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SARS-CoV-2 variants of concern and the biological sex of patients affect the efficacy of molnupiravir, the first orally available drug approved for outpatient use against COVID-19, according to a new study led by researchers in the Center for Translational Antiviral Research in the Institute for Biomedical Sciences at Georgia State University.
SARS-CoV-2, the virus that causes COVID-19, has triggered recurring infection waves worldwide because of the limited longevity of vaccine-induced immunity, hesitancy of various populations to vaccinate and variants of concern (e.g., alpha, beta, gamma, delta and omicron) that are increasingly contagious or aren’t sensitive to vaccines. Omicron has quickly replaced delta as the dominant circulating strain after first appearing in November 2021.
While oral antivirals such as molnupiravir promise to improve disease management, the efficacy and potency of molnupiravir against variants of concern are either questioned or unknown. Though omicron appears to be milder than previous variants, there’s an urgent need for therapeutics to improve disease management because of record-high daily infection rates and elevated hospitalization numbers.
The study, published in the journal Nature Communications, tested molnupiravir against SARS-CoV-2 variants of concern in cultured cells, human airway epithelium organoids, ferrets and a dwarf hamster model of severe COVID-19-like lung injury. The analysis found molnupiravir equally inhibited variants of concern in cells and organoids, and treatment reduced shedding and prevented transmission in ferrets.
In addition, the capacity of SARS-CoV-2 to cause disease in dwarf hamsters was dependent on the variant of concern and was highest for the delta, gamma and omicron variants. All hamsters treated with molnupiravir survived, showing reduction in lung virus load from one order of magnitude for delta to four orders of magnitude for gamma. The effect of treatment varied in individual hamsters infected with omicron, and viral load reduction was significant in males but not females.
“We established in this manuscript a novel SARS-CoV-2 animal model that gives high viral load of omicron, which is currently the variant of concern. None of the other models have done that,” said Richard Plemper, senior author of the study, director of the Center for Translational Antiviral Research and Distinguished University Professor in the Institute for Biomedical Sciences at Georgia State. “We show that dwarf hamsters provide a robust experimental system to explore degrees of pathogenicity of different SARS-CoV-2 variants of concern. Unexpectedly, molnupiravir efficacy against omicron was variable between individual dwarf hamsters. Biological sex of the animals emerged as a correlate for therapeutic benefit of molnupiravir use against omicron, with treated males faring better overall than females. By contrast, biological sex had no effect on treatment benefit when dwarf hamsters were infected with gamma or delta, which matched human trial data reported for these variants of concern.”
Scientists have lacked an efficacy model that mirrors the acute lung injury of life-threatening COVID-19 and a relevant experimental platform to test the effect of molnupiravir on mitigating lung damage caused by different variants of concern. This discovery could enable researchers to explore the impact of treatment on disease outcome.
“Without controlled clinical data assessing the efficacy of molnupiravir against omicron, it’s unclear to what degree the results in dwarf hamsters extend to human therapy,” Plemper said. “However, our study demonstrates that pharmacological mitigation of severe COVID-19 is complex and attempts to predict drug efficacy based on unchanged ex vivo inhibitory concentrations alone may be premature. The dwarf hamster-based results illuminate that variant of concern-specific differences in treatment effect size may be present in vivo, alerting the need to continuously reassess therapeutic benefit of approved antivirals for individual patient subgroups as SARS-CoV-2 evolves and potential future variants of concern may emerge.”
Co-authors of the study include Carolin M. Lieber (co-first author), Robert M. Cox (co-first author), Julien Sourimant, Josef D. Wolf and Richard K. Plemper of the Center for Translational Antiviral Research in the Institute for Biomedical Sciences at Georgia State; Kate Juergens, Quynh Phung and Alexander L. Greninger of the University of Washington; Manohar T. Saindane, Meghan K. Smith, Zachary M. Sticher, Alexander A. Kalykhalov, Michael G. Natchus and George R. Painter of Emory University; and Kaori Sakamotoof the University of Georgia.
The study is funded by the National Institute of Allergy and Infectious Diseases (NIAID) of the National Institutes of Health (NIH).

Black people and women with severe heart failure who might be good candidates for surgery to implant a heart-assisting device have a lower chance of actually getting that operation than white patients, or male patients, a new study finds.
The differences for Black patients cropped up mainly in patients whose chances of benefiting from a left-ventricular assist device (LVAD) were less clear-cut, usually because they had less severe heart failure. That meant it was up to their health care team and the patient to decide if they wanted to have the operation or continue with non-surgical treatment.
The patterns of LVAD use in women, meanwhile, suggests lower access no matter how severe their heart failure.
Differences by race and gender persisted even after the researchers took into account a raft of factors, from patients’ incomes and distance from the hospital to what their neighborhood population mix was like.
That raises the strong possibility that for these patients, the chance of getting an LVAD was influenced by conscious or unconscious race and gender bias on the part of health care providers, the researchers conclude.
And that means hospitals and heart failure teams need to take steps to ensure more equal access to LVAD care for all patients who might benefit, the authors say.
The study, published in JAMA Network Open by a team from the University of Michigan Frankel Cardiovascular Center and Institute for Healthcare Policy and Innovation, is based on data from more than 12,300 patients with traditional Medicare coverage. All had heart failure severe enough to send them to the hospital at least once in the eight-year study period.
The study shows no racial differences in LVAD use among the sickest heart failure patients, those who are the most clear-cut candidates.
Instead, the differences in LVAD use for Black patients clustered among those with a less clear-cut need for the device. That need, based on specific clinical characteristics, is measured with what’s called an LVAD propensity score. In the group whose scores were “on the bubble,” Black patients had much lower chances of getting an LVAD than white or male patients.
The researchers also looked at what happened after patients received an LVAD. Overall, patients survived for at least a year at equal rates, no matter what their race or gender. Black patients in the “on the bubble” group actually had a higher chance of surviving at least a year than white patients (84% vs. 77%), even though they had a slightly higher chance of needing another hospital stay.
“These data show clear racial disparities in cases where there is ‘wiggle room’ for clinicians to decide which patients are most likely to benefit from an LVAD,” says lead author Thomas Cascino, M.D., M.S., a cardiologist and health equity researcher at Michigan Medicine, U-M’s academic medical center. “There is less aggressive use of this life-saving therapy among a subgroup of Black patients and all women with heart failure. While we also need to study the role of patient preference in LVAD decision-making for this group of patients, heart failure providers need to be cognizant of their potential for bias and how it might influence the recommendations we make to patients.”
Cascino and colleagues recently looked at another aspect of heart failure device care — the use of short-term mechanical circulatory support in patients who are candidates for a heart transplant. This analysis also suggested that center-level variation in use plays a major role in this type of care, which could in turn create inequality in a patient’s likelihood of being chosen for a heart transplant when an organ becomes available. The team published the paper in the Journal of Heart and Lung Transplantation.

A unique subset of white blood cells confers fast-acting and lasting protection against ischemic stroke in mice, University of Pittsburgh neurologists and immunologists reported in the Journal of Clinical Investigation today.
This study identified a novel subset of CD8+ regulatory-like T cells, or CD8+TRLs, as “first responders” to stroke. Attracted to the site of ischemic injury by a unique “homing” signal released by dying brain cells, CD8+TRLs reach the brain within 24 hours after stroke onset, where they release molecules that provide direct neuroprotective effects, as well as limit inflammation and secondary brain damage.
“The beauty of CD8+TRLs is in their fast response. They confer very potent protection to the brain, which can last a long time,” said co-corresponding author Xiaoming Hu, M.D., Ph.D., associate professor of neurology at Pitt and a U.S. Department of Veterans Affairs (VA) investigator. “Most importantly, these cells are easily accessible because they circulate in the blood before they enter the injured brain.”
“Creating shelf-stable and ready-to-use CD8+TRLs or developing a cocktail of neuroprotective signaling molecules released by those cells once they reach the brain could present effective future therapies against stroke and offer hope to hundreds of thousands of patients who are ineligible for treatments available to them currently,” said co-senior author Jun Chen, M.D., Ph.D., professor of neurology at Pitt and a U.S. Department of VA investigator.
Stroke affects 800,000 Americans yearly, but only a quarter of those patients will be eligible to receive one of only two Food and Drug Administration-approved treatments: An injection of a blood clot-busting enzyme called tPA or mechanical thrombectomy, a surgical procedure that removes the blood clot in the brain with a stent retriever.
Because those treatments must be administered very early after the stroke, many people, especially those living in remote areas, are ineligible for those therapies. The remaining 600,000 people are left with symptoms-based treatments and are at high risk of developing long-term health complications, including mobility challenges and, in some cases, speech and cognitive pathologies. In addition, the blood clot-busting therapy, in particular, has drawbacks that further limit the number of people benefiting from such therapy.
Immune response plays an important role in stroke. As soon as a blood clot wedges itself in a blood vessel, the brain sends an “SOS” signal to activate the immune system. This rapid immune response aims to clear out the cell debris, limit brain damage and kick-start brain repair processes. However, the function of the immune system is diverse and complex, and different types of immune cells may play distinct beneficial or detrimental roles in a damaged brain.
As Chen, Hu, and their colleagues showed for the first time, the CD8+TRLs enter the brain much faster than any other regulatory immune cells. Within 24 hours after researchers depleted these special CD8+TRLs from the bloodstream of stroke mice, the size of the brain region affected by ischemia expanded by 50% compared to animals whose CD8+TRL levels remained intact.
Even more reassuringly, mice who received a transfusion of purified CD8+TRLs prepared in the lab fared better and recovered faster than those who were untreated for over five weeks. These unique CD8+TRLs, therefore, serve as early responders to rally defenses after stroke and may collaborate with other immune cells to safeguard the brain for a long time.
“Despite the efforts of thousands of people devoting their careers to finding treatments that could benefit stroke patients, therapy options are minimal,” said Chen. “I have been working in this field for more than 30 years, and this is the first time I feel that I am seeing the light at the end of the tunnel, promising future clinical translation that will benefit patients.”
Additional authors of this study are Wei Cai, M.D., Ph.D., Ligen Shi, M.D., Ph.D., Jingyan Zhao, M.D., Ph.D., Fei Xu, B.S., Connor Dufort, B.S., Qing Ye, M.D., Tuo Yang, M.D., Ph.D., Xuejiao Dai, M.D., Ph.D., Junxuan Lyu, M.D., Chenghao Jin, M.D., Hongjian Pu, Ph.D., Fang Yu, M.D., Ph.D., Sulaiman Hassan, B.S., Zeyu Sun, M.D., Ph.D., Wenting Zhang, M.D., Ph.D., T. Kevin Hitchens, Ph.D., Yejie Shi, M.D., Ph.D., and Angus Thomson, Ph.D., all of Pitt; and Rehana Leak, Ph.D., of Duquesne University.
This research was supported by the NIH/NINDS (grants NS105430 and NS094573), the University of Pittsburgh School of Medicine and the UPMC Endowed Chair for stroke research.

Native Americans experienced disproportionately high rates of deaths from COVID-19 due to poverty, crowded housing, high rates of chronic disease, employment in frontline jobs, and limited access to quality health care.
Less is known about the pandemic’s effects on life expectancy for this population, which makes up 2% of the U.S. population.
Noreen Goldman of Princeton University and Theresa Andrasfay, Ph.D. ’20 of the University of Southern California investigated life expectancy at birth in 2020 and 2021 — when COVID-19 rates were surging — compared to 2019.
Life expectancy is a metric of population-level mortality in a given year, and it is sensitive to deaths at younger ages.
Findings
The pandemic set Native Americans further behind other major racial and ethnic groups in terms of life expectancy. For a high-income country, these figures are shockingly low, the researchers said, and far below every country in the Americas except for Haiti. The estimated loss in life expectancy at birth for Native Americans is 4.5 years in 2020 and 6.4 years in 2021 relative to 2019. The pandemic reduced Native American life expectancy at birth from the already low 72 years in 2019 to about 67 years in 2020 and about 65 years in 2021 for both sexes combined. Men and women each experienced around a six-year drop in life expectancy at birth. Women’s life expectancy was 69 in 2021, 71 in 2020 — compared to 75 in 2019. Men’s life expectancy was 62 in 2021, 64 in 2020 — dropping from 69 in 2019. Native Americans experienced a loss in life expectancy at birth in 2020 that is more than three years above that for whites and 1.5 years above losses for Black and Latino populations.

All human tumors originating from various tissues share a series of properties that define them, including the ability to prevent cell death. Instead, healthy organs induce programmed cell death or apoptosis to balance their size and eliminate damaged cells. There is a specific and physiological cell death called ferroptosis that occurs induced by the oxidation of fat mediated by iron content.
Today, an article published in the journal Redox Biology, the journal of reference in the field of free radicals and cancer, by the group of Dr. Manel Esteller, Director of the Josep Carreras Leukaemia Research Institute (IJC), ICREA Research Professor and Chairman of Genetics at the University of Barcelona, and headed by Dr Lucas Pontel, shows that epigenetic changes prevent iron-associated programmed cell death in leukemia and show a new target for treatment with experimental drugs.
“Leukemia cells avoid dying because they have two floats, the metabolism of the biomolecule called glutathione and the FSP1 gene that acts as a shield against this death induced by iron and oxidation.” — comments Dr. Esteller and adds — “Studying all these metabolic pathways we realized that in acute lymphoblastic leukemia (ALL) the activity of the FSP1 gene was epigenetically lost, so these cells were on the edge of the precipice of their programmed death. We only needed to give them a boost and that is what we did by administering them inhibitors of the glutathione pathway, such as L-BSO and RSL3, which rapidly induced the death of these malignant lymphocytes. In other words, this type of leukemia lives on the edge in terms of its tolerance towards ferroptosis and when you eliminate their last lifeline with a drug, these transformed cells die. This weak spot of acute lymphoblastic leukemia can therefore be explored in precision and personalized treatments for this disease, but it could also occur in other cancers. There are few clinical trials in oncology with glutathione inhibitors, but perhaps this type of work will arouse interest in the study and development of these promising experimental agents” — concludes the researcher.
In the same line, Dr. Pontel notes that “by exploring data from T-ALL and B-ALL patients, we detected that FSP1 is under epigenetic control. Thus, by determining the FSP1 epigenetic status in patients, we might be able to anticipate the success of a therapy based on drugs that induced ferroptosis.”
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Falls are a serious public health issue, resulting in tens of thousands of deaths annually and racking up billions of dollars in healthcare costs. While there has been extensive research into the biomechanics of falls, most current approaches study how the legs, joints, and muscles act separately to respond, rather than as a system. The ability to measure how these different levels relate to each other could paint a much clearer picture of why someone falls and precisely how their body compensates. Until recently, however, an integrated measuring approach has been elusive.
In newly published research, Pawel Golyski and his Ph.D. advisor Greg Sawicki, associate professor of mechanical engineering and biological sciences at the Georgia Institute of Technology, investigate whether mechanical energy can be used as a “common currency” to measure how humans use lower limbs to stabilize during walking. Their research, published in the Journal of the Royal Society Interface, lays the groundwork for using mechanical energetics to understand the roles of joints and muscles during unsteady locomotion. The paper also contributed to Golyski’s selection as this year’s recipient of the American Society of Biomechanics’ (ASB) Pre-Doctoral Achievement Award.
Golyski, a graduating member of Sawicki’s Physiology of Wearable Robotics (PoWeR) Lab, previously worked as a research scientist with individuals with lower-limb amputation at Walter Reed National Military Medical Center. For his graduate work at Georgia Tech, his aim was to develop an understanding of how devices and the human body work together, specifically at the intersection of three elements: muscle mechanics, wearable exoskeletons, and stability during walking.
Each of the three elements relates to the others. Exoskeletons affect a person’s stability while also affecting how their muscles work, and vice versa. But to examine how muscles both interact with exoskeletons and affect stability makes for an interesting challenge, Golyski says. Because, while one can observe how muscle dynamics change with the use of an exoskeleton, how those changes relate to stability is not understood. To understand how all three pillars work together to help humans compensate during a fall, Golyski and Sawicki needed to come up with a new framework to measure stability.
Energy Accountants
The researchers knew that for a person walking at a steady speed on level ground, the net mechanical energy of the person and each leg over one stride — from the heel strike of one leg to the next heel strike of that same leg — is zero. They also knew that energy needed to be equal to mechanical energy at all levels of description of the leg, specifically the joints and muscles.
“The idea is that if we can relate stability to a demand in energy, then we can become accountants, and track how the energy — our currency — changes at the level of the person, muscle, and exoskeleton,” Golyski said. “That provides a really powerful framework to relate all three of those areas.”
Golyski and Sawicki designed an experiment with a person walking on a treadmill. Using a split-belt treadmill, they applied short, quick disturbances, known as perturbations, in the form of increases in belt speed to one leg during walking. The purpose was to inject or extract energy during a stride, so that they could then measure how the person’s leg and joint energies change.
For the experiment they used Georgia Tech’s CAREN (Computer Assisted Rehabilitation Environment) — an integrated system used to study stability during movement. It features cameras mounted above a treadmill to track a person’s movement using motion capture markers attached to the person. Using an algorithm designed by Golyski, Sawicki, PoWeR lab Ph.D. student Jennifer Leestma, and a high school mentee, Esmeralda Vazquez, the CAREN can execute perturbations based on a person’s movements — enabling the researchers to initiate perturbations at specific times in the gait cycle. By combining the force of the treadmill with the positional data collected by the CAREN, Golyski and Sawicki can calculate the changes in energy in a person’s individual joints.
Their new framework could assist in determining which part of a person’s body manages responses to destabilizing energy, pointing to specific muscles or joints to target with rehabilitation therapy. It could also open doors to advanced exoskeletons and prostheses that target specific joints to restore stabilizing responses in individuals with impaired balance.
“The body of research that Pawel completed during his doctoral studies is nothing short of impressive. He broke new ground by developing new experimental techniques and a new hip exoskeleton assistive device, making first-of-a-kind muscle imaging measurements, and ultimately answering the question of how exoskeletons modify joint and muscle dynamics to influence human walking stability,” Sawicki said. “I was thrilled that Pawel’s outstanding contributions as a scientist-engineer were recognized by ASB, and I’m even more thrilled that he will return to Walter Reed — his dream job — to apply his new skillset to help people get from here to there.”
This summer, as part of this recognition, Golyski will deliver a research talk during an awards session at the North American Congress on Biomechanics in Ottawa, Ontario. He will also be graduating from Georgia Tech and resuming his work with veterans and active service members at Walter Reed.
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Materials provided by Georgia Institute of Technology. Original written by Catherine Barzler. Note: Content may be edited for style and length.

New findings have uncovered how essential the FOCAD gene is for maintaining a healthy liver, especially in children. In a research study published in Nature Genetics, scientists have found that children carrying loss-of-function mutations in FOCAD are presented with an early onset, paediatric form of liver cirrhosis that can be life-threatening. The study was carried out by scientists from A*STAR’s Genome Institute of Singapore (GIS), in collaboration with hospitals and institutes across seven countries (India, USA, Saudi Arabia, Pakistan, Portugal, Brazil, and France).
Liver disease is becoming a major health concern and is estimated to be the fifth most common cause of death worldwide[1]. A systematic review from the Global Burden of Disease Study identified 1.32 million deaths due to liver cirrhosis in 2017, accounting for more than two percent of the total global deaths. Liver cirrhosis is usually diagnosed late in life, and is traditionally believed to be caused by environmental factors such as poor diet, viral hepatitis or alcohol abuse.
In collaboration with clinicians worldwide, the team combined classical tools such as Mendelian genetics and animal models[2] with modern technology, such as deep sequencing and state-of-the-art gene editing tools to identify that the FOCAD gene is indispensable for maintaining liver health in humans. Mutations in this gene cause an early onset form of liver cirrhosis not documented before. The findings of a single gene, or monogenic, disorder that leads to cirrhosis in childhood establish a strong genetic component for liver disease, which was previously unknown.
In further analysis, they discovered that FOCAD functions as part of a molecular quality control mechanism that assists in translation, a fundamental cellular process by which proteins are made. The main cells of the liver, hepatocytes, were found to rely heavily on this mechanism compared to other cell types. This is the first time that this translation-dependent quality control machinery has been implicated in liver health.
The team also discovered a cytokine[3], CCL2, that is overproduced in FOCAD deficient patients and may play a key role in the progression of liver cirrhosis. Dr Ricardo Moreno Traspas, a postdoctoral fellow from the Laboratory of Human Genetics and Therapeutics at GIS, and first author of the study, explained, “FOCAD mutations lead to an overproduction of a number of proteins that may be key drivers in the progression of the disease. One example is the signalling mediator, CCL2, that attracts immune cells and promotes liver inflammation. Drugs that target this, or similar candidates, are potential therapeutic intervention points for cirrhotic patients.”
Prof Bruno Reversade, Senior Group Leader at GIS and corresponding author of the study, commented, “We report the clinical impact of recessive loss-of-function variants in the FOCAD gene, and provide evidence for the importance of the SKI mRNA surveillance pathway for liver homeostasis. The research also brings forth the first animal model of the human disease, as well as in vitro biological systems that are now being used as platforms to identify and validate new anti-fibrotic therapeutic targets.”
Prof Patrick Tan, Executive Director of GIS, said, “The knowledge and tools generated in this study have the potential to aid in the development of innovative therapies for more common forms of liver diseases such as fatty liver disease and liver cancer. Our clinical data will also help clinicians to identify new patients with this syndrome, better understand the cellular and molecular mechanisms of the disease, and hence, provide a more accurate diagnosis, prognosis, and treatment.”
[1] Williams, R. (2006). Global challenges in liver disease. Hepatology, 44(3), 521-526. https://doi.org/10.1002/hep.21347
[2] Mendel’s experiments of crossing peas to determine whether certain traits are inherited as single genes are so fundamental that they are taught in high school. The enduring power of these principles lies in the fact that they allow us to tie mutations in one specific gene to an important human disease.
[3] A type of protein that is made by certain immune and non-immune cells and has an effect on the immune system.

The effect of ultrasound waves on the function of the human brain has been the key focus of recent research, which has indicated its potential as an effective, non-invasive approach for the modulation of brain activity. While the effects of ultrasound exposure on consciousness and cognition have been extensively explored, little is known about its impact on emotional states such as depression. To add to it, there are limitations in our understanding of neural and molecular mechanisms that underpin emotions.
Fortunately, rats experience pleasant emotions in response to high-frequency ultrasound vocalizations (USVs), making them ideal model organisms to study mechanisms underlying depression.
To this end, a team of researchers led by Professor Akiyoshi Saitoh, including Professor Satoru Miyazaki, Assistant Professor Daisuke Yamada and Ms. Tsugumi Yamauchi from Tokyo University of Science, and Mr. Shoichi Nishino from FUJIMIC, Inc., delved deeper into understanding the effects of ultrasound exposure on depression, by conducting experiments on rats lacking olfactory lobes — organs that regulate neurotransmission. These “olfactory bulbectomized (OB)” rats undergo changes in neurotransmitters, endocrine secretions, and behavior, which are similar to those observed in humans with depression.
Giving further insights into their study, Prof. Saitoh remarked, “Since studies on ultrasound exposure have been primarily conducted on human subjects, we needed to establish robust animal models to elucidate underlying mechanisms using invasive techniques. In our current study, we have used OB rats to study the effects of ultrasound on neural activity and behavior” Their study, published in Volume 33, Issue 10 of NeuroReport on July 6, 2022, is the first of its kind to demonstrate potential anti-depressant effects of ultrasound exposure in rats.
Initially, the team exposed wild type and OB rats to USV for 24 hours, following which they scored them for “hyperemotionality” (agitation and anxiety-like behavior) by studying their responses to getting attacked, getting startled, facing a struggle, and initiating a fight.
Next, they monitored plasma corticosterone (a hormone that is released in response to stress) levels in the blood samples of these rats. In addition, the team assessed anxiety-like behavior of the rodents using the elevated plus maze (EPM) — an approach which triggers behavioral anxiety in rats by exposing them to open spaces in a maze, and causes them to move to closed spaces.
Their findings revealed that OB rats exposed to USV had significantly lower hyperemotionality scores and lower plasma corticosterone levels than unexposed rats. Furthermore, in OB rats with a higher latency initially. i.e., higher inclination to reach the open areas of the maze, ultrasound exposure significantly decreased their latency. Similar effects were observed with a 50-kHz ultrasound frequency which was generated artificially.
This study provides novel evidence on the anti-depressant effects of ultrasound exposure in rodents. “Our findings suggest that OB rats may be a useful animal model for investigating the effects of ultrasound exposure and mechanisms of influence.,” exclaims Prof. Saitoh about the implications of the study.
He further adds, “Unlike drug therapy, ultrasound exposure is non-invasive and easy to use. An ultrasound based therapeutic device may therefore aid the treatment and prevention of mental disorders in patients while they go about their daily lives.”
Let’s hope that these results pave the way for developing ultrasound exposure therapy as a novel treatment to help patients cope with stress and psychiatric disorders.
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A super-Earth planet has been found near the habitable zone of a red dwarf star only 37 light-years from the Earth. This is the first discovery by a new instrument on the Subaru Telescope and offers a chance to investigate the possibility of life on planets around nearby stars. With such a successful first result, we can expect that the Subaru Telescope will discover more, potentially even better, candidates for habitable planets around red dwarfs.
Red dwarfs, stars smaller than the Sun, account for three-quarters of the stars in the Milky Way Galaxy, and are abundant in the neighborhood around the Sun. As such, they are important targets in the search for nearby extra-solar planets and extraterrestrial life. But red dwarfs are cool and don’t emit much visible light compared to other types of stars, making it difficult to study them.
In the infrared wavelengths red dwarfs are brighter. So the Astrobiology Center in Japan developed an infrared observational instrument mounted on the Subaru Telescope to search for signs of planets around red dwarf stars. The instrument is called IRD for Infrared Doppler, the observational method used in this search.
The first fruits of this search are signs of a super-Earth four times the mass of the Earth circling the star Ross 508, located 37 light-years away in the constellation Serpens. This planet, Ross 508 b, has a year of only 11 Earth-days, and lies at the inner edge of the habitable zone around its host star. Interestingly, there are indications that the orbit is elliptical, which would mean that for part of the orbit the planet would be in the habitable zone, the region where conditions would be right for liquid water to exist on the surface of the planet. Whether or not there is actually water or life are questions of further study.
To have the very first planet discovered by this new method be so tantalizingly close to the habitable zone seems too good to be true and bodes well for future discoveries. Bun’ei Sato, a Professor at the Tokyo Institute of Technology and the principal investigator in this search comments, “It has been 14 years since the start of IRD’s development. We have continued our development and research with the hope of finding a planet exactly like Ross 508 b.”
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Chemicals produced in the digestive tract by gut microbes after eating red meat may help explain part of the higher risk of cardiovascular disease associated with red meat consumption, according to new research published today in the American Heart Association’s peer-reviewed journal Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB).
In the United States and around the world, cardiovascular disease is the leading cause of death. While the risk of developing cardiovascular disease, including heart attack and stroke, increases with age, other risk factors are influenced by lifestyle. Lifestyle and behaviors that are known to improve cardiovascular health include eating healthy foods, especially fruits and vegetables; regular physical activity; obtaining sufficient sleep; maintaining a healthy body weight; stopping smoking; and controlling high blood pressure, high cholesterol and high blood sugar.
“Most of the focus on red meat intake and health has been around dietary saturated fat and blood cholesterol levels,” said co-lead author of the study Meng Wang, Ph.D., a postdoctoral fellow at the Friedman School of Nutrition Science and Policy at Tufts University in Boston. “Based on our findings, novel interventions may be helpful to target the interactions between red meat and the gut microbiome to help us find ways to reduce cardiovascular risk.”
Previous research has found that certain metabolites — chemical byproducts of food digestion — are associated with a greater risk of cardiovascular disease . One of these metabolites is TMAO, or trimethylamine N-oxide, which is produced by gut bacteria to digest red meat that contains high amounts of the chemical L-carnitine .
High blood levels of TMAO in humans may be associated with higher risks of CVD, chronic kidney disease and Type 2 diabetes. However, whether TMAO and related metabolites derived from L-carnitine may help explain the effects of red meat intake on cardiovascular risk, and to what extent they may contribute to cardiovascular risk associated with meat consumption, are still unknown.
To understand these questions, the researchers conducting this study measured levels of the metabolites in blood samples. They also examined whether blood sugar, inflammation, blood pressure and blood cholesterol may account for the elevated cardiovascular risk associated with red meat consumption.