”

Previous research by Niculescu resulted in the development of blood tests for pain, depression/bipolar disorder, and post-traumatic stress disorder. This latest study, published in Molecular Psychiatry, employs similar techniques to treat anxiety. The research included three distinct cohorts: discovery, validation, and testing. A blood test would be administered to participants every 3-6 months or whenever a new psychiatric hospitalisation occurred. Researchers could identify a patient’s current state of anxiety and match them with medications and nutraceuticals by examining RNA biomarkers in the blood, demonstrating how effective different options could be for them based on their biology.

“In addition to medications, there are other methods to treat anxiety, such as cognitive behavioural therapy or lifestyle changes,” Niculescu said. “But having something objective like this where we can know what someone’s current state is as well as their future risk and what treatment options match their profile is very powerful in helping people.”

A person’s biomarkers can also change over time. Niculescu said the test can help evaluate a person’s risk of developing higher levels of anxiety in the future as well as how other factors might impact their anxiety, like hormonal changes.

“There are people who have anxiety and it is not properly diagnosed, then they have panic attacks, but think they’re having a heart attack and up in the ER with all sorts of physical symptoms,” Niculescu said. “If we can know that earlier, then we can hopefully avoid this pain and suffering and treat them earlier with something that matches their profile.”

Niculescu said this new test could also be used in combination with the other blood tests his research has led to, providing a more comprehensive view of a patient’s mental health and risk of future mental health concerns. Researchers can also use the test to develop new treatments for anxiety that are more targeted to individual biomarkers.

“This is something that could be a panel test as part of a patient’s regular wellness visits to evaluate their mental health over time and prevent any future distress,” Niculescu said. “Prevention is better in the long run, so our goal is to be able to provide a comprehensive report for patients and their physicians using simply one tube of blood.”

A team of researchers from USC’s Keck School of Medicine has begun to document the actual impact of electric vehicle adoption in the first study to use real-world data to correlate electric cars, air pollution, and health. The researchers analysed a “natural experiment” taking place in California as individuals quickly transitioned to electric cars, or light-duty zero-emission vehicles, using publicly available statistics (ZEVs). The findings were just published in Science of the Total Environment.

Between 2013 and 2019, the researchers examined data from the state’s ZEV registration, air pollution levels, and asthma-related emergency room visits.

Local air pollution levels and emergency department visits decreased as ZEV adoption increased within a given zip code. “When we think about the actions related to climate change, often it’s on a global level,” said Erika Garcia, PhD, MPH, an assistant professor of population and public health sciences at the Keck School of Medicine and the study’s lead author. “But the idea that changes being made at the local level can improve the health of your own community could be a powerful message to the public and to policy makers.”

The researchers also found that while total ZEVs increased over time, adoption was considerably slower in low-resource zip codes — what the researchers refer to as the “adoption gap.” That disparity points to an opportunity to restore environmental justice in communities that are disproportionately affected by pollution and related health problems.

“The impacts of climate change on health can be challenging to talk about because they can feel very scary,” said Sandrah Eckel, PhD, an associate professor of population and public health sciences at the Keck School of Medicine and the study’s senior author. “We’re excited about shifting the conversation towards climate change mitigation and adaptation, and these results suggest that transitioning to ZEVs is a key piece of that.”

To study the effects of electric vehicle adoption, the research team analyzed and compared four different datasets. First, they obtained data on ZEVs (which includes battery electric, plug-in hybrid, and hydrogen fuel cell cars) from the California Department of Motor Vehicles and tabulated the total number registered in each zip code for every year between 2013 and 2019.

They also obtained data from U.S. Environmental Protection Agency air monitoring sites on levels of nitrogen dioxide (NO2), an air pollutant related to traffic, and zip code level asthma-related visits to the emergency room. Asthma is one of the health concerns long linked with air pollutants such as NO2, which can also cause and exacerbate other respiratory diseases, as well as problems with the heart, brain and other organ systems.

Finally, the researchers calculated the percentage of adults in each zip code who held bachelor’s degrees. Educational attainment levels are frequently used as an indicator of a neighborhood’s socioeconomic status.

At the zip code level, for every additional 20 ZEVs per 1,000 people, there was a 3.2% drop in the rate of asthma-related emergency visits and a small suggestive reduction in NO2 levels. On average across zip codes in the state, ZEVs increased from 1.4 to 14.6 per 1,000 people between 2013 and 2019. ZEV adoption was significantly lower in zip codes with lower levels of educational attainment. For example, a zip code with 17% of the population having a bachelor’s degree had, on average, an annual increase of 0.70 ZEVs per 1,000 people compared to an annual increase of 3.6 ZEVs per 1,000 people for a zip code with 47% of the population having a bachelor’s degree.

Past research has shown that underserved communities, such as lower-income neighborhoods, tend to face worse pollution and associated respiratory problems than more affluent areas. If ZEVs replace gas-powered cars in those neighborhoods, they could stand to benefit substantially.

“Should continuing research support our findings, we want to make sure that those communities that are overburdened with the traffic-related air pollution are truly benefiting from this climate mitigation effort,” Garcia said.
While climate change is a massive health threat, mitigating it offers a massive public health opportunity, Eckel said. As one of the first studies to quantify the real-world environmental and health benefits of ZEVs, the research can help demonstrate the power of this mitigation measure, including possibly reduced health care utilization and expenditures.

The findings are promising, Garcia said, but many questions remain. Future studies should consider additional impacts of ZEVs, including emissions related to brake and tire wear, mining of materials for their manufacture, and disposal of old cars. The researchers also hope to study additional types of pollutants and other classes of vehicles, in addition to conducting a follow-up study of the effects of the ever-growing share of ZEVs in the state.

Moving forward, transitioning to ZEVs is just one part of the solution, Eckel said. Shifting to public transport and active transport, including walking and biking, are other key ways to boost environmental and public health.

According to a study, certain T cells that are reactive to microorganisms may also be reactive to common human proteins, leading to autoimmune illness. The discoveries should hasten attempts to develop better autoimmune disease diagnostic tests and therapies.

A team involving researchers from Washington University School of Medicine in St. Louis, Stanford University School of Medicine and Oxford University has developed a way to find crucial protein fragments that drive autoimmunity, as well as the immune cells that respond to them. The findings, published Dec. 7 in Nature, open a promising pathway to diagnose and treat autoimmune diseases.

“Of all genes, the HLA genes have the greatest amount of variation across the human population. There are many, many autoimmune diseases that are associated with specific variants of the HLA genes, and in most cases we don’t know why,” said co-senior author Wayne M. Yokoyama, MD, the Sam J. Levin and Audrey Loew Levin Professor of Arthritis Research at Washington University. “This paper outlines a strategy for figuring out why certain HLA variants are linked to certain diseases. It also provides strong evidence that cross-reactivity between human and microbial proteins drives autoimmunity in at least two diseases and probably many others. Now that we understand the underlying drivers, we can start focusing on the approaches that are most likely to yield benefits for patients.”

The autoimmune diseases ankylosing spondylitis, which involves arthritis in the spine and pelvis, and acute anterior uveitis, which is characterized by inflammation in the eye, are both strongly associated with an HLA variant called HLA-B*27. The link between ankylosing spondylitis and HLA-B*27 was discovered 50 years ago — making it one of the first such associations identified between disease and HLA variants — and it remains one of the strongest known associations between any disease and an HLA variant.

The HLA family of proteins is involved in helping immune cells detect invading pathogens and distinguishing between microbial and human proteins, and is highly variable across individuals. HLA proteins function like hands that pick up fragments of whichever proteins are lying about — microbial or human — and show them to immune cells called T cells to figure out if they’re a sign of danger (microbial) or not (human).

T cells don’t recognize protein fragments by themselves; they recognize the fragment plus the hand that holds it. Scientists have long assumed that the combination of this particular hand — HLA-B*27 — plus a bit of an unknown human protein was being misidentified as dangerous in people with either of the two diseases, triggering autoimmune attacks in the eye or the spine. But for decades, they couldn’t find the fragment. Some scientists began to speculate that the misidentification hypothesis was wrong and some other reason accounted for the association between HLA-B*27 and the two diseases.

Co-corresponding author K. Christopher Garcia, PhD, and co-first author Xinbo Yang, PhD, of Stanford Medicine, along with co-corresponding authors Geraldine M. Gillespie, PhD, and Andrew J. McMichael, PhD, and co-first author Lee Garner, PhD, of Oxford University, collaborated with Yokoyama and co-first author Michael Paley, MD, PhD, of Washington University on a novel way to find the elusive fragment. The research team identified certain T cells that were abundant in the blood and joints of people with ankylosing spondylitis, and in the eyes of people with uveitis.

Garcia and Yang then devised a way to identify protein fragments that drive a T cell response when combined with HLA-B*27, and mapped the fragments against the human genome and five bacterial genomes to identify proteins from which the fragments may have originated. Using that approach, they were able to narrow down the millions of possibilities to a very short list of human and microbial proteins. Then, they determined the structures of the detector molecules — known as T cell receptors — on T cells from both groups of patients and compared them. The similarities were striking.

“This study reveals the power of studying T cell specificity and activity from the ground up; that is, identifying the T cells that are most active in a given response, followed by identifying what they respond to,” Garcia said. “Clearly these patient-derived TCRs are seeing a spectrum of common antigens, and that may be driving the autoimmunity. Proving this in humans is very difficult, but that is our future direction and could lead to therapeutics.”

The findings reveal key aspects of the biological mechanisms underlying ankylosing spondylitis, anterior uveitis and potentially many other autoimmune diseases.

“By combining recently developed technologies, we have revisited an old hypothesis that asks if the traditional antigen-presenting function of HLA-B*27 contributes to disease initiation or pathogenesis in the autoimmune conditions ankylosing spondylitis and uveitis,” Gillespie said. “Our findings that T cells at the sites of pathology recognize HLA-B*27 bound to both self and microbial antigens adds a very important layer of understanding to these complex conditions that also feature strong inflammatory signatures. Our hope is that this work will one day pave the way for more targeted therapies, not only for these conditions but ultimately, for other autoimmune diseases.”

By providing strong support for the idea that T cells that react to microbes also may react to normal human proteins, the findings promise to accelerate efforts to improve diagnostic tools and treatments for autoimmune diseases.

“For ankylosing spondylitis, the average time between initial symptoms and actual diagnosis is seven to eight years,” said Paley, an assistant professor of medicine, of ophthalmology, and of pathology & immunology. “Shortening that time with improved diagnostics could make a dramatic impact on patients’ lives, because treatment could be initiated earlier. As for therapeutics, if we could target these disease-causing T cells for elimination, we could potentially cure a patient or maybe even prevent the disease in people with the high-risk genetic variant. There’s a lot of potential for clinical benefit here.”

Each and every individual has a complicated genome. With numerous variances within each individual, it is comparable to three billion letters of code. Perhaps it is impossible for a human to sit and evaluate all that code.

However, according to a research published in the journal named “Nature Machine Intelligence”, Artificial Intelligence has the ability to spot things that humans may miss through billions of codings. Someday, AI-powered genome readers may even be able to predict the incidence of diseases from cancer to the common cold. Unfortunately, AI’s recent popularity surge has led to a bottleneck in innovation. “It’s like the Wild West right now. Everyone’s just doing whatever the hell they want,” says Cold Spring Harbor Laboratory (CSHL) Assistant Professor Peter Koo. Just like Frankenstein’s monster was a mix of different parts, AI researchers are constantly building new algorithms from various sources. And it’s difficult to judge whether their creations will be good or bad. After all, how can scientists judge “good” and “bad” when dealing with computations that are beyond human capabilities?

That’s where GOPHER, the Koo lab’s newest invention, comes in. GOPHER (short for GenOmic Profile-model compreHensive EvaluatoR) is a new method that helps researchers identify the most efficient AI programs to analyze the genome. “We created a framework where you can compare the algorithms more systematically,” explains Ziqi Tang, a graduate student in Koo’s laboratory.

GOPHER judges AI programs on several criteria: how well they learn the biology of our genome, how accurately they predict important patterns and features, their ability to handle background noise, and how interpretable their decisions are. “AI are these powerful algorithms that are solving questions for us,” says Tang. But, she notes: “One of the major issues with them is that we don’t know how they came up with these answers.”

GOPHER helped Koo and his team dig up the parts of AI algorithms that drive reliability, performance, and accuracy. The findings help define the key building blocks for constructing the most efficient AI algorithms going forward. “We hope this will help people in the future who are new to the field,” says Shushan Toneyan, another graduate student at the Koo lab.

Imagine having a health issue and being able to pinpoint it with the touch of a button. This science fiction cliché may one day become a standard fixture in every doctor’s office thanks to AI. Artificial intelligence (AI) programmes may recognise distinctive features of our genome that result in individualised medicine and treatments, much like video-streaming algorithms that learn users’ preferences based on their viewing history. The Koo team is hoping that GOPHER will aid in refining such AI algorithms so that we can be confident they are picking up the right information for the right purposes.

Toneyan says: “If the algorithm is making predictions for the wrong reasons, they’re not going to be helpful.”

Scripps A novel approach based on nanotechnology has shown promise in early trials for the treatment of autoimmune illnesses, according to research scientists.

The scientists developed “nanoparticles” that resemble cells that only attack the immune cells responsible for an autoimmune response, leaving the rest of the immune system unharmed and functioning normally. Their research was published in the journal ACS Nano.

The nanoparticles significantly postponed, and in some cases even prevented, severe disease in a mouse model of arthritis.

“The potential advantage of this approach is that it would enable safe, long-term treatment for autoimmune diseases where the immune system attacks its own tissues or organs–using a method that won’t cause broad immune suppression, as current treatments do,” says senior study author James Paulson, PhD, Cecil H. and Ida M. Green Chair of Chemistry in the Department of Molecular Medicine at Scripps Research.

Rheumatoid arthritis is an example of an autoimmune illness that develops when the immune system assaults the body’s own tissues or organs. In only the United States, 10 million individuals are thought to be affected by these disorders.

Treatments are available and can benefit many people, but they frequently have unintended adverse effects, including an increased risk of infections and malignancies.

Paulson and his associates have approached the immune system in a more focused manner. Numerous autoimmune disorders are brought on by or made worse by immunological assaults on a particular protein called a “self-antigen” in the patient’s body.

The idea underlying the nanoparticle strategy is to eliminate or deactivate only the immune cells that attack that self-antigen–an approach that could be at least as effective as broad immune suppression, without the side effects.

Autoimmune diseases dominated by immune responses to a single self-antigen include some forms of arthritis, the skin blister disease known as pemphigus and the thyroid ailment Graves’ disease.

The researchers developed nanoparticles that could deactivate two types of immune cells: B cells and T cells, with the help of first author Katarzyna Brzezicka, PhD, a postdoctoral research associate in the Paulson lab, research assistant Britni Arlian, and other lab members.

Each nanoparticle had copies of a target self-antigen on its surface and a sugar-related molecule that can bind to a special “off switch” receptor on B cells called CD22. B cells, which produce antibodies and are specific to different antigens, will effectively shut down if they come into contact with both the antigen they are looking for and the CD22 binding partner at the same time.

Each nanoparticle also was laced with a powerful compound called rapamycin to stimulate the production of immune cells called regulatory T cells.

Treg cells, as they’re also known, are responsible for suppressing other T cells needed to generate an autoimmune attack. The overall aim of the study was to effectively knock out only the B and T cells that recognize the self-antigen, leaving the rest of the B- and T-cell populations intact.

The researchers first demonstrated that their nanoparticle-based strategy could tolerate a chicken protein, ovalbumin, that would otherwise elicit a strong immune response in mice. The strategy was then tested in a widely used mouse model of arthritis in which the mouse immune system is genetically predisposed to attack a self-antigen known as GPI.

The researchers demonstrated that treating mice with GPI-tolerizing nanoparticles at the age of three weeks significantly delayed the development of arthritis symptoms, which would normally appear a week or two later. In fact, approximately one-third of the mice remained arthritis-free for the entire 300-day follow-up period. Tests confirmed that the treatment significantly reduced the mice’s production of anti-GPI antibodies while also increasing their Treg populations.

Paulson says his team plans to follow up these highly promising results with further optimization of the nanoparticle strategy.

“We were able to ‘cure’ a third of these animals in this early demonstration, and I think there’s the potential to combine our nanoparticles with other immune modulator treatments to make it even more effective,” Paulson says. “So that will be our next step–as well as demonstrating our technology against other autoimmune diseases caused by unwanted immune responses to a self-antigen.”

World Aids Day is observed annually on December 1 to promote awareness of the signs, causes, and prevention measures of HIV/AIDS, which has resulted in an unprecedented number of fatalities.

Perhaps the most well-known sign of AIDS awareness throughout the world is the red ribbon, which is worn by individuals all year in memory of those who have passed away from the disease. Understanding why a red ribbon was selected for this use is pretty fascinating. While some believe it is used to symbolise love for everyone who has HIV-positive results, others think it is meant to convey the powerlessness of those who are suffering. Red is the most appropriate colour because it is primarily transmitted through blood.

However, the history of this symbol starts from the year 1988, when as a reaction to the consequences of AIDS on the arts community and as a means of mobilizing artists, arts institutions, and arts audiences towards direct action on AIDS, art professionals created a group called Visual AIDS.

Some of these Visual AIDS artists came together three years later, in 1991, to design a visual symbol to demonstrate compassion for people living with HIV and their caregivers.

After being inspired by the yellow ribbons worn by American soldiers participating in the Gulf War, the artists decided to make a red ribbon to represent support and solidarity for those living with HIV and to remember those who have died from AIDS-related illnesses.

According to the website of UNAIDS, a Switzerland-based non-government organization, the reason for choosing the color red was its, “connection to blood and the idea of passion — not only anger, but love, like a valentine,” the Project founders said. The project was to become known as the Red Ribbon Project.

The Red Ribbon Project volunteers banded together that year to send letters and red ribbons to every Tony Awards attendee in the USA. It was here that actor Jeremy Irons was seen as a red ribbon pinned on his lapel on national television.

On Easter Monday in 1992, during the Freddie Mercury AIDS Awareness Tribute Concert at Wembley Stadium, more than 100,000 red ribbons were distributed, ushering in the symbol’s mass introduction to Europe.

More than one billion individuals in more than 70 different countries watched the television broadcast. In the 1990s, a lot of famous people wore red ribbons as a result of Princess Diana’s well-known AIDS activism.

A quick and effective way to fight the stigma and discrimination related to AIDS is to wear a red ribbon. As a result, the Red Ribbon has come to represent the world’s solidarity with and support for those who are HIV positive.

A recent study from the La Jolla Institute for Immunology (LJI) offers researchers advice on neutralising the Lassa virus using a trio of unique antibodies acquired from Lassa virus survivors.

Lassa virus is a fatal virus native to West Africa that is mostly spread by rodents. The virus causes Lassa fever, a condition that affects up to 300,000 people each year and often begins with flu-like symptoms but can escalate to severe illness, death, and long-term issues such as hearing. The Lassa virus is highly dangerous for pregnant women, with over 90% of infections resulting in death.

LJI researchers can now demonstrate how a mixture of three human antibodies can prevent viral infection. These antibodies may be useful in planned clinical trials for Lassa therapies, and the LJI team intends to use their newly discovered map of the Lassa virus surface glycoprotein to develop a much-needed vaccine.

“We now know where these three therapeutic antibodies act and how exactly they act,” says Kathryn Hastie, Ph.D., an LJI Instructor and the Director of the Antibody Discovery Center at LJI.

The findings were published in Science Translational Medicine as a cover story on October 26, 2022. The research was led by the Saphire Lab at LJI, including Instructor Haoyang Li, Ph.D., Hastie, and Professor Erica Ollmann Saphire, Ph.D., in collaboration with Luis Branco, Ph.D., of Zalgen Labs LLC.

The power of neutralizing antibodies

In 2017, Hastie and her colleagues at Scripps Research’s Saphire Lab published the first structural photos of the Lassa virus glycoprotein. Lassa enters host cells via glycoproteins and initiates infection. The structure of Hastie’s glycoprotein gave researchers a sense of what they were up against.

Hastie’s discovery emerged while researchers searched for the rare human antibodies that could overcome Lassa’s defenses. Researchers hoped to use these neutralizing antibodies to produce Lassa fever treatments or vaccinations.

This hope was realized when Tulane University and Zalgen Labs LLC researchers discovered a promising group of Lassa-fighting antibodies from the blood of Lassa disease survivors. The University of Texas Medical Branch then tested a combination of three neutralizing antibodies in nonhuman primates. This antibody therapy, known as Arevirumab-3, was completely efficient in curing Lassa fever in animals with advanced disease.

“This was a groundbreaking finding,” says Saphire. “The dogma had been that antibodies would not be protective against Lassa virus.”

When it came time to put the combination through human clinical trials, the researchers ran into a snag. The US Food and Drug Administration refused to allow clinical trials to begin unless researchers identified the mechanism that made the therapy so effective. How did these neutralizing antibodies specifically target the Lassa virus glycoprotein and prevent infection?

Researchers needed a more detailed map of Lassa glycoprotein to address the question. Hastie’s original glycoprotein structure required complex molecular engineering to offer enough stability for imaging. Her structure provided scientists with a key peek of the Lassa glycoprotein, but not the complete picture. Furthermore, certain prospective therapeutic antibodies were unable to identify this or any other type of modified Lassa glycoprotein. For additional research, the researchers were required to extract a natural glycoprotein target.

Fortunately, the Saphire Lab had the tools and expertise to reveal these molecular details. Li led the effort to produce a “native” Lassa glycoprotein. Thanks to advances in protein production and three years of perseverance, Li’s version of the glycoprotein was a copy of the real thing and could be recognized by all three antibodies used in Arevirumab-3. Li then used a technique called cryo-electron microscopy single-particle analysis to image the native glycoprotein together with the three antibodies.

“Haoyang’s ingenuity and hard work enabled us to see the structures we couldn’t see before,” says Hastie.

A new map of the Lassa virus targets

The scientists discovered how the three antibodies utilized in Arevirumab-3 neutralize the Lassa virus using high-resolution structures and various functional experiments.

Hastie was taken aback when he saw how antibody 8.9F binds to the very top of the glycoprotein molecule. This region of the glycoprotein is where three molecules (called protomers) combine to form a “trimer,” which Hastie characterizes as a “twisted trefoil.” Lassa would typically use this section of the glycoprotein to attach to host cell receptors, but Li’s structure shows how a single 8.9F leaps in and binds to all three protomers at the same time to prevent infection.

“The structure is really a beautiful illumination of how this antibody essentially mimics the host receptor to block the glycoprotein receptor from binding,” says Hastie. “It’s an absolutely gorgeous structure to see.”

Meanwhile, the neutralizing antibody 12.1F attaches to only one of the three-sided trimer’s protomers. Fortunately, any treatment would have a large number of copies of 12.1F. Each 12.1F antibody can bind to a protomer to aid in virus neutralization when moving as a team of three.

Simultaneously, copies of antibody 37.2D target the Lassa virus by binding in a way that binds adjacent protomers together. This antibody activity is a major issue for Lassa, as the virus has to open up its trimer (where the protomers come together) in order to infect host cells. With 37.2D on the scene, its entry mechanism is rendered inoperable.

“Lassa has another trick. It shields itself using a thick coat of human carbohydrate molecules — like a wolf in sheep’s clothing,” says Saphire, “Haoyang’s structures clearly show how these potent, protective antibodies breach or even utilize the carbohydrates to target and neutralize the virus.”

“The findings fill a critical gap in Lassa virus research and may pave the way for Arevirumab-3 to move into clinical trials,” says Branco, who will lead the Zalgen team to perform future clinical trials.

Also Read: Study finds cutting on carbs may lower risk of diabetes

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A group of academicians devised a method to detect marijuana with a breath analyzer, similar to how an alcohol analyzer detects the presence of alcohol in one’s body through the breath. They are usually used by police to determine if someone is breaking the law by driving while inebriated.

Professor of organic chemistry at UCLA Neil Garg and researchers from the UCLA start-up ElectraTect Inc. describe the method by which THC introduced in a solution into their laboratory-built device can be oxidised, producing an electric current whose strength indicates how much of the psychoactive compound is present.

The research was published in the journal Organic Letters. According to the researchers, the availability of a Breathalyzer-like device could contribute to making roads safer given the recent legalisation or decriminalisation of marijuana in numerous jurisdictions, including California. Marijuana use has been linked to dramatically increased accident risk and has been demonstrated to impair some driving abilities.

In 2020, Garg and UCLA postdoctoral researcher Evan Darzi observed that the bigger THC molecule had a visible colour change when a hydrogen molecule was removed from it. The method, called oxidation, is comparable to how alcohol breath analyzers turn ethanol into an organic chemical molecule by losing hydrogen. This oxidation results in an electric current in the majority of modern alcohol breath analyzer systems, which displays the quantity and concentration of ethanol in the breath.

Since their discovery in 2020, the researchers have been working on creating a THC breath analyzer that functions similarly using their patent-pending oxidation method. The patent rights have been leased exclusively to ElectraTect by UCLA.

How the new device works

Darzi, who is currently the CEO of ElectraTect, Garg, and researchers from ElectraTect describe the operation of their brand-new laboratory-scale THC-powered fuel cell sensor in the new study. THC (technically known as Delta-9-tetrahydrocannabinol) oxidises into a new compound called THCQ when it comes into contact with a negatively charged electrode, or anode, on one side of the device’s H-shaped glass chamber, sending electrons across the chamber to a positively charged electrode, or cathode, on the other, creating a detectable electric current. The current becomes stronger as the amount of THC molecules increases.

THC has never before been utilised to operate a fuel cell sensor, so this development is significant. Researchers are currently working to refine the device to detect and measure THC in exhaled breath and to shrink it to a more compact size suitable for use in a handheld breath analyzer or ignition interlock device–a breath analyzer connected to a vehicle’s ignition that prevents it from starting if THC is detected. The researchers said they expect that the relatively simple, inexpensive technology, once perfected, can be scaled up for economical mass production.

Making marijuana testing easier – and fairer

The technology may also result in increased road safety and more equitable marijuana law enforcement, according to the researchers. THC usage in drivers is typically detected through urine or blood tests. Such roadside tests can be challenging to do, and they aren’t always reliable for detecting intoxicated drivers because the chemical can persist in the body for weeks after marijuana use without having any lasting impact on cognition. Even if a person doesn’t test positive for drugs when tested, this ambiguity might result in penalties, jail time, or loss of work.

These problems, according to the researchers, emphasise the requirement for cutting-edge forensic technology that are simpler to use and more precise for identifying recent marijuana use. Although a commercial marijuana breathalyser based on their research would be a few years away, Darzi and Garg emphasised that such a device would potentially offer advantages beyond those of law enforcement and traffic safety.

Their scientific advancement, they claimed, could eventually be applied in any circumstance where unbiased marijuana testing is necessary, such as at work where employees might be operating machinery or even at home where people might one day be able to use it proactively — before they ever get behind the wheel.

Also Read: Study looks at why late-night eating increases obesity risk

The TB bacteria has a relative you’ve never heard of: MAC. This bacterial complex is present worldwide, yet most people exhibit no symptoms. However, some people become quite ill. Researchers have recently discovered an immunologic flaw that may explain this disparity.

MAC is an “opportunistic” pathogen, explains Cecilia Lindestam Arlehamn, Ph.D., Research Assistant Professor at La Jolla Institute for Immunology (LJI). Some people do have risk factors — such as cystic fibrosis and structural lung diseases, for example — that make them likely to develop symptoms after MAC exposure. The problem is that no one knows exactly why these factors make such a difference. Now Lindestam Arlehamn’s laboratory has uncovered an immune cell defect tied to the risk of developing MAC disease. As her team reports in Frontiers in Immunology, people who show MAC infection symptoms have fewer specialized Th1* (Th1 “star”) cells, which robs them of the ability to mount an effective immune response to the bacteria.

“We think these people have this cellular defect going into MAC exposure,” explains Lindestam Arlehamn, who worked closely on the study with collaborators at the University of Washington.

This research may be a step toward uncovering biomarkers to predict risk of progressive lung disease and responses to treatment in MAC disease patients.

In 2020, Lindestam Arlehamn received funding through a Tullie and Rickey Families SPARK Award to investigate how T cells fight the disease. The hope was that by analyzing T cells from people previously infected with MAC, she could identify key targets, or epitopes, where MAC-infected cells are vulnerable to immune system attacks.

T cells are normally critical for fighting infections, yet to everyone’s surprise, Lindestam Arlehamn’s work revealed that the human body has a very limited T cell response to MAC infection, and she wasn’t able to uncover MAC-specific epitopes.
It’s pretty unusual for a T cell response to a pathogen to be so limited. It was like the MAC-infected study volunteers had barely any “immune memory” of getting the disease. Instead, Lindestam Arlehamn’s SPARK project highlighted an unexpected cellular defect that could explain why some people get sick while others don’t. “This was also very interesting,” says Lindestam Arlehamn.

When Lindestam Arlehamn looked at global gene expression (which genes are “switched on”) in response to MAC infection, she spotted a stark difference in blood samples from people previously infected with MAC and healthy controls.

People who had MAC appeared to have a immunologic defect that leads to low numbers of special “helper” immune cells called Th1* cells in the body. Th1* cells normally help alert the body’s pathogen-fighting cells to danger.

Lindestam Arlehamn and her colleagues were among the first to show that Th1* cells are particularly critical for fighting a Mycobacterium attack, either from MAC or Mycobacterium tuberculosis.

Their work is the first to suggest that this Th1* defect can lead to increased disease susceptibility. They think it’s likely that without enough Th1* cells, some key immune cells never get the message that MAC is trying to invade. This means MAC-susceptible people may have both an over-performing innate immune response (with certain cells driving inflammation early in the disease process) and an under-performing adaptive immune response (a lack of activated T cells to actually stop the disease).

For some people, this lack of an immune defense is too much to bear. For people with cystic fibrosis, for example, thick mucus in the lungs may interfere with the ability of T cells to patrol the tissue and detect MAC. A lack of Th1* cells could then be a double-blow — adding immune system dysfunction to an already weak defense in the lungs. “That could partially explain it,” says Lindestam Arlehamn.

Lindestam Arlehamn now wants to confirm whether the defect leading to fewer Th1* cells is present in people prior to MAC exposure. She plans to look at samples taken from people earlier in the disease progression to see if a lack of Th1* is a feature for them as well. She’d also like to study samples from people who were exposed to the same sources of MAC in the environment.

“If you live together with someone with MAC disease, it’s likely that you are exposed too,” she says. We want to see if we can define specific T cell responses in those individuals and look for the differences between those who get sick and those who don’t.”

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