In the News

Moderate daily caffeine intake during pregnancy may lead to smaller birth size

Thursday, March 25, 2021

Pregnant women who consumed the caffeine equivalent of as little as half a cup of coffee a day on average had slightly smaller babies than pregnant women who did not consume caffeinated beverages, according to a study by researchers at the National Institutes of Health. The researchers found corresponding reductions in size and lean body mass for infants whose mothers consumed below the 200 milligrams of caffeine per day — about two cups of coffee — believed to increase risks to the fetus. Smaller birth size can place infants at higher risk of obesity, heart disease and diabetes later in life.

The researchers were led by Katherine L. Grantz, M.D., M.S., of the Division of Intramural Population Health Research at NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development. The study appears in JAMA Network Open.

“Until we learn more, our results suggest it might be prudent to limit or forego caffeine-containing beverages during pregnancy,” Dr. Grantz said. “It’s also a good idea for women to consult their physicians about caffeine consumption during pregnancy.”

Scientists find evidence that novel coronavirus infects the mouth’s cells

Thursday, March 25, 2021

NIH-funded findings point to a role for saliva in SARS-CoV-2 transmission

An international team of scientists has found evidence that SARS-CoV-2, the virus that causes COVID-19, infects cells in the mouth. While it’s well known that the upper airways and lungs are primary sites of SARS-CoV-2 infection, there are clues the virus can infect cells in other parts of the body, such as the digestive system, blood vessels, kidneys and, as this new study shows, the mouth. The potential of the virus to infect multiple areas of the body might help explain the wide-ranging symptoms experienced by COVID-19 patients, including oral symptoms such as taste loss, dry mouth and blistering. Moreover, the findings point to the possibility that the mouth plays a role in transmitting SARS-CoV-2 to the lungs or digestive system via saliva laden with virus from infected oral cells. A better understanding of the mouth’s involvement could inform strategies to reduce viral transmission within and outside the body. The team was led by researchers at the National Institutes of Health and the University of North Carolina at Chapel Hill.

“Due to NIH’s all-hands-on-deck response to the pandemic, researchers at the National Institute of Dental and Craniofacial Research were able to quickly pivot and apply their expertise in oral biology and medicine to answering key questions about COVID-19,” said NIDCR Director Rena D’Souza, D.D.S., M.S., Ph.D. “The power of this approach is exemplified by the efforts of this scientific team, who identified a likely role for the mouth in SARS-CoV-2 infection and transmission, a finding that adds to knowledge critical for combatting this disease.”

The study, published online March 25, 2021 in Nature Medicine, was led by Blake M. Warner, D.D.S., Ph.D., M.P.H., assistant clinical investigator and chief of NIDCR’s Salivary Disorders Unit, and Kevin M. Byrd, D.D.S., Ph.D., at the time an assistant professor in the Adams School of Dentistry at the University of North Carolina at Chapel Hill. Byrd is now an Anthony R. Volpe Research Scholar at the American Dental Association Science and Research Institute. Ni Huang, Ph.D., of the Wellcome Sanger Institute in Cambridge, U.K., and Paola Perez, Ph.D., of NIDCR, were co-first authors.

NIH-led team sets new bar in retinal imaging

Thursday, March 11, 2021

By eliminating extraneous light, the scientists improved resolution by 33 percent

A team led by scientists at the National Eye Institute (NEI) has noninvasively visualized the light-sensing cells in the back of the eye, known as photoreceptors, in greater detail than ever before. Published in Optica, the researchers report how they improved imaging resolution by a third by selectively blocking the light used to image the eye. NEI is part of the National Institutes of Health.

The achievement is the latest in an evolving strategy to monitor cell changes in retinal tissue that, in turn, will help identify new ways to treat and prevent vision loss from diseases such as age-related macular degeneration, a leading cause of blindness in people age 65 and older.

“Better imaging resolution will enable better tracking of degenerative changes that occur in retinal tissue. The goal of our research is to discern disease-related changes at the cellular level over time, possibly enabling much earlier detection of disease,” said the study’s lead investigator, Johnny Tam, Ph.D., Stadtman Investigator in the Clinical and Translational Imaging Unit at NEI.

Preterm birth, prolonged labor influenced by progesterone balance

Thursday, March 11, 2021

Novel research in mice sheds light on hormone regulation needed in late pregnancy, opens door for therapy

New research by the National Institutes of Health found that unbalanced progesterone signals may cause some pregnant women to experience preterm labor or prolonged labor. The study in mice — published online in the Proceedings of the National Academy of Sciences — provides novel insights for developing treatments.

During pregnancy, the hormone progesterone helps to prevent the uterus from contracting and going into labor prematurely. This occurs through molecular signaling involving progesterone receptor types A and B, referred to as PGR-A and PGR-B. In this first-of-its-kind study, the scientists showed how unbalanced PGR-A and PGR-B signaling can affect pregnancy duration.

“We used genetically engineered mouse models to alter the ratio of PGR-A and PGR-B in the muscle compartment of the uterus, called the myometrium,” said senior author Francesco DeMayo, Ph.D., head of the National Institute of Environmental Health Sciences Reproductive and Developmental Biology Laboratory. “Our team found that PGR-A promotes muscle contraction and PGR-B prevents such contraction, and we identified the biological pathways influenced by both forms.”

Study of mosquito protein could lead to treatments against life-threatening viruses

Wednesday, March 10, 2021

The mosquito protein AEG12 strongly inhibits the family of viruses that cause yellow fever, dengue, West Nile, and Zika and weakly inhibits coronaviruses, according to scientists at the National Institutes of Health (NIH) and their collaborators. The researchers found that AEG12 works by destabilizing the viral envelope, breaking its protective covering. Although the protein does not affect viruses that do not have an envelope, such as those that cause pink eye and bladder infections, the findings could lead to therapeutics against viruses that affect millions of people around the world. The research was published online in PNAS.

Scientists at the National Institute of Environmental Health Sciences (NIEHS), part of NIH, used X-ray crystallography to solve the structure of AEG12. Senior author Geoffrey Mueller, Ph.D., head of the NIEHS Nuclear Magnetic Resonance Group, said at the molecular level, AEG12 rips out the lipids, or the fat-like portions of the membrane that hold the virus together.

"It is as if AEG12 is hungry for the lipids that are in the virus membrane, so it gets rid of some of the lipids it has and exchanges them for the ones it really prefers," Mueller said. "The protein has high affinity for viral lipids and steals them from the virus."

IRP scientists use human cerebral organoid to test drug for deadly brain disease

Tuesday, March 9, 2021

Approximately two years after establishing a human cerebral organoid system to study Creutzfeldt-Jakob disease (CJD), National Institutes of Health researchers have further developed the model to screen drugs for potential CJD treatment. The scientists, from NIH’s National Institute of Allergy and Infectious Diseases (NIAID), describe their work in Scientific Reports.

Human cerebral organoids are small balls of human brain cells ranging in size from a poppy seed to a pea; scientists use human skin cells to create them. CJD, a fatal neurodegenerative brain disease of humans caused by infectious prion proteins, affects about 1 in 1 million people each year. It can arise spontaneously, result from a hereditary mutation within the prion gene, or arise due to infection, for example, from eating contaminated meat products. A notable example of this occurred in the United Kingdom in the mid-1990s following an outbreak of bovine spongiform encephalopathy in cattle. There are no preventive or therapeutic treatments for CJD.

The lack of a completely human CJD model has been a considerable barrier hindering the discovery of potential therapies. Studies in mice have failed to identify treatments that were then effective when tried in patients. The human cerebral organoid CJD model holds promise that this barrier can be eliminated. Cerebral organoids have organization, structure, and electrical signaling systems similar to human brain tissue. Because they can survive in a controlled environment for months to years, cerebral organoids also are ideal for studying nervous system diseases over lengthy periods of time. Cerebral organoids have been used as models to study Zika virus infection, Alzheimer’s disease, and Down syndrome.

IRP scientists discover how DNA fragments can trigger inflammation in sickle cell disease

Thursday, March 4, 2021

Researchers have discovered that DNA from the mitochondria — the cell’s “powerhouses” — acts as a danger signal in the body and triggers inflammation in people with sickle cell disease. A better understanding of mitochondrial DNA, long known to circulate in human blood, may provide vital insight into how to stop the underlying chronic inflammation that marks this inherited red blood cell disorder. It could also lead to new ways to reduce the pain crises suffered by people living with the life-threatening disease.

The study, published in the journal Blood, was supported by the National Heart, Lung, and Blood Institute (NHLBI), part of the National Institutes of Health.

“These study findings suggest that measuring DNA of mitochondrial origin could help us better understand its role in pain crises, destruction of red blood cells, and other inflammatory events in sickle cell disease,” said Swee Lay Thein, M.B., D.Sc., chief of the Sickle Cell Branch at NHLBI. “It could also serve as a marker of disease progression and a way to measure the effectiveness of therapeutic interventions.”

NIH halts trial of COVID-19 convalescent plasma in emergency department patients with mild symptoms

Tuesday, March 2, 2021

Study shows the treatment is safe, but provides no significant benefit in this group

The National Institutes of Health has halted a clinical trial evaluating the safety and effectiveness of COVID-19 convalescent plasma in treating emergency department patients who developed mild to moderate symptoms of COVID-19, the disease caused by the coronavirus SARS-CoV-2.

An independent data and safety monitoring board (DSMB) met on Feb. 25, 2021 for the second planned interim analysis of the trial data and determined that while the convalescent plasma intervention caused no harm, it was unlikely to benefit this group of patients. After the meeting, the DSMB recommended that the National Heart, Lung, and Blood Institute (NHLBI), part of NIH, stop enrolling new patients into the study. NHLBI did so immediately.

Launched in August 2020, the Clinical Trial of COVID-19 Convalescent Plasma of Outpatients (C3PO) was being conducted at 47 hospital emergency departments across the United States and had enrolled 511 of the 900 participant recruitment goal. It was specifically looking at the effectiveness of COVID-19 convalescent plasma – blood plasma derived from patients who have recovered from COVID-19 – in adults who came to an emergency department with mild to moderate symptoms they had for a week or less. These patients also had at least one risk factor associated with severe COVID-19, such as obesity, hypertension, diabetes, heart disease, or chronic lung disease, but none were ill enough at the time to be hospitalized.

IRP study finds that people with SARS-CoV-2 antibodies may have a low risk of future infection

Wednesday, February 24, 2021

People who have had evidence of a prior infection with SARS-CoV-2, the virus that causes COVID-19, appear to be well protected against being reinfected with the virus, at least for a few months, according to a newly published study from the National Cancer Institute (NCI). This finding may explain why reinfection appears to be relatively rare, and it could have important public health implications, including decisions about returning to physical workplaces, school attendance, the prioritization of vaccine distribution, and other activities.

For the study, researchers at NCI, part of the National Institutes of Health, collaborated with two health care data analytics companies (HealthVerity and Aetion, Inc.) and five commercial laboratories. The findings were published on Feb. 24 in JAMA Internal Medicine.

“While cancer research and cancer care remain the primary focus of NCI’s work, we were eager to lend our expertise in serological sciences to help address the global COVID-19 pandemic, at the request of Congress,” said NCI Director Norman E. “Ned” Sharpless, M.D., who was one of the coauthors on the study. “We hope that these results, in combination with those of other studies, will inform future public health efforts and help in setting policy.”

“The data from this study suggest that people who have a positive result from a commercial antibody test appear to have substantial immunity to SARS-CoV-2, which means they may be at lower risk for future infection,” said Lynne Penberthy, M.D., M.P.H., associate director of NCI’s Surveillance Research Program, who led the study. “Additional research is needed to understand how long this protection lasts, who may have limited protection, and how patient characteristics, such as comorbid conditions, may impact protection. We are nevertheless encouraged by this early finding.”

New experiences enhance learning by resetting key brain circuit

Wednesday, February 24, 2021

A study of spatial learning in mice shows that exposure to new experiences dampens established representations in the brain’s hippocampus and prefrontal cortex, allowing the mice to learn new navigation strategies. The study, published in Nature, was supported by the National Institutes of Health.

“The ability to flexibly learn in new situations makes it possible to adapt to an ever-changing world,” noted Joshua A. Gordon, M.D., Ph.D., a senior author on the study and director of the National Institute of Mental Health, part of NIH. “Understanding the neural basis of this flexible learning in animals gives us insight into how this type of learning may become disrupted in humans.”

Dr. Gordon co-supervised the research project with Joseph A. Gogos, M.D., Ph.D., and Alexander Z. Harris, M.D., Ph.D., both of Columbia University, New York City.

Whenever we encounter new information, that information must be consolidated into a stable, lasting memory for us to recall it later. A key mechanism in this memory consolidation process is long-term potentiation, which is a persistent strengthening of neural connections based on recent patterns of activity. Although this strengthening of neural connections may be persistent, it can’t be permanent, or we wouldn’t be able to update memory representations to accommodate new information. In other words, our ability to remember new experiences and learn from them depends on information encoding that is both enduring and flexible.