Publisher Health

Mice fed a diet high in fat, cholesterol and calories, akin to the Western diet, had higher measures of blood lipids associated with elevated levels of inflammation, a new UCLA study finds. Researchers also identified clues to how the microbiology of the intestinal tract impacts disease-causing inflammation, suggesting that targeting the mucus interface between gut bacteria and the cells of the small intestine may be a novel means of preventing systemic inflammation.
The study was published today in the Journal of Lipid Research.
Inflammation is an important process that protects the body from invading infections and toxins. But in individuals who are successfully treated for HIV to the point that their viral load is no longer detectable, the continuing low-grade inflammation in the cells of the intestine contributes to the increased risk of heart attack or stroke in such people. These individuals have been found to have a “leaky gut” with more gut bacterial products in their blood such as the potent pro-inflammatory bacterial product known as lipopolysaccharide, or LPS, which promotes systemic inflammation that can accelerate the disease in arteries that leads to heart attack and stroke.
UCLA researchers previously used mouse models of treated HIV to study this problem. They found that adding a tomato concentrate called Tg6F to the western diet of the mice improved their “leaky gut” and significantly reduced systemic inflammation in the mice. Tg6F contains a peptide mimetic of the main protein in HDL (“good cholesterol”).
To learn more about how diet is related to inflammation, researchers led by Pallavi Mukherjee fed half a group of mice a typical “western diet,” high in fat, cholesterol and calories, while the rest were fed the normal mouse diet, known as a “chow diet,” which is low in fat, cholesterol and calories. The researchers examined dietary phospholipids to identity causes of the associated systemic inflammation.
Normal phospholipids do not induce inflammation, but oxidized phospholipids are known to often induce a strong inflammatory response. Researchers suspected that the high-fat western diet might contain high levels of oxidized phospholipids accounting for the ability of this diet to induce systemic inflammation. Surprisingly, they found the western diet contained very low levels of oxidized phospholipids, while the low-fat chow diet contained much higher levels of oxidized phospholipids.

A new study from The Australian National University (ANU) has revealed the death rate of babies in ancient societies is not a reflection of poor healthcare, disease and other factors, but instead is an indication of the number of babies born in that era.
The findings shed new light on the history of our ancestors and debunk old assumptions that infant mortality rates were consistently high in ancient populations.
The study also opens up the possibility mothers from early human societies may have been much more capable of caring for their children than previously thought.
“It has long been assumed that if there are a lot of deceased babies in a burial sample, then infant mortality must have been high,” lead author Dr Clare McFadden, from the ANU School of Archaeology and Anthropology, said.
“Many have assumed that infant mortality was very high in the past in the absence of modern healthcare.
“When we look at these burial samples, it actually tells us more about the number of babies that were born and tells us very little about the number of babies that were dying, which is counterintuitive to past perceptions.”
The researchers examined United Nations (UN) data from the past decade for 97 countries that looked at infant mortality, fertility and the number of deaths that occurred during infancy. The analysis revealed that fertility had a much greater influence on the proportion of deceased infants than the infant mortality rate.

An international team of researchers from the HEMOCOVID-19 trial have reported in Critical Care that severe COVID-19 patients have alterations in their microcirculation associated with the degree of severity of the disease.
Since the detection of the first Sars-Cov-2 infection cases in November 2019, more than 250 million people worldwide have been diagnosed with the disease, and more than 5 million have died [1].
Although COVID-19 is primarily a respiratory syndrome, it has been observed and detected in other organs. Several studies have shown affections in the circulatory system, where the virus damages the membrane that covers the inside of the heart and blood vessels, known as the endothelium. The correct circulation of blood in the smallest vessels of our body is of crucial importance. The branching network of these microvessels is the end-point of the circulatory system, where the oxygen transfer and the transport and exchange of heat, nutrients or waste products take place.
To further investigate how the disease could affect microcirculation, an international team of researchers put together a clinical study to monitor the endothelium of COVID-19 patients that had been admitted to different intensive care units (ICUs) around the world. They did this by using a non-invasive, portable, wireless, battery-operated near-infrared optical device to observe microvascular health.
After many months of data gathering and analysis, the researchers have published their preliminary results in the journal Critical Care, where they have provided data for the monitoring of healthy adults versus patients with acute respiratory distress syndrome caused by COVID-19, in six different hospitals across Spain, Mexico and Brazil.
Using NIRS to monitor the microcirculation
The researchers used near-infrared spectroscopy (NIRS) to study the local oxygen saturation on the tissues and the blood and the hemoglobin concentration. They also assessed the severity of the disease in the COVID-19 patients.

The use of electrodes placed inside the brains of laboratory specimens has pushed the field of neuroscience to new findings for decades. Common silicon-based electrodes rely on established production methods but are stiff and prone to injuring the brain. More pliable polymer-based electrodes avoid these issues but are difficult to scale, especially when integrating light emitters for neuron stimulation.
Researchers at Lawrence Berkeley National Laboratory developed a technique for assembling optoelectrodes that looks to offer the best of both worlds. In Journal of Vacuum Science & Technology B, by AIP Publishing, the scientists demonstrated it is possible to efficiently create a semiflexible light-emitting electrode by removing the stiff silicon material from underneath the tip of the probe.
The resulting device, called an optoelectrode, can study deep brain tissues with high resolution to record signals from individual nerve cells and stimulate small groups of neurons with state-of-the-art techniques such as optical waveguides.
“It is challenging to implant polymer probes in the brain, but we’ve developed a very simple fabrication technique to address this,” said author Vittorino Lanzio. “They’re less challenging to insert, because they don’t need to be glued to a silicon or tungsten shuttle, which increases the footprint of the device during insertion.”
Optoelectrodes are currently reserved for short-term use in laboratory animals. Despite the new electrode being an important step toward better biocompatibility, much more needs to be developed to bring long-term electrode use to humans.
The minute movements of breathing and pulses of blood flow subtly joggle the brain, even at rest. Microscopic shifts can disrupt an electrode’s performance and damage brain structures. These injuries can alert immune cells that hamper electrode function.
“The consistency of the brain is even more floppy than jelly,” said author Stefano Cabrini.
The optoelectrode is made of oxide glass and nitride initially bound to silicon. The group uses a nanoscale etching technique to remove the silicon underneath the device insertion area.
The team tested the device through experiments in rats and found that the semiflexible device, which packs 64 individual electrodes and high-density photonics into a significantly smaller cross-sectional area, could be inserted into a rat brain without using a silicon or tungsten shuttle.
The researchers hope neuroscientists put the new device to work and integrate more functionality into the electrodes, such as microfluidics to deliver chemicals into the brain, as the field progresses.
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A new study has shown that the airborne transmission of COVID-19 is highly random and suggests that the two-metre rule was a number chosen from a risk ‘continuum’, rather than any concrete measurement of safety.
A team of engineers from the University of Cambridge used computer modelling to quantify how droplets spread when people cough. They found that in the absence of masks, a person with COVID-19 can infect another person at a two-metre distance, even when outdoors.
The team also found that individual coughs vary widely, and that the ‘safe’ distance could have been set at anywhere between one to three or more metres, depending on the risk tolerance of a given public health authority.
The results, published in the journal Physics of Fluids, suggest that social distancing is not an effective mitigation measure on its own, and underline the continued importance of vaccination, ventilation and masks as we head into the winter months in the northern hemisphere.
Despite the focus on hand-washing and surface cleaning in the early days of the pandemic, it’s been clear for nearly two years that COVID-19 spreads through airborne transmission. Infected people can spread the virus through coughing, speaking or even breathing, when they expel larger droplets that eventually settle or smaller aerosols that may float in the air.
“I remember hearing lots about how COVID-19 was spreading via door handles in early 2020, and I thought to myself if that were the case, then the virus must leave an infected person and land on the surface or disperse in the air through fluid mechanical processes,” said Professor Epaminondas Mastorakos from Cambridge’s Department of Engineering, who led the research.

An FDA-approved drug for hepatitis C can increase bacterial sensitivity to antibiotics and reduce the likelihood of antibiotic resistance, according to a new study led by New York University researchers published in Cell Chemical Biology. The drug called telaprevir works by blocking the function of chaperones — important proteins that fold other proteins in the cell — in bacteria.
“Telaprevir is the first previously clinically approved compound that has been shown to inhibit chaperone function in bacteria,” said Tania Lupoli, assistant professor of chemistry at NYU and the study’s senior author. “Our research marks a vital step in developing small molecule chaperone inhibitors that can be used in bacteria to increase the power of antibiotics and slow down the evolution of antibiotic resistance.”
Chaperones exist in almost every cell in every organism, from single-cell bacteria to humans. Due to their critical role in folding other proteins — and what happens when proteins misfold, which can lead to toxicity in the cell — chaperones are the targets of ongoing drug discovery research, but researchers have struggled to find small molecules that can specifically target or bind to chaperones.
In this study, the researchers sought to identify small molecules that could turn off the function of chaperones in disease-causing bacteria. Focusing on Mycobacterium tuberculosis, the microbe that causes tuberculosis, they screened roughly 25,000 compounds — including 1,300 approved drugs — to identify small molecules that inhibit chaperones in mycobacteria.
They landed upon an antiviral drug called telaprevir, which was approved by the FDA to treat hepatitis C. In a series of experiments using model mycobacteria in the lab, they demonstrated that telaprevir binds to mycobacterial chaperones and blocks their ability to fold proteins. This made the mycobacteria more sensitive to antibiotics, including streptomycin, a commonly prescribed tuberculosis drug.
Chaperones can also stabilize the proteins in the cell that cause antibiotic resistance, so using telaprevir to block chaperone function lowered mycobacteria’s resistance against the first-line tuberculosis drug rifampicin. Reducing antibiotic resistance is a major public health priority in the U.S. and around the world, as an increasing number of infections — including tuberculosis — are growing more difficult to treat as antibiotics become less effective.
“In the future, we envision that small molecule chaperone inhibitors could be used in combination with antibiotics to enhance antibiotic potency and lower resistance,” said Lupoli.
While the researchers were excited to identify telaprevir as a chaperone inhibitor, they are continuing to explore hundreds of telaprevir analogs — compounds that are similar in molecular structure — to determine if others bind more tightly to chaperones, a key factor for moving the research into animal or clinical studies. Future work will also explore how to target chaperone inhibitors to only shut down certain chaperones — for instance, blocking chaperones in bacteria, but not human cells.
“Our work contributes to a small but growing list of small molecules that block the function of chaperones and provides a promising avenue for ongoing study of the role that telaprevir and its analogs can play when administered with antibiotics,” said Lupoli.
Additional study authors include Jordan Hosfelt, Aweon Richards, Meng Zheng, Brock Nelson, and Amy Yang of NYU’s Department of Chemistry; Carolina Adura and Fraser Glickman of Rockefeller University; Allison Fay of Sloan Kettering Institute; and William Resager and Beatrix Ueberheide of NYU Grossman School of Medicine. This research was supported by grants from the National Science Foundation (DGE1839302) and the National Institutes of Health (1S10OD010582-01A1).
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Materials provided by New York University. Note: Content may be edited for style and length.

Athletes returning to training following long COVID should undergo a series of tests and seek regular advice from a multi-disciplinary team of specialists to ensure they are fit to resume exercise, according to a new study published in the journal Annals of Medicine.
Researchers from Anglia Ruskin University (ARU) included eight separate studies in an evidence review and made recommendations for athletes returning to training after suffering from long COVID.
The study defined “long COVID” as COVID-19 signs and symptoms lasting for more than four weeks as a result of COVID-19 infection. According to data from the World Health Organisation, 25% of people who have had the virus experience at least four weeks of symptoms.
Researchers recommended that, due to the risk of damage to organs such as the lungs, heart, brain or kidneys from long-term infection, potentially resulting in conditions such as pneumonia or myocarditis, any athlete recovering from long-lasting symptoms should undergo a series of tests to their physical health and regular ongoing assessments. These could include chest x-rays, blood tests, and MRI or ECG scans.
The authors also recommended ongoing monitoring from a multi-disciplinary team of health experts, as long COVID is still a relatively unknown condition and there may be an ongoing risk even after an apparent recovery. The mental health of athletes should also be considered.
Lead author Rosie Lindsay, Postgraduate Researcher at ARU, said: “Long COVID is a complex cluster of conditions that is still not fully understood. However, we know organ damage can result that people may be unaware of before any medical examination.
“Athletes put severe stress on their bodies during competition and so it is particularly important that they manage their return to competition extremely cautiously following a bout of long COVID. This includes a variety of thorough tests, and access to both medical professionals and appropriate health services, including for their mental wellbeing.
“We hope that these recommendations can provide athletes and professionals working with athletes with a guide to help them to manage long-term COVID-19 symptoms.”
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Materials provided by Anglia Ruskin University. Note: Content may be edited for style and length.

Mathematicians have analysed global COVID-19 data to identify two constants which can drastically change a country’s rate of infection.
An international team of researchers led by Professor Alexander Gorban from the University of Leicester used available data from 13 countries to determine the rate of stress response, or ‘mobilisation’ and the rate of spontaneous exhaustion, or ‘demobilisation’.
Their findings, published in Scientific Reports, show that social stress — which varied broadly across the countries studied — drives the multi-wave dynamics of COVID-19 outbreaks.
The study analysed data from China, the USA, UK, Germany, Colombia, Italy, Spain, Israel, Russia, France, Brazil, India, and Iran — and contributed to the research team’s proposed new system of models, which combine the dynamics of the established concept of social stress with classical epidemic models.
Alexander Gorban is a Professor of Applied Mathematics at the University of Leicester, and Director of the Centre for Artificial Intelligence, Data Analysis and Modelling. Professor Gorban said:
“We tried to use the pandemic for research and quantify the social and cultural differences between countries. We measured how variable countries are in two processes: mobilisation of people for rational protective behaviour and exhaustion of this mobilisation with destroying of rational behaviour.

New research by the University of Nottingham has found that drivers touch their face 26 times an hour on average, potentially spreading germs and infection, if handwashing is inadequate.
Researchers, from the University’s Human Factors Research Group, scrutinised 31 hours of archive video footage obtained from two on-road driving studies, documenting 36 experienced drivers.
With little or no conscious self-awareness, drivers were observed to touch on or around their face 26.4 times per hour, with each touch lasting nearly four seconds. The face itself was touched most (79.6%), followed by the hair (10%), neck (8.6%) and shoulders (1.7%).
In 42.5% of occasions, drivers made contact with mucous membranes (inner lining of the lips, nostrils and eyes) approximately every five minutes, with fingertips and thumbs most commonly employed — areas that are frequently missed in handwashing.
Data indicated a lack of differences between genders and different age profiles, suggesting that all drivers are potentially at risk of contamination through face-touching while driving in a road vehicle.
The researchers acknowledge face-touching behaviours (such as nose-picking and ear cleaning) could be much more prevalent than even they observed — particularly when drivers travel alone in the ‘privacy’ of their own vehicle.

Science has the technology to measure the activity of every gene within a single individual cell, and just one experiment can generate thousands of cells worth of data. Researchers at Lund University in Sweden have now revolutionised the way this data is analysed — by using 3D video gaming technology. The study is published in the journal iScience.
Advanced techniques in DNA and RNA sequencing have opened up the possibility of studying individual cells in tissue in a more comprehensive way than was previously possible. The big challenge with these sequencing techniques is that they lead to large amounts of data.
“When you want to distinguish cancer cells from normal cells, for example, you need to examine thousands of cells to get a proper understanding, which translates into enormous amounts of numerical data,” says Shamit Soneji, researcher in computational biology at Lund University.
To make this data comprehensible, each cell is mathematically positioned in three-dimensional space to form a “roadmap” of the cells, and how they relate to each other. However, these maps can be difficult to navigate using a regular desktop computer.
“To be able to walk around your own data and manipulate it intuitively and efficiently gives it a whole new understanding. I would actually go so far as to say that one thinks differently in VR, thanks to the technique’s ability to involve your body in the analysis process,” explains Mattias Wallergård. researcher in interaction design and virtual reality at Lund University.
The Lund University team have developed the software CellexalVR; a virtual reality environment that enables researchers to use intuitive tools to explore all their data in one place. 3D maps of cells that have been calculated from gene activity and other information captured from individual cells can be displayed, and the researcher can clearly see which genes are active when certain cell types are formed.
Using a VR headset, the user has a complete universe of cell populations in front of them, and can more accurately determine how cells relate to one another. Using two hand controllers, they can select cells of interest for further analysis with simple hand gestures as if they were physical objects.
Since space is not an issue, it is possible to have several cellular maps in the same “room” and compare them side by side, something that is difficult on a traditional computer screen. Researchers can also meet in this VR world to analyze data together, despite being in different places geographically.
“Even if you are not familiar with computer programming, this type of analysis is open to everyone. A virtual world is a fast developing area of research that has enormous potential for scientists that need to access and process big-data in a more interactive and collaborative way,” concludes Shamit Soneji.
The software can be downloaded for free at https://www.cellexalvr.med.lu.se/
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Materials provided by Lund University. Note: Content may be edited for style and length.