Publisher Health

The Biden administration is restarting a program to provide free rapid tests through the mail.The Biden administration, looking ahead to a possible winter surge of Covid-19, announced on Wednesday that it was reviving its program of offering Americans free coronavirus tests through the mail and would spend more than $600 million to buy tests from a dozen domestic manufacturers.The website for the program, covidtests.gov, will begin accepting orders on Monday, and households will be able to receive four tests. Dawn O’Connell, the assistant secretary for preparedness and response at the Health and Human Services Department, said the money would fund the purchase of 200 million tests to replenish the nation’s stockpile as tests are sent out.But a byproduct of the program, Ms. O’Connell said, is that it will shore up domestic manufacturing capacity in the event of another serious coronavirus surge. Coronavirus hospitalizations have been on the rise in the United States, though they remain low compared with earlier stretches of the pandemic, and free tests are now harder to come by for many Americans. While private insurers had previously been required to cover up to eight at-home tests per month, that requirement ended when the Biden administration allowed the public health emergency for the coronavirus to expire in May.

The indie-rock singer-songwriter said in a statement on his website that he was expected to recover from the rare neurological condition.Sufjan Stevens, the indie-rock singer-songwriter, said in a statement on his website on Wednesday that he was in recovery from a rare neurological condition called Guillain-Barré syndrome that had taken away his ability to walk, saying he had been hospitalized for several weeks but was expected to recover.“Last month I woke up one morning and couldn’t walk,” Stevens said on his website. “My hands, arms and legs were numb and tingling and I had no strength, no feeling, no mobility.”The musician said that his brother drove him to an emergency room and that neurologists diagnosed him with the autoimmune disorder, which can cause muscle weakness and paralysis. He was treated with immunoglobulin infusions, which he said were effective, and was eventually transferred to rehab for intensive physical therapy, noting that most people with the condition learn to walk again within a year.“My doctors did all the things to keep me alive and stabilize my condition,” Stevens said. “I owe them my life.”Stevens has a new album, called “Javelin,” coming out next month. He noted that his health had prevented him from participating in the album’s promotion.“I’m only in my second week of rehab but it is going really well and I am working really hard to get back on my feet,” he said. “I’m committed to getting better, I’m in good spirits, and I’m surrounded by a really great team.”

In the United States, smoke from wildfires is undoing progress from the Clean Air Act. In poorer countries, the situation is even worse.On the heels of an exceptionally fiery and smoky summer, two new reports released Wednesday confirmed what many Americans have been already seeing and breathing.Smoke from increasingly frequent and increasingly large fires has started to undo decades of hard-won gains in air quality, and the problem is expected to only get worse, not just in the United States but also around the world.More than two billion people were exposed to at least a day of fire-related air pollution each year between 2010 and 2019, a report from researchers in Australia found. And in the United States, wildfires have undone about 25 percent of past progress in cleaning up air pollution in states from coast to coast.“People have known that it’s becoming a bigger issue in the Western states,” said Marissa Childs, a fellow at Harvard University’s Center for the Environment and a co-author of the study that focused on the United States. “But I was really shocked when we were running some of these estimates and seeing that states all the way to the East Coast were being influenced.”

The world’s first study of the increase in pollution from landscape fires across the globe over the past two decades reveals that over 2 billion people are exposed to at least one day of potentially health-impacting environmental hazard annually — a figure that has increased by 6.8 per cent in the last ten years.
The study highlights the severity and scale of the landscape fire-sourced air pollution, its increased impact on the world’s population and associated rise in public health risk. Exposure to fire-sourced air pollution has many adverse health impacts, including increased mortality and morbidity and a global worsening of cardiorespiratory conditions and mental health.
The study, published today (20 September) in Nature led by Australian scientists, estimated the global daily air pollution from all fires from 2000 to 2019 — finding that 2.18 billion people were exposed to at least one day of substantial landscape fire air pollution in each year, with each person in the world having on average 9.9 days of exposure per year, an increase of 2.1 per cent in the last decade. It also found that exposure levels in low-income countries were about four-fold higher than in high income countries.
Led by Professors Yuming Guo and Shanshan Li, from Monash University’s School of Population Health and Preventive Medicine, the study also found that the exposure levels of PM2.5 were particularly high in Central Africa, Southeast Asia, South America and Siberia. The study also looked at global landscape fire-sourced ozone, an important fire-related pollutant has only been estimated for United States.
In the study, landscape fires refer to any fires burning in natural and cultural landscapes, e.g. natural and planted forest, shrub, grass, pastures, agricultural lands and peri-urban areas, including both planned or controlled fires (e.g., prescribed burns, agricultural fires) and wildfires (defined as uncontrolled or unplanned fires burning in wildland vegetation).
The comprehensive assessment of the global population exposures to fire-sourced PM2.5 and ozone during 2000-2019 was calculated using a machine learning approach with inputs from chemical transport models, ground-based monitoring stations, and gridded weather data.
The recent pollution from the Canadian wildfires that spread smoke across North America highlighted the increase in severity and frequency of landscape fires due to climate change. According to Professor Guo, no study to date has looked at the long-range effect of this increase in landscape fires globally and wildfires often impact remote areas where there are few or no air quality monitoring stations. In addition, in many low-income countries, there are no air quality monitoring stations even in urban areas.
“The exposure to air pollution caused by landscape fire smoke travelling hundreds and sometimes even thousands of kilometres can affect much larger populations, and cause much larger public health risks,” he said.
“Mapping and tracking the population exposure to landscape fire-sourced air pollution are essential for monitoring and managing its health impacts, implementing targeted prevention and interventions, and strengthening arguments for mitigation of climate change.”

A team of leading clinicians, engineers, and neuroscientists has made a groundbreaking discovery in the field of treatment-resistant depression. By analyzing the brain activity of patients undergoing deep brain stimulation (DBS), a promising therapy involving implanted electrodes that stimulate the brain, the researchers identified a unique pattern in brain activity that reflects the recovery process in patients with treatment-resistant depression. This pattern, known as a biomarker, serves as a measurable indicator of disease recovery and represents a significant advance in treatment for the most severe and untreatable forms of depression.
The team’s findings, published online in the journal Natureon September 20, offer the first window into the intricate workings and mechanistic effects of DBS on the brain during treatment for severe depression.
DBS involves implanting thin electrodes in a specific brain area to deliver small electrical pulses, similar to a pacemaker. Although DBS has been approved and used for movement disorders such as Parkinson’s disease for many years, it remains experimental for depression. This study is a crucial step toward using objective data collected directly from the brain via the DBS device to inform clinicians about the patient’s response to treatment. This information can help guide adjustments to DBS therapy, tailoring it to each patient’s unique response and optimizing their treatment outcomes.
Now, the researchers have shown it’s possible to monitor that antidepressant effect throughout the course of treatment, offering clinicians a tool somewhat analogous to a blood glucose test for diabetes or blood pressure monitoring for heart disease: a readout of the disease state at any given time. Importantly, it distinguishes between typical day-to-day mood fluctuations and the possibility of an impending relapse of the depressive episode.
The research team, which includes experts from the Georgia Institute of Technology, the Icahn School of Medicine at Mount Sinai, and Emory University School of Medicine, used artificial intelligence (AI) to detect shifts in brain activity that coincided with patients’ recovery.
The study, funded by the National Institutes of Health Brain Research Through Advancing Innovative Neurotechnologies ®, or the BRAIN Initiative ®, involved 10 patients with severe treatment-resistant depression, all of whom underwent the DBS procedure at Emory University. The study team used a new DBS device that allowed brain activity to be recorded. Analysis of these brain recordings over six months led to the identification of a common biomarker that changed as each patient recovered from their depression. After six months of DBS therapy, 90 percent of the subjects exhibited a significant improvement in their depression symptoms and 70 percent no longer met the criteria for depression.
The high response rates in this study cohort enabled the researchers to develop algorithms known as “explainable artificial intelligence” that allow humans to understand the decision-making process of AI systems. This technique helped the team identify and understand the unique brain patterns that differentiated a “depressed” brain from a “recovered” brain.

A research team led by scientists from City University of Hong Kong (CityU) has achieved a significant breakthrough by inventing a new class of near-infrared-activated photo-oxidants that can effectively kill cancer cells without requiring oxygen. The photo-oxidants induce a unique form of cancer cell death that can overcome cancer cell resistance. The findings offer a new strategy, called ‘photo-oxidation therapy’, and provide a promising direction for the development of anti-cancer drugs.
Photodynamic therapy, an innovative cancer treatment approach, utilizes photosensitizers to generate reactive oxygen species (ROSs), which when irradiated by light, selectively kill cancer cells. However, most existing photodynamic therapies rely on the presence of oxygen, while solid cancer tumours often feature a hypoxic microenvironment with very low oxygen levels, limiting the therapeutic efficiency of this approach.
To address this limitation, a research team led by Professor Zhu Guangyu, in the Department of Chemistry, and Professor He Mingliang, in the Department of Biomedical Sciences (BMS) at CityU, discovered an effect called “metal-enhanced photo-oxidation.” By conjugating metals like platinum with organic photosensitive ligands, they significantly enhanced the photo-oxidation capability. This breakthrough led them to develop a new class of near-infrared-activated platinum(IV) photo-oxidants (Pt(IV) photo-oxidants) that can be activated by near-infrared (NIR) light to directly oxidize biomolecules and effectively kill cancer cells without the need for oxygen.
In their experiments, the team administered Pt(IV) photo-oxidants to mice with tumours through intravenous injection. Four hours later, they applied near-infrared radiation to the mice to activate the photo-oxidants to attack the cancer cells. The results demonstrated a significant reduction in tumour volume and weight of 89% and 76%, respectively, indicating the potent tumour-inhibitory effect of the Pt(IV) photo-oxidants.
“Intriguingly, we found that the ‘death mode’ of cancer cells induced by the Pt(IV) photo-oxidants differs from that of any other anticancer agents,” said Professor Zhu. “A unique mode of cancer cell destruction was initiated through the dual-action effect of strong intracellular oxidative stress and reduced intracellular pH value.”
Their experimental data show that after the Pt(IV) photo-oxidants that accumulated in the endoplasmic reticulum inside the cancer cells were activated by near-infrared radiation, they vigorously oxidized crucial biomolecules inside the cancer cells without requiring oxygen, generating ROSs, lipid peroxides and protons. The ROSs and lipid peroxides then triggered intensive oxidative bursts, while the protons lowered the intracellular pH value, creating an unfavourable acidic microenvironment for the cancer cells.
Moreover, their experiments confirmed that Pt(IV) photo-oxidants effectively activate the immune system in both in vitro and in vivo settings. The Pt(IV) photo-oxidants triggered immunogenic cell death, stimulating the proliferation and activation of immune cells. The number of T helper and T killer cells, which are crucial for triggering the body’s immune response, in the mice treated with photoactivated Pt(IV) photo-oxidants increased by 7- and 23-fold, respectively, compared to the control group.

Among available immunotherapies, the use of “CAR-T” cells is proving extremely effective against certain blood cancers, but only in half of patients. A main reason for this is the premature dysfunction of these immune cells, which have been artificially modified in vitro. A team from the Universities of Geneva (UNIGE), Lausanne (UNIL), the Geneva University Hospitals (HUG) and the Vaud University Hospital (CHUV), all part of the Swiss Cancer Center Léman (SCCL), has discovered how to prolong the functionality of CAR-T cells. By inhibiting a very specific metabolic mechanism, the team has succeeded in creating CAR-T cells with enhanced immune memory, capable of fighting tumour cells for much longer. These are very promising results, to be read in the journal Nature.
CAR-T cell immunotherapy involves taking immune cells — usually T lymphocytes — from a person suffering from cancer, modifying them in the laboratory to increase their ability to recognise and fight tumour cells, then readministering them to the patient. However, as with other types of immunotherapies, many patients do not respond to the treatment or relapse.
”CAR-T cells must be massively multiplied before they can be administered,” explains Mathias Wenes, a research fellow who coordinated this research in the laboratory of Pr Denis Migliorini, Department of Medicine at the UNIGE Faculty of Medicine and Department of Oncology at HUG. ”But the disease history of the patient, in combination with the amplification process, exhausts the cells: they reach a state of terminal differentiation that precipitates the end of their life cycle without leaving them time to act on the length.”
A mechanism common to cancer cells and immune cells
In the absence of oxygen, cancer cells resort to a very specific survival mechanism: they metabolise the amino acid glutamine as an alternative source of energy through a chemical reaction known as ”reductive carboxylation”. ”Immune cells and cancer cells have a fairly similar metabolism, which enables them to proliferate very rapidly. We have indeed discovered here that T cells also used this mechanism,” explains Alison Jaccard, a PhD student in Professor Ping-Chih Ho’s laboratory in the UNIL-CHUV Department of Oncology and the study’s first author.
To investigate the role of reductive carboxylation, the scientists inhibited this mechanism in CAR-T cells in mouse models of leukemia and multiple myeloma, two blood cancers. ”Our modified CAR-T cells multiplied normally and did not lose their capacity to attack, indicating that reductive carboxylation is not essential for them,” Mathias Wenes sums up.
Mice cured with these CAR-T
What’s more, the mice treated in this way were virtually cured of their cancer, a result well beyond the research team’s expectations. ”Without reductive carboxylation, the cells no longer differentiate as much and maintain their anti-tumor function for longer. And even, and this is the heart of our discovery, they tend to transform into memory T lymphocytes, a type of immune cell that retains the memory of the tumour elements that needs to be attacked.”

Patients living with fibromyalgia (FM) — a disease that predominantly affects women and is characterized by chronic pain, fatigue and brain fog — often find limited treatment options and a scarcity of explanations for their symptoms. Research led by Mass General Brigham investigators has found that cognitive behavioral therapy (CBT) can significantly reduce the burden of FM by, in part, reducing pain-catastrophizing, a negative cognitive and emotional response that can intensify pain through feelings of helplessness, rumination and intrusive thoughts. This finding is backed by neuroimaging data, evidencing reduced connectivity between regions of the brain associated with self-awareness, pain and emotional processing. Results are published on September 20in Arthritis & Rheumatology.
“In this study, we looked at the interplay between psychological processes and the brain’s connectivity patterns in response to pain,” said co-senior author Robert Edwards, PhD, a clinical psychologist in the Department of Anesthesiology, Perioperative & Pain Medicine at Brigham and Women’s Hospital, a founding member of the Mass General Brigham healthcare system. “We wanted to explore how CBT, a talk therapy aimed at combatting maladaptive thoughts, can enhance individuals’ daily functioning and alter the brain’s processing of pain-related information.”
Edwards explains that CBT can reduce negative cognitive and emotional responses to pain. He says that while these responses are normal, they can amplify the disabling effects of chronic pain, and make conditions like FM more burdensome.
The research team for the study included researchers from three Mass General Brigham members: Spaulding Rehabilitation Hospital, Brigham and Women’s Hospital and Massachusetts General Hospital. Mass General Brigham brings together 16 member institutions, including academic medical centers, top-tier specialty hospitals, community hospitals and more. Research that spans more than one of these entities is more than the sum of its parts, helping to provide insights and unique perspectives from multiple settings and areas of expertise.
Researchers recruited 98 women, randomly assigning 64 to a treatment group receiving CBT and 34 to a control group that received education about FM and chronic pain but was not taught specific CBT techniques. All participants were between 18 and 75 years old and had a confirmed FM diagnosis for at least six months. To collect baseline data, all participants completed several validated pain and quality of life questionnaires.
Each group participated in eight intervention sessions, consisting of 60-75-minute visits with a licensed mental health provider. Participants were primarily assessed for their levels of pain interference, or a measure of how much their pain disrupted their daily activities, pain catastrophizing, pain severity and the overall impact FM had on patients’ quality of life.
Results demonstrated that those who underwent CBT experienced significantly greater reductions in pain interference. CBT participants also exhibited significantly less pain catastrophizing and reported that their FM symptoms had significantly less impact on their daily lives.

A research team at the University of Basel and the SIB Swiss Institute of Bioinformatics uncovered a treasure trove of uncharacterised proteins. Embracing the recent deep learning revolution, they discovered hundreds of new protein families and even a novel predicted protein fold. The study has now been published in Nature.
In the past years, AlphaFold has revolutionised protein science. This Artificial Intelligence (AI) tool was trained on protein data collected by life scientists for over 50 years, and is able to predict the 3D shape of proteins with high accuracy. Its success prompted the modelling of an astounding 215 million proteins last year, providing insights into the shapes of almost any protein. This is particularly interesting for proteins that have not been studied experimentally, a complex and time-consuming process.
“There are now many sources of protein information, enclosing valuable insights into how proteins evolve and work” says Joana Pereira, the leader of the study. Nevertheless, research has long been faced with a data jungle. The research team led by Professor Torsten Schwede, group leader at the Biozentrum, University of Basel, and the Swiss Institute of Bioinformatics (SIB), has now succeeded in decrypting some of the concealed information.
A bird’s eye view reveals new protein families and folds
The researchers constructed an interactive network of 53 million proteins with high quality AlphaFold structures. “This network serves as a valuable source for theoretically predicting unknown protein families and their functions on a large scale,” underlines Dr. Janani Durairaj, the first author. The team was able to identify 290 new protein families and one new protein fold that resembles the shape of a flower.
Building on the expertise of the Schwede group in developing and maintaining the leading software SWISS-MODEL, they made the network available as an interactive web resource, termed the “Protein Universe Atlas.”
AI as a valuable tool in research
The team has employed Deep Learning-based tools for finding novelties in this network, paving the way to innovations in life sciences, from basic to applied research. “Understanding the structure and function of proteins is typically one of the first steps to develop a new drug, or modify their functions by protein engineering, for example,” says Pereira. The work was supported by a ‘kickstarter’ grant from SIB to encourage the adoption of AI in life science resources. It underscores the transformative potential of Deep Learning and intelligent algorithms in research.
With the Protein Universe Atlas, scientists can now learn more about proteins relevant to their research. “We hope this resource will help not only researchers and biocurators but also students and teachers by providing a new platform for learning about protein diversity, from structure, to function, to evolution,” says Janani Durairaj.

Hearing the sound of a newborn’s wail can trigger the release of oxytocin, a brain chemical that controls breast-milk release in mothers, a new study in rodents shows. Researchers found that once prompted, this flood of hormones continues for roughly five minutes before tapering off, enabling mothers to feed their young until they are sated or begin crying again.
Led by researchers at NYU Grossman School of Medicine, the study explored a centuries-old observation in humans and other mammals that when a baby begins a feeding session, its cries alone can prompt its mother to release breast milk. Studies dating back decades have shown that such calls for food, and not suckling itself, prompts the largest oxytocin surges. However, the mechanisms behind and purpose for this wail-to-milk pipeline had until now remained unclear.
According to the findings, publishing online Sept. 20 in the journal Nature, when a mouse pup starts crying, sound information travels to an area of its mother’s brain called the posterior intralaminar nucleus of the thalamus (PIL). This sensory hub then sends signals to oxytocin-releasing brain cells (neurons) in another region called the hypothalamus, a control center for hormone activity.
Most of the time these hypothalamus neurons are “locked down” by proteins that act as gatekeepers to prevent false alarms and wasted milk. After 30 seconds of continuous crying, however, signals from the PIL were found to build up and overpower these inhibitory proteins, setting off oxytocin release.
“Our findings uncover how a crying infant primes its mother’s brain to ready her body for nursing,” said study co-lead author Habon Issa, a graduate student at NYU Langone Health. “Without such preparation, there can be a delay of several minutes between suckling and milk flow, potentially leading to a frustrated baby and stressed parent.”
The results also revealed that the oxytocin boost only occurs in mother mice and not in females who have never given birth. In addition, the mothers’ brain circuitry only responded to her pups’ cries and not to computer-generated tones designed to mimic natural wails.
According to Issa, the study offers the first description of how sensory experiences like hearing directly activate oxytocin neurons in mothers. She notes that the scientists used a relatively new kind of molecular sensor called iTango to measure actual oxytocin release from brain cells in real time. Previously, she says, researchers could only take indirect measurements using proxies because the hormone degrades quickly given its small size.