Publisher Health

A new analysis suggests that the Nutri-Score — a label indicating the overall nutritional quality of a food product — can counteract the misleading effects of sugar claims. Kristin Jürkenbeck and colleagues of the University of Göttingent, Germany, present these findings in the open-access journal PLOS ONE on August 17, 2022.
High consumption of sugar has been linked to an increased risk of becoming overweight and other health issues. Some companies therefore label products with claims about sugar content, such as “without added sugar” or “less sweet.” However, consumers may interpret such claims to mean that a food product is healthier than it really is.
Another type of label, the Nutri-Score, is increasingly being used in European countries to inform consumers of the overall nutritional quality of food products. Previous research shows that the Nutri-Score can indeed guide consumers to make healthier food purchases.
Now, Jürkenbeck and colleagues have examined how the Nutri-Score might interact with sugar-content labels. In October 2020, they conducted an online survey of 1,103 German participants. The survey asked participants for their perceptions after being presented with images of the packaging of three hypothetical products — instant cappuccino, chocolate muesli, and an oat drink — with different combinations of sugar claims and Nutri-Score labels.
Statistical analysis of the survey results suggests that, when a Nutri-Score was not present, claims about reduced sugar did indeed mislead participants into believing that hypothetical products were healthier than they actually were. However, the presence of a Nutri-Score counteracted those effects, reducing misconceptions about the healthiness of less nutritional foods.
On the basis of these findings, the researchers call for restricted use of sugar content claims and similar labels, and mandatory use of the Nutri-Score by companies that do make such claims. They also call for future research to evaluate the effects of the Nutri-Score for additional food categories and in the context of other advertising claims that could mislead consumers about food healthiness.
The authors add: “Nutrition or taste claims about sugar on the front of packages can improve the health perception of foods with poor health images.”
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Our many different organ systems are in constant communication with each other. During exercise, for example, muscles send out signals to fat and liver tissue to release their energy sources. While these communication networks play a critical role in our bodies every day, it has been historically difficult to uncover such pathways. Scientists at Scripps Research, University of Southern California and elsewhere have now successfully created a model to label and track the protein signals that enable organ-to-organ communication.
As the researchers described in Open Biology on August 10, 2022, their new mouse model marks the proteins that a cell secretes and tracks their movement throughout the body. This novel technology could shape our molecular understanding of healthy versus diseased tissue, as well as the role that inter-organ communication plays in disease onset and progression.
“This new model can be likened to establishing a passport system in the body, as we are identifying where proteins are coming from and where they’re going,” says study co-first author Ilia Droujinine, PhD, Scripps fellow and principial investigator in the Department of Molecular Medicine at Scripps Research. “We can finally bring these interconnected communications networks to light, and then develop treatments based on this new knowledge.”
Researchers have used other methods, such as viral approaches, to understand protein secretion and the ways that organs communicate with each other. While these techniques have provided invaluable insight into the proteins expressed in an organism, they aren’t sensitive enough to label low-abundance proteins, or the origin and ultimate destination of protein interactions. But with this new model, scientists are now able to understand the exact path a particular protein takes.
In the study, the researchers used an enzyme called BirA*G3, which labels secreted proteins with a biotin tag. These biotin labels were then detected in live mice using a method called quantitative mass spectrometry proteomics, which is used to measure proteins in a sample. This revealed where the proteins originated from and where they traveled to in the body.
When BirA*G3 was broadly activated throughout the body, the researchers found that all secreted proteins were successfully labeled, even low-abundance proteins with hormone-like properties. Likewise, when BirA*G3 was activated solely in the liver, only secreted proteins related to that organ system were highlighted — displaying the high specificity of the model as well.
“Given the central role of key secreted proteins such as insulin, there is a great deal of interest in identifying novel secreted proteins,” said Andrew McMahon, PhD, senior author of the study and chair of the Department of Stem Cell Biology and Regenerative Medicine at the University of Southern California. “Genome studies are suggesting that many new proteins remain to be characterized. We’re looking forward to a deep dive into this area now that we have validated the technology.”
There are countless research applications for this technology, Droujinine notes. With this type of model, scientists can start to map unexplored disease pathways and ultimately develop targeted treatments, as many diseases originate in a single organ and then eventually spread to others. Cancer, with its metastatic properties, is one example. For another, studies have shown that many of the health complications that arise from obesity could be due to faulty organ communication, yet many of the molecular mechanisms remain unknown.
“Any protein we discover that plays a role in disease has the potential be translated into a therapeutic,” adds Droujinine.
In addition to Droujinine and McMahon, authors of the study, “A genetic model for in vivo proximity labelling of the mammalian secretome,” include Rui Yang, Amanda S. Meyer, Jinjin Guo, Jill A. McMahon of the University of Southern California (USC); Namrata D. Udeshi, Dominique K. Carey, Charles Xu and Steven A. Carr of Broad Institute of Harvard and MIT; Yanhui Hu, David Rocco and Norbert Perrimon of Harvard Medical School; Qiao Fang of University of Toronto; Jihui Sha and James Wohlschlege of UCLA; Shishang Qin of Peking University; and Alice Y. Ting of Chan Zuckerberg Biohub.
This work was supported by a NIH Transformative R01 grant 5R01DK121409 to A.P.M., A.Y.T., S.A.C. and N.P., and HHMI funding to N.P. I.A.D. acknowledges support from the Ellen Browning Scripps Foundation.

Findings from a new study at the Marshall University Joan C. Edwards School of Medicine show that a thymidine phosphorylase (TYMP) inhibitor could help slow thrombosis in COVID-19 patients.
Expression of TYMP, the gene that plays an important role in platelet activation, thrombosis and inflammation, is significantly increased in COVID-19 patients. The increase of TYMP occurs earlier than other inflammation markers, such as C-reactive protein, and is positively correlated to D-dimer, a marker of thrombotic event, as well as COVID-19 severity. This suggests that SARS-CoV-2 binding to host cells via its spike protein may enhance or trigger thrombosis. In addition, all COVID-19 vaccines, which use SARS-CoV-2 spike protein as an antigen to generate anti-SARS-CoV-2 antibody, also reportedly have thrombotic side effects. Control of SARS-CoV-2 associated thrombosis has significantly reduced COVID-19 mortality.
“This study is the first to demonstrate that the SARS-CoV-2 spike protein is sufficient to enhance expression of TYMP as well as activation of NF-kB, the major pro-inflammatory transcription factor in human bronchial epithelial cells,” said Wei Li, Ph.D., associate professor of biomedical sciences at the Joan C. Edwards School of Medicine and lead author on the study. “Our study also indicates that TYMP could be a novel biomarker for diagnosing COVID-19 and a therapeutic target for COVID-19-associated thrombotic complication.”
Li and his team presented the research last month at the International Society on Thrombosis and Haemostasis (ISTH) during its 2022 Congress, the leading international meeting in the field of thrombosis and hemostasis, held in London, England.
Using a human ACE2 gene, which mediates SARS-CoV-2 invading host cells, transgenic mice and a murine thrombosis model, the researchers observed, for the first time, that intraperitoneal injection of the SARS-CoV-2 spike protein to mice enhances thrombosis, which can be inhibited by tipiracil, a selective TYMP inhibitor and FDA-approved drug.
In addition to Li, Renat Roytenberg, Autumn DeHart, Krista Denning, Ph.D., and Hong Yue, Ph.D., served as co-authors on the study. This work is supported by the Marshall University Institute Start Fund, the National Institutes of Health (R15HL145573), the West Virginia IDeA Network of Biomedical Research Excellence (WV-INBRE) (P20GM103434), and the West Virginia Clinical and Translational Science Institute-Pop-Up COVID-19 Fund supported by the National Institute of General Medical Sciences (U54GM104942). A patent (WO2022159429 — METHODS FOR DIAGNOSIS AND TREATMENT OF COVID-19) associated with this project was published on July 28, 2022.
The researchers are seeking collaborators and collect patient samples to develop TYMP as a biomarker for diagnosing COVID-19 severity. Additional studies are ongoing to clarify the mechanisms that mediate SARS-CoV-2 spike protein increased TYMP expression as well as the potential effect of TYMP in long COVID-19.

For some smokers, the first cigarette of the day is just not as satisfying without a cup of coffee. That could be more than just a morning habit: Chemical compounds in roasted coffee beans may help lighten the effects of morning nicotine cravings, University of Florida researchers have found.
In a cell-based study, the researchers identified two compounds in coffee that directly affect certain high-sensitivity nicotine receptors in the brain. In smokers, these brain receptors can be hypersensitive after a night of nicotine withdrawal.
The recently published findings have yet to be tested in humans but are an important step toward better understanding how coffee and cigarettes affect nicotine receptors in the brain, said Roger L. Papke, Ph.D., a pharmacology professor in the UF College of Medicine. Caffeine is coffee’s feel-good ingredient for most people but smokers may get another kind of boost.
“Many people like caffeine in the morning but there are other molecules in coffee that may explain why cigarette smokers want their coffee,” Papke said.
The researchers applied a dark-roasted coffee solution to cells that express a particular human nicotine receptor. An organic chemical compound in coffee may help restore the nicotine receptor dysfunction that leads to nicotine cravings in smokers, the researchers concluded.
The findings have led Papke to a broader hypothesis: One of the compounds in brewed coffee, known as n-MP, may help to quell morning nicotine cravings.
Papke said he was intrigued by the idea that nicotine-dependent smokers associate tobacco use with coffee in the morning and alcohol in the evening. While alcohol’s effect on nicotine receptors in the brain has been thoroughly researched, the receptors’ interaction with coffee has been studied less.
“Many people look for coffee in the morning because of the caffeine. But was the coffee doing anything else to smokers? We wanted to know if there were other things in coffee that were affecting the brain’s nicotine receptors,” Papke said.
The findings, he said, provide a good foundation for behavioral scientists who could further study nicotine withdrawal in animal models.
Funding for the research was provided by the National Institutes of Health.
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With antibiotic-resistant bacteria on the rise, scientists have been searching for ways to shut down the Type IV secretion system (T4SS), a protein complex on the outer envelope of bacterial cells that helps them to exchange DNA with neighboring bacteria and resist antibiotics.
Now a collaboration between UT Southwestern computational biologist Qian Cong, Ph.D., and molecular biologists at the University of London has elucidated the structure of the T4SS complex, providing a blueprint that could help researchers design drugs that slow development of antibiotic resistance. Their findings were published in Nature.
“For the first time, we determined the 3D structure of the entire T4SS complex,” said Dr. Cong, Assistant Professor of Biophysics and in the Eugene McDermott Center for Human Growth and Development at UTSW.
The team in London was led by Gabriel Waksman, Ph.D., whose lab has been working for more than two decades to understand T4SS, especially how it forms a thin, hollow structure called a pilus, which connects to nearby bacteria to share genes. For this project, his team used cryo-electron microscopy (cryo-EM) — a process that freezes proteins and uses beams of electrons to obtain high-resolution microscopic images — to elucidate the structure of T4SS. This was no small feat since the T4SS complex is larger than 99.6% of all those included to date in the worldwide library of protein structures.
Dr. Cong then used her background in statistics and machine learning to analyze T4SS protein sequences from several bacteria to generate structural predictions, which were compared to the cryo-EM data. Her computational analysis supported the cryo-EM data and suggested a hypothesis about the function of T4SS. While it was already known that T4SS is involved in pilus assembly, she predicted how it occurs. With that prediction in hand, Dr. Waksman’s team was able to make specific mutations within the relevant pieces of the complex and validate Dr. Cong’s hypothesis in live bacteria.
“In addition to the contribution we have made toward the development of drugs to slow the spread of antibiotic resistance genes, this study showcases the power of modern computational methods to validate experimental results and suggest functional insights beyond available experimental data,” said Dr. Cong, a Southwestern Medical Foundation Scholar in Biomedical Research.
Other researchers who contributed to this study include Ke?vin Mace?, Abhinav K. Vadakkepat, Adam Redzej, Natalya Lukoyanova, Clasien Oomen, Nathalie Braun, Marta Ukleja, Fang Lu, Tiago R. D. Costa, and Elena V. Orlova of the Institute of Structural and Molecular Biology, Birkbeck College, University of London; and David Baker of the University of Washington.
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Among other flaws, the public guidance during the coronavirus pandemic was “confusing and overwhelming,” the agency said.Dr. Rochelle P. Walensky, the director of the Centers for Disease Control and Prevention, on Wednesday delivered a sweeping rebuke of her agency’s handling of the coronavirus pandemic, saying it had failed to respond quickly enough and needed to be overhauled.In a meeting with senior staff, Dr. Walensky outlined in broad terms a plan to reorganize the agency’s structure to prioritize public health needs and efforts to curb continuing outbreaks, and to put less emphasis on publication of scientific papers about rare diseases.The steps announced on Wednesday grew out of an external review Dr. Walensky had ordered in April, after months of scathing criticism of the C.D.C.’s response to the pandemic. Its public messages on masking and other mitigation measures were sometimes so confusing or abruptly modified that they seemed more like internal drafts than carefully considered proclamations.The public guidance has been “confusing and overwhelming,” according to a briefing document provided by the agency.Leaders of the agency’s Covid team rotated out after only a few months, leaving other senior federal health officials unsure about who was in charge. And important data were sometimes inexplicably released too late to inform federal decisions, including some data on breakthrough infections that could have influenced a recommendation on whether to authorize a round of booster shots.“For 75 years, C.D.C. and public health have been preparing for Covid-19, and in our big moment, our performance did not reliably meet expectations,” Dr. Walensky said in a startling acknowledgment of the agency’s failings. “My goal is a new, public health, action-oriented culture at C.D.C. that emphasizes accountability, collaboration, communication and timeliness.”Her plan, which was also described in a video to the agency’s more than 11,000 employees, was short on specifics. But it was welcomed by at least some of the agency’s two dozen senior staff members, as well as by outside public health specialists.The agency has been criticized for years as too insular and academic. Many of its experts are accustomed to conducting narrowly focused research that undergoes lengthy reviews, and they are uneasy with the kind of urgent action needed to address the coronavirus, and now the monkeypox outbreak.A coronavirus testing site in Houston in July 2020. Dr. Walensky ordered an external review this year, after months of scathing criticism of the C.D.C.’s response to the pandemic. Callaghan O’Hare for The New York TimesIn an interview on Monday, Dr. Walensky said she had repeatedly pushed staff members to turn around Covid-19 data as fast as possible. “Some of the data are messy, and some of the data take time,” she said. “I’ve really tried hard to push data out when we had it.”The external review Dr. Walensky ordered was led by James Macrae, who has held senior positions at the Department of Health and Human Services, which oversees the C.D.C. He interviewed about 120 people inside and outside the agency. His report was not released; one official said it was being completed.The changes Dr. Walensky described include the appointment of a former Obama administration health official, Mary K. Wakefield, to lead the C.D.C.’s shift to a stronger public health focus. Two scientific divisions will now report directly to Dr. Walensky’s office, and the agency will cut down review time for urgently needed studies. The agency is also altering its promotion system so that it rewards efforts to make an impact on public health and is less heavily based on the number of scientific papers published.The briefing document said that Dr. Walensky wanted staff members to “produce data for action” as opposed to “data for publication.”Importantly, the agency will beef up the team that responds to public health emergencies and require those officials to remain in their positions for at least six months, aides said. Previously, they were allowed to rotate out after only a few months, a system that senior federal officials said sowed confusion and took up valuable time during the pandemic.A new executive team will be created to set priorities and make decisions about how to spend the agency’s annual budget of about $12 billion, “with a bias toward public health impact,” the briefing document said.And the C.D.C. is working on improving its public messaging. Dr. Walensky, who has already shaken up the agency’s communications division, wants to make sure guidance is issued in “plain language, easy to understand,” the document said.

The impact of environmental conditions on the dynamic structures of RNAs in living cells has been revealed by innovative technology developed by researchers at the John Innes Centre.
The research, the result of a collaboration between the groups of Professor Dame Caroline Dean FRS and Dr Yiliang Ding, increases our understanding of what happens at cellular level in response to environmental signals. This raises the possibility that we may use this knowledge to fine-tune crops or develop RNA-based therapies for diseases such as COVID-19 (SARS-COV-2.)
Previous research by these groups showed that two important genetic elements COOLAIR and FLC interplay to regulate plant molecular responses to warm and cold.
But it was unclear how the RNA structure of COOLAIR contributes to the regulation of FLC – a genetic brake on flowering in plants.
Researchers in the Ding group developed a new technology which is capable of profiling RNA structure at the resolution of a single molecule in live cells.
Using this technique allowed them to observe RNA structural changes. In warm conditions COOLAIR RNA adopts three predominant structures and these shapes and proportions changed after the plants were exposed to cold temperatures.

A first-in-human multicenter trial involving Mayo Clinic used a new ablation technique for patients with ventricular tachycardia, an abnormally rapid heart rhythm that is a leading cause of sudden cardiac death worldwide.
The trial tested needle ablation using in-catheter, heated, saline-enhanced, radio frequency energy, also known as SERF, to substantially increase heat transfer, compared to conventional ablation methods. The new process produces deeper, controllable lesion scars at sites inside the heart muscle. The catheter can accurately control the ablation size and treat tissue that is deeper in the heart wall, which is where life-threatening arrhythmias that cause ventricular tachycardia are often found.
Therapies of medication and traditional ablation, which uses heat or cold to scar small areas of heart tissue, may not be enough to prevent ventricular tachycardia. Therefore, many patients also have an implantable cardioverter-defibrillator (ICD) to address dangerous arrhythmias. While an ICD shock corrects the heart’s rhythm, it does not prevent arrhythmia. In the trial, researchers used several methods to directly eliminate abnormal heart tissue that causes life-threatening rhythm.
“This preliminary trial is important because it suggests that there is a new way to treat problematic ventricular tachycardia by reducing or eliminating the shocks that ICDs deliver. It appears to be effective in achieving this goal,” says Douglas Packer, M.D., a cardiac electrophysiologist at Mayo Clinic, first author and principal investigator of the study. “For clinicians, it provides hope that treatment in the electrophysiology lab may be effective, even if other treatments failed. For patients, it provides hope that their quality of life can be improved.”
The innovative catheter was developed by Michael Curley, Ph.D., of Boston-based Thermedical Inc., with funding from the National Institutes of Health (NIH). Dr. Curley is senior author of the research findings that are published in Circulation: Arrhythmia and Electrophysiology.
In the trial, 32 participants from six centers underwent needle electrode ablation. Each had experienced multiple episodes of ventricular tachycardia that did not respond to drug therapy after an ICD was implanted and standard ablation was done. These patients had about 45 shocks from their defibrillator in the six months before their procedure.

Researchers have developed a label-free and non-invasive Raman spectroscopy approach that can acquire microscopic images of biological samples and identify a wide range of biomolecules with unprecedented speed and sensitivity.
“Our work could lead to a non-invasive, label-free and user-friendly device for clinical use,” said research team leader Dario Polli from Politecnico di Milano in Italy. “This innovative microscope, coupled with deep learning-based algorithms, could eventually make it easier and faster to diagnose cancer by allowing the visualization of the chemical constituents of human tissues and cells.”
In the Optica Publishing Group journal Optics Express, the researchers describe their new technique, which is based on coherent anti-stokes Raman scattering (CARS) microscopy. CARS microscopy produces images based on the vibrational signatures of molecules by exploiting the interaction between ultrashort laser pulses and biological samples.
The new approach provides access to the hard-to-detect region of the vibrational spectrum known as the fingerprint region, which spans from 400 to 1800 cm?1. Although many individual compounds can be identified using their vibrational fingerprints in this region, it tends to produce weak signals that are difficult to detect.
“Commonly used techniques in biomedical sciences often require staining, which is not only cumbersome but can also introduce structural and chemical alterations that can lead to artifacts, or errors, in imaging and data processing,” said Polli. “Because our system can distinguish between many different chemical species in biological tissues without labels, it could be useful for live cell imaging and analyzing tissue biopsies.”
Lower repetition rate, faster imaging
This new work is part of the CRIMSON project funded by the European Commission, which aims to develop a turnkey imaging device that uses vibrational spectroscopy for fast cell and tissue classification. The project’s goal is to transform the study of the cellular origin of diseases to enable new approaches that could advance personalized therapy.

The majority of people who were likely infected with the Omicron variant of SARS-CoV-2, the virus that causes COVID-19, didn’t know they had the virus, according to a new study from Cedars-Sinai investigators. The findings are published in JAMA Network Open.
“More than one in every two people who were infected with Omicron didn’t know they had it,” said Susan Cheng, MD, MPH, director of the Institute for Research on Healthy Aging in the Department of Cardiology at the Smidt Heart Institute at Cedars-Sinai and corresponding author of the study. “Awareness will be key for allowing us to move beyond this pandemic.”
Prior studies have estimated that at least 25% and possibly as many as 80% of people infected with SARS-CoV-2 may not experience symptoms. Compared to other SARS-CoV-2 variants, the Omicron variant is associated with generally less severe symptoms that may include fatigue, cough, headache, sore throat or a runny nose.
“Our study findings add to evidence that undiagnosed infections can increase transmission of the virus,” said Sandy Y. Joung, MHDS, an investigator at Cedars-Sinai and first author of the study. “A low level of infection awareness has likely contributed to the fast spread of Omicron.”
As part of research into the effects of COVID-19 and the impact of vaccines, the investigators began collecting blood samples from healthcare workers more than two years ago. In the fall of 2021, just before the start of the omicron variant surge, the investigators were able to expand enrollment to include patients, thanks to study infrastructure and biospecimen processing support provided by Sapient Bioanalytics.
Of the healthcare workers and patients who have participated in the research, investigators identified 2,479 people who had contributed blood samples just prior to or after the start of the Omicron surge. The investigators identified 210 people who likely were infected with the Omicron variant based on newly positive levels of antibodies to SARS-CoV-2 in their blood.