Publisher Health

In 2020, more than 1.5 million people around the world died of tuberculosis, marking the first time in more than a decade that annual TB deaths had increased and demonstrating the global need for better access to treatments. To address that problem, scientists at the UNC School of Medicine, the UNC Institute for Global Health and Infectious Diseases, and the International Center for the Advancement of Translational Science developed a long-acting injectable formulation of the anti-TB drug rifabutin.
Published in the journal Nature Communications, research in animal models showed the potential of delivering a TB drug with one injection that lasts at least four months, in lieu of the current standard treatment requiring constant adherence to a daily drug regimen.
“We think our approach could dramatically change TB treatment,” said Martina Kovarova, PhD, associate professor of medicine at UNC “Affordable long-acting formulations with generic anti-TB drugs would help ease the burden of this disease on low-income communities around the world where better access to treatment is most needed.”
Co-author Miriam Braunstein, PhD, professor of Microbiology and Immunology at the UNC School of Medicine and member of the UNC Institute for Global Health and Infectious Diseases, added, “During the COVID-19 pandemic, we witnessed more deaths due to TB because of disruption or reallocation of health services, setting us back at least five to eight years in the global fight against TB. We think long-acting formulations could be a game-changer, whether it’s for preventative therapy or treatment of disease.”
Tuberculosis, which is caused by Mycobacterium tuberculosis (Mtb), affects an estimated 10 million people a year, according to the World Health Organization, which also estimates that about one-quarter of the world population has a latent TB infection with the potential for reactivation, leading to symptoms such as weakness, weight loss, fever, coughing, chest pain, and coughing up blood.
Not adhering to strict drug regimens can lead to treatment failure and drug resistance. To overcome this, UNC researchers sought to create a therapeutic delivery system that would provide an effective way to improve adherence to medications.
Co-first authors Manse Kim, PhD, a postdoctoral researcher at UNC-Chapel Hill, and UNC graduate student Claire Johnson, led experiments to combine rifabutin with biodegradable polymers and non-toxic solvents that solidify in the body after subcutaneous injection. The researchers also added a compound to this formula to significantly increase the amount of rifabutin that could be included.
Using mouse models, the researchers observed how the solidified implant slowly eroded over the course of 16 weeks, releasing their drug payload in a sustained fashion throughout. This long-acting formulation prevented infection in mice that were exposed to TB. Also, the single injection cleared infection from lungs and other tissues in mice that had been previously infected with TB. The researchers observed no adverse effects in the mice, but if side effects arise, the implant is removable.
This type of long-acting technology has already been FDA-approved for other conditions, such as cancers, schizophrenia, and opioid dependency.
“We think this technology could be leveraged in our battle against tuberculosis world-wide,” Kovarova said. “More research is needed before phase 1 trials in humans, but our study provides an important step toward a much-needed long-acting treatment and prevention strategy against TB.”
J. Victor Garcia, PhD, professor of medicine at the UNC School of Medicine, is co-senior author. Other authors are Alan Schmalstig, PhD, Ayano Annis, Sarah Wessel, Brian van Horne, Amanda Schauer, and Angela Wahl, PhD, all at UNC-Chapel Hill, Agata Exner, PhD, at Case Western University, and Jason Stout, MD, at Duke University.
Core facilities were essential in the completion of this research: The UNC Nanomedicines Characterization Core Facility, the UNC Animal Histopathology and Laboratory Medicine Core, the UNC Microscopy Services Laboratory, and the Clinical Pharmacology and Analytic Chemistry Core.

Excessively hot nights caused by climate change are predicted to increase the mortality rate around the world by up to 60% by the end of the century, according to a new international study that features research from the UNC Gillings School of Global Public Health.
Ambient heat during the night may interrupt the normal physiology of sleep. Less sleep can then lead to immune system damage and a higher risk of cardiovascular disease, chronic illnesses, inflammation and mental health conditions. Results show that the average intensity of hot night events will nearly double by 2090, from 20.4℃ (68.7℉) to 39.7℃ (103.5℉) across 28 cities from east Asia, increasing the burden of disease due to excessive heat that disrupts normal sleeping patterns.
This is the first study to estimate the impact of hotter nights on climate change-related mortality risk. The findings show that the burden of mortality could be significantly higher than estimated by average daily temperature increase, suggesting that warming from climate change could have a troubling impact, even under restrictions from the Paris Climate Agreement.
“The risks of increasing temperature at night were frequently neglected,” said study co-author Yuqiang Zhang, PhD, a climate scientist in the Department of Environmental Sciences and Engineering at the Gillings School. “However, in our study, we found that the occurrences of hot night excess (HNE) are projected to occur more rapidly than the daily mean temperature changes. The frequency and mean intensity of hot nights would increase more than 30% and 60% by the 2100s, respectively, compared with less than 20% increase for the daily mean temperature.”
The study, published in The Lancet Planetary Health, was co-authored by a group of researchers in China, South Korea, Japan, Germany and the United States. The team estimated the mortality due to excess heat in 28 cities in China, South Korea and Japan between 1980 and 2015 and applied it to two climate change modeling scenarios that aligned with carbon-reduction scenarios adapted by the respective national governments.
Through this model, the team was able to estimate that between 2016and 2100, the risk of death from excessively hot nights would increase nearly six-fold. This prediction is much higher than the mortality risk from daily average warming suggested by climate change models.
“From our study, we highlight that, in assessing the disease burden due to non-optimum temperature, governments and local policymakers should consider the extra health impacts of the disproportional intra-day temperature variations. A more complete health risk assessment of future climate change can help policymakers for better resource allocation and priority setting,” said Haidong Kan, PhD, who is a professor at Fudan University in China and the study’s corresponding author.
In this study, the authors also found that regional differences in temperature accounted for many of the variances in nighttime temperature, and areas with the lowest average temperature were projected to have the largest warming potential.
“To combat the health risk raised by the temperature increases from climate change, we should design efficient ways to help people adapt,” said Zhang. “Locally, heat during the night should be taken into account when designing the future heatwave warning system, especially for vulnerable populations and low-income communities who may not be able to afford the additional expense of air conditioning. Also, stronger mitigation strategies, including global collaborations, should be considered to reduce future impacts of warming.”
Since the study only included 28 cities from three countries, Zhang said that “extrapolation of these results to the whole East Asia region or other regions should be cautious. Currently, based on these findings, authors are trying to extend the analysis to a global dataset. Then we could have a global picture of the deadly nighttime heat on health under climate change scenarios.”

Cystic fibrosis remains an incurable genetic disorder which impairs lung function and significantly reduces life expectancy. A new combination drug therapy which addresses the disorder’s underlying defects offers a promising new treatment approach. The use of this therapy had previously been limited to adolescents and adults. Designed to meet the highest standards of clinical practice, a study co-led by Charité — Universitätsmedizin Berlin has now confirmed that this combination therapy regimen is also beneficial to primary school-aged children. Earlier treatment means disease progression is likely to be significantly slowed. The researchers’ findings have been published in the American Journal of Respiratory and Critical Care Medicine.
Characterized by the build-up of thick, sticky mucus, cystic fibrosis, also known as mucoviszidosis, is the most common fatal genetic disease in Germany. A defect in the CFTR ion channel (which sits on the surface of airway epithelial cells and transports salt and water) disrupts the normal fluid balance, resulting in highly viscous mucus. Cystic fibrosis primarily impairs the lungs, which get clogged by this viscous mucus and thus become less effective at clearing away pathogens. The result is chronic infection and airway inflammation, progressively impaired lung function, and difficulty breathing. In severe cases, a lung transplant may become necessary. People affected by the disease used to die before reaching adulthood. Today, average life expectancy is around 55 years. These gains in life expectancy are mainly due to improvements in symptomatic treatment.
Drugs which target not just the disease’s symptoms but also its underlying molecular defects by improving CFTR channel function — known as CFTR modulators — only became available a few years ago. In approximately 90 percent of patients with cystic fibrosis, the underlying CFTR channel defect is caused by a specific fault in the CFTR gene known as the F508del mutation. A triple therapy combining three CFTR modulators (elexacaftor, tezacaftor and ivacaftor) has been available in Europe since August 2020. In patients with one copy of the F508del mutation, this triple combination therapy can restore ion channel function to approximately half the normal level, thereby producing noticeable improvements in lung function and quality of life. “It was a milestone in the treatment of cystic fibrosis,” explains first author Prof. Dr. Marcus Mall, Head of Charité’s Department of Pediatric Respiratory Medicine, Immunology and Critical Care Medicine and Charité’s Cystic Fibrosis Center. He adds: “Unfortunately, until now, this treatment has only been available to patients aged 12 and over. This is because, traditionally, new drugs are first tested on and then authorized for use in adults. What we want to do, however, is administer this causal treatment as early as possible during the course of the disease in order to prevent irreversible lung damage. This is of course only possible if treatment starts during childhood. What we have been able to do now is to show that this can be done both safely and very effectively in primary school-aged children.”
Prof. Mall and his international research partners studied the effects of this triple combination therapy in 121 children with cystic fibrosis. Participants were aged between 6 and 11 years and had at least one copy of the F508del mutation. The children were randomized to receive either the triple combination regimen or placebo for a duration of approximately six months. The study, which was conducted at centers in ten different countries, was designed as a randomized controlled trial — the gold standard in clinical research. “This type of clinical study remains too much of a rarity in pediatric drug development,” says Prof. Mall, Einstein Professor at Charité and cystic fibrosis research lead at the German Center for Lung Research (DZL). “The inclusion of control groups is often neglected in pediatric research. Instead, adult data are used to extrapolate effects from adults to children. But children are not simply small adults. High-quality studies are therefore crucial to the development of safe and effective drugs for children.”
Their recently published study showed that treatment significantly improved CFTR channel function, thereby enhancing the children’s lung function and quality of life. The treatment had a good overall safety profile and was well tolerated, with side effects comparable to those observed in older patients. “I was both surprised and delighted to see that, even this early in the disease trajectory and despite the brief treatment duration, the children experienced noticeable improvements,” says Prof. Mall. “These findings contributed to the decision by the European Medicines Agency to expand the marketing authorization for this triple combination regimen to include children aged 6 and over. That means we are already in a position to treat children in this age group. I expect that the earlier initiation of treatment targeting the disease’s causative defect will produce significant improvements to the long-term health of patients with cystic fibrosis.”
As a next step, the research team plan to test whether the drug combination might be suitable for use in even younger children. Given cystic fibrosis forms part of the newborn screening program, the disease can now be diagnosed within the first few weeks of life. “That would place us in a position to start causal treatment for cystic fibrosis as early as early infancy, which would hopefully prevent even early-stage damage to the lungs and possibly even other organs like the pancreas. Very gradually, we are working our way closer to this target. Currently, we are testing the safety and efficacy of this triple combination therapy in children aged between 2 and 5 years,” explains Prof. Mall.
About this study The study discussed here was the first randomized, double-blind, placebo-controlled multicenter clinical trial to evaluate the safety and efficacy of the elexacaftor/tezacaftor/ivacaftor triple combination regimen in children with cystic fibrosis who were aged between 6 and 11 years and had at least one copy of the F508del mutation in addition to a second CFTR mutation which is unaffected by this treatment. A phase 3b clinical trial, the study was conducted across 34 trial centers in Germany, France, Spain, Denmark, the Netherlands, Switzerland, the United Kindgom, Australia, Canada and Israel. The study is registered on ClinicalTrials.gov (NCT 04353817). The clinical trial sponsor is Vertex Pharmaceuticals. Prof. Mall is one of three international study leads.

Before young children learn to speak, crying is their only means of vocal communication. But do adults know when a baby is in pain as opposed to being mildly uncomfortable? A new study reported in Current Biology on August 8, 2022 finds that the answer to this question is that it depends.
“We found that the ability to detect pain in cries — that is, to identify a pain cry from a mere discomfort cry — is modulated by experience of caring for babies,” says Nicolas Mathevon, University of Saint-Etienne, France. “Current parents of young babies can identify a baby’s pain cries even if they have never heard this baby before, whereas inexperienced individuals are typically unable to do so.”
The findings show that humans’ ability to interpret babies’ cries isn’t innate but learned from experience. Parenting young babies shapes our ability to decode the information conveyed by babies’ communication signals.
Mathevon and his University of Saint-Etienne colleagues including David Reby and Roland Peyron made this discovery as part of a broader research program investigating how information is encoded in babies’ cries and how human listeners extract this information. In the new study, they wanted to find out how prior caregiving experience with babies shaped the ability to identify when they were in pain.
They recruited people with different amounts of experience caring for babies, ranging from people with no experience at all to current parents of young children. They also included people with occasional experience babysitting and non-parents with more extensive professional experience in caregiving.
Next, they gave everyone in the study a short training phase in which they heard eight discomfort cries from one baby over a couple of days. Next, their ability to decode the cries as discomfort or pain was put to the test.
And it turned out that experience was everything. People with little to no experience couldn’t tell the difference between cries any better than chance. Those with a small amount of experience performed slightly better.
Current parents and professionals did better than chance. But parents of younger babies were the clear winners. They were able to identify the crying contexts of babies even when they’d never heard the cries of that youngster before. Parents of older kids and those with professional experience didn’t do well with unfamiliar cries.
“Only parents of younger babies were also able to identify the crying contexts of an unknown baby they had never heard before,” says first author of the study Siloe Corvin.
“Professional pediatric caregivers are less successful at extending this ability to unknown babies,” says study co-author Camille Fauchon. “This was surprising at first, but it is consistent with the idea that experienced listeners may develop a resistance that decreases their sensitivity to acoustic cues of pain.”
The findings show that babies’ cries contain important information that’s encoded in their acoustic structure. While adults are attuned to that information, our ability to decode it and identify when a baby is in pain gets better with exposure and experience.
The researchers hope that learning more about how babies communicate pain may help parents learn how to recognize and respond to it even better. They’re now conducting neuroimaging studies to further explore how experience and parenthood shape brain activity when babies cry.
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Hot summer temperatures may have you reaching for a fan and an iced drink in your quest to keep cool. But now, researchers from Japan have found that some mutant proteins are even less tolerant of the heat, getting trapped in a cycle of activation that can have deadly consequences.
In a study soon to be published in Proceedings of the National Academy of Sciences, a team of researchers led by Osaka University reveals that malignant hyperthermia (MH) is caused by heat-hypersensitive mutant calcium channel proteins.
MH is a condition in which the body temperature rises uncontrollably in response to anesthesia. The body temperature can increase rapidly, sometimes to over 42°C, causing symptoms that can be fatal if not treated immediately.
“Most human MH-associated mutations have been identified in the ryanodine receptor type 1 (RyR1) gene and cause increased calcium release from the sarcoplasmic reticulum, leading to hyperthermia,” explains Kotaro Oyama, one of the lead authors on the study. “Some studies have suggested that there is a positive feedback loop between calcium release and thermogenesis, but it was still unclear how this loop might work.”
To investigate this, the researchers precisely heated cultured cells expressing mutant RyR1 proteins with an infrared laser beam and assessed changes in calcium flow using fluorescence calcium imaging. This approach enabled them to quantitatively evaluate the cellular response to heat.
“The results were very clear,” says Madoka Suzuki, senior author on the study. “A local heat pulse induced an intracellular calcium burst, but even a weak heat pulse induced this response in cells expressing mutant forms of the RyR1 channels, demonstrating their hypersensitivity to heat compared with the unmutated channel.” The team named this novel response “Heat-Induced Ca2+ Release (HICR).” The HICR was also observed in skeletal muscles isolated from a mouse model of MH.
Importantly, the calcium that is released into the intracellular environment in response to heat via the HICR mechanism could possibly accelerate further thermogenesis in the cell, creating a cascade effect.
“Our findings suggest that, when calcium leakage through RyR1 mutant channels is enhanced by MH inducers such as anesthetics, a positive feedback loop is created that leads to the release of more and more calcium. One plausible explanation for the calcium leakage is that the mutant proteins are easily destabilized by heat,” states lead author Kotaro Oyama.
Given that recent studies suggest that there is a close relationship between malignant hyperthermia and heat stroke, the findings from this study could also provide insight into how exertional heat stroke occurs under extreme environmental conditions. A better understanding of this condition could help develop preventive and treatment strategies.
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In 2015, Andrea Sheardown was diagnosed with a rare liver cancer and given just six weeks to live. But against all the odds, in an attempt to inspire her family and reframe her attitude, Andrea decided to take on a series of challenges. She’s taken part in a firewalking event, climbed several mountains including Kilamanjaro and Everest and has raised nearly £100,000 for a cancer charity.Filmed and produced by Fay Nurse

Inflammation is an essential part of the body’s healing process. But when it persists, it can contribute to a wide range of complex diseases including type 2 diabetes, heart disease, and autoimmune diseases.
Now, world-first genetic research from the University of South Australia shows a direct link between low levels of vitamin D and high levels of inflammation, providing an important biomarker to identify people at higher risk of or severity of chronic illnesses with an inflammatory component.
The study examined the genetic data of 294,970 participants in the UK Biobank, using Mendelian randomization to show the association between vitamin D and C-reactive protein levels, an indicator of inflammation.
Lead researcher, UniSA’s Dr Ang Zhou, says the findings suggest that boosting vitamin D in people with a deficiency may reduce chronic inflammation.
“Inflammation is your body’s way of protecting your tissues if you’ve been injured or have an infection,” Dr Zhou says.
“High levels of C-reactive protein are generated by the liver in response to inflammation, so when your body is experiencing chronic inflammation, it also shows higher levels of C-reactive protein.
“This study examined vitamin D and C-reactive proteins and found a one-way relationship between low levels of vitamin D and high levels of C-reactive protein, expressed as inflammation.
“Boosting vitamin D in people with deficiencies may reduce chronic inflammation, helping them avoid a number of related diseases.”
Supported by the National Health and Medical Research Council and published in the International Journal of Epidemiology the study also raises the possibility that having adequate vitamin D concentrations may mitigate complications arising from obesity and reduce the risk or severity of chronic illnesses with an inflammatory component, such as CVDs, diabetes, and autoimmune diseases.
Senior investigator and Director of UniSA’s Australian Centre for Precision Health, Professor Elina Hyppönen, says these results are important and provide an explanation for some of the controversies in reported associations with vitamin D.
“We have repeatedly seen evidence for health benefits for increasing vitamin D concentrations in individuals with very low levels, while for others, there appears to be little to no benefit.” Prof Hyppönen says.
“These findings highlight the importance of avoiding clinical vitamin D deficiency, and provide further evidence for the wide-ranging effects of hormonal vitamin D.”
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Implantable devices that release insulin into the body hold promise as an alternative way to treat diabetes without insulin injections or cannula insertions. However, one obstacle that has prevented their use so far is that the immune system attacks them after implantation, forming a thick layer of scar tissue that blocks insulin release.
This phenomenon, known as the foreign body response, can also interfere with many other types of implantable medical devices. However, a team of MIT engineers and collaborators has now devised a way to overcome this response. In a study of mice, they showed that when they incorporated mechanical actuation into a soft robotic device, the device remained functional for much longer than a typical drug-delivery implant.
The device is repeatedly inflated and deflated for five minutes every 12 hours, and this mechanical deflection prevents immune cells from accumulating around the device, the researchers found.
“We’re using this type of motion to extend the lifetime and the efficacy of these implanted reservoirs that can deliver drugs like insulin, and we think this platform can be extended beyond this application,” says Ellen Roche, the Latham Family Career Development Associate Professor of Mechanical Engineering and a member of MIT’s Institute for Medical Engineering and Science.
Among other possible applications, the researchers now plan to see if they can use the device to deliver pancreatic islet cells that could act as an “bioartificial pancreas” to help treat diabetes.
Roche is the co-senior author of the study, with Eimear Dolan, a former postdoc in her lab who is now a faculty member at the National University of Ireland at Galway. Garry Duffy, also a professor at NUI Galway, is a key collaborator on the work, which appears in Nature Communications. MIT postdocs William Whyte and Debkalpa Goswami, and visiting scholar Sophie Wang, are the lead authors of the paper.

To study the relationship between age and fatigue, Kessler Foundation researchers conducted a novel study using neuroimaging and self-report data. Their findings were published online on May 9, 2022, in Frontiers in Human Neuroscience in the open access article, “Fatigue across the lifespan in men and women: State vs. trait.”
The authors are Glenn Wylie, DPhil, Amanda Pra Sisto, Helen M. Genova, PhD, and John DeLuca, PhD, of Kessler Foundation. All have faculty appointments at Rutgers New Jersey Medical School. Dr. Wylie is also a research scientist at The Department of Veterans’ Affairs War-related Injury and Illness Study Center at the New Jersey Healthcare System.
Their study is the first to report the effects of gender and age on both ‘state’ and ‘trait’ fatigue, and the first to report fatigue-related differences in brain activation across the lifespan and across gender during a cognitively fatiguing task. “State” measure of fatigue assesses a subject’s instantaneous experience of fatigue at the time of testing; “trait” measure of fatigue assesses how much fatigue a subject experienced over a longer period of time, such as the previous four weeks.
Researchers collected data on trait fatigue and state fatigue from 43 healthy men and women aged 20 to 63 years. State fatigue was measured during fMRI scans while participants performed a cognitively challenging task. The study was conducted at the Rocco Ortenzio Neuroimaging Center at Kessler Foundation, a specialized facility dedicated solely to rehabilitation research. They found that older individuals reported less state fatigue.
Dr. Wylie, director of the Ortenzio Center, commented: “Our neuroimaging data show that the role of middle frontal areas of the brain changes with age. Younger individuals may use these areas to combat fatigue, but this is not the case with older individuals. Moreover, these results suggest that women show greater resilience when faced with a fatiguing task.”
“This study is an important first step toward explaining some of the differences reported in the literature of fatigue, by showing that state and trait measures of fatigue measure different aspects of fatigue, and that age and gender both appear to affect the relationship between state fatigue and brain activation,” Dr. Wyle concluded.
Funding: National MS Society (RG 4232A1), New Jersey Commission for Brain Injury Research (10.005.BIR1), Department of Veterans’ Affairs (5I01CX000893), and Kessler Foundation
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A new way of injecting monkeypox vaccine could stretch the nation’s supply of shots, but some experts argue that the approach has not been sufficiently studied.WASHINGTON — It sounded like a simple solution to the shortage of monkeypox vaccine: Merely by changing the way doses are injected, the federal government could vaccinate five times as many people with the supply it has in hand.But the approach — injecting one-fifth of the current dose into the skin instead of a full dose into underlying fat — is not actually all that simple, experts say. And some federal officials are concerned about changing the method without more research, even though Dr. Robert M. Califf, the head of the Food and Drug Administration, described the proposal on Thursday as promising.Some outside experts, too, are urging caution. “From a basic science perspective, this should work,” said Dr. Jay K. Varma, the director of the Cornell Center for Pandemic Prevention and Response. “But, of course, there are lots of things in life, in science, that we think should work, and then when we actually do them, they don’t.”Stretching out doses of the vaccine, Jynneos, could help the federal government resolve a predicament partly of its own making. Even though it invested more than $1 billion developing the two-dose vaccine that to use against both monkeypox and smallpox, the government only has 1.1 million shots on hand, partly because it was slow to order bulk vaccine stocks to be processed into vials.That supply is enough to cover 550,000 people, but about three times as many doses are needed to cover the 1.6 million to 1.7 million Americans who, according to the Centers for Disease Control and Prevention, are at high risk of monkeypox. For now, the virus has been spreading primarily through skin-to-skin contact during sex among gay and bisexual men, the C.D.C. has said.Some federal officials are hoping that by injecting a smaller dose of the vaccine between skin layers, called an intradermal shot, the Biden administration could tamp down the outbreak before it spreads more widely.But some experts argue that this approach has not been sufficiently studied. They also warn that some vaccinators will need training to properly deliver the shots, which could slow vaccination efforts. Otherwise, the government could end up wasting doses, not saving them.Intradermal injection involves carefully guiding a needle into skin layers, a thin space with immune cells. If a vaccinator goes too deep and inserts the dose into fat, the patient might not receive enough vaccine, experts say. But if the needle is not inserted far enough, some of the vaccine could leak back out.“If you’re giving a lower dose and you don’t inject it properly into the skin — you might inject it into the wrong place — you may not be giving a protective vaccine,” said Dr. Phil Krause, who retired as a senior F.D.A. vaccine regulator last year and worked on the agency’s licensing of Jynneos. “If you ask this to be done nationwide in millions of doses, it’s a lot easier for there to be mistakes made in the administration of the vaccine.”On the other hand, the method has a track record. It has been used in polio vaccination campaigns when doses have been limited, as well as for rabies and for tuberculosis skin tests.What to Know About the Monkeypox VirusCard 1 of 7What is monkeypox?