It’s the first study of individualized brain stimulation to treat severe depression. Sarah’s case raises the possibility the method may help people who don’t respond to other therapies.Driving home from work in Northern California five years ago, a young woman was so overwhelmed with depression that all she could think about was ending her life.“I couldn’t stop crying,” recalled Sarah, now 38. “The thought that consumed me the entire way on that road was just driving my car into the marshland so I can drown.”She made it home, but soon after, moved in with her parents because doctors considered it unsafe for her to live alone. No longer able to function at work, she quit her health technology job.She tried nearly every treatment: roughly 20 different medications, months in a hospital day program, electroconvulsive therapy, transcranial magnetic stimulation. But as with nearly a third of the more than 250 million people with depression worldwide, her symptoms persisted. Then Sarah became the first participant in an unusual study of an experimental therapy. Now, her depression is so manageable that she’s taking data analysis classes, has moved to her own place and helps care for her mother, who suffered a fall.“Within a few weeks, the suicidal thoughts just disappeared,” said Sarah, who asked to be identified by only her first name to protect her privacy. “Then it was just a gradual process where it was like my lens on the world changed.”Researchers at the University of California, San Francisco surgically implanted a battery-operated, matchbook-sized device in Sarah’s brain — a “pacemaker for the brain” some call it — calibrated to detect the neural activity pattern that occurs when she is becoming depressed. It then delivers pulses of electrical stimulation to stave off depression.Twelve days after Sarah’s device was fully operational in August 2020, her score on a standard depression scale dropped to 14 from 33, and several months later, it fell below 10, essentially signaling remission, the researchers reported.“The device has kept my depression at bay, allowing me to return to my best self and rebuild a life worth living,” Sarah said.Sarah’s is the first documented case of personalizing a technique called deep brain stimulation to successfully treat depression. Much more research is needed before it’s clear how effective the approach could be and for how many patients. But several teams of scientists are now working on ways to essentially match the electrical stimulation to what happens in an individual patient’s brain.Deep brain stimulation is used to treat Parkinson’s disease and several other disorders, but isn’t approved by federal regulators for depression because results have been inconsistent. While some previous studies suggested benefits, two trials sponsored by U.S. device companies were stopped in the last decade because stimulation seemed no better than the placebo effect of a “sham” implant that provided no stimulation.But those studies didn’t target individualized locations or patterns of electrical activity in people’s brains. It was “one size fits all,” said Dr. Darin Dougherty, director of neurotherapeutics at Massachusetts General Hospital, who worked on one of the halted trials. He called the personalized approach with Sarah, which he wasn’t involved in, “very exciting.”“One person’s depression might look very different from another person’s depression,” said Dr. Katherine Scangos, an assistant professor of psychiatry at U.C.S.F. and an author of a report about Sarah’s case, published Monday in the journal Nature Medicine. The senior authors were Dr. Andrew Krystal, an expert in neuro-modulation and mood disorders, and Dr. Edward Chang, whose work includes brain implants for paralyzed patients who cannot speak.To identify the specific brain activity pattern linked to Sarah’s depression, researchers conducted an intensive 10-day exploration of Sarah’s brain, placing multiple electrodes in it and asking about her feelings when they applied stimulation to different locations in varying doses.“One person’s depression might look very different from another person’s depression,” said Dr. Katherine Scangos, a researcher on a new study using deep brain stimulation as a personalized treatment.Mike Kai Chen for The New York TimesSarah remembers an “aha moment” when she felt like “the Pillsbury Doughboy,” emitting a “giant belly laugh,” which she said was “the first time I spontaneously laughed and smiled” in five years. Another feeling resembled “being in front of warm fire and reading a comforting book,” while a negative sensation felt like “nails on a chalkboard.”Eventually, the team identified a specific pattern of electrical activity that coincided with Sarah becoming depressed.The exploratory phase guided the researchers to place the stimulation device in Sarah’s right brain hemisphere linked to electrodes in two regions. One was the the ventral striatum, involved in emotion, motivation and reward, where stimulation “consistently eliminated her feelings of depression,” and the other the amygdala, where changes could “predict when her symptoms were most severe,” Dr. Scangos said.While deep brain stimulation is typically delivered continuously, Sarah’s device is set to supply only a six-second burst when it recognizes her depression-linked brain activity pattern. The goal, said Dr. Dougherty, is that stimulation will disrupt or shift the neural activity to produce a healthier pattern that will ease depressive symptoms.Sarah has continued taking psychiatric medications, and the stimulation hasn’t eliminated depression-causing activity in her brain. But she can manage her illness much better, she said, instead of being unable to make even the smallest decisions, like what to eat.Now, “you’re experiencing that whole negative, depressive, whatever the triggering thing is, and then it’s like suddenly the ultra-rational side of you comes on and those emotions can be separated,” she said in an interview, wearing a T-shirt that said “Take it easy lemon squeezy.”That separation helps her productively use tools from talk therapy, like staying calm and maintaining perspective.About 30 percent of people with depression don’t respond to standard treatments or find the side effects intolerable. Deep brain stimulation wouldn’t be appropriate for all because it costs tens of thousands of dollars and brain surgery to implant the device carries risks like infection. But if the new attempts work, it might help a significant number, experts said. Dr. Chang said the research may also lead to noninvasive approaches that would help more people.“Our job now is really to figure out what is it that identifies who needs this kind of intervention,” said Dr. Helen Mayberg, director of the Center for Advanced Circuit Therapeutics at the Icahn School of Medicine in New York City, who pioneered the concept of deep brain stimulation for depression nearly 20 years ago.Dr. Mayberg uses a different method of individualization. With imaging, she finds the location in each person’s brain where four white matter bundles intersect near a key depression-related region. After implanting electrodes and a stimulation device, “we pretty much set it and forget it,” delivering stimulation continuously, while also helping patients with conventional therapy.Dr. Scangos examined a graph of Sarah’s brain activity. Mike Kai Chen for The New York TimesNeural activity is monitored “to learn the brain signature that heralds an impending depressive relapse or need for a dose adjustment or just indicates that the person is just having a bad week,” Dr. Mayberg said. She led one of the halted trials, but her work has also allowed patients to experience improvements that continue for years if stimulation is sustained.In another approach, Dr. Sameer Sheth, an associate professor of neurosurgery at Baylor College of Medicine, and colleagues study a patient’s specific brain activity pattern to identify which of billions of combinations of stimulation characteristics, like frequency and amplitude, improve that patient’s depression.He then tunes electrodes in two regions and applies that specific combination as continuous stimulation.Dr. Sheth said the first patient, given the device in March 2020, “is remarkably well” now, maintaining a relationship and becoming a father. To test for a placebo effect, researchers gradually stopped stimulation to one brain region without the patient knowing when. His depression “got worse and worse” said Dr. Sheth, until he needed “rescue.” After stimulation restarted, he improved, suggesting the effect “is definitely stimulation-related.”Several months ago, Sarah needed a rescue too. Shortly after entering a study phase where the device is either turned off or left on for six weeks without the participant knowing which, “the suicidal thoughts were back,” Sarah said. Her family tried to get her hospitalized, but hospitals were full. “Things were really bad,” Sarah said.“She did have a very severe worsening of her depression,” said Dr. Scangos. She said she couldn’t disclose whether stimulation had been off or on, but said a device company technician was sent to Sarah’s home to “make a rescue change.”Afterward, Sarah said, she improved again.Over the year, the number of times a day that Sarah’s device has detected depression-linked brain activity and delivered stimulation has decreased somewhat, but is still substantial, Dr. Scangos said. Still, some days Sarah doesn’t need the maximum amount the device is set to provide: 300 times or 30 total minutes daily. (It automatically stops around 6 p.m. because evening stimulation made her too alert to sleep.)Longer-term and more detailed data on Sarah will be published later, said the researchers, who have two other participants so far. The device is intentionally tuned so Sarah cannot feel the stimulation, but she believes she knows that it’s occurred because she subsequently develops a sense of “emotional distance” that keeps negative feelings “compartmentalized,” she said.Also, “I feel alert,” she said. “I feel present.” That’s “a really good sign,” said Dr. Dougherty, who is considering using a similar approach for depression and possibly addiction. “The emotions are still there, but instead of sticking like mud, it’s running off like water.”To help researchers correlate brain activity with emotional states, two or three times a day, Sarah holds a doughnut-shaped magnet to her head, triggering the device to save the next 90 seconds of neural activity, and she completes a mental health survey. She’s been encouraged to pick moments “when she’s in a very good mood or a bad mood,” Dr. Scangos said. Also, twice daily, 12 minutes of neural data are automatically relayed to the device company and researchers.One question, experts said, is whether Sarah’s results support the theory that stimulating briefly whenever depression begins works because it keeps the brain from becoming accustomed to the treatment. Or, Dr. Sheth asked, does Sarah’s need for many daily doses after a year suggest continuous stimulation would be as or more effective?Another question is whether the therapy can prompt lasting brain changes to eventually avert depression with little or no continuing stimulation.Because of her implanted device that delivers deep brain stimulation, Sarah has been able to move to her own apartment and take classes in data analysis.Ruth Fremson/The New York TimesResearchers, several of whom consult for device companies or have patents related to deep brain stimulation, expect it will take years to learn if individualized approaches are effective enough to be approved. Different methods might work for different people’s depression, and individualized stimulation might eventually help other psychiatric disorders, researcher say. The most elemental things have improved for Sarah, who said she’s started to “relearn my life” and that “hobbies I used to distract myself from suicidal thoughts suddenly became pleasurable again.” When depressed, Sarah, a passionate cook and foodie, had such slow reflexes and trouble functioning that she’d cut or burn herself in the kitchen and doctors told her it wasn’t safe to cook anymore. Foods had little flavor. But after receiving the device, she ate Vietnamese pho in the hospital cafeteria and was thrilled she could taste “the brightness and the herbs,” she said. While being driven home from the hospital, she saw the marshes and exclaimed: “God, the color differentiation is gorgeous.” Now, she said, she’s “seeing things that are beautiful in the world, and when I was in the depths of depression, all I saw was what was ugly.”If you are having thoughts of suicide, call the National Suicide Prevention Lifeline at 1-800-273-8255 (TALK) or go to SpeakingOfSuicide.com/resources for a list of additional resources.

By observing mice hair follicles, scientists discovered an unexpected mechanism of aging. “If I didn’t see it with my own eyes I wouldn’t believe it,” one said.Every person, every mouse, every dog, has one unmistakable sign of aging: hair loss. But why does that happen?Rui Yi, a professor of pathology at Northwestern University, set out to answer the question.A generally accepted hypothesis about stem cells says they replenish tissues and organs, including hair, but they will eventually be exhausted and then die in place. This process is seen as an integral part of aging.Instead Dr. Yi and his colleagues made a surprising discovery that, at least in the hair of aging animals, stem cells escape from the structures that house them.“It’s a new way of thinking about aging,” said Dr. Cheng-Ming Chuong, a skin cell researcher and professor of pathology at the University of Southern California, who was not involved in Dr. Yi’s study, which was published on Monday in the journal Nature Aging.The study also identifies two genes involved in the aging of hair, opening up new possibilities for stopping the process by preventing stem cells from escaping.Charles K.F. Chan, a stem cell researcher at Stanford University, called the paper “very important,” noting that “in science, everything about aging seems so complicated we don’t know where to start.” By showing a pathway and a mechanism for explaining aging hair, Dr. Yi and colleagues may have provided a toehold.Stem cells play a crucial role in the growth of hair in mice and in humans. Hair follicles, the tunnel-shaped miniature organs from which hairs grow, go through cyclical periods of growth in which a population of stem cells living in a specialized region called the bulge divide and become rapidly growing hair cells.Sarah Millar, director of the Black Family Stem Cell Institute at the Icahn School of Medicine at Mount Sinai, who was not involved in Dr. Yi’s paper, explained that those cells give rise to the hair shaft and its sheath. Then, after a period of time, which is short for human body hair and much longer for hair on a person’s head, the follicle becomes inactive and its lower part degenerates. The hair shaft stops growing and is shed, only to be replaced by a new strand of hair as the cycle repeats.But while the rest of the follicle dies, a collection of stem cells remains in the bulge, ready to start turning into hair cells to grow a new strand of hair.Dr. Yi, like most scientists, had assumed that with age the stem cells died in a process known as stem cell exhaustion. He expected that the death of a hair follicle’s stem cells meant that the hair would turn white and, when enough stem cells were lost, the strand of hair would die. But this hypothesis had not been fully tested.Together with a graduate student, Chi Zhang, Dr. Yi decided that to understand the aging process in hair, he needed to watch individual strands of hair as they grew and aged.Ordinarily, researchers who study aging take chunks of tissue from animals of different ages and examine the changes. There are two drawbacks to this approach, Dr. Yi said. First, the tissue is already dead. And it is not clear what led to the changes that are observed or what will come after them.He decided his team would use a different method. They watched the growth of individual hair follicles in the ears of mice using a long wavelength laser that can penetrate deep into tissue. They labeled hair follicles with a green fluorescent protein, anesthetized the animals so they did not move, put their ear under the microscope and went back again and again to watch what was happening to the same hair follicle.Colored arrows point to escaping stem cells on a hair follicle. (Rui Yi)Rui YiWhat they saw was a surprise: When the animals started to grow old and gray and lose their hair, their stem cells started to escape their little homes in the bulge. The cells changed their shapes from round to amoeba-like and squeezed out of tiny holes in the follicle. Then they recovered their normal shapes and darted away.Sometimes, the escaping stem cells leapt long distances, in cellular terms, from the niche where they lived.“If I did not see it for myself I would not have believed it,” Dr. Yi said. “It’s almost crazy in my mind.”The stem cells then vanished, perhaps consumed by the immune system.Dr. Chan compared an animal’s body to a car. “If you run it long enough and don’t replace parts, things wear out,” he said. In the body, stem cells are like a mechanic, providing replacement parts, and in some organs like hair, blood and bone, the replacement is continual.But with hair, it now looks as if the mechanic — the stem cells — simply walks off the job one day.Researchers manipulated the genes of this mouse. By 18 months old, it had rapid hair loss, but was otherwise healthy.Rui Yi and Chi ZhangBut why? Dr. Yi and his colleagues’ next step was to ask if genes are controlling the process. They discovered two — FOXC1 and NFATC1 — that were less active in older hair follicle cells. Their role was to imprison stem cells in the bulge. So the researchers bred mice that lacked those genes to see if they were the master controllers.By the time the mice were 4 to 5 months old, they started losing hair. By age 16 months, when the animals were middle-aged, they looked ancient: They had lost a lot of hair and the sparse strands remaining were gray.Now the researchers want to save the hair stem cells in aging mice.This story of the discovery of a completely unexpected natural process makes Dr. Chuong wonder what remains to be learned about living creatures.“Nature has endless surprises waiting for us,” he said. “You can see fantastic things.”

Mind and body form a two-way street.It’s no surprise that when a person gets a diagnosis of heart disease, cancer or some other life-limiting or life-threatening physical ailment, they become anxious of depressed. But the reverse can also be true: Undue anxiety or depression can foster the development of a serious physical disease, and even impede the ability to withstand or recover from one. The potential consequences are particularly timely, as the ongoing stress and disruptions of the pandemic continue to take a toll on mental health.The human organism does not recognize the medical profession’s artificial separation of mental and physical ills. Rather, mind and body form a two-way street. What happens inside a person’s head can have damaging effects throughout the body, as well as the other way around. An untreated mental illness can significantly increase the risk of becoming physically ill, and physical disorders may result in behaviors that make mental conditions worse.In studies that tracked how patients with breast cancer fared, for example, Dr. David Spiegel and his colleagues at Stanford University School of Medicine showed decades ago that women whose depression was easing lived longer than those whose depression was getting worse. His research and other studies have clearly shown that “the brain is intimately connected to the body and the body to the brain,” Dr. Spiegel said in an interview. “The body tends to react to mental stress as if it was a physical stress.”Despite such evidence, he and other experts say, chronic emotional distress is too often overlooked by doctors. Commonly, a physician will prescribe a therapy for physical ailments like heart disease or diabetes, only to wonder why some patients get worse instead of better.Many people are reluctant to seek treatment for emotional ills. Some people with anxiety or depression may fear being stigmatized, even if they recognize they have a serious psychological problem. Many attempt to self-treat their emotional distress by adopting behaviors like drinking too much or abusing drugs, which only adds insult to their pre-existing injury.And sometimes, family and friends inadvertently reinforce a person’s denial of mental distress by labeling it as “that’s just the way he is” and do nothing to encourage them to seek professional help.How common are anxiety and depression?Anxiety disorders affect nearly 20 percent of American adults. That means millions are beset by an overabundance of the fight-or-flight response that primes the body for action. When you’re stressed, the brain responds by prompting the release of cortisol, nature’s built-in alarm system. It evolved to help animals facing physical threats by increasing respiration, raising the heart rate and redirecting blood flow from abdominal organs to muscles that assist in confronting or escaping danger.These protective actions stem from the neurotransmitters epinephrine and norepinephrine, which stimulate the sympathetic nervous system and put the body on high alert. But when they are invoked too often and indiscriminately, the chronic overstimulation can result in all manner of physical ills, including digestive symptoms like indigestion, cramps, diarrhea or constipation, and an increased risk of heart attack or stroke.Depression, while less common than chronic anxiety, can have even more devastating effects on physical health. While it’s normal to feel depressed from time to time, more than 6 percent of adults have such persistent feelings of depression that it disrupts personal relationships, interferes with work and play, and impairs their ability to cope with the challenges of daily life. Persistent depression can also exacerbate a person’s perception of pain and increase their chances of developing chronic pain.“Depression diminishes a person’s capacity to analyze and respond rationally to stress,” Dr. Spiegel said. “They end up on a vicious cycle with limited capacity to get out of a negative mental state.”Potentially making matters worse, undue anxiety and depression often coexist, leaving people vulnerable to a panoply of physical ailments and an inability to adopt and stick with needed therapy.A study of 1,204 elderly Korean men and women initially evaluated for depression and anxiety found that two years later, these emotional disorders increased their risk of physical disorders and disability. Anxiety alone was linked with heart disease, depression alone was linked with asthma, and the two together were linked with eyesight problems, persistent cough, asthma, hypertension, heart disease and gastrointestinal problems.Treatment can counter emotional tollsAlthough persistent anxiety and depression are highly treatable with medications, cognitive behavioral therapy and talk therapy, without treatment these conditions tend to get worse. According to Dr. John Frownfelter, treatment for any condition works better when doctors understand “the pressures patients face that affect their behavior and result in clinical harm.”Dr. Frownfelter is an internist and chief medical officer of a start-up called Jvion. The organization uses artificial intelligence to identify not just medical factors but psychological, social and behavioral ones as well that can impact the effectiveness of treatment on patients’ health. Its aim is to foster more holistic approaches to treatment that address the whole patient, body and mind combined.The analyses used by Jvion, a Hindi word meaning life-giving, could alert a doctor when underlying depression might be hindering the effectiveness of prescribed treatments for another condition. For example, patients being treated for diabetes who are feeling hopeless may fail to improve because they take their prescribed medication only sporadically and don’t follow a proper diet, Dr. Frownfelter said.“We often talk about depression as a complication of chronic illness,” Dr. Frownfelter wrote in Medpage Today in July. “But what we don’t talk about enough is how depression can lead to chronic disease. Patients with depression may not have the motivation to exercise regularly or cook healthy meals. Many also have trouble getting adequate sleep.”Some changes to medical care during the pandemic have greatly increased patient access to depression and anxiety treatment. The expansion of telehealth has enabled patients to access treatment by psychotherapists who may be as far as a continent away.Patients may also be able to treat themselves without the direct help of a therapist. For example, Dr. Spiegel and his co-workers created an app called Reveri that teaches people self-hypnosis techniques designed to help reduce stress and anxiety, improve sleep, reduce pain and suppress or quit smoking.Improving sleep is especially helpful, Dr. Spiegel said, because “it enhances a person’s ability to regulate the stress response system and not get stuck in a mental rut.” Data demonstrating the effectiveness of the Reveri app has been collected but not yet published, he said.

Throughout the COVID-19 pandemic, there has been much uncertainty about how long immunity lasts after someone who is unvaccinated is infected with SARS-CoV-2.
Now a team of scientists led by faculty at Yale School of Public Health and the University of North Carolina at Charlotte have an answer. Strong protection following natural infection is short-lived.
“Reinfection can reasonably happen in three months or less,” said Jeffrey Townsend, the Elihu Professor of Biostatistics at the Yale School of Public Health and a lead author of the study. “Therefore, those who have been naturally infected should get vaccinated. Previous infection alone can offer very little long-term protection against subsequent infections.”
The study, published in the journal The Lancet Microbe, is the first to determine the likelihood of reinfection following natural infection and without vaccination.
Townsend and his team analyzed known reinfection and immunological data from the close viral relatives of SARS-CoV-2 that cause “common colds” — along with immunological data from SARS-CoV-1 and Middle East Respiratory Syndrome. Leveraging evolutionary principles, the team was able to model the risk of COVID-19 reinfection over time.
Reinfections can and have happened, even shortly after recovery. And they will become increasingly common as immunity wanes and new SARS-CoV-2 variants arise.
“We tend to think about immunity as being immune or not immune. Our study cautions that we instead should be more focused on the risk of reinfection through time,” said Alex Dornburg, assistant professor of bioinformatics and genomics at the University of North Carolina at Charlotte, who co-led the study with Townsend. “As new variants arise, previous immune responses become less effective at combating the virus. Those who were naturally infected early in the pandemic are increasingly likely to become reinfected in the near future.”
The team’s data-driven model reveals striking similarities to the reinfection risks over time between SARS-CoV-2 and endemic coronaviruses.
“Just like common colds, from one year to the next you may get reinfected with the same virus. The difference is that, during its emergence in this pandemic, COVID-19 has proven to be much more deadly.” said Townsend.
“Due to the ability of SARS-CoV-2 to evolve and reinfect, it, too, is likely to transition from pandemic to an endemic disease,” added Dornburg.
“A hallmark of the modern world is going to be the evolution of new threats to human health,” said Townsend. “Evolutionary biology — which provided the theoretical foundations for these analyses — is traditionally considered a historical discipline. However, our findings underscore its important role in informing decision-making, and provide a crucial stepping stone toward robust knowledge of our prospects of resistance to SARS-CoV-2 reinfection.”
Co-authors include researchers from Temple University. Funding for the research was provided by the U.S. National Science Foundation.
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JILA scientists have boosted the sensitivity of their decade-old frequency comb breathalyzer a thousandfold and can detect additional biomarkers of disease — four now, with the potential for six more. When validated and engineered into a portable design, the comb system could offer real-time, noninvasive analysis of human breath to detect and monitor diseases. JILA is jointly operated by the National Institute of Standards and Technology (NIST) and the University of Colorado Boulder.
The JILA system “fingerprints” chemicals by measuring the colors and amounts of light absorbed as a laser frequency comb passes back and forth through breath samples loaded into a mirrored glass tube. Recent upgrades include a shift in the light spectrum analyzed from the near-infrared to the mid-infrared band, where more molecules absorb light, and advances in optical coatings and several other technologies to achieve detection sensitivity up to the parts-per-trillion level.
As described in Proceedings of the National Academy of Sciences, NIST/JILA Fellows Jun Ye and David Nesbitt detected and monitored four biomarkers — methanol (CH3OH), methane (CH4), water (H2O) and a form of heavy water (HDO) — in the breath of a volunteer. These are indicators of health conditions such as, in the case of methane, intestinal problems.
The researchers say it is feasible to use the same apparatus to detect six more chemicals: formaldehyde, ethane, carbonyl sulfide, ethylene, carbon disulfide and ammonia. In addition, extending the comb lasers further into the infrared should greatly expand the detection capability and enable the identification of many hundreds of trace breath chemicals.
JILA researchers demonstrated a prototype comb breathalyzer in 2008 but did not develop it further at that time. They have now refocused on it, prompted by the possibility of eventually testing for COVID-19.
“We are really quite optimistic and committed to pushing this technology to real medical applications,” Ye said.
The most widely used analytical technique in breath research is gas chromatography combined with mass spectrometry, which can detect hundreds of exhaled molecules but works slowly, requiring tens of minutes. Most optical breath tests approved by the U.S. Food and Drug Administration detect only one chemical. JILA is the only institution that has published research on comb breathalyzers, Ye said.
Breath analysis is the leading medical application for frequency combs. Combs offer a combination of broad spectral coverage, high resolution and high sensitivity, potentially detecting tens of chemicals simultaneously. Among other advantages, the comb system would not require chemical reagents and complex laboratory facilities.
Ye and Nesbitt are now working with other NIST researchers to engineer a compact version of the breathalyzer. The tube is only 55 centimeters (21.7 inches) long, but the laser comb is custom-made and somewhat bulky.
The work is funded by the Air Force Office of Scientific Research, the National Science Foundation and NIST.

A previously unknown virus that can infect humans and cause disease has been identified by scientists in Japan. The novel infectious virus, named Yezo virus and transmitted by tick bites, causes a disease characterized by fever and a reduction in blood platelets and leucocytes. The discovery was made by researchers at Hokkaido University and colleagues, and the results have been published in the journal Nature Communications.
Keita Matsuno, a virologist at Hokkaido University’s International Institute for Zoonosis Control, said: “At least seven people have been infected with this new virus in Japan since 2014, but, so far, no deaths have been confirmed.”
The Yezo virus was discovered after a 41-year-old man was admitted to the hospital in 2019 with fever and leg pain after being bitten by an arthropod believed to be a tick while he was walking in a local forest in Hokkaido. He was treated and discharged after two weeks, but tests showed he had not been infected with any known viruses carried by ticks in the region. A second patient showed up with similar symptoms after a tick bite the following year.
Genetic analysis of viruses isolated from blood samples of the two patients found a new type of orthonairovirus, a class of nairovirus, that includes pathogens such as the Crimean-Congo haemorrhagic fever virus. The scientists named it Yezo virus, after a historical Japanese name for Hokkaido, a large island in the north of the country where the virus was discovered. The novel virus was found most closely related to Sulina virus and Tamdy virus, detected in Romania and Uzbekistan, respectively, the latter of which reportedly caused acute fever in humans recently in China.
The scientists then checked blood samples collected from hospital patients who showed similar symptoms after tick bites since 2014. They found additional positive samples from five patients. These patients, including the first two, had a fever and reduced blood platelets and leucocytes, and showed indicators of abnormal liver function.
To determine the likely source of the virus, the research team screened samples collected from wild animals in the area between 2010 and 2020. They found antibodies for the virus in Hokkaido shika deer and raccoons. They also found the virus RNA in three major species of ticks in Hokkaido. Matsuno says, “The Yezo virus seems to have established its distribution in Hokkaido, and it is highly likely that the virus causes the illness when it is transmitted to humans from animals via ticks.”
As the Covid-19 pandemic so dramatically demonstrates, animals carry many unknown viruses and some of these can go on to infect people. “All of the cases of Yezo virus infection we know of so far did not turn into fatalities, but it’s very likely that the disease is found beyond Hokkaido, so we need to urgently investigate its spread,”said Matsuno.
The research team now plans to track the possible nationwide distribution of the novel virus in wild animals and patients. And they say more hospitals should test for the virus in patients who complain of the symptoms.
The study was carried out in collaboration with researchers at the Graduate School of Veterinary Medicine and One Health Research Center of Hokkaido University, Sapporo City General Hospital, Nagaoka Red Cross Hospital, Hokkaido Institute of Public Health, National Institute of Infectious Diseases, Nagasaki University, Rakuno Gakuen University, Health Sciences University of Hokkaido, and the University of Liverpool.
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Patients with psoriasis have reported that glycerin, an inexpensive, harmless, slightly sweet liquid high on the list of ingredients in many skin lotions, is effective at combatting their psoriasis and now scientists have objective evidence to support their reports.
They found that whether applied topically or ingested in drinking water, glycerin, or glycerol, helps calm the classic scaly, red, raised and itchy patches in their psoriasis model, Dr. Wendy Bollag, cell physiologist and skin researcher at the Medical College of Georgia and Charlie Norwood VA Medical Center and her colleagues report in the International Journal of Molecular Sciences.
The studies also provide more evidence of the different ways glycerin enables the healthy maturation of skin cells through four stages that result in a smooth, protective skin layer. Psoriasis is an immune-mediated problem that typically surfaces in young adults in which skin cells instead multiply rapidly, piling up into inflamed patches.
“We have experimental data now to show what these patients with psoriasis are reporting,” says Bollag, who nearly 20 years ago first reported in The Journal of Investigative Dermatology that glycerin, a natural alcohol and water attractor known to help the skin look better, also safely helped it function better by helping skin cells mature properly.
Bollag’s early report led to many anecdotal reports from individuals and their reports ultimately led to the newly published study.
Topically, glycerin is known to have a soothing, emollient effect. But another key part of its magic, which Dr. Bollag has helped delineate, is its conversion to the lipid, or fat, phosphatidylglycerol, which ultimately regulates the function of keratinocytes, our major skin cell type, and suppresses inflammation in the skin.

A new Tel Aviv University study examined for the first time the development of a glioblastoma cancerous tumor in animal models with a normal immune system, in order to best simulate the development of the tumor in humans. The findings of the study showed that there are immune system cells that, despite the fact that their primary function is to attack and kill the cancer cells, actually act as “double agents” that increase and intensify the aggressiveness and threat of the tumor.
The study was led by Dr. Dinorah Friedmann-Morvinski of the George S. Wise Faculty of Life Sciences and Sagol School of Neuroscience, and her PhD student and Prerna Magod Also participating in the study were Dr. Liat Rousso-Noori and Ignacio Mastandrea, also from the Faculty of Life Sciences, as well as other researchers from the Sackler Faculty of Medicine at Tel Aviv University and the Weizmann Institute of Science. The study was published in the journal Cell Reports.
Glioblastoma is the most common type of brain cancer, and one of the most violent and deadly cancers in humans; the average life expectancy of glioblastoma patients is 12 to 15 months from the moment of detection. The researchers explain that usually, the scientific monitoring of the development of the cancerous tumor in animal models is carried out without an active immune system, in order to enable the absorption and growth of cancer cells in the body. The disadvantage of this commonly-used model lies in the fact that the immune system either does not exist or does not function properly, which prevents researchers from monitoring the interaction between it and the tumor cells.
The study, which was conducted in Dr. Friedmann-Morvinski’s laboratory, used a model that examined the development of cancer cells in animal models with functioning immune systems. This allowed the cancer to grow gradually, to the point of the development of a massive tumor, which enabled the close monitoring of its development, and throughout the process, of the interaction between the cancer cells and different immune system cells.
In the study, the researchers found that cells called neutrophils play a critical role in interacting with the cancerous growth. Neutrophils are immune system cells that originate in the bone marrow, and whose purpose is to “swallow” or kill bacteria and fungi and fight the infections caused by them. “Neutrophils are the front-line soldiers of the immune system,” says Dr. Friedmann-Morvinski. “When a tumor begins to develop, the neutrophils are among the first to mobilize and attack it in order to eliminate it.”
The researchers also found that the neutrophils remain in close proximity to the tumor throughout its development, and are continuously and consistently recruited from the bone marrow. The surprising thing that was discovered during this study is that the neutrophils “change sides:” Whereas at first, with the onset of the initial tumor, the neutrophils fight it, over time the neutrophils recruited to the cancerous area begin to support its development.
Dr. Friedmann-Morvinski: “We learned that the neutrophils actually change their role. They are mobilized by the tumor itself, and from being anti-cancerous, become pro-cancerous; as a result, they aggravate the damage that the tumor itself creates.”
Moreover, the researchers found that the process by which the neutrophils change their properties can take place remotely, even before they progress towards the tumor itself.
“The study showed that the change in the properties of neutrophils takes place in the bone marrow itself — where there is no tumor at all: the cancerous tumor is located only in the brain, and from there it succeeds in changing the properties of the cells it recruits,” adds Dr. Friedmann-Morvinski. “The new findings of this study may also shed light on immunotherapeutic therapies, which have been gaining a lot of momentum in recent years. In one type of immunotherapy treatment, T cells are removed from the patient’s body, processed, and returned to the body with increased healing abilities. One of the major problems today is that even these cells that have been sent to heal are suppressed and their actions stifled. If we know how to change the interaction between neutrophils and T cells so that they are not suppressed, this will have implications for the effectiveness of immunotherapy.”
It is not inconceivable that these revelations are the first step towards deciphering the mechanism of interaction between the immune system and violent cancerous tumors that, as mentioned, claim the lives of so many.
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Materials provided by Tel-Aviv University. Note: Content may be edited for style and length.

New research led by University of Limerick in Ireland has revealed a direct link between fatty tissue and Crohn’s disease.
The study, carried out by researchers at UL along with a team from University Hospital Limerick, is suggesting for the first time that Crohn’s disease, which is an inflammatory bowel condition, may in fact be a fatty intestine condition.
The research, published in leading journal Scientific Reports, has been described as “an exciting starting point” for the further exploration of Crohn’s disease, which affects thousands of people every year in Ireland and internationally.
The study involved body composition analysis of patients with Crohn’s disease using equipment hosted on the UL campus, with the UL team collaborating with gastroenterology and surgical specialists in UHL.
“People with Crohn’s disease incorporate fat into their body in a way that is different to people who do not have Crohn’s, and appear to preferentially lay down fat on the lower parts of their body rather than the abdomen,” explained Professor Colum Dunne, Foundation Chair and Director of Research at the UL School of Medicine.
“In our study it was evident that, in the abdominal areas where the intestines are located, Crohn’s related ulcers or lesions and inflammation are associated with higher depositions of fat. More simply, in that part of their body that has relatively less overall fat, disease shows up as linked with fatty tissue surrounding the gut,” explained Professor Dunne, who led the study along with Professor Phil Jakeman in Physical Education and Sport Sciences at UL, Professor J Calvin Coffey in the UL School of Medicine and Dr Maeve Skelly in UHL.

New research indicates that an overload of various inflammatory molecules, literally “trapped” inside insoluble microscopic blood clots (micro clots), might be the cause of some of the lingering symptoms experienced by individuals with Long COVID.
This unexpected finding was made by Prof Resia Pretorius, a researcher in the Department of Physiological Science at Stellenbosch University (SU), when she started looking at micro clots and their molecular content in blood samples from individuals with Long COVID. The findings have since been peer-reviewed and published in the journal Cardiovascular Diabetology in August 2021.
“We found high levels of various inflammatory molecules trapped in micro clots present in the blood of individuals with Long COVID. Some of the trapped molecules contain clotting proteins such as fibrinogen, as well as alpha(2)-antiplasmin,” Prof Pretorius explains.
Alpha(2)-antiplasmin is a molecule that prevents the breakdown of blood clots, while fibrinogen is the main clotting protein. Under normal conditions the body’s plasmin-antiplasmin system maintains a fine balance between blood clotting (the process by which blood thickens and coagulate to prevent blood loss after an injury) and fibrinolysis (the process of breaking down the fibrin in the coagulated blood to prevent blood clots from forming).
With high levels of alpha(2)-antiplasmin in the blood of COVID-19 patients and individuals suffering from Long COVID, the body’s ability to break down the clots are significantly inhibited.
The insolubility of the micro clots became apparent when Dr Maré Vlok, a senior analyst in the Mass Spectrometry Unit at SU’s Central Analytical Facilities, noted that the blood plasma samples from individuals with acute COVID and Long COVID continued to deposit insoluble pellets at the bottom of the tubes after dilution (a process called trypsinization).
He alerted Prof Pretorius to this observation and she investigated it further. They are now the first research group to have reported on finding micro clots in the blood samples from individuals with Long COVID, using fluorescence microscopy and proteomics analysis, thereby solving yet another puzzle associated with the disease.
“Of particular interest is the simultaneous presence of persistent anomalous micro clots and a pathological fibrinolytic system,” they write in the research paper. This implies that the plasmin and antiplasmin balance may be central to pathologies in Long COVID, and provides further evidence that COVID-19, and now Long COVID, have significant cardiovascular and clotting pathologies.
Further research is recommended into a regime of therapies to support clotting and fibrinolytic system function in individuals with lingering Long COVID symptoms.
Working with vascular internist Dr Jaco Laubscher from Mediclinic Stellenbosch (a co-author on the article), they now plan to perform the same analysis on a larger sample of patients. To date they have collected blood from one hundred Long COVID individuals who participated in the Long COVID registry which launched in May 2021, as well as from 30 healthy individuals. The research is funded by the Long COVID Research Charitable Trust, a trust established with an initial donation made by Mr Koos Pretorius from ENSafrica. It is intended that this trust will be used as a vehicle to raise further funds for research into the causes and effective treatment of people suffering from Long COVID.
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Materials provided by Stellenbosch University. Original written by Wiida Fourie-Basson. Note: Content may be edited for style and length.