Publisher Health

A new mouse model identified by virologists from the University of Pittsburgh might revolutionize development of therapies targeting brain inflammation caused by Rift Valley Fever virus (RVFV).
As the first mouse model that faithfully mimics brain damage caused by severe RVFV infection, it will permit the study of disease mechanisms in detail and provide an opportunity to conduct high-throughput preclinical testing of next-generation drugs, enabling development of therapies for a virus that is present throughout Africa. The study was published today in PLOS Pathogens.
“Rift Valley Fever can sweep across villages causing devastating consequences, but there are no drugs or vaccines that we can offer to people,” said senior author Anita McElroy, M.D., Ph.D., virologist and pediatric infectious diseases physician at Pitt’s School of Medicine and UPMC Children’s Hospital of Pittsburgh. “Before IV acyclovir became available in the 1990s, the outcome of herpes simplex virus encephalitis in newborns was horrible. But acyclovir turned that trend on its heel, and we would love to have the same success with RVFV encephalitis.”
A virus that mosquitoes transmit between animals and people, RVFV is endemic to the African continent and belongs to a family of viruses identified by the National Institute of Allergy and Infectious Diseases (NIAID) workgroup on pandemic preparedness as likely to give rise to future pandemics.
Unlike other mosquito-borne infectious diseases such as malaria, RVFV can be spread by many species of mosquitos, expanding its potential to sweep across large distances and reach many hosts. Some blood sample surveys suggest that by adulthood, up to 50% of Africans living in endemic areas have been exposed to the virus in their lifetime. Even though the overall mortality rate of RVFV infection is relatively low, estimated between 1% to 3%, this virus causes major economic and public health impacts across Africa.
RVFV is spread by mosquitos from infected animals, especially livestock, eventually finding its way into people. Because the virus can also spread via bodily fluids across mucous membranes and through skin cuts and abrasions, farmers and butchers are particularly vulnerable to infection.
Once the virus infects a human, it can spread into the liver and the brain and cause hepatitis, encephalitis or both. Yet, despite the virus’s economic and human toll, a vaccine for RVFV has not been made commercially available, and efforts to develop an effective therapy have historically been stymied by the lack of an appropriate preclinical model.
Unlike humans, whose genetic diversity likely explains why some people develop mild disease and some succumb to liver failure or brain damage, common strains of mice injected with RVFV tend to die from liver disease.
To address this challenge and map out genetic differences that dictate how the infection presents itself in the body, McElroy and colleagues sought to identify a genetically diverse but stable mouse model by testing mice with different genetic backgrounds and measuring their susceptibility to RVFV infection. One strain, labeled CC057/Unc, consistently developed late-onset encephalitis and had a high viral load in the brain without developing severe acute hepatitis, making it particularly suitable to study the neurological form of the RVFV disease.
“It is impossible to study how RVFV causes brain disease if the animals die of liver failure,” said McElroy. “This new model is a critical step on the quest to figure out why some people who get infected with the virus recover and others die and how we can best help them.”
Additional authors of the paper include Haley Cartwright, Ph.D., Dominique Barbeau, M.S., Joshua Doyle, M.D., Ph.D., and Ed Klein, Ph.D., all of Pitt; and Mark Heise, Ph.D., and Martin Ferris, Ph.D., both of the University of North Carolina at Chapel Hill.
This study was funded by the RK Mellon Institute for Pediatric Research, Pediatric Infectious Disease Society Stanley and Susan Plotkin and Sanofi Pasteur Fellowship Award, UPMC Children’s Hospital of Pittsburgh, and the Burroughs Wellcome Fund (CAMS 1013362.01).

The loss of the male sex chromosome as many men age causes the heart muscle to scar and can lead to deadly heart failure, new research from the University of Virginia School of Medicine shows. The finding may help explain why men die, on average, several years younger than women.
UVA researcher Kenneth Walsh, PhD, says the new discovery suggests that men who suffer Y chromosome loss — estimated to include 40% of 70-year-olds — may particularly benefit from an existing drug that targets dangerous tissue scarring. The drug, he suspects, may help counteract the harmful effects of the chromosome loss — effects that may manifest not just in the heart but in other parts of the body as well.
On average, women live five years longer than men in the United States. The new finding, Walsh estimates, may explain nearly four of the five-year difference.
“Particularly past age 60, men die more rapidly than women. It’s as if they biologically age more quickly,” said Walsh, the director of UVA’s Hematovascular Biology Center. “There are more than 160 million males in the United States alone. The years of life lost due to the survival disadvantage of maleness is staggering. This new research provides clues as to why men have shorter lifespans than women.”
Chromosome Loss and Heart Health
While women have two X chromosomes, men have an X and a Y. But many men begin to lose their Y chromosome in a fraction of their cells as they age. This appears to be particularly true for smokers. The loss occurs predominantly in cells that undergo rapid turnover, such as blood cells. (Loss of the Y chromosome does not occur in male reproductive cells, so it is not inherited by the children of men who exhibit Y chromosome loss.) Scientists previously observed that men who suffer Y chromosome loss are more likely to die at a younger age and suffer age-associated maladies such as Alzheimer’s disease. Walsh’s new research, however, is believed to be the first hard evidence that the chromosome loss directly causes harmful effects on men’s health.

Pox viruses are able to get a head start on infecting a host by delivering a package of proteins that directly interferes with the body’s innate immune system.
According to a new study by researchers at the University of Birmingham and ETH Zurich, the pox virus starts to do this immediately after infection -even before it has begun to replicate — using proteins specifically designed to target key components of a host’s immune response.
In a new paper, published in PLOS Pathogens, the interdisciplinary team have identified these proteins for the first time, uncovering the molecular mechanisms at work and in turn opening up new avenues for the development of anti- poxvirus treatments.
Co-Lead researcher Professor Jason Mercer, of the University of Birmingham, said: “Our current arsenal of pox anti-viral agents is limited and only available for emergency use, so new anti-viral treatments would be extremely valuable. Our research identifies a highly unusual ability to bring immunosuppressing proteins into the host right at the start of the infection. By understanding what proteins the virus brings and how they work, we can start to investigate how to exploit them for new treatments.”
In the study, the researchers used mass spectrometry-based proteotyping and super-resolution microscopy to identify and characterise relevant proteins in vaccinia virus, the smallpox vaccine, which is a member of the same virus family as monkeypox virus and the smallpox virus, variola.
While all viruses have the goal of invading cells and successfully replicating, they must also find ways to evade the body’s innate immune system — the broad-spectrum defences against invading pathogens. In most viruses, this is by producing proteins during replication which can evade and attack the immune system. Pox viruses, in contrast, are unusual in that they contain and deliver immune-modulating proteins right at the start.
The research team identified 15 new proteins within the viral delivery packets called lateral bodies. Importantly, they found five ‘redox’ proteins, which are designed to interact with immune system elements called Reactive Oxygen Species.
Reactive Oxygen Species (ROS) are highly reactive molecules which play a key role destroying pathogens identified by the body’s innate immune system. The redox proteins within the pox virus are released at the start of the infection specifically to seek out and suppress ROS.
“Identifying the precise nature of the proteins contained with the lateral bodies was a complicated process because poxviruses are highly complex molecular structures,” added Professor Bernd Wollscheid, of ETH Zurich. “This work represents a big step in advancing our understanding of the molecular mode of action of this important family of viruses which is timely/relevant considering the current multi-country monkeypox outbreak in non-endemic countries.”
Next steps for the UK & Swiss research team will include testing the protein mechanisms in animal models to find out how they work individually and together to combat the host immune response.
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A groundbreaking study, led by Professors Yossi Buganim at the Hebrew University of Jerusalem (HU) Faculty of Medicine’s Institute for Medical Research and Tommy Kaplan at HU’s School of Computer Science and Engineering and Department of Computational Biology, has uncovered 14,000 unique sites in DNA that together form the most elementary blueprint for embryogenesis — the creation of embryos. Their findings were published in Nature Communications.
In 2006, Japanese scientists inserted four embryonic genes into skin cells and successfully reprogrammed those skin cells to act like embryonic stem cells. Artificial embryonic stem cells made from skin cells are identical to natural stem cells that develop at the earliest stages of the embryonic development process and are responsible for the development of all the cells of a fetus. However, they cannot create extra-embryonic tissues, such as the placenta.
In 2015, Prof. Buganim and his team were first to discover how to create artificial placental stem cells from skin cells. This step enabled scientists to create the two earliest types of stem cells in the embryonic development process that happens right after sperm fertilize an egg. In this current study, the HU research team, which included PhD students Mohammad Jaber, Ahmed Radwan and Netanel Loyfer, closely examined the process that skin cells undergo to transform themselves into either embryonic or placental stem cells.
“We analyzed the changes that skin cells undergo to change their identity and become one of the two earliest types of stem cells. We looked at changes in gene expression of the skin cell, in the accessibility and activity of the DNA within the nucleus of the changing skin cell, and in epigenetic markers (i.e. marks that decorate the DNA and responsible for gene expression). These are all critical when trying to convert a skin cell into an artificial embryonic or placental stem cell,” Buganim explained.
The researchers found that the changes that take place in skin cells to become either embryonic or placental artificial stem cells were entirely different from one another at every level, despite the fact that both started out as skin cells.
When a skin cell transforms into an artificial embryonic stem cell, the parts of DNA that are responsible to create the brain, heart and liver began to reorganize and prepare themselves to differentiate- given the right signal- into brain, heart or liver cells. On the other hand, when those same cells were transforming into an artificial placental stem cell, the DNA sites began reorganizing themselves to allow the changing cell to implant itself and attract blood vessels, a phenomenon that occurs naturally, allowing the embryo to implant into the uterus.
The most remarkable discovery came when the team compared the two processes side-by-side and looked at a chemical molecule called methyl, which interacts with specific areas of the DNA and is responsible for silencing their expression. “We discovered that artificial placental stem cells contained close to 14,000 DNA sites with methyl but were nowhere to be seen in the artificial embryonic stem cells,” shared Buganim.
When the research team tried to understand the significance of those DNA areas, they found that they are responsible to create all the organs and cells in developing embryos — from the brain, heart, liver and kidneys to the skeleton, spinal cord and connective tissues.
Going forward, this significant discovery may help explain the embryonic defense system, which prevents early placental cells from developing into embryonic cells. “Since placental cells are susceptible to damage and infection, the body’s natural defense mechanism prevents placental cells that migrating to the developing embryo and attaching to it to become part of the embryo,” Buganim explained. Overall, this study illuminates key features that characterize our ability to reprogram cells and provides a powerful tool to study cellular plasticity and cell-fate decisions.
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Women tend to live longer than men but typically have higher rates of illness. Now, new research from University of Georgia suggests these higher rates of illness can be improved by a better diet, one that is high in pigmented carotenoids such as yams, kale, spinach, watermelon, bell peppers, tomatoes, oranges and carrots. These bright-colored fruits and vegetables are particularly important in preventing visual and cognitive loss.
“The idea is that men get a lot of the diseases that tend to kill you, but women get those diseases less often or later so they perseverate but with illnesses that are debilitating,” said Billy R. Hammond, a professor in UGA’s Franklin College of Arts and Sciences department of psychology behavioral and brains sciences program and co-author of the study. “For example, of all of the existing cases of macular degeneration and dementia in the world, two-thirds are women … these diseases that women suffer for years are the very ones most amenable to prevention through lifestyle.”
The study, which reviewed and analyzed data from previous studies, detailed several degenerative conditions, from autoimmune diseases to dementia that, even controlling for lifespan differences, women experience at much higher rates than men. “If you take all the autoimmune diseases collectively, women account for nearly 80%. So, because of this vulnerability, linked directly to biology, women need extra preventive care,” Hammond said.
How does gender affect health?
One of the reasons for this vulnerability has to do with the way women store vitamins and minerals in their bodies. Hammond points out that women have, on average, more body fat than men. Body fat serves as a significant sink for many dietary vitamins and minerals, which creates a useful reservoir for women during pregnancy. This availability, however, means less is available for the retina and the brain, putting women at more risk for degenerative problems.
Dietary intake of pigmented carotenoids act as antioxidants for humans. Two specific carotenoids, lutein and zeaxanthin, are found in specific tissues of the eye and brain and have been shown to directly improve central nervous system degeneration.
“Men and women eat about the same amount of these carotenoids, but the requirements for women are much higher,” said Hammond.
“The recommendations should be different, but there are, generally, not any recommendations for men or women for dietary components that are not directly linked to deficiency disease (like vitamin C and scurvy),” Hammond said. “Part of the idea for the article is that recommendations need to be changed so that women are aware that they have these vulnerabilities that they have to proactively address, so they don’t have these problems later in life.”
Carotenoids are also available via supplements, and the National Institutes of Health has focused resources on specific carotenoids through the National Eye Institute program. And though supplements of lutein and zeaxanthin are a way of increasing intake, Hammond said getting them through food is a much better strategy.
“Components of diet influence the brain, from things like personality to even our concept of self. I don’t think people quite realize what a profound effect diet has on basically who they are, their mood, even their propensity to anger,” Hammond said. “And now of course this is extended to the microbiome and the bacteria that make up your gut — all of these components work together to create the building blocks that compose our brain and the neurotransmitters that mediate its use.”
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Materials provided by University of Georgia. Original written by Alan Flurry. Note: Content may be edited for style and length.

To date most research on obesity has focused on studying those with a high body mass index (BMI), but a research group in China is taking a different approach. In a study published July 14 in the journal Cell Metabolism, the scientists looked at individuals with a very low BMI. Their findings reveal that these individuals are actually considerably less active than people with a BMI in the normal range, contrary to speculation that they have a metabolism that makes them naturally more active. Additionally, they eat less food than those with a normal BMI.
“We expected to find that these people are really active and to have high activity metabolic rates matched by high food intakes,” says corresponding author John Speakman, a professor at the Shenzhen Institutes of Advanced Technology in China and the University of Aberdeen in the UK. “It turns out that something rather different is going on. They had lower food intakes and lower activity, as well as surprisingly higher-than-expected resting metabolic rates linked to elevated levels of their thyroid hormones.”
The investigators recruited 173 people with a normal BMI (range 21.5 to 25) and 150 who they classified as “healthy underweight” (with a BMI below 18.5). They used established questionnaires to screen out people with eating disorders as well as those who said they intentionally restrained their eating and those who were infected with HIV. They also excluded individuals who had lost weight in the past six months potentially related to illness or were on any kind of medication. They did not rule out those who said they “exercised in a driven way,” but only 4 of 150 said they did.
The participants were monitored for two weeks. Their food intake was measured with an isotope-based technique called the doubly-labeled water method, which assesses energy expenditure based on the difference between the turnover rates of hydrogen and oxygen in body water as a function of carbon dioxide production. Their physical activity was measured using an accelerometry-based motion detector.
The investigators found that compared with a control group that had normal BMIs, the healthy underweight individuals consumed 12% less food. They were also considerably less active, by 23%. At the same time, these individuals had higher resting metabolic rates, including an elevated resting energy expenditure and elevated thyroid activity.
“Although these very lean people had low levels of activity, their markers of heart health, including cholesterol and blood pressure, were very good,” says first author Sumei Hu, currently at the Beijing Technology and Business University. “This suggests that low body fat may trump physical activity when it comes to downstream consequences.”
The investigators acknowledge some limitations on this research, including the fact that although they measured food intake, they didn’t measure what the participants were actually eating or their feelings of satiation or satiety.
The team is now expanding its research, including studies that include these measures. They also plan to look at genetic differences between normal weight and healthy underweight individuals. Preliminary analysis suggests single nucleotide polymorphisms in certain genes that might play a role. When these genetic changes were replicated in mice, the animals had some aspects of the phenotype that was observed in human subjects.
“The next stage is to understand more about the phenotype itself and understand the mechanisms that generate it more clearly,” says Speakman.
This research was funded by the National Key R&D Program of China and the National Natural Science Foundation of China.
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Research by the University of Southampton shows future choices about trade, diet and climate change will be crucial in securing micronutrient food supplies for the UK.
Scientists conclude that factors such as Brexit, a move to plant-based diets and any further disruption from the COVID-19 pandemic will be major influences on our food supply and in-turn the range and level of micronutrients available to people through their food.
The UK is not self-sufficient in several key vitamins (A and C) and minerals (calcium, zinc and iron). We rely on imports, rather than domestic produce, to provide enough of these micronutrients to ensure the population can receive their recommended daily allowance.
“The pandemic has shown the importance of nutrition in keeping healthy and fighting off infection. It is important for public health that people can maintain a healthy diet through readily available food sources,” said lead researcher, Professor Guy Poppy, who is also Deputy Executive Chair of the Biotechnology and Biological Sciences Research Council (BBSRC). “If the UK is to become more nutrient self-sufficient, it will require a range of actions to change production and how much is grown domestically, coupled with some significant changes in consumer food preferences.”
The researchers examined data from a number of sources showing how micronutrient security has varied between 1961 and 2017. They also analysed 2017 overseas trade data from HM Revenue and Customs to assess overseas food supply prior to the exit from the EU and ran future scenarios around domestic production, imports and supply of animal and plant food sources.
Findings, published in the journal Nature Food, show that since the 1960’s the UK has become much more reliant on imports to secure micronutrients. For example, prior to joining the EU, most of our vitamin C was domestically produced, but we now import the majority in the form of fruit and vegetables. About half of all these imports are from European countries, with Spain and the Netherlands the most significant contributors. The research also highlighted that over the last sixty years, trade agreements have affected the supply of key micronutrients, emphasising the importance of trade on food supply as the UK negotiates post-Brexit deals.
Co-author of the paper, Dr Jenny Baverstock added: “There is an increasing call for a more plant based-diet to help address climate change — but this will be a challenge based on current patterns, and especially if we continue to rely on imports of fruit and vegetables which can’t be grown in the UK.
“This increase in vegetarianism and veganism will require careful policy and decision making, as the bioavailability of micronutrients from meat and dairy is something not easily replicated by plants. Consideration will be needed over how to ‘eat for the health of the human’ as well as ‘eat for the health of the planet’.”
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Changes in DNA can lead to the development and progression of cancer. DNA serves as a template for an intermediary molecule called RNA that, in turn, codes for proteins that control all cellular processes. Most cancer research and available anticancer drugs focus on the impact of DNA and protein alterations that contribute to cancer; however, it is now understood that RNA molecules can also both positively and negatively impact the development of cancer. In a new article published in Cancer Research, a journal of the American Association for Cancer Research, Moffitt Cancer Center researchers describe how RNA molecules promote the development of melanoma metastasis by impacting anti-tumor microRNA.
MicroRNA (miRNA) molecules are small segments of nonprotein coding RNA that can silence other protein-coding RNA molecules and regulate the production of proteins. When the activity of miRNA molecules is perturbed, diseases such as cancer can develop. Recently, it has been shown that this regulation also works in the opposite direction, where protein coding RNAs act as “sponges” to bind to miRNA molecules and block their function. RNAs affecting the function of miRNAs are called competitive endogenous RNA (ceRNA) and are thought to play an important role in cancer development independent of their protein-coding activity.
The existence of ceRNA has been known since approximately 2010, but its impact on cancer development is not well understood. Since DNA copy number alterations impact cancer, Moffitt researchers wanted to determine whether these DNA alterations can drive cancer development through ceRNAs.
The team analyzed chromosome alterations and discovered that gains in chromosome segment 1q were very common among a panel of metastatic melanoma cases. A more in-depth analysis revealed that three key genes called CEP170, NUCKS1andZC3H11A present on chromosome 1q are amplified in metastatic melanoma cases and associated with disease progression.
Given the potential clinical implications of these alterations, the researchers wanted to understand the molecular contributions of CEP170, NUCKS1andZC3H11Ato melanoma development. They performed a series of laboratory experiments and discovered that the RNA sequences of CEP170, NUCKS1andZC3H11A promote cell growth, migration and invasion in melanoma cell lines, and stimulated metastasis growth in mouse models of melanoma, independent of their protein-coding activity. Mechanistically, the researchers discovered that the RNA sequences of the three genes act as ceRNAs that sponge miRNA molecules that function to inhibit tumor growth and development. Therefore, by “soaking up” the miRNA molecules and their blocking antitumor activity, the ceRNA molecules drive tumor growth and metastasis. Importantly, the researchers discovered that copy number alterations of CEP170, NUCKS1andZC3H11A were present in other tumor types, including breast, colon, liver and lung cancer, suggesting that these alterations may be important for other cancer types as well.
These results will likely change the widely held view that the key to cancer primarily relies on the structure and function of proteins and opens avenues for new investigations into a biological area that is only beginning to be studied.
“Our study challenges the notion that somatic copy number alterations promote cancer predominantly through their encoded proteins and establishes ceRNAs as potent drivers underlying the oncogenicity of somatic copy number alterations,” said Florian Karreth, Ph.D., study author and assistant member of the Molecular Oncology Department.
This study was supported by the National Institutes of Health (R03CA227349, R01CA259046 and P30CA076292) and the Melanoma Research Alliance (500655).
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In cancer research, it all comes down to a single cell.
Over the last decade, cancer researchers have homed in on the fact that an individual cell from a tumor can be used to perform molecular analyses that reveal important clues about how the cancer developed, how it spreads and how it may be targeted.
With this in mind, a team of researchers at Brown University has developed an advanced way to isolate single cells from complex tissues. In a study published in Scientific Reports, they show how the approach not only results in high-quality, intact single cells, but is also superior to standard isolation methods in terms of labor, cost and efficiency.
The challenge was to develop a technology to enable researchers to more quickly and easily isolate cells from biopsied cancer tissue to ready it for analysis, said Anubhav Tripathi, study author and director of biomedical engineering at Brown.
“From a technology standpoint, there’s nothing like this available on the market right now,” Tripathi said. “This technology will be useful for those looking for answers using genomics, proteomics, transcriptomics — it will not only make those diagnostic and therapeutic investigations easier, but will also save researchers time and effort.”
Tripathi added that beyond clinical applications, the technology will be useful in biomedical applications like tissue engineering and cell culture.

Clinical trial results from the DRCR Retina Network suggest that a specific step strategy, in which patients with diabetic macular edema start with a less expensive medicine and switch to a more expensive medicine if vision does not improve sufficiently, gives results similar to starting off with the higher-priced drug. The main complication of diabetic macular edema, fluid build-up in the retina that causes vision loss, is commonly treated with anti-vascular endothelial growth factor (VEGF) drugs.
The trial was funded by the National Eye Institute (NEI) and the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), both part of National Institutes of Health. Results of the trial, which examined a stepped regimen of anti-VEFG drugs Avastin (bevacizumab) and Eylea (aflibercept), were published today in the New England Journal of Medicine.
“Our study showed that switching treatments when needed is a reasonable strategy,” said Chirag Jhaveri, M.D., Austin Research Center for Retina, Texas, the lead study author. “Insurance companies often require clinicians to start with the less expensive treatment, so we really wanted to see how a specific treatment strategy using this approach would affect patient care.”
Diabetic macular edema is caused by diabetes-related alterations to retinal blood vessels. Symptoms include blurred vision. If untreated, vision loss can become permanent and progress to blindness. Retinal injections of anti-VEGF drugs can restore vision. The DRCR Retina Network previously showed that Avastin and Eylea improve visual acuity in people with diabetic macular edema. However, while Eylea is approved by the U.S. Food and Drug Administration to treat diabetic macular edema and results in better visual outcomes on average, off-label Avastin is much less expensive and is sometimes required by insurers as a first-line treatment.
The study enrolled 270 participants with diabetic macular edema, some of whom received treatments in both eyes. At enrollment, all had best-corrected visual acuity between 20/50 and 20/320. Half the study eyes were assigned to Eylea from the start, and half were assigned to start with Avastin. For participants who needed treatment in both eyes, each eye started treatment with a different drug. Participants received either Avastin or Eylea injections every four weeks for 24 weeks. If eyes assigned Avastin failed to reach the pre-set improvement benchmarks starting at 12 weeks, the eye was switched to Eylea.
After 24 weeks, physicians could taper down the frequency of injections as appropriate to maintain visual acuity. The study collected information about participants’ retinal structure and visual acuity for two years.
After two years, eyes in both groups had similar visual acuity outcomes, improving on average approximately three lines on an eye chart, compared to the trial’s start. In the Avastin group, 70% of eyes switched to Eylea during the study.
“While most participants on Avastin eventually switched to Eylea, they still had improvement during those initial weeks, even if they didn’t hit our pre-set benchmarks,” said Adam Glassman of the Jaeb Center for Health Research and director of the DRCR Retina Network coordinating center. “There are large cost disparities between these drugs, so differences in treatment strategies may have substantial cost implications.”
“We’ve demonstrated here one method to managing a step treatment, where the outcomes are similar to the best existing treatment protocol with Eylea,” said Jennifer Sun, M.D., M.P.H., of Joslin Diabetes Center and Harvard Medical School, Boston, and chair of diabetes initiatives for the DRCR Retina Network. “Any time we can add to a clinician’s toolbox, whether it’s a new medication or a new approach to using existing medications, as in this study, it’s a benefit for patients.”
The study was supported by NEI (EY014231) and NIDDK through the Special Diabetes Program for Type 1 Diabetes Research. Clinical trial number NCT03321513.
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