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Scientists Crack Lyme Disease’s Genetic Code, Paving the Way for Better Diagnosis and Treatment

A groundbreaking genetic analysis of Lyme disease bacteria has paved the way for more accurate diagnostics, treatments, and vaccines.

By sequencing the genomes of 47 strains, researchers can now identify specific bacteria that cause the disease, allowing for more targeted interventions.

Mapping the Genetic Landscape of Lyme Disease

A genetic analysis of Lyme disease bacteria may pave the way for improved diagnosis, treatment, and prevention of the tick-borne ailment.

By mapping the complete genetic makeup of 47 strains of Lyme disease-causing bacteria from around the world, the international team has created a powerful resource for identifying the specific bacterial strains that infect patients. Researchers said this could enable more accurate diagnostic tests and treatments tailored to the exact type or types of bacteria causing each patient’s illness.

“This comprehensive, high-quality sequencing investigation of Lyme disease and related bacteria provides the foundation to propel the field forward,” said Steven Schutzer, a Rutgers New Jersey Medical School professor and coauthor of the study published in mBio . “Every modern research project — from clinical to public health to ecology and evolution to bacterial physiology to medical-tool development to host-bacteria interaction — will benefit from this work.

Unveiling the Evolution of Lyme Disease Bacteria

Researchers said the genetic information uncovered in this study — which explains how the bacteria evolves and spreads and the genes are essential for survival — may help scientists develop more effective vaccines against Lyme disease.

Lyme disease is the most prevalent tick-borne illness in North America and Europe, impacting hundreds of thousands of people annually. This disease is caused by bacteria from the Borrelia burgdorferi sensu lato group, which are transmitted to humans through the bite of infected ticks. Symptoms often include fever, headache, fatigue, and a distinctive skin rash. Without treatment, the infection can progress, leading to more serious complications affecting the joints, heart, and nervous system.

Case numbers are increasing steadily, with 476,000 new cases each year in the US, and may grow faster with climate change, according to the researchers.

Sequencing the Genomes of Lyme Bacteria

The research team sequenced the complete genomes of Lyme disease bacteria representing all 23 known species in the group. Most of these hadn’t been sequenced before this effort. The National Institutes of Health -funded project included multiple strains of the bacteria most commonly associated with human infections and species not previously known to cause disease in humans.

By comparing these genomes, the researchers reconstructed the evolutionary history of Lyme disease bacteria, tracing the origins back millions of years. They discovered the bacteria likely originated before the breakup of the ancient supercontinent Pangea, explaining the current worldwide distribution.

Genetic Exchange and Adaptation in Bacteria

The study also revealed how these bacteria exchange genetic material within and between species. This process, known as recombination, allows the bacteria to evolve rapidly and adapt to new environments. The researchers identified specific hot spots in the bacterial genomes where this genetic exchange occurs most frequently, often involving genes that help the bacteria interact with their tick vectors and animal hosts.

“By understanding how these bacteria evolve and exchange genetic material, we’re better equipped to predict and respond to changes in their behavior, including potential shifts in their ability to cause disease in humans,” said Weigang Qiu, a professor of biology at City University of New York and senior author of the study.

Tools for Future Research and Combatting Lyme Disease

To facilitate ongoing research, the team has developed web-based software tools (BorreliaBase.org) that allow scientists to compare Borrelia genomes and identify determinants of its ability to infect humans.

Looking ahead, the researchers plan to analyze more strains of Lyme disease bacteria, particularly from understudied regions. They also aim to investigate the functions of genes unique to disease-causing strains, which could reveal new targets for therapeutic interventions.

As factors such as climate change help Lyme disease expand its geographic range, this research provides valuable tools and insights for combating this rising public health threat.

“This is a seminal study, a body of work that provides researchers with data and tools going forward to better tailor treatment against all causes of Lyme disease and provides a framework toward similar approaches against other infectious diseases caused by pathogens,” said Benjamin Luft, the Edmund D. Pellegrino Professor of Medicine at the Renaissance School of Medicine at Stony Brook University.

For more on this research, see Lyme Disease DNA Mapping: The Breakthrough That Could Revolutionize Treatment .

Reference: “Natural selection and recombination at host-interacting lipoprotein loci drive genome diversification of Lyme disease and related bacteria” by Saymon Akther, Emmanuel F. Mongodin, Richard D. Morgan, Lia Di, Xiaohua Yang, Maryna Golovchenko, Natalie Rudenko, Gabriele Margos, Sabrina Hepner, Volker Fingerle, Hiroki Kawabata, Ana Cláudia Norte, Isabel Lopes de Carvalho, Maria Sofia Núncio, Adriana Marques, Steven E. Schutzer, Claire M. Fraser, Benjamin J. Luft, Sherwood R. Casjens and Weigang Qiu, 15 August 2024, mBio . DOI: 10.1128/mbio.01749-24

Other scientists among the study’s 20 authors were Claire Fraser and Emmanuel Mongodin of the University of Maryland School of Medicine and Sherwood Casjens of the University of Utah School of Medicine. The research was also supported by the Steve and Alexandra Cohen Foundation.

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Herpes cure with gene editing makes progress in laboratory studies

SEATTLE — May 13, 2024 — Researchers at Fred Hutch Cancer Center have found in pre-clinical studies that an experimental gene therapy for genital and oral herpes removed 90% or more of the infection and suppressed how much virus can be released from an infected individual, which suggests that the therapy would also reduce the spread of the virus.

“Herpes is very sneaky. It hides out among nerve cells and then reawakens and causes painful skin blisters,” said Keith Jerome, MD, PhD , professor in the Vaccine and Infectious Disease Division at Fred Hutch. “Our aim is to cure people of this infection, so that they don’t have to live with the worry of outbreaks or of transmitting it to another person.”

Published May 13 in Nature Communications , Jerome and his Fred Hutch team report an encouraging step toward a gene therapy for herpes.

The experimental gene therapy involves injecting into the blood a mixture of gene editing molecules that seek out where the herpes virus resides in the body. The mixture includes laboratory-modified viruses called a vector — commonly used in gene therapies — plus enzymes that work like molecular scissors. Once the vector reaches the clusters of nerves where the herpes virus hangs out, the molecular scissors snip away at the herpes virus’s genes to damage them or remove the virus entirely.

“We are using a meganuclease enzyme that cuts in two different places in the herpes virus’s DNA,” said first author Martine Aubert, PhD , principal staff scientist at Fred Hutch. “These cuts damage the virus so much that it can’t repair itself. Then the body’s own repair systems recognize the damaged DNA as foreign and get rid of it.”

Using mouse models of the infection, the experimental therapy eliminated 90% of herpes simplex virus 1 (HSV-1) after facial infection, also known as oral herpes, and 97% of herpes HSV-1 after genital infection. It took about a month for the treated mice to show these reductions, and the reduction of virus seemed to get more complete over time.

In addition, the researchers found that the HSV-1 gene therapy had a significant reduction in both the frequency and amount of viral shedding.

“If you talk to people living with herpes, many are worried about whether their infection will transmit to others,” Jerome said. “Our new study shows that we can reduce both the amount of virus within the body and how much virus is shed.”

The Fred Hutch team also simplified their gene editing treatment, making it safer and easier to make. In a 2020 study , they used three vectors and two different meganucleases. The latest study uses just one vector and one meganuclease capable of cutting the virus DNA in two places.

“Our streamlined gene editing approach is effective at eliminating the herpes virus and has less side effects to the liver and nerves,” Jerome said. “This suggests that the therapy will be safer for people and easier to make, since it has fewer ingredients.”

While the Fred Hutch scientists are encouraged by how well the gene therapy works in animal models and are eager to translate the findings to treatments for people, they are also careful about the steps needed to prepare for clinical trials. They also noted that though the current study examined HSV-1 infections, they are working on adapting the gene editing technology to target HSV-2 infections. 

“We’re collaborating with numerous partners as we approach clinical trials so we align with federal regulators to ensure safety and effectiveness of the gene therapy,” Jerome said. “We deeply appreciate the support of herpes advocates as they share our vision for curing this infection.” 

Herpes simplex virus (HSV) is a common infection that lasts a lifetime once people are infected. Current therapies can only suppress but not completely eliminate symptoms, which include painful blisters. According to the World Health Organization , an estimated 3.7 billion people under the age of 50 (67%) have HSV-1, which is the main cause of oral herpes. An estimated 491 million people aged 15-49 (13%) worldwide have HSV-2, which is the main cause of genital herpes.

Herpes can create other harms to people’s health. HSV-2 increases the risk of acquiring HIV infection. Other studies have linked dementia with HSV-1.

The work was funded by the National Institutes of Health, the Caladan Foundation and more than 2,000 individual donors. The meganucleases used in this research are derivatives of commercially-available meganucleases. 

Note: Scientists at Fred Hutch played a role in developing these discoveries, and Fred Hutch and certain of its scientists may benefit financially from this work in the future.

Media contact: Molly McElroy [email protected]

Fred Hutchinson Cancer Center unites individualized care and advanced research to provide the latest cancer treatment options while accelerating discoveries that prevent, treat and cure cancer and infectious diseases worldwide.

Based in Seattle, Fred Hutch is an independent, nonprofit organization and the only National Cancer Institute-designated cancer center in Washington. We have earned a global reputation for our track record of discoveries in cancer, infectious disease and basic research, including important advances in bone marrow transplantation, immunotherapy, HIV/AIDS prevention and COVID-19 vaccines. Fred Hutch operates eight clinical care sites that provide medical oncology, infusion, radiation, proton therapy and related services. Fred Hutch also serves as UW Medicine’s cancer program.

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In two studies, experimental drugs for cholesterol show ‘revolutionary’ promise

New, experimental drugs designed to drive down dangerous levels of cholesterol were shown to be safe and effective in two groundbreaking bodies of research presented Sunday at an annual meeting of the American Heart Association.

Both medications target people born with a genetic predisposition to high cholesterol. While drugs like statins , as well as diet and exercise, can help these individuals manage cholesterol, they cannot change the underlying genetic cause.

The two new approaches work in different ways, but with a singular mission: go after genes responsible for raising cholesterol to change the trajectory of a person’s risk for heart attack and stroke .

Neither treatment had ever been tested in humans before. And both will need years of additional research before they'd be considered for approval by the Food and Drug Administration. Still, experts are impressed with the results.

"There is no way to categorize this other than revolutionary," said Dr. Hugh Cassiere, director for critical care services at South Shore University Hospital, Northwell Cardiovascular Institute in New York. Cassiere was not involved with either study.

A tiny change to a gene

One of the treatments, from Boston-based Verve Therapeutics, uses a gene-editing approach called base editing. It involves an IV infusion of a drug that targets the PCSK9 gene, which is instrumental in the production of LDL, often called "bad" cholesterol .

When the drug zeroes in on PCSK9, it makes a tiny change to the gene. The effect is akin to a permanent eraser, removing its ability to raise cholesterol, said Dr. Sekar Kathiresan, Verve's co-founder and chief executive officer.

In theory, the one-time treatment should last a lifetime. Patients so far have only been followed for six months.

Verve's preliminary study, which was presented on Sunday, was meant to test the safety of the drug. Ten patients participated. Most received doses that didn't make a measurable difference in their LDL levels, but were found to be safe.

Three patients, however, were given higher doses — and their LDL cholesterol levels were reduced by more than half. Additional studies will be needed to ensure the treatment remains safe, without unexpected side effects, and effective.

Verve's research was limited to people with a genetic condition called heterozygous familial hypercholesterolemia , in which cholesterol levels are sky-high from birth. Many people affected suffer heart attacks at young ages, in their 30s or 40s.

Kathiresan, a cardiologist who previously worked at Massachusetts General Hospital and was a professor of medicine at Harvard Medical School, has long focused his research on understanding why some people have heart attacks at young ages, and why others do not. He has a strong family history of high cholesterol. In 2012, his brother died from a heart attack at age 40.

That's when Kathiresan decided "to try to develop a therapy that could avert tragedies like what's happened in my family."

It is unclear whether the approach will make a measurable impact on heart attack and stroke risk — that remains to be seen in future studies.

Experts were still optimistic about the technology.

"While larger and longer-term studies are required to assess both effectiveness, durability and safety, this should be the dawn of an era of therapeutic gene targeting for cardiovascular disease," said Dr. Sahil Parikh, director of endovascular services at Columbia University Irving Medical Center in New York. Parikh was not involved with Verve's research.

Shooting the messenger

Findings on a second novel therapy were also presented on Sunday.

The results, though early, offer a promising glimpse of what could be the first treatment for a particularly dangerous type of cholesterol called lipoprotein(a).

People with high levels of Lp(a) are at extremely high risk of having fats and cholesterol build up in their arteries.

That's because Lp(a) gloms onto LDL cholesterol, making those LDL particles even stickier and more likely to cause plaque.

It's like adding super glue to duct tape. And it's purely genetic, meaning that people are born with this elevated risk. Diet and exercise have no impact on Lp(a) levels.

"It is essentially untreatable," said study author Dr. Steven Nissen, chief academic officer of the Heart, Vascular & Thoracic Institute at Cleveland Clinic. "The only way to target such a genetic risk factor is to find a way to interfere with the product of the gene."

Nissen and colleagues used a novel approach to correcting how that gene acts.

They used a drug called lepodisiran, which targets mRNA. If that sounds familiar, it should: Most Covid vaccines use mRNA to prompt the body to make an antibody against SARS-CoV-2.

In this case, the mRNA in question tells the body to produce Lp(a). The drug stops this from happening, essentially shooting the messenger.

Nissen's study was meant to test the safety of lepodisiran. It was small, including just 48 adults in the U.S. and Singapore. All had very high levels of Lp(a). Overall, the drug was found to be safe, with no major side effects, Nissen said.

But it also dramatically lowered their Lp(a) levels. A single shot of lepodisiran drove down Lp(a) by more than 94% for nearly one year, the study found.

The results of the study, which was sponsored by drugmaker Eli Lilly, were published Sunday in the Journal of the American Medical Association .

"This really offers a lot of hope for patients with elevated lipoprotein(a)," Nissen said. "We're working as fast as we can because there are patients dying every day because of this disorder. We've not been able to treat it, and we need to change that."

As many as 64 million Americans have elevated Lp(a) levels, most commonly people of African and South Asian descent.

Additional research is critical. An important question moving forward is whether lowering Lp(a) actually cuts heart risks.

"We've had to wait until this generation of therapeutics where we can directly and specifically target Lp(a) and do it safely to see whether that will also result in fewer heart attacks and strokes," said Dr. Donald Lloyd-Jones, professor and chair of the department of preventive medicine Northwestern Feinberg School of Medicine in Chicago. Lloyd-Jones, also a past president of the American Heart Association, was not involved with the lepodisiran study.

Nissen predicts that the treatment could someday be used as an "annual vaccine-like treatment for this previously untreatable disorder."

While many heart problems may be avoided with lifestyle changes such as exercise and healthy diets, Lloyd-Jones said, the medical community needs therapies to help people whose genes put them at greater risk for heart attacks and stroke.

"We'll always need some medication for people who are at very high risk," he said.

Follow  NBC HEALTH  on  Twitter  &  Facebook .

Erika Edwards is a health and medical news writer and reporter for NBC News and "TODAY."

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Experimental depression treatment is nearly 80% effective in controlled study

In a double-blind controlled study, high doses of magnetic brain stimulation, given on an accelerated timeline and individually targeted, caused remission in 79% of trial participants with severe depression.

October 28, 2021 - By Mandy Erickson

Since receiving an experimental depression treatment at Stanford, Tommy Van Brocklin has been walking Scout for "the sheer joy of it." Nellie Van Brocklin

A new type of magnetic brain stimulation brought rapid remission to almost 80% of participants with severe depression in a study conducted at the  Stanford University School of Medicine .

The treatment, known as Stanford accelerated intelligent neuromodulation therapy (SAINT) or simply Stanford neuromodulation therapy, is an intensive, individualized form of transcranial magnetic stimulation. In the study, remission typically occurred within days and lasted months. The only side effects were temporary fatigue and headaches.

“It works well, it works quickly and it’s noninvasive,” said  Nolan Williams , MD, an assistant professor of psychiatry and behavioral sciences. “It could be a game changer.” Williams is the senior author of the study, which was published Oct. 29 in the  American Journal of Psychiatry .

Twenty-nine people with treatment-resistant depression participated in the study: About half received SAINT, and the rest underwent a placebo procedure that mimicked the real treatment. After five days of treatment, 78.6% of the participants in the treatment group were no longer depressed, according to several standard methods of evaluation. “It’s quite a dramatic effect, and it’s quite sustained,” said  Alan Schatzberg , MD, the Kenneth T. Norris, Jr. Professor in Psychiatry and Behavioral Sciences, who was a co-author of the study.

A lifetime of depression

Tommy Van Brocklin, 60, has suffered from depression since he was 15. “In 1975, they didn’t have the medication and understanding they do now,” he said. “I was told I wasn’t trying hard enough.”

“I’ve functioned all these years, but it’s been very difficult at times,” the civil engineer added. Talk therapy helped “for about half a day after an appointment.” When selective serotonin reuptake inhibitors became available in the 1990s, he started on paroxetine, commonly sold under the brand name Paxil.

“It worked like a miracle drug,” he said, but after 10 or 15 years it started to lose its effect. After 25 years, it stopped working entirely. He tried other medications, but none helped; one even made him suicidal. 

His sister, who lives near Stanford, connected him with the researchers studying SAINT. He flew from his home in Memphis, Tennessee, and underwent the treatment in September. He felt nothing the first day; on day two, he began feeling emotional — “I felt the struggle of what I’d been through all these years.”

“The next day, all of a sudden, it broke through,” he said. “I felt so much better, and it’s stuck with me.”

Specialized magnetic stimulation

The transcranial magnetic stimulation treatment currently approved by the Food and Drug Administration requires six weeks of once-daily sessions. Only about half of patients who undergo the treatment improve, and only about a third experience remission from depression.

SAINT advances that treatment by targeting the magnetic pulses according to each patient’s neurocircuitry and providing a greater number of pulses at a faster pace.

In the study, the researchers first used MRI to locate the best location to target within each participant’s dorsolateral prefrontal cortex, which regulates executive functions, such as problem solving and inhibiting unwanted responses. They applied the stimulation in a subregion that has the strongest relationship with the subgenual cingulate, a part of the brain that is overactive in people experiencing depression. The transcranial magnetic stimulation strengthens the connection between the two regions, facilitating dorsolateral prefrontal cortex control of the activity in the subgenual cingulate.

The researchers also used 1,800 pulses per session instead of 600. (The larger amount has been used safely in other forms of brain stimulation for neurological disorders such as Parkinson’s disease.) And instead of providing one treatment a day, they gave participants 10 10-minute treatments, with 50-minute breaks in between.

For the control group, the researchers disguised the treatment with a magnetic coil that mimicked the experience of the magnetic pulse; both the control and active treatment groups wore noise-canceling earphones and received a topical ointment to dull sensation. Neither the researcher administering the procedure nor the participant knew whether the participant was receiving real treatment.

A hard-to-treat group

The trial participants ranged in age from 22 to 80; on average, they had suffered depression for nine years. They had tried medications, but either they had had no effect or they had stopped working. During the trial, participants who were on medication maintained their regular dosage; participants who weren’t taking medications did not start any.

Nolan Williams demonstrates SAINT, the magnetic brain stimulation therapy he and his colleagues developed, on Deirdre Lehman, a participant in a previous study of the treatment. Steve Fisch

Within four weeks after treatment, 12 of the 14 participants who had received the treatment improved, and 11 of them met FDA criteria for remission. In contrast, only two of the 15 participants who had received the placebo met the criteria for remission.

Because the study participants typically felt better within days of starting SAINT, the researchers are hoping it can be used to quickly treat patients who are at a crisis point. Patients who start taking medication for depression typically don’t experience any reduction of symptoms for a month.

“We want to get this into emergency departments and psychiatric wards where we can treat people who are in a psychiatric emergency,” Williams said. “The period right after hospitalization is when there’s the highest risk of suicide.”

Van Brocklin said that since he returned home following treatment, he’s made some radical changes. “I have a really strong desire to get my life together,” he said.

“I don’t procrastinate anymore,” he added. “I’m sleeping better. I completely quit alcohol. I’m walking my dog and playing the guitar again, for nothing more than the sheer joy of it.”

Most importantly, he said, “I’m remaining positive and being respectful of others. These are big changes in my life.”

Other Stanford scientists who contributed to the study are former postdoctoral scholars Eleanor Cole, PhD, and Angela Phillips, PhD; Brandon Bentzley, MD, PhD, David Carreon, MD, Jennifer Keller, PhD, Kristin Raj, MD, and Flint Espil, PhD, all clinical assistant professors of psychiatry and behavioral sciences; clinical research coordinators Katy Stimpson, Romina Nejad, Clive Veerapal, Nicole Odenwald and Maureen Chang; former clinical research coordinators Fahim Barmak, MD, Naushaba Khan and Rachel Rapier; postdoctoral scholars Kirsten Cherian, PhD, James Bishop, PhD, Azeezat Azeez, PhD, and John Coetzee, PhD; life science research professional Heather Pankow; clinical research manager Jessica Hawkins; Charles DeBattista, MD, professor of psychiatry and behavioral sciences; and Booil Jo, PhD, associate professor of psychiatry and behavioral sciences.

Scientists from the U.S. Department of Veterans Affairs; Palo Alto University; the Centre for Neuroimaging and Cognitive Genomics at the National University of Ireland; and the School of Medicine at Southern Illinois University, Carbondale, contributed to the research.

The research was funded by a Brain and Behavior Research Foundation Young Investigator Award, Charles R. Schwab, the David and Amanda Chao Fund II, the Amy Roth PhD Fund, the Neuromodulation Research Fund, the Lehman Family, the Still Charitable Trust, the Marshall and Dee Ann Payne Fund, and the Gordie Brookstone Fund.

Stanford’s Department of Psychiatry and Behavioral Sciences also contributed to the work.

If you're interested in participating in a study, please email [email protected] .

About Stanford Medicine

Stanford Medicine is an integrated academic health system comprising the Stanford School of Medicine and adult and pediatric health care delivery systems. Together, they harness the full potential of biomedicine through collaborative research, education and clinical care for patients. For more information, please visit med.stanford.edu .

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Nih research matters.

February 9, 2021

Experimental treatment helps patients hospitalized with COPD

At a glance.

• A pilot study found that hyaluronan, a sugar naturally produced by the body, improved lung function in hospitalized COPD patients.
• If confirmed in larger trials, the treatment would expand therapeutic options for severe COPD.

People with chronic obstructive pulmonary disease (COPD) can no longer take in all the air they need. COPD often causes shortness of breath, wheezing, and chest tightness. People may also cough up large amounts of mucus. Smoking and air pollution are the main causes of the lung disease. 

Current COPD treatments include inhaled steroids, antibiotics, and drugs called bronchodilators that help open the airways. Scientists are interested in developing new drugs for COPD. A research team led by Drs. Stavros Garantziotis of NIH’s National Institute of Environmental Health Sciences (NIEHS) and Raffaele Incalzi of Campus Bio-Medico University and Teaching Hospital in Rome, Italy, investigated the use of hyaluronan.

Hyaluronan is a long-chain sugar that’s naturally secreted by many tissues, including within the lungs. Part of the supporting scaffold that forms outside of cells, it plays an important role in wound healing and reducing inflammation. Hyaluronan has both lubricating and hydrating properties. It’s used in cosmetics as a skin moisturizer and in nasal sprays to moisturize airways. In animal studies, inhaled hyaluronan treatment has been shown to reverse some types of COPD.

The researchers examined whether inhaled hyaluronan might benefit hospitalized COPD patients who needed breathing support. Their findings were published in Respiratory Research , on February 1, 2021.

The team randomly assigned 41 participants to receive inhaled hyaluronan or an identical-looking placebo. The study was conducted in Italy, where hyaluronan is approved for airway moisturization. Patients in the study had been hospitalized for severe breathing trouble related to COPD. All required ventilation through a mask. The patients inhaled hyaluronan or a placebo twice daily.

The researchers found that inhaled hyaluronan treatment shortened the amount of time that patients needed support from the ventilator and improved their lung function. Those receiving hyaluronan also had lower levels of inflammation in their blood.

To understand how hyaluronan might work, the team conducted studies in the lab with lung cells from COPD patients and healthy donors. The researchers suspected that hyaluronan might help move the thick mucus that collects in the lungs of people with COPD. Healthy cells exposed to cigarette smoke in culture and cells from COPD patients in culture both developed less thick mucus after receiving hyaluronan.

Earlier studies from the researchers give insight into why inhaled hyaluronan may be an effective COPD treatment. Exposure to pollution causes hyaluronan in the lungs to break down into smaller fragments. These fragments irritate lung tissue and activate the immune system. This leads to constriction and inflammation of the airways. Reintroducing full-length hyaluronan may restore balance, reducing inflammation and helping to slow COPD.

“Studying the effect of pollution on the lungs helped us discover treatments for lung disease,” Garantziotis explains, “because pollution-induced lung damage and chronic lung disease share many characteristics, like the role of hyaluronan.”

“Inhaled hyaluronan…is safe and easy to administer,” Incalzi says. “Furthermore, it acts locally, only in the bronchial tree, and thus cannot interfere with any systemic drug.”

Larger studies are planned to further test hyaluronan for COPD other lung diseases and to determine the doses and conditions that may produce the most benefit.

Related Links

• Diagnosing COPD
• Altered Lung Structure May Increase COPD Risk
• Long-Term Oxygen for COPD
• COPD Learn More Breathe Better
• Chronic Obstructive Pulmonary Disease (COPD)
• Ventilator/Ventilator Support

References:  Inhaled high molecular weight hyaluronan ameliorates respiratory failure in acute COPD exacerbation: a pilot study. Galdi F, Pedone C, McGee CA, George M, Rice AB, Hussain SS, Vijaykumar K, Boitet ER, Tearney GJ, McGrath JA, Brown AR, Rowe SM, Incalzi RA, Garantziotis S. Respir Res. 2021 Feb 1;22(1):30. doi: 10.1186/s12931-020-01610-x. PMID: 33517896.

Funding:  NIH’s National Institute of Environmental Health Sciences (NIEHS), National Heart, Lung, and Blood Institute (NHLBI), and National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK).

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• Beauty sleep:...

Beauty sleep: experimental study on the perceived health and attractiveness of sleep deprived people

• Related content
• Peer review
• John Axelsson , researcher 1 2 ,
• Tina Sundelin , research assistant and MSc student 2 ,
• Michael Ingre , statistician and PhD student 3 ,
• Eus J W Van Someren , researcher 4 ,
• Andreas Olsson , researcher 2 ,
• Mats Lekander , researcher 1 3
• 1 Osher Center for Integrative Medicine, Department of Clinical Neuroscience, Karolinska Institutet, 17177 Stockholm, Sweden
• 2 Division for Psychology, Department of Clinical Neuroscience, Karolinska Institutet
• 3 Stress Research Institute, Stockholm University, Stockholm
• 4 Netherlands Institute for Neuroscience, an Institute of the Royal Netherlands Academy of Arts and Sciences, and VU Medical Center, Amsterdam, Netherlands
• Correspondence to: J Axelsson john.axelsson{at}ki.se
• Accepted 22 October 2010

Objective To investigate whether sleep deprived people are perceived as less healthy, less attractive, and more tired than after a normal night’s sleep.

Design Experimental study.

Setting Sleep laboratory in Stockholm, Sweden.

Participants 23 healthy, sleep deprived adults (age 18-31) who were photographed and 65 untrained observers (age 18-61) who rated the photographs.

Intervention Participants were photographed after a normal night’s sleep (eight hours) and after sleep deprivation (31 hours of wakefulness after a night of reduced sleep). The photographs were presented in a randomised order and rated by untrained observers.

Main outcome measure Difference in observer ratings of perceived health, attractiveness, and tiredness between sleep deprived and well rested participants using a visual analogue scale (100 mm).

Results Sleep deprived people were rated as less healthy (visual analogue scale scores, mean 63 (SE 2) v 68 (SE 2), P<0.001), more tired (53 (SE 3) v 44 (SE 3), P<0.001), and less attractive (38 (SE 2) v 40 (SE 2), P<0.001) than after a normal night’s sleep. The decrease in rated health was associated with ratings of increased tiredness and decreased attractiveness.

Conclusion Our findings show that sleep deprived people appear less healthy, less attractive, and more tired compared with when they are well rested. This suggests that humans are sensitive to sleep related facial cues, with potential implications for social and clinical judgments and behaviour. Studies are warranted for understanding how these effects may affect clinical decision making and can add knowledge with direct implications in a medical context.

Introduction

The recognition [of the case] depends in great measure on the accurate and rapid appreciation of small points in which the diseased differs from the healthy state Joseph Bell (1837-1911)

Good clinical judgment is an important skill in medical practice. This is well illustrated in the quote by Joseph Bell, 1 who demonstrated impressive observational and deductive skills. Bell was one of Sir Arthur Conan Doyle’s teachers and served as a model for the fictitious detective Sherlock Holmes. 2 Generally, human judgment involves complex processes, whereby ingrained, often less consciously deliberated responses from perceptual cues are mixed with semantic calculations to affect decision making. 3 Thus all social interactions, including diagnosis in clinical practice, are influenced by reflexive as well as reflective processes in human cognition and communication.

Sleep is an essential homeostatic process with well established effects on an individual’s physiological, cognitive, and behavioural functionality 4 5 6 7 and long term health, 8 but with only anecdotal support of a role in social perception, such as that underlying judgments of attractiveness and health. As illustrated by the common expression “beauty sleep,” an individual’s sleep history may play an integral part in the perception and judgments of his or her attractiveness and health. To date, the concept of beauty sleep has lacked scientific support, but the biological importance of sleep may have favoured a sensitivity to perceive sleep related cues in others. It seems warranted to explore such sensitivity, as sleep disorders and disturbed sleep are increasingly common in today’s 24 hour society and often coexist with some of the most common health problems, such as hypertension 9 10 and inflammatory conditions. 11

To describe the relation between sleep deprivation and perceived health and attractiveness we asked untrained observers to rate the faces of people who had been photographed after a normal night’s sleep and after a night of sleep deprivation. We chose facial photographs as the human face is the primary source of information in social communication. 12 A perceiver’s response to facial cues, signalling the bearer’s emotional state, intentions, and potential mate value, serves to guide actions in social contexts and may ultimately promote survival. 13 14 15 We hypothesised that untrained observers would perceive sleep deprived people as more tired, less healthy, and less attractive compared with after a normal night’s sleep.

Using an experimental design we photographed the faces of 23 adults (mean age 23, range 18-31 years, 11 women) between 14.00 and 15.00 under two conditions in a balanced design: after a normal night’s sleep (at least eight hours of sleep between 23.00-07.00 and seven hours of wakefulness) and after sleep deprivation (sleep 02.00-07.00 and 31 hours of wakefulness). We advertised for participants at four universities in the Stockholm area. Twenty of 44 potentially eligible people were excluded. Reasons for exclusion were reported sleep disturbances, abnormal sleep requirements (for example, sleep need out of the 7-9 hour range), health problems, or availability on study days (the main reason). We also excluded smokers and those who had consumed alcohol within two days of the protocol. One woman failed to participate in both conditions. Overall, we enrolled 12 women and 12 men.

The participants slept in their own homes. Sleep times were confirmed with sleep diaries and text messages. The sleep diaries (Karolinska sleep diary) included information on sleep latency, quality, duration, and sleepiness. Participants sent a text message to the research assistant by mobile phone (SMS) at bedtime and when they got up on the night before sleep deprivation. They had been instructed not to nap. During the normal sleep condition the participants’ mean duration of sleep, estimated from sleep diaries, was 8.45 (SE 0.20) hours. The sleep deprivation condition started with a restriction of sleep to five hours in bed; the participants sent text messages (SMS) when they went to sleep and when they woke up. The mean duration of sleep during this night, estimated from sleep diaries and text messages, was 5.06 (SE 0.04) hours. For the following night of total sleep deprivation, the participants were monitored in the sleep laboratory at all times. Thus, for the sleep deprivation condition, participants came to the laboratory at 22.00 (after 15 hours of wakefulness) to be monitored, and stayed awake for a further 16 hours. We therefore did not observe the participants during the first 15 hours of wakefulness, when they had had a slightly restricted sleep, but had good control over the last 16 hours of wakefulness when sleepiness increased in magnitude. For the sleep condition, participants came to the laboratory at 12.00 (after five hours of wakefulness). They were kept indoors two hours before being photographed to avoid the effects of exposure to sunlight and the weather. We had a series of five or six photographs (resolution 3872×2592 pixels) taken in a well lit room, with a constant white balance (×900l; colour temperature 4200 K, Nikon D80; Nikon, Tokyo). The white balance was differently set during the two days of the study and affected seven photographs (four taken during sleep deprivation and three during a normal night’s sleep). Removing these participants from the analyses did not affect the results. The distance from camera to head was fixed, as was the focal length, within 14 mm (between 44 and 58 mm). To ensure a fixed surface area of each face on the photograph, the focal length was adapted to the head size of each participant.

For the photo shoot, participants wore no makeup, had their hair loose (combed backwards if long), underwent similar cleaning or shaving procedures for both conditions, and were instructed to “sit with a straight back and look straight into the camera with a neutral, relaxed facial expression.” Although the photographer was not blinded to the sleep conditions, she followed a highly standardised procedure during each photo shoot, including minimal interaction with the participants. A blinded rater chose the most typical photograph from each series of photographs. This process resulted in 46 photographs; two (one from each sleep condition) of each of the 23 participants. This part of the study took place between June and September 2007.

In October 2007 the photographs were presented at a fixed interval of six seconds in a randomised order to 65 observers (mainly students at the Karolinska Institute, mean age 30 (range 18-61) years, 40 women), who were unaware of the conditions of the study. They rated the faces for attractiveness (very unattractive to very attractive), health (very sick to very healthy), and tiredness (not at all tired to very tired) on a 100 mm visual analogue scale. After every 23 photographs a brief intermission was allowed, including a working memory task lasting 23 seconds to prevent the faces being memorised. To ensure that the observers were not primed to tiredness when rating health and attractiveness they rated the photographs for attractiveness and health in the first two sessions and tiredness in the last. To avoid the influence of possible order effects we presented the photographs in a balanced order between conditions for each session.

Statistical analyses

Data were analysed using multilevel mixed effects linear regression, with two crossed independent random effects accounting for random variation between observers and participants using the xtmixed procedure in Stata 9.2. We present the effect of condition as a percentage of change from the baseline condition as the reference using the absolute value in millimetres (rated on the visual analogue scale). No data were missing in the analyses.

Sixty five observers rated each of the 46 photographs for attractiveness, health, and tiredness: 138 ratings by each observer and 2990 ratings for each of the three factors rated. When sleep deprived, people were rated as less healthy (visual analogue scale scores, mean 63 (SE 2) v 68 (SE 2)), more tired (53 (SE 3) v 44 (SE 3)), and less attractive (38 (SE 2) v 40 (SE 2); P<0.001 for all) than after a normal night’s sleep (table 1 ⇓ ). Compared with the normal sleep condition, perceptions of health and attractiveness in the sleep deprived condition decreased on average by 6% and 4% and tiredness increased by 19%.

 Multilevel mixed effects regression on effect of how sleep deprived people are perceived with respect to attractiveness, health, and tiredness

• View inline

A 10 mm increase in tiredness was associated with a −3.0 mm change in health, a 10 mm increase in health increased attractiveness by 2.4 mm, and a 10 mm increase in tiredness reduced attractiveness by 1.2 mm (table 2 ⇓ ). These findings were also presented as correlation, suggesting that faces with perceived attractiveness are positively associated with perceived health (r=0.42, fig 1 ⇓ ) and negatively with perceived tiredness (r=−0.28, fig 1). In addition, the average decrease (for each face) in attractiveness as a result of deprived sleep was associated with changes in tiredness (−0.53, n=23, P=0.03) and in health (0.50, n=23, P=0.01). Moreover, a strong negative association was found between the respective perceptions of tiredness and health (r=−0.54, fig 1). Figure 2 ⇓ shows an example of observer rated faces.

 Associations between health, tiredness, and attractiveness

Fig 1  Relations between health, tiredness, and attractiveness of 46 photographs (two each of 23 participants) rated by 65 observers on 100 mm visual analogue scales, with variation between observers removed using empirical Bayes’ estimates

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Fig 2  Participant after a normal night’s sleep (left) and after sleep deprivation (right). Faces were presented in a counterbalanced order

To evaluate the mediation effects of sleep loss on attractiveness and health, tiredness was added to the models presented in table 1 following recommendations. 16 The effect of sleep loss was significantly mediated by tiredness on both health (P<0.001) and attractiveness (P<0.001). When tiredness was added to the model (table 1) with an estimated coefficient of −2.9 (SE 0.1; P<0.001) the independent effect of sleep loss on health decreased from −4.2 to −1.8 (SE 0.5; P<0.001). The effect of sleep loss on attractiveness decreased from −1.6 (table 1) to −0.62 (SE 0.4; P=0.133), with tiredness estimated at −1.1 (SE 0.1; P<0.001). The same approach applied to the model of attractiveness and health (table 2), with a decrease in the association from 2.4 to 2.1 (SE 0.1; P<0.001) with tiredness estimated at −0.56 (SE 0.1; P<0.001).

Sleep deprived people are perceived as less attractive, less healthy, and more tired compared with when they are well rested. Apparent tiredness was strongly related to looking less healthy and less attractive, which was also supported by the mediating analyses, indicating that a large part of the found effects and relations on appearing healthy and attractive were mediated by looking tired. The fact that untrained observers detected the effects of sleep loss in others not only provides evidence for a perceptual ability not previously subjected to experimental control, but also supports the notion that sleep history gives rise to socially relevant signals that provide information about the bearer. The adaptiveness of an ability to detect sleep related facial cues resonates well with other research, showing that small deviations from the average sleep duration in the long term are associated with an increased risk of health problems and with a decreased longevity. 8 17 Indeed, even a few hours of sleep deprivation inflict an array of physiological changes, including neural, endocrinological, immunological, and cellular functioning, that if sustained are relevant for long term health. 7 18 19 20 Here, we show that such physiological changes are paralleled by detectable facial changes.

These results are related to photographs taken in an artificial setting and presented to the observers for only six seconds. It is likely that the effects reported here would be larger in real life person to person situations, when overt behaviour and interactions add further information. Blink interval and blink duration are known to be indicators of sleepiness, 21 and trained observers are able to evaluate reliably the drowsiness of drivers by watching their videotaped faces. 22 In addition, a few of the people were perceived as healthier, less tired, and more attractive during the sleep deprived condition. It remains to be evaluated in follow-up research whether this is due to random error noise in judgments, or associated with specific characteristics of observers or the sleep deprived people they judge. Nevertheless, we believe that the present findings can be generalised to a wide variety of settings, but further studies will have to investigate the impact on clinical studies and other social situations.

Importantly, our findings suggest a prominent role of sleep history in several domains of interpersonal perception and judgment, in which sleep history has previously not been considered of importance, such as in clinical judgment. In addition, because attractiveness motivates sexual behaviour, collaboration, and superior treatment, 13 sleep loss may have consequences in other social contexts. For example, it has been proposed that facial cues perceived as attractive are signals of good health and that this recognition has been selected evolutionarily to guide choice of mate and successful transmission of genes. 13 The fact that good sleep supports a healthy look and poor sleep the reverse may be of particular relevance in the medical setting, where health estimates are an essential part. It is possible that people with sleep disturbances, clinical or otherwise, would be judged as more unhealthy, whereas those who have had an unusually good night’s sleep may be perceived as rather healthy. Compared with the sleep deprivation used in the present investigation, further studies are needed to investigate the effects of less drastic acute reductions of sleep as well as long term clinical effects.

Conclusions

People are capable of detecting sleep loss related facial cues, and these cues modify judgments of another’s health and attractiveness. These conclusions agree well with existing models describing a link between sleep and good health, 18 23 as well as a link between attractiveness and health. 13 Future studies should focus on the relevance of these facial cues in clinical settings. These could investigate whether clinicians are better than the average population at detecting sleep or health related facial cues, and whether patients with a clinical diagnosis exhibit more tiredness and are less healthy looking than healthy people. Perhaps the more successful doctors are those who pick up on these details and act accordingly.

Taken together, our results provide important insights into judgments about health and attractiveness that are reminiscent of the anecdotal wisdom harboured in Bell’s words, and in the colloquial notion of “beauty sleep.”

What is already known on this topic

Short or disturbed sleep and fatigue constitute major risk factors for health and safety

Complaints of short or disturbed sleep are common among patients seeking healthcare

The human face is the main source of information for social signalling

What this study adds

The facial cues of sleep deprived people are sufficient for others to judge them as more tired, less healthy, and less attractive, lending the first scientific support to the concept of “beauty sleep”

By affecting doctors’ general perception of health, the sleep history of a patient may affect clinical decisions and diagnostic precision

Cite this as: BMJ 2010;341:c6614

We thank B Karshikoff for support with data acquisition and M Ingvar for comments on an earlier draft of the manuscript, both without compensation and working at the Department for Clinical Neuroscience, Karolinska Institutet, Sweden.

Contributors: JA designed the data collection, supervised and monitored data collection, wrote the statistical analysis plan, carried out the statistical analyses, obtained funding, drafted and revised the manuscript, and is guarantor. TS designed and carried out the data collection, cleaned the data, drafted, revised the manuscript, and had final approval of the manuscript. JA and TS contributed equally to the work. MI wrote the statistical analysis plan, carried out the statistical analyses, drafted the manuscript, and critically revised the manuscript. EJWVS provided statistical advice, advised on data handling, and critically revised the manuscript. AO provided advice on the methods and critically revised the manuscript. ML provided administrative support, drafted the manuscript, and critically revised the manuscript. All authors approved the final version of the manuscript.

Funding: This study was funded by the Swedish Society for Medical Research, Rut and Arvid Wolff’s Memory Fund, and the Osher Center for Integrative Medicine.

Competing interests: All authors have completed the Unified Competing Interest form at www.icmje.org/coi_disclosure.pdf (available on request from the corresponding author) and declare: no support from any company for the submitted work; no financial relationships with any companies that might have an interest in the submitted work in the previous 3 years; no other relationships or activities that could appear to have influenced the submitted work.

Ethical approval: This study was approved by the Karolinska Institutet’s ethical committee. Participants were compensated for their participation.

Participant consent: Participant’s consent obtained.

Data sharing: Statistical code and dataset of ratings are available from the corresponding author at john.axelsson{at}ki.se .

This is an open-access article distributed under the terms of the Creative Commons Attribution Non-commercial License, which permits use, distribution, and reproduction in any medium, provided the original work is properly cited, the use is non commercial and is otherwise in compliance with the license. See: http://creativecommons.org/licenses/by-nc/2.0/ and http://creativecommons.org/licenses/by-nc/2.0/legalcode .

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University of Kansas awarded $26 million for new Engineering Research Center from National Science Foundation

Wed, 08/21/2024

Cody Howard

LAWRENCE — The National Science Foundation (NSF) has awarded the University of Kansas $26 million to establish a new Gen-4 Engineering Research Center (ERC) — Environmentally Applied Refrigerant Technology Hub (EARTH) — that will create a sustainable and circular refrigerant economy.

NSF’s Engineering Research Centers bring universities and businesses together to strengthen the competitive position of American industry in the global marketplace.

“NSF's Engineering Research Centers ask big questions in order to catalyze solutions with far-reaching impacts,” NSF Director Sethuraman Panchanathan said. “NSF Engineering Research Centers are powerhouses of discovery and innovation, bringing America's great engineering minds to bear on our toughest challenges. By collaborating with industry and training the workforce of the future, ERCs create an innovation ecosystem that can accelerate engineering innovations, producing tremendous economic and societal benefits for the nation.”

KU’s ERC EARTH was selected from among hundreds of proposed centers.

“Working closely with industry partners, EARTH will have the resources and expertise to solve the technical, environmental and economic challenges required to create a sustainable refrigerant lifecycle that will benefit Kansans, the nation and the world. In doing this work, the center is a prime example of how the University of Kansas is driving economic development in Kansas," said Douglas A. Girod, University of Kansas chancellor.

KU is well positioned to lead this effort.

“The University of Kansas has a talented workforce and robust research capabilities,” said Kansas Sen. Jerry Moran. “This new research center will allow Kansans to lead the way in developing the next generation of refrigerant technology, increasing U.S. competitiveness in an important technology and industry. Through my leadership role on the Senate Appropriations subcommittee which funds federal scientific priorities, I am pleased to help fund the U.S. National Science Foundation, which is critical to advancing U.S. research and development.”  

KU is the lead institution and is joined by partners at the University of Notre Dame, University of Maryland, University of Hawai'i, University of South Dakota and Lehigh University. 

Mark Shiflett serves as director for ERC EARTH. Shiflett is a KU Foundation Distinguished Professor in the Department of Chemical & Petroleum Engineering and director of the Wonderful Institute for Sustainable Engineering.

“EARTH’s operational design will cultivate inclusive, interdisciplinary research collaborations and foster workforce development. The EARTH team will partner with community colleges and technical schools to ensure availability of the needed workforce at all levels,” Shiflett said. 

At the heart of ERC EARTH’s work is reimagining the process for heating, ventilation, air-conditioning and refrigeration (HVACR) systems across the globe. EARTH will develop sustainable, accessible and equitable refrigerant technologies and practices through research, education and innovation that will improve quality of life and combat climate change. 

HVACR systems are widespread throughout society, enabling transportation and preservation of fresh foods, storage of medicines and cooling of buildings. Most current refrigerants are hydrofluorocarbons (HFCs), which have high global-warming potential. As a result of leaks from existing systems and the energy required to operate them, HFCs account for nearly 8% of global greenhouse-gas emissions.

In response, the U.S. and 170 other countries are phasing down HFCs in accordance with domestic and international agreements signed in recent years, which creates a tremendous challenge to responsibly and sustainably replace billions of kilograms of refrigerants.

ERC EARTH will take a multifaceted approach to address this challenge.

“Multidisciplinary research teams will focus on three key areas: promoting the recycling and repurposing of refrigerants, developing transformative refrigerants and creating next-generation cooling and heating technologies with higher energy efficiency,” Shiflett said.

At its core, ERC EARTH will address a critical challenge facing society.

“There is a tremendous need to develop cooling/heating technologies that use less energy and new refrigerants that are safe for the environment. EARTH will be a critical national resource to address these challenges. The University of Kansas School of Engineering is proud to be leading this collaboration, which leverages multiple academic and industrial partners,” said Mary Rezac, dean of the KU School of Engineering.

This is one of the largest federally funded grants in KU history, with the potential to become the largest if the renewal option is successful. The project is renewable after five years for another $26 million dollars, for a total of 10 years and $52 million.

Media Contacts

Erinn Barcomb-Peterson

KU News Service

785-864-8858

Mark Shiflett

Department of Chemical & Petroleum Engineering

[email protected]

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New experimental drug offered at Philadelphia-area vet clinic could extend a dog's life

By Stephanie Stahl , Nate Sylves

Updated on: August 20, 2024 / 3:21 PM EDT / CBS Philadelphia

PHILADELPHIA (CBS) — Helping dogs live longer, better lives –  that's the aim of a new experimental drug . It's a pill that's designed to slow down the aging process, so our beloved dogs can be with us a little longer.

It was love at first sight when Brent Sheldon's family first saw Riley.

"He does not fail to put a smile on our face every day," Sheldon said.

Hoping to keep him around as long as possible, the 10-and-a-half-year-old corgi is part of a clinical trial for an experimental drug made by a biotech company called Loyal, designed to improve and extend the lives of dogs.

"I didn't even have to think about it," Sheldon said.

"That obviously is every dog owner's dream. It's how can I keep my best friend alive and healthier and happy longer," said Dr. Sam Geller of Quakertown Veterinary Clinic.

Geller said so far, he's enrolled about 50 dogs and is accepting more to test the daily pill.

"It helps with potentially preventing insulin resistance," Geller said. "It helps with managing fats in your body. It helps with managing lipids in the bloodstream."

The way the study is designed has half of the dogs getting the drug, and the other half getting a placebo. So we don't know which one Riley is getting.

"The FDA wants you to show that your drug is better than a sugar pill," Geller said.

The FDA said there's a "reasonable expectation of effectiveness" for one of Loyal's other drugs and is now seeking it for the new one.

"This medication is intended to help preserve metabolic health," said Dr. Brennen McKenzie, director of veterinary medicine at Loyal.

McKenzie said the drug works on the principle of calorie restriction that's been shown to help canine and human health, but there's no limit on what the dogs eat.

"The way that this drug works is essentially to activate some of the same pathways in the body that caloric restriction activates, but in a way that is safer and more convenient. Because none of us want to starve our dogs in order to make them live longer," McKenzie said. 

The study is aiming to include more than 1,000 dogs. Sheldon is hopeful it will keep Riley around as long as possible.

"As long as it doesn't change the way he acts, his quality of life," he said.

Researchers don't know how long this could extend life, months or years– that's what the four-year research will examine. The nationwide study is currently enrolling larger dogs who are at least 10 years old.

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Stephanie Stahl is an Emmy Award-winning health reporter. She can be seen daily on CBS News Philadelphia and Philly57.

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