Publisher Health

Changing the structure of a dietary fibre commonly found in a range of food products has been found to promote healthy gut bacteria and reduce gas formation, a finding that could help people with intolerances to fibre and irritable bowel conditions.
A team of scientists from the University of Nottingham, Quadram Institute Biosciences and the University of East Anglia examined psyllium, a type of natural dietary fibre that is used in a range of products including cereals and yoghurts. They showed that the physical state of the fibre has a major impact on gas production which often is linked to bowel discomfort. The findings have been published in Food Hydrocolloids.
The team performed in vitro fermentation experiments seeded with human stool. They conducted analysis of fermentation products and evaluated the impact of different structures on the broad categories of microorganisms.
Dr Gleb Yakubov, Associate Professor in Food Physics at the University of Nottingham was one of the lead researchers on the study, he explains: “Although fibre is an important part of any diet, for many people it can cause bowel discomfort and for people with IBS or IBD fibre can be a trigger. This is because some foods cause bacterial interactions in the gut that create gas that can lead to pain or discomfort. Our study shows that the physical state of the fibre has a major impact on gas production by creating beneficial compounds that promote the creation of the good bacteria in the gut.”
Psyllium fibre comes from the seeds of Plantago ovata plants, known by many common names such as blond plantain. These seeds produce a jelly-like material called mucilage, which comes in a variety of shapes and forms and these feature long-chain sugars, called polysaccharides. It is these polysaccharides that lead to the production of beneficial short-chain fatty acids that positively contribute to gut health and systemic metabolism. This study shows that different physical states of fibre impact the way dietary fibre breaks down and that microbes ‘colonise fibre’ during fermentation.
Professor Yakubov continues: “These findings show that there are new opportunities for designing targeted structures using psyllium, either through seed processing or selective breeding, to achieve new fibre materials with clear clinical benefit above that of unrefined psyllium powders aiding in the treatment of gastrointestinal discomfort.”
Research is already underway at the University if Nottingham with the School of Medicine to use this new knowledge to create and test psyllium-mimicking materials as medical nutrition which could provide a source of fibre for people with some bowel conditions and trials will be starting in the Spring.

Betalains are a class of plant pigments that are responsible for the characteristic red-violet (betacyanin) or yellow (betaxanthin) color of certain fruits and vegetables. These naturally occurring, water-soluble, and nitrogen-containing pigments are commonly used as food coloring agents. Recently, research findings have brought to the forefront, the strong antioxidant potential of betalains, making them potential candidates to produce health foods and combat various diseases. At present, betalains are only produced in plants of the order Caryophyllales and higher fungi. Hence, metabolic engineering has been explored to genetically modify cultivable non-Caryophyllales plants, to enhance the production and scalability of these pigments.
Although transgenic betalain-accumulating plants have been developed over the years, their applications in producing healthcare food resources are yet to be explored.
To address this gap, a collaborative research team from Tokyo University of Science (TUS) and Iwate Biotechnology Research Center, Japan, led by Professor Gen-ichiro Arimura from TUS, attempted to genetically modify potato and tomato plants to produce betacyanin. Their aim was to test the therapeutic efficacy of betacyanin producing tomatoes and potatoes against murine models of colitis and inflammation-inducing macrophages. Their findings were published in Biotechnology & Bioengineering on January 26, 2023. Discussing the results of this study, Prof. Arimura says, “We successfully engineered potato tubers and tomato fruits to co-express betacyanin biosynthesis genes [genes for CYP76AD1 from Beta vulgaris, DOD (DOPA 4,5-dioxygenase) and 5GT (cyclo-DOPA 5-O-glucosyltransferase) from Mirabilis jalapa] under the control of suitable promoters. This enhanced the endogenous accumulation of betanin and isobetanin — two common types of betacyanin — in these transgenic vegetables. The accumulation of these pigments made them appear dark red in color upon maturation, as compared to their wild-type counterparts.”
Since macrophages play an important role in several inflammatory diseases, the team further tested the therapeutic efficacy of these transgenic vegetables in macrophage-like cells (RAW264.7), following immune response stimulation by lipopolysaccharides (LPS). They observed that the extracts of the transgenic tomato fruit exerted higher anti-inflammatory activity compared to their wild-type counterparts. This was attributed to a decrease in the LPS-stimulated transcription of the proinflammatory cytokine gene — a Tnf-? gene, within transgenic cells.
“These findings were in line with the anti-inflammatory effects of transgenic tomato that we observed in the intestines of murine models with dextran sulfate sodium (DSS)-induced colitis. A marked improvement in their body weight loss and disease activity index was observed through the suppression of the DSS-stimulated transcription of proinflammatory genes — genes for Tnf-?, Il6 and Cox-2,” adds Prof. Arimura, while discussing the results derived from the other experiment in mice. Moreover, the additive and synergistic action of betacyanin with natural fruit components (such as lycopene in tomato) further boosted the amelioration of colitis in murine models. Interestingly, while significant anti-inflammatory effects were observed with transgenic tomato extracts at 100-1000-fold dilutions, this was not the case with transgenic potatoes, despite substantial production of betanin and isobetanin. The reason for this is speculated to be the presence of unknown antagonists in transgenic potatoes that work against betacyanin’s anti-inflammatory function, but is yet to be confirmed.
“Tomatoes genetically engineered to produce betacyanins were found to have substantial health promoting effects. Although natural plant sources of betalains such as beetroots exist, these pigments demonstrate poor stability in high temperatures and extreme pH. This indicates that betacyanin producing transgenic tomato lines are more likely to be effective as health foods when ingested in their raw state,” summarizes Prof. Arimura.
What are the potential applications of these findings? He further adds, “Although there is no commercial cultivation of edible genetically modified crops in Japan, we expect that their applications as health foods through production in enclosed plant factories and other facilities will lead to the widespread use of recombinant plants in Japan.”
We are confident that betalain engineering will soon become a promising avenue to improve the commercial production of health foods, that boost food supply while simultaneously conferring health benefits to its consumers.

Electrostatic adsorption is an important complement to mechanical filtration for high-efficiency air filtering in the use of face masks. However, the electrostatic charge of the filters decays over time, particularly in humid conditions. A research team at City University of Hong Kong (CityU) successfully engineered a breath-to-charge electrostatic face mask that can “self-charge” through the user’s breathing and continuously replenish its electrostatic charge as the user wears and breathes through the mask. This significantly increase the filtering performance in prolonged use of the mask for up to 60 hours, compared to four hours for a conventional surgical mask. This also benefits the environment.
Face masks are an easy, cost-effective method of preventing COVID-19 and other airborne diseases. Most face masks have three functional layers: a core melt-blown polypropylene (PP) layer as the filter medium and two spun-bonding nonwoven fabrics (generally PP or polyethylene (PE)) as the supporting layers, including a hydrophilic layer, worn inwards, to absorb moisture from breathing and a hydrophobic layer, worn outwards, to repel fluid.
Tackling the problem of electrostatic adsorption efficacy decline
Electrospinning provides better mechanical filtration than the melt-blown technology extensively used in the industry. But mechanical filtration alone does not provide enough protection. One solution is to introduce an electric field to give the filter medium an electrostatic charge, which facilitates ultrafine particle trapping. However, the electrostatic adsorption efficacy declines over time, especially in a humid environment when moisture is exhaled in breathing.
“Although many reports work on replenishing the charge for long-lasting electrostatic adsorption efficacy, an extra power source is generally needed, which is cumbersome and inconvenient,” explained Dr Yang Zhengbao, Associate Professor in the Department of Mechanical Engineering and the Department of Materials Science and Engineering at CityU, who led the research. “We have developed an efficient, durable, low-cost air filter that can continuously replenish the electrostatic charge in a self-charging manner.”
The research team introduced a self-charging air filter (SAF), which leverages the triboelectric effect and achieves efficient and prolonged airborne particle removal. By sandwiching the electrospun polyvinylidene fluoride (PVDF) nanofiber filter medium between two triboelectric nylon fabric layers, the SAF continuously generates electrostatic charges excited by breathing. As a result, the SAF provides durable particle removal performance, maintaining high efficiency of 95.8% after 60 hours of testing (including 30 hours of wearing).

“As the middle layer moves forth and back between the lateral layers with breathing, a charge transfer occurs between PVDF and nylon due to their large difference in electron affinity, resulting in the PVDF layer being negatively charged and the nylon layers positively charged,” explained Dr Yang. “This self-charging process enables the continuous replenishment of the electrostatic charges and prolonged electrostatic adsorption.”
“Self-charging” driven by the user’s breath
The raw material cost of SAF for making one mask is as low as HK$0.47, making it the most cost-effective option among the commonly used masks, such as surgical, N95, KF94 and KN95 masks.
The findings were published in Nature Communications under the title “Self-charging electrostatic face masks leveraging triboelectrification for prolonged air filtration.”
This promising strategy of self-charging to leverage the triboelectric effect paves a new path for the development of high-efficiency, long-lifespan air-filtering techniques. “Surgical masks are suggested to be changed every four hours in a high-risk environment, but the vast number of discarded masks results in severe environmental challenges,” said Dr Yang. “We expect this self-charging strategy to significantly prolong the service life of face masks, enhance the protection effectiveness against the coronavirus, and reduce the environmental burden caused by discarded masks.”
The research also established a quantitative relationship between filtration efficiency and surface electrostatic potential, which is important for standardised, high-efficiency industrial production.
The first author of the paper is Dr Peng Zehua, CityU postdoc in the Department of Mechanical Engineering. Dr Yang is the corresponding author. Other collaborators from CityU include Professor Michael Leung Kwok-hi, Shun Hing Education and Charity Fund Professor of Energy and Environment, Professor Li Wenjung, Chair Professor and Mr Shi Jihong, Ph.D. student in the Department of Mechanical Engineering, and researchers from Dr Yang’s group, including Dr Hong Ying, Dr Li Xuemu and Dr Zhang Weiwei.
The research was funded by CityU, the Hong Kong Research Grants Council, the Hong Kong Innovation and Technology Fund, the Shenzhen Fundamental Research Program, and the National Natural Science Foundation of China.

The so-called isolated REM-sleep behavior disorder is a condition that can provide an indication of Parkinson’s disease well in advance. A research team headed by Professor Dr Erdem Gültekin Tamgüney from Heinrich Heine University Düsseldorf (HHU) has shown that a greater concentration of α-synuclein aggregates can be detected in the stool samples of sufferers. In the scientific journal npj Parkinson’s Disease, which is published by the NatureSpringer group, they now present a method for detecting these aggregates, which they have developed in collaboration with the University Hospital Cologne, Jülich Research Center (FZJ) and the company attyloid GmbH.
There are two forms of Parkinson’s disease (for short: PD). In 70% of cases, it originates in the central nervous system. However, in around 30% of cases it originates in the nervous system of the intestine (“enteric nervous system”). The latter form is referred to as “body-first Parkinson’s disease” (for short: body-first PD) and the characteristic deposits of aggregates of the body’s own α-synuclein protein are formed in the neurons in the intestine.
A preliminary form of body-first PD is the so-called isolated REM-sleep behavior disorder (for short: iBRD). It causes in part complex movements during a specific phase of sleep — REM-sleep — insofar as the patient experiences vivid and disturbing dreams. These movements can endanger the sufferer themselves or others.
A research team headed by Professor Erdem Gültekin Tamgüney from the Institute of Physical Biology at HHU now reports that it is possible to detect an elevated level of α-synuclein aggregates in the stool samples of patients. To achieve this, the team used a new surface-based fluorescence intensity distribution analysis (sFIDA) to detect and quantify individual particles of α-synuclein aggregates.
Professor Tamgüney: “We are the first to prove the presence of α-synuclein aggregates in stool samples. Our results show a significantly higher level of α-synuclein aggregates in iRBD patients compared with healthy individuals or patients with Parkinson’s. These findings could lead to a non-invasive diagnostic tool for prodromal synucleinopathies — including Parkinson’s — which could in turn enable therapies to be initiated at an early stage before symptoms occur.” However, more research is required before the process can find its way into clinical practice, for example investigation into why the level is lower in Parkinson’s patients.
The study was conducted in collaboration with the Institute of Biological Information Processing — Structural Biochemistry (IBI-7) at Jülich Research Center (FZJ), the Department of Neurology at the University Hospital Cologne and the HHU/FZJ spin-off attyloid GmbH. HHU worked with the University Hospital Cologne to establish a biobank with stool samples from patients and control subjects, and with FZJ to develop the test procedure and conduct the tests on the samples. attyloid GmbH is a cooperation partner and is working towards the commercial exploitation of the results. It is necessary to verify that the test procedure is safe and can be used in normal operations in order to gain a license.
Background
In body-first PD, the deposits of fibrils of the body’s own α-synuclein protein, which are characteristic of Parkinson’s, are first formed in the neurons of the enteric nervous system, which serves the gastrointestinal tract. The aggregates then spread to the central nervous system in a way similar to prions, i.e. an existing aggregate combines individual α-synuclein proteins in its vicinity into further aggregates in a nucleation process; these aggregates then spread further through the body.
The influence of what happens in the gastrointestinal tract on the brain is referred to as the “gut-brain axis.” The gastrointestinal tract is exposed to the environment and it is possible that harmful substances such as chemicals, bacteria or viruses ingested directly with food or via interaction with the microbiome of the gastrointestinal tract may trigger the pathological formation of α-synuclein aggregates.

The first white woman to head the pediatrics unit at Harlem Hospital, she was challenged by the epidemics of crack cocaine and H.I.V.Dr. Margaret Heagarty was familiar enough with poverty and disease when she went to work in Harlem in 1978. She had grown up in the hardscrabble coal fields of West Virginia, where her father was a physician to miners and their families. She had also been separated from her parents, like many children in Harlem, and placed in an orphanage.But for all the similarities, the contrasts were striking: She was the first white doctor and the first woman appointed director of pediatrics at Harlem Hospital Center. Dr. Heagarty, who died on Dec. 23 at her home in the Bronx at 88, won Harlem over. Her death was confirmed by William Burgan, her brother-in-law.In her 22 years at Harlem Hospital, a public institution run by New York City’s Health and Hospitals Corporation and affiliated with Columbia University’s College of Physicians and Surgeons, Dr. Heagarty made a name for herself as an eloquent and effective champion for children’s health. She fought for causes like reducing teenage pregnancies and playground injuries.Thanks in part to her efforts and other community programs, the infant mortality rate in Central Harlem dropped dramatically during her tenure. From 1990 to 2008, the number of babies born there who died before their first birthday plunged from about 28 a year to fewer than seven.She also enlisted Diana, Princess of Wales; Barbara Bush, the first lady; and Dr. C. Everett Koop, the surgeon general, to rally public support nationally for combating two of the newest scourges her department faced: cocaine-exposed babies abandoned by drug-addicted parents, and H.I.V.-infected infants and young people.Dr. Heagarty enlisted Princess Diana, center, who visited the hospital in 1989, to help bring attention to the struggles it faced.John Sotomayor/The New York Times“She was a mountain of an Irishwoman, a mother superior in disguise,” said Dr. Stephen W. Nicholas, who succeeded Dr. Heagarty as the director of pediatrics at Harlem Hospital and is now president of the Children’s Global Health Fund. “In her no-nonsense way, she captured the imagination of many, including a princess, a first lady and a surgeon general, to address the plight of children in Harlem during the ravages of AIDS and crack during the 1980s.” Hundreds of miles divided West Virginia from Harlem. But Dr. Heagarty discovered that the common cause of helping the next generation survive trumped any disparities in distance, race or gender.Margaret Caroline Heagarty was born on Sept. 8, 1934, in Charleston, W.Va., the oldest of three children of Dr. John Patrick Heagarty, who practiced in Ward, a tiny company-owned coal town, and Margaret Caroline (Walsh) Heagarty, a nurse. The household was racked by alcohol abuse and addiction, Mr. Burgan said, and she and her sister were placed in an orphanage when they were teenagers.After earning a bachelor’s degree from Seton Hill College in Greensburg, Pa. (formerly a Roman Catholic women’s college and now Seton Hill University), she became one of two women attending West Virginia University’s two-year School of Medicine and then earned her medical degree from the University of Pennsylvania in 1961.She completed a pediatric residency at Temple University with St. Christopher’s Hospital for Children in Philadelphia in 1964. She then accepted a fellowship in child health at Harvard University and served as director of pediatric ambulatory care services of what is now NewYork-Presbyterian Hospital before joining Harlem Hospital.Dr. Heagarty inherited a department with an infant mortality rate more than three times the national average, a demoralized faculty, decrepit facilities and new challenges posed by the epidemics of crack cocaine and AIDS.“It’s one thing to preach from the ivory tower what’s good for the poor,” said Dr. Janet Stewart Claman, associate professor emerita of pediatrics at the University of Colorado School of Medicine, who met Dr. Heagarty when they were both residents. “It’s another to go into one of the poorest hospitals in America in one of the most afflicted neighborhoods and try to accomplish something.”“Maggie was a doer,” Dr. Claman said by email. “She believed it was better to err by commission than omission. She was often underestimated; she could play the role of a country girl from West Virginia to the hilt, and she physically reminded one of a maiden aunt. But Maggie had a mind like a steel trap, and she always knew her facts.”Not long after Dr. Heagarty arrived, as many as 15 percent of the babies born at Harlem Hospital were testing positive for cocaine, ingested by their mothers, and as many as 4 percent of the pregnant women were infected with H.I.V. Babies languished for months because foster parents feared contagion, stigma and behavioral issues related to addiction. In her early years at the hospital, Dr. Nicholas said, admissions for gunshots and stabbings quadrupled.“There are times when my wards look more like a battlefield than a pediatric unit,” Dr. Heagarty once wrote.But if caring for Harlem’s children was a battle, she was an unrelenting fighter.She helped reduce the hospital’s infant mortality rate to the New York City norm. To care for children with AIDS, she, along with Msgr. Tom Leonard, Sister Una McCormack and the real estate developer and philanthropist Jack Rudin, founded Incarnation Children’s Center. She also established a network of five neighborhood satellite health clinics in Harlem and a group home for H.I.V.-infected children.In 1989, she escorted Princess Diana on a tour of the hospital’s pediatric AIDS unit, an event depicted in the Netflix series “The Crown.” The princess was quoted as asking, “When you have a problem with the drugs, how on earth do you deal with AIDS as well?”Her response, Dr. Nicholas recalled, was: “It is bad enough to have a fatal disease, but with poverty and drugs, you have a very bad problem indeed. It is easy to say that these mothers are irresponsible, but still, I have seen them grieving over their dying children. These mothers love their children the same as you love your little princes.”In 1993, Dr. Heagarty, who was also a professor of pediatrics at Columbia University, received a Ronald McDonald House Charities award of $100,000. She donated it to the Harlem Hospital pediatrics unit.Dr. Heagarty never married. In addition to Mr. Burgan, her survivors include several nieces and nephews.Dr. Heagarty’s strategy could be unorthodox, her manner blunt. Dr. Nicholas recalled that when Dr. Heagarty was president of the hospital’s medical board from 1992 to 1995, she strongly disagreed with a new department director, who was Black.The director turned to a Columbia dean, Dr. Nicholas recalled, and asked, “Is Dr. Heagarty racist?”“Oh, no,” the dean replied. “Dr. Heagarty’s not racist. She treats everyone that way.”

In a potential game changer for the treatment of superbugs, a new class of antibiotics was developed that cured mice infected with bacteria deemed nearly “untreatable” in humans — and resistance to the drug was virtually undetectable.
Developed by a research team of UC Santa Barbara scientists, the study was published in the journal eBioMedicine. The drug works by disrupting many bacterial functions simultaneously — which may explain how it killed every pathogen tested and why low-level of bacterial resistance was observed after prolonged drug exposure.
The project was led by professors Michael Mahan, David Low, Chuck Samuel and their research team, Douglas Heithoff, Scott Mahan, Lucien Barnes and Cyril George. Additional contributors include professors Guillermo Bazan (UC Santa Barbara) and Andrei Osterman (Sanford Burnham Prebys Medical Discovery Institute).
The discovery was serendipitous. The U.S. Army had a pressing need to charge cell phones while in the field — essential for soldier survival. Because bacteria are miniature power plants, compounds were designed by Bazan’s group to harness bacterial energy as a “‘microbial”‘ battery. Later the idea arose to re-purpose these compounds as potential antibiotics.
“When asked to determine if the chemical compounds could serve as antibiotics, we thought they would be highly toxic to human cells similar to bleach,” said Mahan, the project lead investigator. “Most were toxic — but one was not — and it could kill every bacterial pathogen we tested.”
What makes the drug unique is the failure of bacteria to become resistant to it. And bacterial resistance is typically a major barrier to antibiotic development since it limits a drug’s potential value in the marketplace.
“The key finding was that bacterial resistance to the drug was virtually undetectable,” said lead author Heithoff. “Most drugs fail at this stage of development and never get to clinical practice.”
The antibiotic has a unique mechanism of action. Contrary to most drugs (like penicillin) that target a specific germ function, the new drug targets many functions simultaneously.
“The drug appears to affect the bacterial membrane which, in turn, disrupts multiple bacterial functions,” explained Low, the co-project lead. “This may account for the broad-spectrum antibacterial activity and low level of bacterial resistance.”
“This class of antibiotics has potential as a new versatile therapy for antimicrobial resistant pathogens,” Samuel said.
Additional drug safety and efficacy studies will need to be conducted to fully understand the clinical benefits and risks before the drug can be used in clinical practice.

Location, location, location is the key for psychedelic drugs that could treat mental illness by rapidly rebuilding connections between nerve cells. In a paper published Feb. 17 in Science, researchers at the University of California, Davis show that engaging serotonin 2A receptors inside neurons promotes growth of new connections but engaging the same receptor on the surface of nerve cells does not.
The findings will help guide efforts to discover new drugs for depression, PTSD and other disorders, said senior author David E. Olson, associate professor of chemistry, biochemistry and molecular medicine and director of the Institute for Psychedelics and Neurotherapeutics at UC Davis.
Drugs such as LSD, MDMA and psilocybin show great promise for treating a wide range of mental disorders that are characterized by a loss of neural connections. In laboratory studies, a single dose of these drugs can cause rapid growth of new dendrites — branches — from nerve cells, and formation of new spines on those dendrites.
Olson calls this group of drugs “psychoplastogens” because of their ability to regrow and remodel connections in the brain.
Earlier work from Olson’s and other labs showed that psychedelic drugs work by engaging the serotonin 2A receptor (5-HT2AR). But other drugs that engage the same receptor, including serotonin, do not have the same growth effects.
Maxemiliano Vargas, a graduate student in Olson’s lab, Olson and colleagues experimented with chemically tweaking drugs and using transporters to make it easier or harder for compounds to slip across cell membranes. Serotonin itself is polar, meaning it dissolves well in water but does not easily cross the lipid membranes that surround cells. The psychedelics, on the other hand, are much less polar and can easily enter the interior of a cell.
They found that the growth-promoting ability of compounds was correlated with the ability to cross cell membranes.
Drug receptors are usually thought of as being on the cell membrane, facing out. But the researchers found that in nerve cells, serotonin 2A receptors were concentrated inside cells, mostly around a structure called the Golgi body, with some receptors on the cell surface. Other types of signaling receptors in the same class were on the surface.
The results show that there is a location bias in how these drugs work, Olson said. Engaging the serotonin 2A receptor when it is inside a cell produces a different effect from triggering it when it is on the outside.
“It gives us deeper mechanistic insight into how the receptor promotes plasticity, and allows us to design better drugs,” Olson said.
Additional authors on the paper include: from UC Davis, Lee Dunlap, Chunyang Dong, Samuel Carter, Robert Tombari, Lin Tian, John Gray, Shekib Jami, Seona Patel, Lindsay Cameron and Hannah Saeger; Joseph Hennessey and John McCorvy from the Medical College of Wisconsin, Milwaukee. The work was supported by grants from the National Institutes of Health and the Camille and Henry Dreyfus Foundation, and by a sponsored research agreement with Delix Therapeutics.

Yale scientists have for the first time identified a volatile pheromone emitted by the tsetse fly, a blood-sucking insect that spreads diseases in both humans and animals across much of sub-Saharan Africa. The discovery offers new insights into how the flies communicate with one another and could yield new methods for controlling their populations and the harmful diseases they carry.
The findings were published Feb. 16 in Science.
Tsetse flies are known to carry parasites called African trypanosomes. When the insects bite humans or animals, they transmit these parasites, spreading diseases such as African sleeping sickness, which can be fatal to humans, and nagana, a disease that affects livestock and other animals.
“African sleeping sickness is a dreadful disease that’s hard to treat. Our immune systems have a hard time clearing trypanosomes and most of the drugs we have to kill them are toxic,” said John Carlson, the Eugene Higgins Professor of Molecular, Cellular, and Developmental Biology in Yale’s Faculty of Arts and Sciences and senior author of the study. “And nagana, which affects livestock, has had terrible economic impacts in the region.”
Further, with climate change projected to expand the areas in which tsetse flies can survive, more humans and animals are expected to be affected by these diseases in the coming years.
One strategy identified as a way to control the spread of tsetse flies is to use their own pheromones — particularly volatile pheromones, or pheromones that work over distances rather than through direct contact — to attract and trap the insects.

To identify volatile pheromones that might be used for this purpose, the Yale research team took tsetse flies — of the species G. morsitans — and placed them in a liquid to collect any chemicals they might be emitting. They then ran those extracts through a device called a gas chromatograph-mass spectrometer, which can identify specific compounds from a mixed sample.
The researchers found several chemicals that had never previously been reported, including three that elicited responses from tsetse flies. One in particular, a chemical called methyl palmitoleate (MPO), had the strongest effects.
Specifically, in a series of experiments led by first author Shimaa Ebrahim, a postdoctoral fellow in Carlson’s lab, researchers found that MPO attracted male tsetse flies, caused them to stop and remain where they were for some time, and acted as an aphrodisiac. A drop of liquid containing MPO attracted male tsetse flies to knots in yarn that only resembled flies and to females of another tsetse fly species that they would not typically interact with.
To better understand how MPO mediated behavior, the researchers then tested whether neurons on the flies’ antennae responded to MPO. Indeed, they identified a subpopulation of olfactory neurons on the antennae that increased their firing rates when exposed to the pheromone.
Together, the findings indicate that MPO is a tsetse fly attractant, say the researchers, and therefore, it may be useful in slowing disease spread.

Currently, the most effective method of controlling tsetse fly populations is through traps that use odors from the animals the flies prefer to feed on.
“Now we’ve found this pheromone that could be used in combination with the host odors,” said Carlson. “Especially since MPO not only attracts the flies but causes them to freeze where they are.”
While animal odors have the benefit of attracting tsetse flies across large distances, they tend to fade quickly. MPO works at shorter distances but is effective for longer periods of time, Carlson added.
“MPO could be one more tool in the toolbox when it comes to combatting tsetse flies and the diseases they spread,” he said.
The team is now working with collaborators in Kenya to test whether MPO is useful in traps in the real world, not just in a lab setting.
Additionally, the researchers want to understand what causes tsetse flies infected with trypanosomes to emit an entirely different set of chemicals — something else they identified in the study — and how that affects fly communication.
Other Yale authors include Hany Dweck and Brian Weiss.

The Strategically Focused Research Network (SFRN) on Obesity, funded by the American Heart Association (AHA) to study obesity and train future obesity-focused investigators, has published its findings in a Journal of the American Heart Association special report, which hails the group’s work as “the beginning of innovative science, and, importantly, the birth of new collaborations and research partnerships to propel the field forward.”
Vanderbilt University Medical Center (VUMC) and Vanderbilt University (VU) collaborated with Johns Hopkins University School of Medicine, New York University Grossman School of Medicine and the University of Alabama at Birmingham on a four-year, $15 million award from the AHA, funded in 2017 to study aspects of obesity that contribute to disorders such as Type 2 diabetes and heart disease that reduce quality of life and life span,
The Centers for Disease Control and Prevention (CDC) reports the prevalence of obesity in the U.S. was 42.4% in 2018, with current estimates indicating the global prevalence of overweight and obesity may exceed 57% by 2030.
“The importance of sharply focused scientific collaborations such as the SFRN on Obesity cannot be overstated, particularly as the prevalence of overweight and obesity continues to escalate throughout the world,” said Kevin Niswender, MD, PhD, associate professor of Medicine at VUMC and director of the Vanderbilt center.
“As a result of this AHA-supported network, we have collectively taken several significant steps forward as we seek to more fully understand the causes of obesity, discover new therapeutic interventions and identify biomarkers to more precisely track both obesity and the success of weight loss,” he said.
A goal of the VUMC center research was to further advance precision medicine approaches to treating obesity while reducing cardiovascular disease risk.

The investigators focused on a particular drug target for diabetes and obesity, the glucagon-like peptide-1 receptor (GLP-1R), which has been shown to protect the heart and its arteries rather than increase the risk for cardiovascular disease.
As a result of the research of the VUMC team, it was determined that:
• Changes in the way the GLP-1R signals or communicates with cells, caused either by genetic variation or drug-like molecules, improve how cells respond to metabolic stress.
• GLP-1R activation does not directly alter how blood vessels function but does improve other markers of cardiovascular disease risk.
• Using electronic health record data, curated for cardiometabolic outcomes, together with linked genotyping, offers novel approaches to understanding obesity and cardiometabolic risk heterogeneity.
The SFRN was also tasked with developing a training program for investigators to pursue obesity-related investigations. AHA fellows were recruited at every center who presented their research at national and international conferences.
“This center accomplished many of the important goals of both VUMC and the AHA,” said Joshua Beckman, MD, professor of Medicine, who served as a training co-director for the center.
“New knowledge was created that will advance our understanding of the interface between obesity and cardiovascular disease. New teams of investigators were brought together to attack these issues from basic, translational and clinical perspectives. New investigators were provided training in multiple disciplines to position them well to advance their careers and the science they will discover. All in all, it was a very VUMC-like effort — coming together to do big things,” he said
SFRN on Obesity researchers at VUMC include Niswender; training directors Alyssa Hasty, PhD, and Beckman; James Luther, MD, MSCI; former chair of the VUMC Department of Medicine Nancy Brown, MD; Nancy Cox, PhD; Quinn Wells, MD, PharmD, MSCI; and postdoctoral fellows Megan Shuey-Henthorn, MSc, PhD; Rebecca Levinson, PhD; Megan Vogel, PhD; Mona Mashayekhi, MD, PhD; and Monica Bhanot, MD, PhD. Four Vanderbilt University undergraduate students also participated in the project.