Publisher Health

Despite the Centers for Disease Control and Prevention warning this year will be potentially dangerous for respiratory illnesses, a third of Americans are not concerned about the threat, according to a new national survey by The Ohio State University Wexner Medical Center.
The survey found that while the majority of those polled (87%) said they do everything they can to avoid spreading seasonal viruses, one-third think their vaccine decision doesn’t affect others and that they don’t need vaccines for the flu or COVID-19 if they’re not at high risk.
“Unfortunately, respiratory viruses can cause really severe and life-changing disease for some people, even among the young and very healthy. The best way to help prevent a virus from really upending your life or others is to get vaccinated. Our vaccines are safe and very effective in preventing you from getting very sick and that’s an important outcome,” said Megan Conroy, MD, a pulmonologist and critical care specialist at the Ohio State Wexner Medical Center and clinical assistant professor in the College of Medicine.
Along with the flu and respiratory syncytial virus (RSV), COVID-19 has become part of the respiratory virus season, resulting in strain on the healthcare system. The CDC projects the total number of hospitalizations will be higher this year than in seasons before the COVID-19 pandemic.
“Unfortunately, the flu kills tens of thousands of Americans every year. We get an idea of how bad a respiratory illness season the U.S. will have by looking at what happened in the southern hemisphere where flu season is during our summer. Australia had almost a record setting influenza season. That’s concerning and a sign that we may have higher flu numbers than average and certainly higher than in recent years since universal masking has gone by the wayside,” Conroy said.
Who should get a vaccination
When it comes to flu and COVID-19 vaccinations, it’s recommended everyone 6 months and older get both vaccines every season with rare exceptions. It’s safe to get both at the same time, and clinical trials are underway on whether both vaccines can be combined into a single shot, Conroy said.

Findings from a multi-center, international clinical trial reported by a Cleveland Clinic physician show that semaglutide reduced cardiovascular events by 20% in adults with overweight or obesity and established cardiovascular disease who do not have diabetes.
Semaglutide is primarily prescribed for adults with type 2 diabetes but is also approved for chronic weight management in adults with obesity or overweight and have at least one other health issue. In the trial, patients treated with semaglutide lost an average of 9.4% of their body weight and experienced improvements in other risk factors for cardiovascular disease.
Results from the “SELECT — Semaglutide and Cardiovascular Outcomes in Patients with Overweight or Obesity Who Do Not Have Diabetes” trial were presented today during a late-breaking science session at the American Heart Association’s Scientific Sessions 2023 and simultaneously published in the New England Journal of Medicine.
In the trial, for patients with preexisting cardiovascular disease and overweight or obesity but without diabetes, weekly injections of semaglutide at a dose of 2.4 mg was superior to placebo in reducing the risk of death from cardiovascular causes, nonfatal heart attack, or nonfatal stroke over an average follow-up of 40 months.
“It is known that overweight and obesity increase a person’s risk of cardiovascular events. Yet while reducing cardiovascular disease by treating high cholesterol, high blood pressure, and diabetes is standard practice, the concept of treating obesity to reduce cardiovascular complications has been hampered by the lack of evidence that lifestyle or pharmacologic interventions for overweight or obesity improve cardiovascular outcomes,” said Michael Lincoff, M.D., SELECT’s lead author and vice chair for research in Cleveland Clinic’s Department of Cardiovascular Medicine. “This marks the first pharmacologic intervention for overweight or obesity that’s been shown in a rigorous fashion to reduce the risk of cardiovascular events.”
More than half the world population is projected to have overweight or obesity by the year 2035. High body-mass index (BMI) is estimated to have accounted for 4 million deaths globally in 2015, more than two thirds of which were caused by cardiovascular diseases.
Semaglutide, a GLP-1 receptor agonist medication initially approved and most frequently prescribed for adults with type 2 diabetes, was also FDA-approved in 2021 for chronic weight management in adults with obesity or overweight with at least one weight-related comorbidity. While the weight loss effects of semaglutide appear to occur primarily through appetite suppression, this drug has other actions which may reduce cardiovascular risk, including improvements in glucose levels, decreases in blood pressure and cholesterol levels and reductions in inflammation, and beneficial effects on heart muscle and blood vessels.

Nearly everyone can lower their blood pressure, even people currently on blood pressure-reducing drugs, by lowering their sodium intake, reports a new study from Northwestern Medicine, Vanderbilt University Medical Center and the University of Alabama at Birmingham.
“In the study, middle-aged to elderly participants reduced their salt intake by about 1 teaspoon a day compared with their usual diet. The result was a decline in systolic blood pressure by about 6 millimeters of mercury (mm Hg), which is comparable to the effect produced by a commonly utilized first-line medication for high blood pressure,” said Dr. Deepak Gupta, associate professor of medicine at Vanderbilt University Medical Center and co-principal investigator.
“We found that 70-75% of all people, regardless of whether they are already on blood pressure medications or not, are likely to see a reduction in their blood pressure if they lower the sodium in their diet,” said co-principal investigator Norrina Allen, professor of preventive medicine at Northwestern University Feinberg School of Medicine.
This is one of the largest studies to investigate the effect of reducing sodium in the diet on blood pressure to include people with hypertension and already on medications.
“We previously didn’t know if people already on blood pressure medication could actually lower their blood pressure more by reducing their sodium,” said Allen, also the Quentin D. Young Professor of Health Policy and director of the Center for Epidemiology and Population Health.
The study will be published Nov. 11 in the Journal of the American Medical Association and presented at the American Heart Association Scientific Sessions 2023 in Philadelphia.
The total daily sodium intake recommended by the AHA is to be below 1,500 milligrams and this study was designed to decrease it even lower than that, Allen said. “It can be challenging but reducing your sodium in any amount will be beneficial,” she said.

The ventilation technique, also known as rescue breathing, commonly used during cardiopulmonary resuscitation (CPR) for people with cardiac arrest is often performed poorly by professional emergency responders, and this ineffective strategy is linked to significantly worse patient survival rates, according to a study supported by the National Institutes of Health. Ventilation involves administering breaths to a patient to provide life-sustaining oxygen and inflate the lungs when they stop breathing or during cardiac arrest, when the heart suddenly stops pumping blood. Among the nearly 2,000 people in the study who received CPR for out-of-hospital cardiac arrests, those who were given a higher number of effective ventilations had survival rates three times greater than those who were given fewer ventilations.
The study, funded largely by the National Heart, Lung, and Blood Institute (NHLBI), part of NIH, could lead to improved CPR guidelines and practices among emergency responders and potentially save more lives. Its findings were published in the journal Circulation andsimultaneously presented at the American Heart Association’s Resuscitation Science Symposium 2023 in Philadelphia.
“This is one of the first studies to measure the quality and frequency of ventilations used during CPR,” said study leader Ahamed Idris, M.D., director of emergency medicine research at the University of Texas Southwestern Medical Center in Dallas. “While we suspected that better ventilation was going to show some benefit to patients, the result that we got was much more than we expected. It was very surprising.”
Each year in the United States, more than 356,000 people have out-of-hospital cardiac arrests, and only about 10% of them survive, according to the American Heart Association. Idris estimated that if more emergency responders performed CPR according to resuscitation guidelines — that is, giving four effective ventilations per minute and using proper techniques — about 15,000 more people might get to the hospital alive and leave alive. However, many responders are falling short of that goal, showing effective lung ventilations as few as two over 10 minutes, with potentially serious consequences, according to the study.
For the study, the researchers analyzed cardiac defibrillator readings, including measurements of ventilation frequency, that were recorded for 1,976 people who were given standard CPR by emergency responders from June 2011 to May 2015 in six cities in the United States and Canada. Standard CPR is defined as 30 cycles of chest compressions interrupted by brief pauses, during which two breaths are administered through a bag-mask device, which is a portable instrument used by professionals that delivers oxygen through a face mask using a squeezable air bag.
From the start of chest compressions to the placement of an advanced airway device — a tube placed directly in the airway to keep it open — the average duration of the CPR procedure ranged from 10 to 15 minutes.
The researchers then compared the ventilation measurements to the patients’ health outcomes after reaching the hospital. To do this, they divided the patients — 66% male and 65 years old on average — into two groups: Patients who received a higher number of ventilations (about 12 on average during the CPR session) and patients who received a lower number of ventilations (about two on average per session). Patients in the group with the higher number of ventilations had better clinical outcomes, including a three times higher rate of survival-to-hospital discharge, compared to the group with lower ventilation numbers (13.5% vs 4.1%).

For the first time, scientists have used the concept of evolutionary traps on human societies at large. They find that humankind risks getting stuck in 14 evolutionary dead ends, ranging from global climate tipping points to misaligned artificial intelligence, chemical pollution, and accelerating infectious diseases.
The evolution of humankind has been an extraordinary success story. But the Anthropocene — the proposed geological epoch shaped by us humans — is showing more and more cracks. Multiple global crises, such as the Covid-19 pandemic, climate change, food insecurity, financial crises, and conflicts have started to occur simultaneously in something which scientists refer to as a polycrisis.
“Humans are incredibly creative as a species. We are able to innovate and adapt to many circumstances and can cooperate on surprisingly large scales. But these capabilities turn out to have unintentional consequences. Simply speaking, you could say that the human species has been too successful and, in some ways, too smart for its own future good,” says Peter Søgaard Jørgensen, researcher at the Stockholm Resilience Centre at Stockholm University and at the Royal Swedish Academy of Sciences’ Global Economic Dynamics and the Biosphere programme and Anthropocene laboratory.
He is the lead author of a new landmark study published today as part of a larger assessment in the journal Philosophical Transactions of the Royal Society B. The assessment gathers insights from a wide range of different scientific disciplines across the natural and social sciences and humanities, to understand how the Anthropocene evolved and how global sustainability can continue to evolve in the future.
The new study shows how humanity could get stuck in “evolutionary traps” — dead ends that occur from initially successful innovations. In a first scoping effort, they identify 14 of these, including the simplification of agriculture, economic growth that does not deliver benefits for humans or the environment, the instability of global cooperation, climate tipping points, and artificial intelligence (for a full list of traps see table further down).
“Evolutionary traps are a well-known concept in the animal world. Just like many insects are attracted by light, an evolutionary reflex that can get them killed in the modern world, humankind is at risk of responding to new phenomena in harmful ways,” explains Peter Søgaard Jørgensen.
The simplification of agricultural systems is an example of such a trap. Relying on a few highly productive crops such as wheat, rice, maize, and soya, has meant that calories produced have skyrocketed over the past century. But it also meant that the food system has become very vulnerable to environmental change, such as weather extremes, or new diseases. Of the 14 evolutionary traps, 12 are in an advanced state, meaning that humankind is on the verge of getting stuck to a degree where it becomes very difficult to get out. What’s more, societies are continuing to move in the wrong direction in 10 of these 14. Alarmingly, these evolutionary traps tend to reinforce each other. If societies get stuck in one dead end, they are more likely to get stuck in others as well. The two dead ends which currently are less advanced are the autonomy of technology — AI and robotics — and a loss of social capital through digitalization.

A joint research team at KAIST developed an intravenous (IV) needle that softens upon insertion, minimizing risk of damage to blood vessels and tissues. Once used, it remains soft even at room temperature, preventing accidental needle stick injuries and unethical multiple use of needle. A thin-film temperature sensor can be embedded with this needle, enabling real-time monitoring of the patient’s core body temperature, or detection of unintended fluid leakage, during IV medication.
Intravenous (IV) injection is a method commonly used in patient’s treatment worldwide as it induces rapid effects and allows treatment through continuous administration of medication by directly injecting drugs into the blood vessel. However, medical IV needles, made of hard materials such as stainless steel or plastic which do not mechanically match the soft biological tissues of the body, can cause critical problems in healthcare settings, starting from minor tissue damages in the injection sites to serious inflammations.
The structure and dexterity of rigid medical IV devices also enable unethical reuse of needles for reduction of injection costs, leading to transmission of deadly blood-borne disease infections such as human immunodeficiency virus (HIV) and hepatitis B/C viruses. Furthermore, unintended needlestick injuries are frequently occurring in medical settings worldwide, that are viable sources of such infections, with IV needles having the greatest susceptibility of being the medium of transmissible diseases. For these reasons, the World Health Organization (WHO) in 2015 launched a policy on safe injection practices to encourage the development and use of “smart” syringes that have features to prevent re-use, after a tremendous increase in the number of deadly infectious disease worldwide due to medical-sharps related issues.
KAIST announced on the 13th that Professor Jae-Woong Jeong and his research team of its School of Electrical Engineering succeeded in developing the Phase-Convertible, Adapting and non-REusable (P-CARE) needle with variable stiffness that can improve patient health and ensure the safety of medical staff through convergent joint research with another team led by Professor Won-Il Jeong of the Graduate School of Medical Sciences.
The new technology is expected to allow patients to move without worrying about pain at the injection site as it reduces the risk of damage to the wall of the blood vessel as patients receive IV medication. This is possible with the needle’s stiffness-tunable characteristics which will make it soft and flexible upon insertion into the body due to increased temperature, adapting to the movement of thin-walled vein. It is also expected to prevent blood-borne disease infections caused by accidental needlestick injuries or unethical re-using of syringes as the deformed needle remains perpetually soft even after it is retracted from the injection site.
The results of this research, in which Karen-Christian Agno, a doctoral researcher of the School of Electrical Engineering at and Dr. Keungmo Yang of the Graduate School of Medical Sciences participated as co-first authors, was published in Nature Biomedical Engineering on October 30. 
“We’ve developed this special needle using advanced materials and micro/nano engineering techniques, and it can solve many global problems related to conventional medical needles used in healthcare worldwide,” said Jae-Woong Jeong, Ph.D., an associate professor of Electrical Engineering at KAIST and a lead senior author of the study.

Researchers at the University of Leicester have discovered the mechanism by which cholesterol in our diet is absorbed into our cells.
This discovery, which has just been published in the journal Science opens up new opportunities for therapeutic intervention to control cholesterol uptake that could complement other therapies and potentially save lives.
The research, conducted with colleagues from the USA, China and Australia, has shown that two proteins (called Aster B and Aster C) play a key role in transporting cholesterol from the membrane of the cells lining our intestine to the internal compartment where it is modified prior to circulation.
Funding came from the Leducq Foundation which awarded $6 million to eight laboratories across the USA and Europe for collaborative research into how cholesterol is transported in our bodies.
University of Leicester researchers from the Institute of Structural and Chemical Biology, used their expertise to reveal how Ezetimibe, a cholesterol lowering drug, blocks the ability of Aster B and C to transport cholesterol.
Professor John Schwabe, Director of the Institute for Structural and Chemical Biology, said: “This breakthrough is the result of a long-lasting collaboration and forms part of an international effort to identify ways in which we can combat cardiovascular disease and stroke. A better understanding of important areas of cholesterol absorption and metabolism and, particularly, how cholesterol moves within cells and tissues is essential. This knowledge will allow us to design new drugs and therapies that target specific proteins involved in these pathways to combat most pressing public health problems such as heart attacks and stroke.
Cholesterol is a natural fatty substance found in the blood. Produced in the liver, it is also found in some of the foods we eat such as red meat and dairy products. Frying our food can also add to cholesterol in our diet.

From plants to animals, all living things depend on proteins to help their cells function properly. In certain cases, like when under stress in response to heat or toxins, some proteins within the cell condense into liquid-like droplets called condensates. This process is hypothesized to occur via phase separation and provides a quick way for the cell to assemble certain components. Research in Syracuse University Professor Carlos Castañeda’s lab has recently shown that protein quality control (PQC) components are important for many of these condensates.
Castañeda, associate professor of biology and chemistry in the College of Arts and Sciences (A&S), is among a team of researchers working to understand how protein quality control works in cells. Similar to the way computers use coding as a set of instructions, the PQC receives its instructions from polyubiquitin chains. Ubiquitin (Ub) is a regulatory protein found in all eukaryotic cells (cells containing a defined nucleus) and polyubiquitin is an assembly containing at least a few ubiquitin molecules.
Under normal operating conditions, condensates form and react to a stressor, and then dissolve after the stress is relieved. But when this system becomes disrupted, it can result in protein clumping or aggregation, which can cause cells, especially those in the nervous system, to die. These abnormal protein aggregates are markers for neurological diseases like amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease. By understanding the circumstances that lead to dysregulation of the PQC, scientists hope this research will one day lead to a cure for such neurodegenerative diseases.
In a paper published last year in EMBO Reports, Castañeda and his collaborators established a framework for how polyubiquitin chains regulate the formation and disassembly of a condensate made of Ubiquilin-2 (UBQLN2) proteins, whose dysregulation is implicated in ALS. Polyubiquitin is important for UBQLN2 function and the two bind noncovalently, meaning that the interaction between them is weaker than a covalent chemical bond. Following up on that work, the researchers wanted to further explore the specific conditions that affect assembly of these condensates.
“While working on the EMBO Reports project, we started to see that more extended polyubiquitin chains favored phase separation (condensate formation) with UBQLN2,” says Castañeda. “So, we wondered if this is always true. We decided to make even more extended chains.”
Through the Research Experience for Undergraduates (REU) program, Castañeda welcomed students Suzanne Enos and Antara Chaudhuri into his lab in 2021. The NSF-sponsored REU program brings undergraduate students from across the country to Syracuse’s campus to participate in research over the summer.
In Castañeda’s lab, the team engineered and designed different types of polyubiquitin chains with variable lengths and topologies. Enos and Chaudhuri then helped test how well these chains phase separated with UBQLN2. After further design-work by Sarasi Galagedera, a former postdoctoral researcher in Castañeda’s lab; Thuy Dao, a lab manager in the Department of Chemistry; and Jeremy Schmit, a professor of physics at Kansas State University, the team found there was a “sweet spot” — or specific spacing between Ub units — where condensate formation was optimized. Fittingly coined as “goldilocks,” the group’s findings were recently published in Proceedings of the National Academy of Sciences (PNAS).

For years, researchers and clinicians have known that lupus, an autoimmune condition, occurs in women at a rate nine times higher than in men. Some of the factors that cause the disease’s high prevalence in women have eluded discovery, but in a new study investigating the immune system processes in lupus and the X chromosome, Johns Hopkins Medicine researchers have uncovered answers about the disease’s frequency in females.
A number of dysregulated genetic and biological pathways contribute to the development of lupus and its varied symptoms of muscle and joint pain, skin rashes, kidney problems and other complications throughout the body. One such pathway involves a protein in the immune system called toll-like receptor 7 (TLR7), which, in lupus, reacts to the body’s own RNA, molecules that act as messengers of genetic information. TLR7’s reaction to RNA triggers an immune response that damages healthy tissue.
In the full article, published in the October volume of the Journal of Clinical Investigation Insight, researchers honed in on this TLR7 immune response in lupus, looking specifically at how a piece of genetic material only found in women, known as X-inactive specific transcript (XIST), could trigger TLR7’s immune system response. XIST is a type of RNA that plays a crucial role in inactivating one of the two X chromosomes found in female cells so that females do not have imbalanced gene expression.
“XIST has previously been implicated in autoimmunity, but more as something that could prevent autoimmune conditions like lupus, rather than drive the disease’s development,” says study author Erika Darrah, Ph.D., adjunct professor of medicine at the Johns Hopkins University school of Medicine. She has since left the university, but led the project. “Our findings show the opposite, that XIST actually plays a role in promoting autoimmunity — increasing the susceptibility to lupus and its severity in women.”
The research team first tested whether XIST could bind to TLR7 and initiate the receptor’s immune response using cellular experiments. They observed that XIST could strongly bind to TLR7 and trigger the production of molecules called interferons, an immune system protein seen at high levels in lupus that contributes to tissue damage in this disease. Rather than protect from TLR7 and interferon’s negative effects on the body, these tests illustrated that XIST drove the process of an overactive immune response and therefore contributed to lupus development.
“XIST has now taken on a different role, an alarm signal related to autoimmunity,” says study author Brendan Antiochos, M.D., assistant professor of medicine at the Johns Hopkins University School of Medicine. “The immune system activation through XIST and TLR7 is female-specific, helping explain the observation that lupus is so much more common in women compared to men.”
To further study XIST’s role in lupus, researchers also examined XIST levels in patients from two lupus cohorts. The team tested blood samples from patients at the Johns Hopkins Lupus Center for XIST levels, and also used publicly available data from another study that showed XIST and interferon levels in white blood cells taken from the kidneys of people with lupus. They assessed that not only did the levels of XIST in the kidney correlate with higher interferon levels, but also, those with more XIST in their blood cells experienced greater disease severity and worsened lupus symptoms.

Having healthy mitochondria, the organelles that produce energy in all our cells, usually portends a long healthy life whether in humans or in C. elegans, a tiny, short-lived nematode worm often used to study the aging process. Researchers at the Buck Institute have identified a new drug-like molecule that keeps mitochondria healthy via mitophagy, a process that removes and recycles damaged mitochondria in multicellular organisms. The compound, dubbed MIC, is a natural compound that extended lifespan in C. elegans, ameliorated pathology in neurodegenerative disease models of C. elegans, and improved mitochondrial function in mouse muscle cells. Results are published in the November 13, 2023, edition of Nature Aging.
The impact of mitochondrial dysfunction in age-related disease
Defective mitophagy is implicated in many age-related diseases. It’s tied to neurodegenerative disorders such as Parkinson’s and Alzheimer’s; it plays a role in cardiovascular diseases including heart failure; it influences metabolic disorders including obesity and type 2 diabetes; it is implicated in muscle wasting and sarcopenia and has a complex relationship with cancer progression. Even though interventions that restore mitophagy and facilitate the elimination of damaged mitochondria hold great promise for addressing these conditions, not one treatment has been approved for human use despite advances in the field.
What’s MIC?
MIC (Mitophagy-Inducing Compound) is a coumarin, which are naturally bioactive compounds that have anticoagulant, antibacterial, antifungal, antiviral, anticancer, and antihyperglycemic properties (among others) as well as being an antioxidant with neuroprotective effects. Coumarin is found in many plants and is found in high concentrations in certain types of cinnamon, which is one of the most frequent sources for human exposure to the substance.
A new mechanism of action in mitophagy
The project started in a mouse model of Parkinson’s disease where researchers in the laboratory of Julie Andersen, PhD, a senior author of the paper, were looking at known enhancers of mitophagy, including rapamycin. “Co-author Shankar Chinta, PhD, started screening natural compounds in neuronal cells and MIC came up as a major hit,” she said. “Rather than taking MIC immediately into a mouse model we wanted to understand its impact on overall aging and identify its mechanism of action, so we took the work into the worm where we found that MIC is in a different class of molecules that enhance the expression of a key protein, TFEB.”
In an effort spearheaded by Andersen and research scientist Manish Chamoli, PhD, lead author of the study, researchers found that MIC enhanced the activity of transcription factor TFEB, which is a master regulator of genes involved in autophagy and lysosomal functions. Autophagy is the intracellular recycling process whereby cells clean up damaged proteins; it derives its abilities from the lysosome. Researchers found that MIC robustly increased the lifespan of C. elegans while also preventing mitochondrial dysfunction in mammalian cells.