A new study showed that a wearable computer vision device can reduce collisions for both people who are blind or those who are visually impaired and using a long cane and/or guide dog by 37 percent, compared to using other mobility aids alone.
People who have visual impairments are at a significantly higher risk for collisions and falls. Commonly used mobility aids like long canes and guide dogs can offer benefits, but come with limitations in effectiveness and costs, respectively. While some electronic devices are marketed direct-to-consumer claiming to warn wearers of surrounding objects, there has been little evidence of their effectiveness in actual daily mobility settings. This is one of the first randomized-controlled trials to look at the potential benefit of the devices at home and outside of a controlled lab environment. The new study led by vision rehabilitation researchers at Mass Eye and Ear, a member of Mass General Brigham was published July 22 in JAMA Ophthalmology.
“Independent travel is an essential part of daily life for many people who are visually impaired, but they face a greater risk of bumping into obstacles when they walk on their own,” said Gang Luo, PhD, an associate scientist at the Schepens Eye Research Institute of Mass Eye and Ear, and an associate professor of ophthalmology at Harvard Medical School. “Although many blind individuals use long canes to detect obstacles, collision risks are not completely eliminated. We sought to develop and test a device that can augment these everyday mobility aids, further improving their safety.”
Vibrating wearable device prototype put to test
The experimental device used in the trial was created by Dr. Luo and colleagues in his vision rehabilitation lab, including the lead author Shrinivas Pundlik, PhD, who designed the computer vision algorithm. The device and data recording unit were enclosed in a sling backpack with a chest-mounted, wide-angle camera on the strap, and two Bluetooth-connected wristbands worn by the user. The camera is connected to a processing unit that captures images and analyzes collision risk based on the relative movement of incoming and surrounding objects in the camera’s field of view. If an imminent collision is detected on the left or right side, the corresponding wristband will vibrate; a head-on collision will cause both wristbands to vibrate. Unlike other devices that simply warn of nearby objects whether or not a user is moving toward the objects, this device analyzes relative motion, warning only of approaching obstacles that pose a collision risk, and ignoring objects not on a collision course.
The new study included 31 blind and visually impaired adults who use either a long cane or guide dog (or both) to aid their daily mobility. After being trained to use the device, they used it for about a month at home in conjunction with their typical mobility device (mostly a long cane). The device was randomized to switch between active mode, in which the users could receive vibrating alerts for imminent collisions, and silent mode, in which the device still processed and recorded images, but did not give users any warning even if potential collisions were detected. The silent mode is equivalent to the placebo condition in many clinical trials testing drugs. The wearers and researchers would not know when the device modes changed during the testing and analysis. Collisions were analyzed by researchers from the recorded videos. The effectiveness of the device was evaluated by comparing collision incidents that occurred during active and silent modes. The study found that the collision frequency in active mode was 37 percent less than that in silent mode.

Some antibiotics appear to be effective against a form of skin cancer known as melanoma. Researchers at KU Leuven, Belgium, examined the effect of these antibiotics on patient-derived tumours in mice. Their findings were published in the Journal of Experimental Medicine.
Researchers from KU Leuven may have found a new weapon in the fight against melanoma: antibiotics that target the ‘power plants’ of cancer cells. These antibiotics exploit a vulnerability that arises in tumour cells when they try to survive cancer therapy.
“As the cancer evolves, some melanoma cells may escape the treatment and stop proliferating to ‘hide’ from the immune system. These are the cells that have the potential to form a new tumour mass at a later stage” explains cancer researcher and RNA biologist Eleonora Leucci (KU Leuven). “In order to survive the cancer treatment however, those inactive cells need to keep their ‘power plants’ — the mitochondria — switched on at all times.” As mitochondria derive from bacteria that, over time, started living inside cells, they are very vulnerable to a specific class of antibiotics. This is what gave us the idea to use these antibiotics as anti-melanoma agents.”
The researchers implanted patient-derived tumours into mice, which were then treated with antibiotics — either as the only treatment or in combination with existing anti-melanoma therapies. Leucci: “The antibiotics quickly killed many cancer cells and could thus be used to buy the precious time needed for immunotherapy to kick in. In tumours that were no longer responding to targeted therapies, the antibiotics extended the lifespan of — and in some cases even cured — the mice.”
The researchers worked with antibiotics that are now, because of rising antibiotic resistance, only rarely used in bacterial infection. However, this resistance has no effect on the efficacy of the treatment in this study, explains Leucci. “The cancer cells show high sensitivity to these antibiotics, so we can now look to repurpose them to treat cancer instead of bacterial infections.”
However, patients with melanoma shouldn’t start experimenting, warns Leucci. “Our findings are based on research in mice, so we don’t know how effective this treatment is in human beings. Our study mentions only one human case where a melanoma patient received antibiotics to treat a bacterial infection, and this re-sensitised a resistant melanoma lesion to standard therapy. This result is cause for optimism, but we need more research and clinical studies to examine the use of antibiotics to treat cancer patients. Together with oncologist Oliver Bechter (KU Leuven/UZ Leuven), who is a co-author of this study, we are currently exploring our options.”
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Participation in elite adult rugby may be associated with changes in brain structure. This is the finding of a study of 44 elite rugby players, almost half of whom had recently sustained a mild head injury while playing.
The study, part of the Drake Rugby Biomarker Study, was led by Imperial College London and published in the journal Brain Communications.
The research found a significant proportion of the rugby players had signs of abnormalities to the white matter, in addition to abnormal changes in white matter volume over time.
White matter is the ‘wiring’ of the brain, and helps brain cells communicate with each other. The research team say more work is now needed to investigate the long-term effects of professional rugby on brain health.
Professor David Sharp, senior author from Imperial’s Department of Brain Sciences, said: “Despite relatively high rates of head injury and an increasing focus on prevention, there has been relatively little research investigating the long-term effects of rugby participation. More objective measures of the effects of sporting head injuries on the brain are needed to assist with the assessment and management of individual players.
“Our research using advanced magnetic resonance imaging suggests that professional rugby participation can be associated with structural changes in the brain that may be missed using conventional brain scans. What is not clear at this stage is the long-term clinical impact of these changes. Further research is needed to understand the long-term implications of repeated head injuries experienced during a rugby career and to provide more accurate ways to assess risk for an individual.”
The work, in collaboration with University College London, was funded and instigated by The Drake Foundation, who brought together academia and sport for this pioneering study, and was additionally supported by the National Institute for Health Imperial Biomedical Research Centre, the UK Dementia Research Institute and the Rugby Football Union.

An international collaborative study led by University of Helsinki has conducted a holistic study to investigate the effects of COVID-19 restrictions on several air quality pollutants for the Po Valley region in northern Italy. The area is well known to have one of the worst air quality standards in Europe and is highly influenced by anthropogenic (human-led) activities. The study was done between research groups in Finland, Italy and Switzerland and the results were published in the journal Environmental Science: Atmospheres.
Scientists have combined air quality measurements and computer simulation data over several locations in the region. The resulting studies show that reduced emissions from traffic lead to a strong reduction of nitrogen oxides, while have had limited impact on aerosol concentrations, contributing to a better understanding of how the air pollution is formed in the Po Valley.
The studies show that despite the large reduction in mobility of people and emissions from cars (which raise for instance nitrogen oxides concentrations), aerosols concentrations remained almost unchanged compared to previous years. Secondary formed pollutants like ozone, on the other hand, showed an increase in concentrations. These findings were confirmed by a computer model simulation that simulates the COVID-19 restriction on traffic, indicating that the increased overall oxidation capacity of the atmosphere might have enhanced the formation of new aerosols.
Furthermore, model simulations indicated that as nitrogen oxides emissions were largely reduced, chemical reactions of organic gases against atmospheric oxidants increased, slightly favoring the formation of new organic particles.
“You can think of the Po Valley region as a massive batch reactor with all sort of chemicals. Altering one of the “ingredients” can trigger non-linear responses in air pollutants concentrations,” says Dr Federico Bianchi from the Institute for Atmospheric and Earth System Research (INAR) of University of Helsinki.
These studies shade new lights on the formation of air pollutants in the Po Valley region and on their sources. The conclusion is that the reduction in traffic emissions had little impact on particulate matter concentrations, possibly highlighting the importance of other emissions sources in the Po Valley area.
Carefully characterizing the evolution of such emission categories are of a vital importance to improve the understanding of the air pollution and to reduce the uncertainties in future air quality scenarios.
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Materials provided by University of Helsinki. Original written by Paavo Ihalainen. Note: Content may be edited for style and length.

Targeted removals can be effective in suppressing the number of invasive lionfish found within protected coastlines around the Mediterranean Sea.
However, if they are to really be successful they need to be combined with better long-term monitoring by communities and conservationists to ensure their timing and location achieve the best results.
Those are the key findings of a new study, one of the first of its kind to examine the effectiveness of targeted lionfish removals from both an ecological and a socio-economic perspective.
Scientists working as part of the European Union-funded RELIONMED project teamed up with specially trained divers and citizen scientists to conduct a series of removal events and surveys over a six-month period.
Focussed on three marine protected areas on the coast of Cyprus — the Zenobia shipwreck off Larnaca, and two popular diving sites within the Cape Greco Marine Protected Area — between 35 and 119 lionfish were removed per day by divers at each protected site.
Those sites were then monitored by divers over several months which showed that, in some locations, population numbers recovered within three months.

UT Southwestern researchers report the first structural confirmation that endogenous — or self-made — molecules can set off innate immunity in mammals via a pair of immune cell proteins called the TLR4-MD-2 receptor complex. The work has wide-ranging implications for finding ways to treat and possibly prevent autoimmune diseases such as multiple sclerosis and antiphospholipid syndrome.
The TLR4-MD-2 receptor complex is well known for its role in the body’s response to infection by gram-negative bacteria. Its role in autoimmunity had been long suspected, although direct proof was lacking. The team, led by Nobel Laureate Bruce Beutler, M.D., director of the Center for the Genetics of Host Defense (CGHD), identified lipids called sulfatides that can activate the innate immunity sensor TLR4, located on a cell’s membrane. His discovery of the genes behind the TLR4 receptor and its role in the body’s earliest response to infection — innate immunity — led to his 2011 Nobel Prize in Physiology or Medicine.
Beutler is corresponding author of the study published this week in the Proceedings of the National Academy of Sciences that used X-ray crystallography to confirm how sulfatides bind to the receptor complex. Lead author Lijing Su, Ph.D., a CGHD assistant professor with a secondary appointment in biophysics, conducted the X-ray crystallography at UT Southwestern’s Structural Biology Core Facility and at Argonne National Laboratory in Illinois.
“For many years, the question of whether endogenous — or self — molecules can activate innate immune receptors has been an important one,” says Beutler, a professor of immunology and internal medicine. “Scientists had observed that our own nucleic acids can activate TLRs 3, 7, 8, and 9, causing inflammation and autoimmunity. Many endogenous ligands for TLR4, most of them proteins, have been proposed. This is the first study to substantiate the existence of such a TLR4 ligand, meaning a molecule that fits into the receptor, by structural studies.”
The team’s structural studies of mouse TLR4-MD-2 in complex with sulfatides gave a detailed look at how sulfatides bind to the U-shaped side of the receptor complex in order to activate it. That binding sets off biological pathways that lead to the body’s inflammatory response.
The study, which raises new and important questions, includes some observations about differences in the way the receptor responds in mice and humans. It also raises new questions about how the chemical makeup of individual sulfatides might affect the way they interact with the receptor complex to activate or suppress the immune response.
“Our work demonstrates that these, or perhaps other endogenous lipids, may indeed trigger activation of TLR4,” Beutler says, adding that TLR4 usually acts as a sensor of lipopolysaccharide (a lipid plus sugar molecule) — also known as endotoxin — that resides on gram-negative bacteria. TLR4-LPS binding is implicated in sepsis, a potentially deadly condition in which the immune system goes into overdrive in response to infection.
Su adds that she and others in the Beutler lab previously reported that TLR4 and its co-receptor MD-2 can be activated by a synthetic small molecule called neoseptin-3, created in collaboration with the laboratory of Dale Boger, Ph.D., at The Scripps Research Institute, which shares no structural similarity to the natural microbial ligand, LPS.
“Our crystal structure of mouse TLR4-MD-2 in complex with neoseptin-3 revealed that this receptor complex might accommodate multiple small molecules rather than a big molecule like LPS,” Su explains. “This result led us to look for natural lipids that might bind and activate TLR4-MD-2 signaling. Among early candidates were phosphoceramides, but these failed to activate the receptor. Structural features of sulfatides, and their great abundance in some tissues, led us to test them instead, and we confirmed that some sulfatides do indeed activate TLR4.”
UTSW co-authors include Ying Wang, Tao Yue, Jianhui Wang, and Eva Marie Y. Moresco. Researchers from Israel, Pittsburgh, Pennsylvania, and Germany also participated in the work.
The investigation received support from the National Institutes of Health (grants AI125581 and AI100627), the Lyda Hill Foundation, the Israel Cancer Association (grant 20180115), the Israel Science Foundation (grant 2142/20), and the Ministry of Science of Israel. The work at Argonne received support from the U.S. Department of Energy (contract DE-AC02-06CH11357). The research also received support from the Office of the Director, NIH (award S10OD025018).
Beutler, a Regental Professor, holds the Raymond and Ellen Willie Distinguished Chair in Cancer Research, in Honor of Laverne and Raymond Willie, Sr.

With the application of a novel three-dimensional imaging technology, researchers at Karolinska Institutet in Sweden have discovered that one portion of the autonomic nervous system in the liver undergoes severe degeneration in non-alcoholic fatty liver disease. The study, which is conducted in mice and human liver tissue, shows that the degeneration of nerves is correlated with the severity of liver pathology. The results are being published in the journal Science Advances.
Non-alcoholic fatty liver disease is the most common hepatic disorder, with prevalence around 25 percent globally. Approximately one third of all fatty liver cases will develop to steatohepatitis, which is a severe disease seriously affecting the entire metabolism.
In the current paper, researchers explore the nervous system in fatty liver using volume immuno-imaging and light sheet microscopy ? a novel imaging technique, which altogether offer large-scale 3D visualization with cellular resolution. According to the study, this technology can reveal even early, minor or hidden structural impairments of the liver.
“Now we know that nerves in the liver have multiple subtle regulatory roles” says Csaba Adori, researcher at the Department of Neuroscience, who led the study. “Their role, however, may be more essential during the fight-or-flight response or when subjected to metabolic challenges. Degeneration of liver sympathetic nerves and abnormal operation of the remaining nerve fibres in the fatty liver could compromise all these functions, which may contribute to further aggravation of the disease, as part of a vicious cycle.”
According to the study, alterations in the liver innervation occurs already in early stages of fatty liver disease. With progression to the more severe steatohepatitis, these impairments turn to a pronounced degeneration of the nerves. The nerve pathology is also similar in mouse model of fatty liver and in human fatty liver samples. The research team now hopes that the study results will open the door for new therapeutic approaches in the treatment of steatohepatitis and portal hypertension, by targeting the liver sympathetic nervous system.
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As cities worldwide expand their networks of cycling paths and more cyclists take to the streets, the chances of cycling accidents and potential collisions increase as well, underscoring the need for proper cycling safety in dense urban areas.
According to a World Health Organisation report in 2020, more than 60 per cent of the reported bicycle-related deaths and long-term disabilities are a result of accidents with head injuries.
Researchers from Nanyang Technological University, Singapore (NTU Singapore), in collaboration with French specialty materials leader Arkema, have developed a tougher, safer bicycle helmet using a combination of materials. The new helmet prototype has higher energy absorption, reducing the amount of energy transferred to a cyclist’s head in the event of an accident and lowering the chances of serious injury.
Led by Associate Professor Leong Kah Fai from the School of Mechanical and Aerospace Engineering, the team, comprising research fellow Dr Bhudolia Somen Kumar, research associate Goram Gohel and MSc student Elisetty Shanmuga, created the composite helmet with an outer shell made primarily of a new type of acrylic thermoplastic resin, reinforced with carbon fibre.
The new thermoplastic resin, named Elium®, was developed by Arkema, one of NTU’s industry partners. The NTU team worked with Arkema engineers to develop a moulding process for Elium® to manufacture stronger bicycle helmets.
“Our partnership with Arkema is driven by the desire to develop a new type of helmet that is stronger and safer for cyclists,” said Assoc Prof Leong. “Helmets have been proven time and time again to play a critical role in reducing the severity of injuries and number of fatalities. Our prototype helmet has been subjected to a barrage of internationally benchmarked tests and has demonstrated the ability to provide greater protection for cyclists compared to conventional helmets.”
The findings by the research team were published in the peer-reviewed journal Composites Part B: Engineering in May.

A research team led by Wim Annaert (VIB-KU Leuven) uncovered the early assembly of gamma-secretase, a protein complex linked to numerous cellular processes including the development of Alzheimer’s disease. In a first step, two dimeric subcomplexes are formed, which independently exit the ER and only afterwards assemble into a four-subunit complex. This ‘buckle up’ mechanism is thought to prevent premature assembly and activity. The new insights are very relevant, as gamma-secretase is an important potential therapeutic target for Alzheimer’s and other conditions.
An enzyme complex involved in plaque production
Gamma-secretase is best known as the enzyme that cleaves the amyloid precursor protein, generating a small peptide called amyloid beta, the main constituent of the plaques found in the brains of people affected by Alzheimer’s disease. Ever since the discovery of its implication in disease, gamma-secretase has been studied and tested as a potential therapeutic target, but its role in the body is much broader than producing amyloid.
We now know that gamma-secretase is a complex made up of four components, two of which have multiple homologues, resulting in variety of complexes with distinct subcellular distributions, providing a basis for substrate selectivity. All four gamma-secretase components are transmembrane proteins that are co-translationally inserted into the endoplasmic reticulum (ER). But how these four subunits get assembled in such stable enzyme complexes remained unknown until now.
Dissecting the assembly line
The Annaert lab at the VIB-KU Leuven Center for Brain & Disease Research is specialized in membrane trafficking and has a long track record of studying the gamma-secretase complex. By combining biochemistry and high-resolution imaging, they have now uncovered the early steps of the gamma-secretase assembly process.
“To dissect the assembly steps, we used a method developed by Randy Schekman of UC Berkeley (who won the Noble Prize in Medicine in 2013), and with whom we collaborated on this endeavor. This approach unveiled that in fact dimers of two out of the four subunits are formed in the ER, in this way preventing the premature breakdown of individual subunits,” says Wim Annaert. “These dimers only get fully assembled into gamma-secretase complexes shortly thereafter, between ER-exit and their transition to the Golgi complex.”
Only fully assembled complexes are transported through the Golgi onto their final destination in different cellular compartments.
Interestingly, the dimer assembly signature remains visible in the high-resolution structure of gamma-secretase, suggesting a ‘buckle up model’ for dimer assembly: one side of the dimers act as ‘buckles’, while the other side functions as the belt through interactions keeping the full complex in place.
“This ‘buckle up’ mechanism could prevent the untimely processing of substrates,” says Annaert. “Given the broad range of substrates and pathways controlled by gamma-secretase -from developmental processes to cancer and Alzheimer, the precise tuning of this assembly process allows for further spatiotemporal regulation of gamma-secretase activity.”
The insights are extremely relevant, as problems during complex assembly may also have a significant impact on the many physiological and pathological processes regulated by gamma-secretase.
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Materials provided by VIB (the Flanders Institute for Biotechnology). Note: Content may be edited for style and length.

Scientists have developed a ‘nanobody’ — a small fragment of a llama antibody — that is capable of chasing out human cytomegalovirus (HCMV) as it hides away from the immune system. This then enables immune cells to seek out and destroy this potentially deadly virus.
Around four out of five people in the UK are thought to be infected with HCMV, and in developing countries this can be as high as 95%. For the majority of people, the virus remains dormant, hidden away inside white blood cells, where it can remain undisturbed and undetected for decades. If the virus reactivates in a healthy individual, it does not usually cause symptoms. However, for people who are immunocompromised — for example, transplant recipients who need to take immunosuppressant drugs to prevent organ rejection — HCMV reactivation can be devastating.
At present, there is no effective vaccine against HCMV, and anti-viral drugs often prove ineffective or have very serious side-effects.
Now, in a study published in Nature Communications, researchers at Vrije Universiteit Amsterdam in the Netherlands and at the University of Cambridge have found a way to chase the virus from its hiding place using a special type of antibody known as a nanobody.
Nanobodies were first identified in camels and exist in all camelids — a family of animals that also includes dromedary, llamas and alpacas. Human antibodies consist of two heavy and two light chains of molecules, which together recognise and bind to markers on the surface of a cell or virus known as antigens. For this special class of camelid antibodies, however, only a single fragment of the antibody — often referred to as single domain antibody or nanobody — is sufficient to properly recognize antigens.
Dr Timo De Groof from Vrije Universiteit Amsterdam, the study’s joint first author, said: “As the name suggests, nanobodies are much smaller than regular antibodies, which make them perfectly suited for particular types of antigens and relatively easy to manufacture and adjust. That’s why they’re being hailed as having the potential to revolutionise antibody therapies.”
The first nanobody has been approved and introduced onto the market by biopharmaceutical company Ablynx, while other nanobodies are already in clinical trials for diseases like rheumatoid arthritis and certain cancers. Now, the team in The Netherlands and the UK have developed nanobodies that target a specific virus protein (US28), one of the few elements detectable on the surface of a HCMV latently infected cell and a main driver of this latent state.
Dr Ian Groves from the Department of Medicine at the University of Cambridge said: “Our team has shown that nanobodies derived from llamas have the potential to outwit human cytomegalovirus. This could be very important as the virus can cause life threating complications in people whose immune systems are not functioning properly.”
In laboratory experiments using blood infected with the virus, the team showed that the nanobody binds to the US28 protein and interrupts the signals established through the protein that help keep the virus in its dormant state. Once this control is broken, the local immune cells are able to ‘see’ that the cell is infected, enabling the host’s immune cells to hunt down and kill the virus, purging the latent reservoir and clearing the blood of the virus.
Dr Elizabeth Elder, joint first author, who carried out her work while at the University of Cambridge, said: “The beauty of this approach is that it reactivates the virus just enough to make it visible to the immune system, but not enough for it to do what a virus normally does — replicating and spreading. The virus is forced to put its head above the parapet where it can then be killed by the immune system.”
Professor Martine Smit, also from from the Vrije Universiteit Amsterdam, added: “We believe our approach could lead to a much-needed new type of treatment for reducing — and potentially even preventing — CMV infectious in patients eligible for organ and stem cell transplants.”
The research was funded by the Dutch Research Council (NWO), Wellcome and the Medical Research Council, with support from the NIHR Cambridge Biomedical Research Centre.