Publisher Health

WASHINGTON — Prominent social media users and conservative voices have amplified a baseless theory promoted by Russian state media accusing the United States of funding biological weapons laboratories in Ukraine.There is no evidence to support the claims, which President Volodymyr Zelensky of Ukraine, the White House, the Pentagon and the State Department have all unequivocally denied.There are biological laboratories inside Ukraine, and since 2005, the United States has provided backing to a number of institutions to prevent the production of biological weapons. But Tucker Carlson, the Fox News host, and others have misleadingly cited remarks from American officials as proof that the labs are producing or conducting research on biological weapons.“Out of nowhere, the Biden official in charge of Ukraine confirmed the story,” Mr. Carlson said on his program Thursday night. “Victoria Nuland, the under secretary of state, casually mentioned in a Senate hearing on Tuesday that actually, yes, the Biden administration does fund a series of biolabs in Ukraine.”Representative Thomas Massie, Republican of Kentucky, characterized Ms. Nuland’s remarks as a “serious admission.” Donald Trump Jr., the son of the former president, tweeted that her comments propelled the claim from “conspiracy theory to fact.”Mr. Carlson also pointed to an interview with Robert Pope, the director of the Pentagon’s Cooperative Threat Reduction Program, which helps countries in the former Soviet Union secure or eliminate nuclear and chemical weapons.“As Pope put it, scientists are scientists, they don’t want to destroy all the bioweapons,” Mr. Carlson continued in his segment. “Instead, they’re using them to conduct new bioweapons research — that’s what he said.”Mr. Carlson mischaracterized those remarks from Ms. Nuland and Mr. Pope.In congressional testimony this week, Ms. Nuland, the under secretary of state for political affairs, was asked by Senator Marco Rubio, Republican of Florida, whether Ukraine has chemical or biological weapons.“Ukraine has biological research facilities which, in fact, we are now quite concerned Russian troops, Russian forces, may be seeking to gain control of,” she responded. “So we are working with the Ukrainians on how they can prevent any of those research materials from falling into the hands of Russian forces should they approach.”If there were a biological or chemical weapon attack inside Ukraine, Mr. Rubio asked, would there be any doubt that Russia was behind it?“There is no doubt in my mind, senator, and it is classic Russian technique to blame the other guy what they’re planning to do themselves,” Ms. Nuland responded.The State Department said Ms. Nuland was referring to Ukrainian diagnostic and biodefense laboratories during her testimony, which are different from biological weapons facilities. Rather, these biodefense laboratories counter biological threats throughout the country, the department said.Mr. Rubio made the same clarification in another congressional hearing on Thursday, noting that “there’s a difference between a bioweapons facility and one that’s doing research.”In referring to Mr. Pope on Thursday, Mr. Carlson was distorting a February interview Mr. Pope gave to the Bulletin of the Atomic Scientists, a nonprofit organization and publication.Mr. Pope had warned that Russia’s invasion of Ukraine may damage laboratories in the country that conduct research and disease surveillance and are supported by the United States. He noted that some of the facilities may contain pathogens once used for Soviet-era bioweapons programs, but he emphasized that the Ukrainian labs currently did not have the ability to manufacture bioweapons.“There is no place that still has any of the sort of infrastructure for researching or producing biological weapons,” Mr. Pope said. “Scientists being scientists, it wouldn’t surprise me if some of these strain collections in some of these laboratories still have pathogen strains that go all the way back to the origins of that program.”In a March interview with the Bulletin of the Atomic Scientists, Mr. Pope also echoed Ms. Nuland’s concerns about the laboratories falling into Russia’s hands. He spoke specifically about the Pentagon’s support of 14 veterinary laboratories that provide Ukraine with sampling and diagnostic abilities to detect infectious diseases.Russia-Ukraine War: Key Things to KnowCard 1 of 4On the ground.

Briefly blocking a key molecule when administering the only approved vaccine for tuberculosis vastly improves long-term protection against the devastating disease in mice, researchers from Texas Biomedical Research Institute report this week in the Journal of Immunology. The finding, if it continues to hold true in nonhuman primates and clinical trials, has the potential to save millions of lives.
Tuberculosis (TB) infects more than 10 million people a year, killing more than 1 million a year. The Bacillus Calmette-Guérin (BCG) vaccine is widely used to inoculate children against TB, but its effectiveness wanes over time. Researchers around the world are hunting for more effective vaccines and treatments.
“We are very excited that we can reverse BCG’s waning effectiveness by combining it with a host-directed therapy into one dose, which makes it very practical for the clinic,” says Joanne Turner, PhD, Texas Biomed’s Executive Vice President, Research, and senior paper author.
Decades of research
Turner emphasized the finding builds on more than 20 years of research. Throughout her career, she has been investigating the role of a molecule, interleukin-10 (IL-10) on TB. IL-10 typically helps dampen excessive inflammation during infection, but through numerous studies, Turner and her colleagues have found IL-10 does more harm than good in TB, definitively showing it drives TB infection.
In previous studies, Turner and her colleagues blocked IL-10 at different times during infection — late into infection, the first three weeks during infection — and have knocked out IL-10 completely. All signs pointed to improved TB control and longer survival. In the current study, the team looked at what happens if they temporarily block IL-10 before infection occurs, at the same time as giving the BCG vaccine.

Physicists, chemists and immunologists at McMaster University have teamed up to modify red blood cells to transport viral agents which can safely trigger the immune system to protect the body against SARS-CoV-2, creating a promising new vehicle for vaccine delivery.
Developing new strategies and vaccine technologies is critical for controlling the pandemic and preparing for future outbreaks as the coronavirus continues to evolve and mutate, say the researchers.
The new method, described in the journal PLOS ONE, is an entirely unique approach to vaccination. Red blood-cell membranes are embedded with SARS-CoV-2 spike proteins, which then form virus-like particles.
“We take red blood cells and remove everything from the inside. We then attach spike proteins to their outside to mimic a corona virus,” explains graduate student Isabella Passos-Gastaldo, a lead author on the paper.
The particles, shown to activate the immune system and produce antibodies in mice, are completely harmless.
“Current vaccine delivery methods often cause drastic immune system reactions and have short-lived responses,” says Maikel Rheinstadter, a senior supervisor on the paper and a professor in the Department of Physics & Astronomy at McMaster.

Research carried out by RCSI University of Medicine and Health Sciences has revealed new information about how blood clots are formed during wound healing.
The research, published tomorrow in Science Advances, examines the behaviour of platelets at a wound site, specifically their ability to sense where within a blood clot they are and remodel their surroundings accordingly.
Platelets are key to initiating wound healing and the formation of blood clots (thrombus). Fibroblasts are connective tissue cells that are essential for the later stages of wound healing. Fibroblasts invade the clot that has been formed and produce vital proteins, including fibronectin, that then forma structural framework to build the new tissue needed to heal.
This new study indicates that platelets can also form a provisional fibronectin matrix in their surroundings, similar to what fibroblasts do in the later stages of wound healing. This has potential implications for how the integrity of blood clots might be maintained during vascular repair.
The study’s lead author is Dr Ingmar Schoen from the School of Pharmacy and Biomolecular Sciences at RCSI.
Commenting on the discovery, Dr Schoen said: “We have identified an additional unexpected role for the most prominent platelet adhesion receptor. Our results show that platelets not only form the clot but also can initiate its remodelling by erecting a fibrous scaffold. This finding challenges some existing paradigms in the field of wound healing, which is dominated by research on fibroblasts.”
Key to this research was the use of superresolution microscopy, which enables sharper images of structures inside or around cells to be captured and observed in vitro, in a laboratory. Observation of this platelet behaviour in a living organism (in vivo) will be required to further develop this finding.
“Without super-resolution microscopy, this discovery would not have been possible,” Dr Schoen noted.
The research was carried out in collaboration with researchers at ETH Zurich, Julius-Maximilians-University Würzburg, University of Freiburg and University Hospital Zurich.
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Autoimmune diseases are the molecular equivalent of “friendly fire”: the body attacks itself instead of harmful invaders. Now, researchers from Japan have found that interrupting the complex interplay between different immune cell types can help prevent the damage that this friendly fire causes in one type of autoimmune disease.
In a study published in this month in Annals of Neurology, researchers from Osaka University have revealed that treatment with an antibody to a protein called repulsive guidance molecule-a (RGMa) dramatically improves symptoms of neuromyelitis optica, a devastating autoimmune disorder, in an experimental rat model.
Neuromyelitis optica (NMO) is an inflammatory disorder that can cause pain, paralysis, and even death. In most cases, NMO is caused by antibodies that the body develops to a protein called aquaporin-4 (AQP4). These anti-AQP4 antibodies leak into the tissue at sites of nerve damage that also show massive accumulation of neutrophils. This neutrophil build-up is associated with the death of cells called astrocytes, which ultimately causes NMO symptoms.
“We recently found that injecting rats with an antibody to RGMa can decrease the severity of NMO symptoms,” says lead author of the study Shosuke Iwamoto. “However, it was still unclear how this treatment works mechanistically, whether by affecting AQP4, astrocytes, or some other factor.”
To address this, the researchers used a clinically relevant rat model of NMO to test the effects of the anti-RGMa antibody on disease symptoms, as well as gene and protein expression.
“Our findings revealed a new molecular mechanism of NMO pathophysiology in which RGMa stimulates macrophages to attract neutrophils to the lesions, where they kill off astrocytes,” explains Toshihide Yamashita, senior author.
Importantly, treating rats with an antibody to RGMa prevented these effects, resulting in fewer neutrophils around nerve lesions, less astrocyte killing, and a decrease in symptoms like movement problems and pain.
“Our findings suggest that anti-RGMa antibodies may represent an effective therapeutic strategy for NMO-associated neuropathic pain and motor deficits in patients with NMO,” says Iwamoto.
Given that the severity of acute NMO attacks greatly affects patients’ long-term outcomes, treatments targeting RGMa that help reduce the severity of the attack or enhance the recovery process are crucial for improving their quality of life. Treatment with an anti-RGMa antibody could potentially even be helpful in preventing NMO relapses in the chronic stage of the disease.
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Tiny structures called nanoparticles can be used to carry substances to certain parts of the body — for example, to deliver a chemotherapy drug to a tumor. Although such “nanomedicine” offered hope for improving cancer therapeutics, the survival benefits of clinically approved nanomedicines are often modest when compared with conventional chemotherapy. New research published in the Journal of Controlled Release indicates that nanomedicine may provide additional benefits if it’s administered at lower, more frequent doses — called metronomic dosing — rather than the standard maximum tolerated dose of current treatments.
“Nanomedicine and metronomic therapy have been regarded as two different approaches to treat cancer. Our analysis suggests that these two approaches can be viewed using the same unified framework as strategies to enhance treatment,” says co-corresponding author Rakesh K. Jain, PhD, director of the E.L. Steele Laboratories for Tumor Biology at Massachusetts General Hospital and the Andrew Werk Cook Professor of Radiation Oncology at Harvard Medical School.
Jain explains that metronomic therapy seems to help normalize the tumor microenvironment — meaning that it helps correct some of the abnormalities that develop around tumors that protect the tumor and foster its growth and spread. For example, while tumors can send out signals that compromise normal blood flow and block immune cell responses (both of which make them hard to treat), metronomic therapy appears to improve blood vessel function and immune activation within a tumor. Recent preclinical studies suggest that nanomedicines can cause similar changes in the tumor microenvironment.
“In this study, we hypothesized that nanoparticle formulations, given the controlled release of their payload and the long blood circulation time, can trigger the same cascade of activities as metronomic therapy,” says Jain.
Using a mathematical framework and experiments conducted in mice, the team showed that both approaches can serve as “normalization strategies” to affect the tumor microenvironment and improve cancer treatments. Also, in mice with triple negative breast cancer or fibrosarcoma, Doxil — a nanomedicine that is approved to treat metastatic breast cancer and consists of doxorubicin encapsulated in a lipid sphere — administered through a metronomic schedule could overcome tumor resistance typically seen when Doxil is given through a standard dosing schedule. A metronomic schedule also improved the efficacy of the combination of Doxil plus a type of immunotherapy called an immune checkpoint inhibitor.
“Nano-immunotherapy, which combines nanomedicines with immunotherapy, has high potential to improve patient outcomes, and for this reason, understanding the mechanisms of resistance to and development of strategies to enhance nano-immunotherapy in breast and other cancer types is urgently needed,” says co-corresponding author Triantafyllos Stylianopoulos, PhD, director of the Cancer Biophysics Laboratory and associate professor at the University of Cyprus. “The results of this work could be a basis for the planning of future clinical studies to improve the efficacy of nano-immunotherapy regimens.”
The results suggest that combining nanomedicines with metronomic scheduling can lead to a powerful attack against hard-to-treat tumors. By acting together to normalize the tumor microenvironment, these two strategies give drugs a better chance of reaching cancer cells and targeting them effectively.
The study’s co-authors include Fotios Mpekris and Myrofora Panagi (University of Cyprus), Chrysovalantis Voutouri (Massachusetts General Hospital) and James W. Baish (Bucknell University).
This work was supported by grants from the National Foundation for Cancer Research, the Ludwig Center at Harvard; the Jane’s Trust Foundation; Nile Albright Medical Research Foundation; the U.S. National Cancer Institute grants R35-CA197743, R01-CA208205, R01-CA259253, R01NS118929, U01CA224348, U01CA261842 (to R.K.J.); the European Research Council (ERC-2013-StG-336839, ERC-2019-CoG-863955); and the Cyprus Research and Innovation Foundation (INFRASTRUCTURE/1216/0052, POST-DOC/0718/0084) (to T.S.), a Marie Sk?odowska Curie Actions Individual Fellowship Global (MSCA-IF-GF-2020-101028945) (to C.V.) and Grant R01 HL128168 (to J.W.B.).
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A clinical trial conducted by researchers from RCSI University of Medicine and Health Sciences and Beaumont Hospital Dublin has indicated an effective treatment for critically ill COVID-19 patients.
The study, published today in Med, investigates the effects of using an anti-inflammatory protein, alpha-1 antitryspin (AAT), to treat COVID-19 patients who have progressed to acute respiratory distress syndrome (ARDS).
ARDS is a highly inflammatory state hallmarked by airway damage, respiratory failure and increased risk of death. Treatment options for COVID-19 patients who have ARDS are particularly limited.
AAT is a naturally occurring human protein produced by the liver and released into the bloodstream which normally acts to protect the lungs from the destructive actions of common illnesses.
In this randomized controlled trial, AAT that had been purified from the blood of healthy donors was administered to patients with COVID-19-associated ARDS, with the aim of reducing inflammation.
The results indicated that treatment with AAT led to decreased inflammation after one week. The study also found that the treatment was safe and well tolerated, and did not interfere with patients’ ability to generate their own protective response to COVID-19.
This discovery suggests a potentially important role for AAT in the treatment of ARDS and other inflammatory diseases associated with COVID-19.
The study’s co-lead author, Dr Oliver McElvaney from the RCSI Department of Medicine and Beaumont Hospital, commented on these novel findings: “We know that patients who are critically ill with COVID-19 are more prone to developing severe inflammation throughout the body, with a disproportionately high rate of progression to ARDS and other serious respiratory issues. We think AAT might be able to provide some protection against the more harmful types of inflammation that arise in severe COVID-19 and other conditions with a similar inflammatory profile.”
Natalie McEvoy, Senior Clinical Research Nurse in the Department of Critical Care and Anaesthesia at the RCSI and Beaumont Hospital and the paper’s co-lead author, commented: “This study is the first randomized control trial of AAT for acute respiratory distress syndrome, the first randomized control trial of AAT in the intensive care unit and the first such trial of a COVID-19 therapeutic in Ireland.”
Senior author on the paper, Professor Ger Curley from the RCSI Department of Anaesthetics and Critical Care and Beaumont Hospital, noted the national significance of the study: “It is only through clinical trials we will be able to determine if new treatments are effective and safe in critically ill patients with COVID-19. This study is the first Irish-led clinical trial of a medicine for COVID-19. The rationale for the study, its design and the recruitment of critically ill patients was all carried out by researchers from RCSI, Beaumont Hospital and St James’s Hospital on patients here in Ireland.”
Professor Gerry McElvaney, RCSI Department of Medicine and Beaumont Hospital, and senior author on the paper, commented: “These early results are encouraging, and will we hope form the basis for a larger trial to see how much of an effect reducing inflammation using AAT has on clinical outcomes such as mortality.”
The study was a collaboration between RCSI University of Medicine and Health Sciences, Beaumont Hospital, Dublin and St James’s Hospital, Dublin.
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It is well known that methane, a greenhouse gas, is produced by special microorganisms, for example in the intestines of cows, or in rice fields. For some years, scientists had also observed the production of methane in plants and fungi, without finding an explanation. Now researchers from Heidelberg and the Max Planck Institute for Terrestrial Microbiology in Marburg have shed light on the underlying mechanism. Their findings suggest that all organisms release methane.
Methane is a potent greenhouse gas, so the study of its natural and anthropogenic biogeochemical sources and sinks is of enormous interest. For many years, scientists considered methane to be produced only by single-celled microbes called Archaea, upon decomposition of organic matter in the absence of oxygen (anaerobic).
Now, a collaboration of earth and life scientists led by Frank Keppler and Ilka Bischofs has shown that an enzyme is potentially not necessary for methane formation, as the process can also take place via a purely chemical mechanism. “Methane formation triggered by reactive oxygen species most likely occurs in all organisms,” explains Leonard Ernst, an interdisciplinarily trained junior researcher who conducted the study. The scientists verified the reactive oxygen species-driven formation of methane in more than 30 model organisms, ranging from bacteria and archaea to yeasts, plant cells and human cell lines.
It was a sensation when Max Planck researchers discovered the release of methane from plants in the presence of oxygen (aerobic) 16 years ago. However, initially the results were doubted, since methane formation could not be explained with the then existing knowledge about plants. When researchers observed that also fungi, algae and cyanobacteria (formerly blue-green algae) formed methane under aerobic conditions, enzymatic activities were assumed to be responsible. However, the researchers never found a corresponding enzyme in any of these organisms. “This study is therefore a milestone in our understanding of aerobic methane formation in the environment,” said Frank Keppler, a geoscientist at Heidelberg University. “This universal mechanism also explains the observations of our previous study on the release of methane from plants,” adds Keppler.
High cell activity leads to more methane
As the researchers have now been able to show using the bacterium Bacillus subtilis, there is a close connection between metabolic activity and extent of methane formation. Metabolic activity, especially under the influence of oxygen, leads to the formation of reactive oxygen species in cells, which include hydrogen peroxide and hydroxyl radicals. In interaction with the essential element iron, the Fenton reaction takes place — a reaction between reduced iron and hydrogen peroxide that leads to the formation of highly reactive tetravalent iron compounds and hydroxyl radicals.
The latter molecules drive the cleavage of a methyl radical from methylated sulfur and nitrogen compounds, e.g., the amino acid methionine. In a subsequent reaction of the methyl radical with a hydrogen atom, methane is finally formed. All reactions can take place under physiological conditions in a test tube and are significantly enhanced by biomolecules such as ATP and NADH, which are generated by cellular metabolism.
Oxidative stress boosts methane formation
Additional oxidative stress, triggered by physical and chemical factors, e.g. higher ambient temperatures or the addition of reactive oxygen species-forming substances, also led to an increase in methane formation in the examined organisms. In contrast, the addition of antioxidants and the scavenging of free radicals reduced the formation of methane — an interaction that probably controls the formation of methane in organisms.
The study therefore also helps to explain why methane production by a certain organism can vary by several orders of magnitude and why stress factors particularly affect the amount of production. Shifts in environmental and temperature conditions caused by climate change could potentially influence the stress levels of many organisms and thus their atmospheric methane emissions. Conversely, variations in the methane content of the breath could indicate age- or stress-related changes in cellular metabolism.
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Acral melanoma is a rare subtype that represents roughly 3% of all melanoma cases. Unlike typical melanoma that occurs on sun-exposed skin, acral melanoma develops on the nonhair bearing skin of the soles, palm and nail beds. There is very little information known about the development of acral melanoma. But in a new article published in Clinical Cancer Research, researchers from Moffitt Cancer Center’s Donald A. Adam Melanoma and Skin Cancer Center of Excellence reveal key differences in the cellular and molecular composition of acral melanoma compared to melanoma. Their findings may lead to new potential therapeutic targets for this rare disease.
Acral melanoma is most common among people of Asian, Hispanic and African American heritage. Those who develop the disease are often diagnosed at a late, more advanced stage and therefore have poorer outcomes. Additionally, some of the common genetic alterations observed in melanoma are not seen in acral melanoma. Despite these differences, acral melanoma is treated with the same therapies used for melanoma and are often unsuccessful.
The Moffitt team, led by Keiran Smalley, Ph.D., and Y. Ann Chen, Ph.D., sought to identify the characteristics that distinguish acral melanoma from melanoma to better understand the disease and design more effective therapies. They analyzed the molecular and cellular composition of acral melanoma patient samples, including those from primary tumors and sites of metastatic spread. They also compared these samples to patient samples from those with melanoma.
The researchers discovered several key characteristics of acral melanoma that may be potential therapeutic targets. There are differences between the gene expression patterns of primary tumors and those from metastatic sites, including alterations in immune signaling and metabolic pathways. Acral melanoma was associated with a suppressive immune environment when compared to melanoma. Acral melanoma had fewer infiltrating immune cells than melanoma, with significant differences observed for CD8 T cells, natural killer cells and γδ T cells. Acral melanoma had higher levels of the proteins VISTA and ADORA2, which are involved in suppressing immune responses. These combined immune characteristics of acral melanoma would lead to fewer active immune cells targeting cancer cells and could be one reason why patients have poorer responses to therapy.The researchers hope that their identification of these key differences will lead to more effective treatments for acral melanoma patients in the future.
“We have undertaken the first comprehensive analysis of the immune/tumor transcriptional landscape of acral melanoma. Our study identified unique features of the immune environment of acral melanoma, including immune checkpoints of translational interest that could represent novel therapeutic targets for this neglected disease,” said Smalley.
This study was supported by the National Cancer Institute (P30CA076292), the Melanoma Research Alliance, the Florida Department of Health (9LA03) and the Moffitt Foundation.
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By uncovering the subtle difference between two varieties of a protein, researchers from the Perelman School of Medicine at the University of Pennsylvania may have discovered how to eliminate the risk of weight gain from a certain type of diabetes medication. Through this, it’s possible that more patients with diabetes could get more effective treatment from modified thiazolidinediones, which many likely avoid in their current form due to side effects. These findings were published in Genes & Development.
“One small, undiscovered difference between the two forms of a single protein proved to be extremely significant,” said study senior author Mitchell Lazar, MD, PhD,the Willard and Rhoda Ware Professor in Diabetes and Metabolic Diseases at Penn. “Our findings suggest a way to improve on the mechanism of action of thiazolidinedione drugs, which holds promise for eliminating the side effect of weight gain.”
The popularity of diabetes drugs called thiazolidinediones, which are also known as glitazones, has been reduced because of side effects such as weight gain. They work by activating a fat cell protein called PPARgamma (PPARγ). The protein occurs in two forms, PPARγ1 and PPARγ2, whose functional differences have been unclear. But when the Penn researchers examined each form of the protein on its own, they found that activating just PPARγ2 with a thiazolidinedione drug protects mice from diabetes-like metabolic changes — without causing weight gain.
Type 2 diabetes is characterized by the progressive dysfunction of the insulin hormone signaling system in the body, resulting in chronic, high levels of glucose (sugar) in the blood. This, in turn, contributes to the hardening of arteries, high blood pressure, heart attacks, strokes, and other serious diseases. Thought to arise largely due to obesity, poor diets, and modern sedentary lifestyles, type 2 diabetes has become epidemic in many countries. The U.S. Centers for Disease Control and Prevention has estimated that, in the United States alone, about 35 million people, roughly 10 percent of the population, are living with the disorder.
Thiazolidinediones, which include rosiglitazone (under the brand name Avandia), were introduced in the 1990s and, for many years, were widely used as diabetes drugs. They have since become less popular due to side effects. This has led some researchers to investigate whether new compounds could be developed that retain these drugs’ therapeutic effects while having fewer side effects.
In their study, Lazar and his team approached this problem by taking a closer look at thiazolidinediones’ target, PPARγ, which helps control fat cell production. The scientists studied two lines of mice: One greatly deficient in one form of the protein, PPARγ1, the other greatly deficient in PPARγ2. In the mice, the scientists showed that activating PPARγ1 or PPARγ2 with a thiazolidinedione had an anti-diabetic effect in each case, protecting mice from the metabolic harm of a high-fat diet.
However, the researchers discovered that activation of these two forms has subtly different downstream effects on gene activity. Specifically, in the PPARγ1-deficient mice (in which most of the present PPARγ takes the form of PPARγ2), the thiazolidinedione treatment caused no weight gain.
The finding therefore suggests that it may be possible to realize the benefits of thiazolidinediones without the weight gain side effect, by activating only PPARγ2 and not PPARγ1.
“We’re now studying in more detail how PPARγ1 and PPARγ2 work and how they differ, in the hope of finding ways to selectively activate PPARγ2,” Lazar said.
The research was supported by the American Diabetes Association, the American Heart Association, Cox Medical Institute, the JPB Foundation, and the National Institutes of Health.