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A new study by Indiana University found women, younger individuals, those with lower levels of formal education, and people of color are being hit hardest by the COVID-19 pandemic.

The study, published in the Proceedings of the National Academy of Sciences journal, found that Black adults were three times as likely as whites to report food insecurity, being laid off, or being unemployed during the pandemic. Additionally, residents without a college degree were twice as likely to report food insecurity (compared to those with some college) while those not completing high school are four times as likely to report it, compared to those with a bachelor's degree.

These patterns persisted even after taking into account employment status and financial hardship before the pandemic, suggesting that the gap between the "haves" and "have nots" is being widened by the crisis.

The study found that younger adults and women were also more likely to report economic hardships.

"It is clear that the pandemic has had an extraordinary impact on the economic security of individuals who were already vulnerable and among disadvantaged groups," said Bernice Pescosolido, a distinguished professor of sociology at IU and co-author of the study. "This work demonstrates the need for strategically deployed relief efforts and longer-term policy reforms to challenge the perennial and unequal impact of disasters."

Researchers utilized the Person to Person Health Interview Study (P2P) - a statewide representative, face-to-face survey - to interview nearly 1,000 Indiana residents before (October 2018-March 2020) and during the initial stay at home order in (March-May 2020). Their goal was to determine differences in experiences of economic hardship among historically advantaged and disadvantaged groups following the COVID-19 lockdown. The authors measured four self-reported indicators of economic precarity: housing insecurity, food insecurity, general financial insecurity, and unemployment or job loss.

Previous research has shown national and global crises tend to disproportionally impact those who were already struggling financially, and it takes more vulnerable communities significantly longer to recover from disasters.

These previous findings are in line with the IU study, which shows Indiana residents already concerned with their housing, food and finances reported greater concerns with these economic hardships due to the COVID-19 pandemic.

"Providing basic resources to all Americans, such as generous unemployment benefits, paid family leave, affordable federal housing and universal preschool will help communities better weather crisis," said Brea Perry, professor of sociology at IU and co-author of the study. "We need to rethink how we intervene in disasters and also strengthen our social safety net for everyone."

Perry and her team have plans to follow up after the pandemic to understand the long-term impact that COVID-19 has had on individuals and their families. While the impact may not be fully understood at this time, she said we do know that rebuilding public health and other social structures will not only assist disadvantaged groups in times of need, it will also help society at large.

Progressive vision loss, and eventually blindness, are the hallmarks of juvenile neuronal ceroid lipofuscinosis (JNCL) or CLN3-Batten disease. New research shows how the mutation associated with the disease could potentially lead to degeneration of light sensing photoreceptor cells in the retina, and subsequent vision loss.

"The prominence and early onset of retinal degeneration in JNCL makes it likely that cellular processes that are compromised in JNCL are critical for health and function of the retina," said Ruchira Signh, Ph.D., an associate professor in the Department of Ophthalmology and Center for Visual Science and lead author of the study which appears in the journal Communications Biology. "It is important to understand how vision loss is triggered in this disease, what is primary and what is secondary, and this will allow us to develop new therapeutic strategies."

Batten disease is caused by a mutation in the CLN3 gene, which is found on chromosome 16. Most children suffering from JNCL have a missing part in the gene which inhibits the production of certain proteins. Rapidly progressive vision loss can start in children as young as 4 and eventually develop learning and behavior problems, slow cognitive decline, seizures, and loss of motor control. Most patients with the disease die between the ages of 15 and 30.

It has been well established that vision loss in JNCL is due to degeneration of the light-sensing tissue in the retina. The vision loss associated with JNCL can precede other neurological symptoms by many years in some instances, which often leads to patients being misdiagnosed with other more common retinal degenerations. However, one of the barriers to studying vision loss in Batten disease is that mouse models of CLN3 gene mutation do not produce the retinal degeneration or vision loss found in humans. Additionally, examination of eye tissue after death reveals extensive degeneration of retinal cells which does not allow researchers to understand the precise mechanisms that lead to vision loss.

URMC is a hub for Batten disease research. The Medical Center is home to the University of Rochester Batten Center (URBC), one of the nation's premier centers dedicated to the study and treatment of this condition. The URBC is led by pediatric neurologist Jonathon Mink, M.D., Ph.D., who is a co-author of the study. Batten disease is also one of the key research projects that will be undertaken by the National Institute of Child Health and Human Development-supported University of Rochester Intellectual and Development Diseases Research Center.

To study Batten disease in patient's own cells, the research team reengineered skin cells from patients and unaffected family members to create human-induced pluripotent stem cells. These cells, in turn, were used to create retinal cells which possessed the CLN3 mutation. Using this new human cell model of the disease, the new study shows for the first time that proper function of CLN3 is necessary for retinal pigment epithelium cell structure, the cell layer in the retina that nourishes light sensing photoreceptor cells in the retina and is critical for their survival and function and thereby vision.

Singh points out that understanding how RPE cell dysfunction contributes to photoreceptor cell loss in Batten disease is important first step, and it will enable researchers to target specific cell type in the eye using potential future gene therapies, cell transplantation, and drug-based interventions.

Researchers from Kumamoto University (Japan) have clarified the mechanism by which blood and lymph vessels remain segregated from one another after development. The characteristics and structures of these two vessel types are very similar, and how they maintain separation has remained unexplained for many years. In this study, researchers found that the molecule Folliculin (FLCN) in vascular endothelial cells acts as a gatekeeper to maintain that separation.

Blood and lymphatic vessels form independent networks until the final confluence at the left and right venous angles in the neck. Blood vessels act as a pipeline that transports oxygen from the lungs to tissues throughout the body. Lymphatic vessels, on the other hand, take in tissue fluids that cannot be collected by blood vessels and act as part of the immune system. However, blood and lymph vessel characteristics and structures are very similar so how they maintain separation from each other has long been a mystery. The elucidation of this mechanism could provide the foundation for the development of novel therapeutic approaches to human lymphatic disorders. For example, the creation of a bypass (a venous-lymphatic shunt) allowing clogged lymphatic flow to return directly to veins would become an innovative therapy for postoperative lymphedema. Thus, researchers around the world have been looking into blood-lymphatic vessel separation mechanisms, but it is still not completely understood.

In this study, researchers first focused on FLCN, the causative gene of a genetic disorder with typical symptoms of multiple lung cysts, kidney cancer, and benign skin tumors (Birt-Hogg-Dube syndrome). They found that mice that were missing the Flcn gene in vascular endothelial cells had abnormal anastomosis between blood and lymph vessels that resulted in fetal death. Furthermore, even in postnatal mice with normal blood and lymphatic vessel separation, induced Flcn gene depletion in endothelial cells caused abnormal anastomosis between the two vessel types.

Flcn deficiency gives rise to lymphatic-biased vascular endothelial cells. These cells cause anastomosis between blood and lymphatic vessels. Prox1* is a central transcription factor in the regulation of lymphangiogenesis and its expression is suppressed by Flcn in venous endothelial cells to maintain the identity of vascular endothelial cells. However, when Flcn regulation in vascular endothelial cells is lost, Prox1 becomes expressed, making venous endothelial cells lymphatic biased. Researchers also found that deletion of Flcn results in the translocation of the transcription factor Tfe3, which is normally in the cytoplasm, into the nucleus where it directly upregulated Prox1 expression. In fact, when Flcn knockout mice were crossed with Tfe3 knockout mice, Prox1 was not expressed in the absence of both Tfe3 and Flcn, and lymphatic biased venous endothelial cells were not seen. These results demonstrate that FLCN acts as a gatekeeper that regulates the plasticity and maintains the separation of blood and lymphatic vessels.

"These results are of great academic importance in that they have clarified a biological question that has gone unanswered for many years: Why do two very similar circulatory systems in the body, blood and lymph vessels, form and maintain independent networks? From a clinical point of view, this has the potential to provide clues on the mechanism of cancer metastasis and can potentially be developed into a treatment for lymphedema," said Associate Professor Masaya Baba, who led the study. "In cancer surgery, lymph node removal can result in serious edema in the upper and lower limbs due to decreased ability to drain lymphatic fluid. Physical therapy, elastic stockings, and lymphovenous anastomosis are listed as treatment methods, but even with skilled microsurgery techniques, it is difficult to treat sufficiently. Out of this research, we envision a future innovative treatment for lymphedema where we can pharmaceutically intervene in the signaling pathway of FLCN to artificially create a shunt that locally connects veins and lymph vessels."

This research was posted online in Nature Communications on 9 December 2020 and was selected as one of Nature Communications Editor's Highlights. The link to the featured article can be found an the translational and clinical research page.

*Prox1 (prospero-related homeobox 1) is a transcription factor that is essential for the development of lymphatic endothelial cells from vascular endothelium cells during development. It is normally expressed specifically in lymphatic endothelial cells and Prox1 is a master gene for the formation of lymphatic vessels. Artificially expressing Prox1 in blood vessels is known to induce their differentiation into lymphatic vessels.

This is the finding of an 18-year-study of over 300,000 people with diabetes in England, from scientists from Imperial College London and published in the journal The Lancet Diabetes & Endocrinology.

Thursday Feb 4th is World Cancer Day.

The research, funded by the Wellcome Trust, reveals that between 2001-2018 heart disease and stroke were no longer the leading causes of death among people with diabetes, as they were 18 years ago.

Diabetes affects 4.7 million people in the UK, and is caused by the body being unable to regulate blood sugar levels. Around 90 per cent have type 2 diabetes, which is associated with lifestyle factors such as high blood pressure and excess weight.

The remainder have type 1 diabetes, which is caused by the body attacking the cells that produce insulin, the hormone that controls blood sugar.

In the study, researchers from Imperial's School of Public Health looked at anonymised primary care data from 313,907 people in England with diabetes between 2001-2018, and linked this with death data from the Office of National Statistics.

The study revealed death rates for those with diabetes declined in the study period by 32 per cent for men, and 31 per cent for women.

The team explain deaths from heart disease and stroke have reduced across the whole population, including those without diabetes.

Dr Jonathan Pearson-Stuttard, lead author of the study, said: "Improvements in risk factors such as smoking and blood pressure, along with progress in medical treatments have contributed to large falls in deaths from heart disease and stroke. The improvements have been even greater in those with diabetes. This has resulted in vascular conditions accounting for around 25 per cent of all deaths in those with diabetes compared to 45 per cent 20 years ago.

"In contrast, improvements in cancer death rates have been much more modest, with improvements in those with diabetes lagging behind the general population. It is striking that cancer is now the leading cause of death in England among people with diabetes and the leading contributor to excess death compared to those without diabetes. Added to this is the fact the UK continues to lag behind other EU countries in terms of cancer survival rates."

The findings also showed people with diabetes were more likely to die from dementia, liver disease, or respiratory disease in 2018 than people without diabetes.

Death rates were higher in those with diabetes compared to those without in almost all causes studied. Death rates for liver disease and dementia were twice as high in those with diabetes compared to those without in 2018, while respiratory death rates were 80 per cent higher.

he research team say individuals with diabetes have up to a two-fold increased risk of dementia compared with those without diabetes. The precise link for this is unclear but there are several shared risk factors such as smoking, obesity and poor diet between diabetes and dementia.

The increase in liver disease could be due to the high levels of obesity among people with diabetes, and a higher alcohol consumption.

The team call for guidance around the treatment of diabetes to be updated, to ensure patients and clinicians are aware of the breadth of conditions they are at higher risk of including cancer, dementia and liver disease.

They add that the reasons for cancer being the leading cause of death are unclear, but could be linked to the fact people with diabetes are more likely to be overweight, and excess weight is a leading risk factor for cancer.

The team also highlight limitations of the study, such as the inability to differentiate between type one and two diabetes in the data, and the fact around 20 per cent of people with diabetes in the UK are undiagnosed.

Professor Edward Gregg, senior author of the study added: "This study is another reminder that as people die less from cardiovascular diseases, diabetes still leads to a wide range of other problems. The diversification of the big contributors to death here included cancers, dementia and respiratory diseases. This, and the current experience with COVID-19, is a reminder that we need to take an increasingly broad view about what prevention means for people with diabetes."

Researchers at Flinders University are working to remedy this situation by identifying what triggers this chronic pain in the female reproductive tract.

Dr Joel Castro Kraftchenko - Head of Endometriosis Research for the Visceral Pain Group (VIPER), with the College of Medicine and Public Health at Flinders University - is leading research into the pain attached to Dyspareunia, also known as vaginal hyperalgesia or painful intercourse, which is one of the most debilitating symptoms experienced by women with endometriosis and vulvodynia.

Pain is detected by specialised proteins (called ion channels) that are present in sensory nerves and project from peripheral organs to the central nervous system.

"Very little is known about which ion channels are in charge of detecting painful stimuli from the female reproductive tract; and how pain is transmitted via peripheral sensory nerves (innervating these organs) to the central nervous system," says Dr Castro Kraftchenko.

"Also, little is known about how mechanical stimuli is detected and transmitted from female reproductive organs to the Central Nervous System.

"This lack in knowledge provides a limiting factor for developing treatments for painful intercourse associated with endometriosis and vulvodynia.

"The aim of our study is to fill this gap in knowledge. this study provides novel findings advancing the understanding of vaginal sensation that can be used to recognise and explore changes in states of chronic pelvic pain associated with endometriosis and vulvodynia."

The study - Pharmacological modulation of voltage-gated sodium (NaV) channels alters nociception arising from the female reproductive tract, by Joel Castro Kraftchenko, Jessica Maddern, Andelain Erickson, Ashlee Caldwell, Luke Grundy, Andrea Harrington and Stuart Brierley, published in the journal Pain (DOI: 10.1097/j.pain.0000000000002036) - describes how sensory nerves innervating a vagina (tested on mice) respond to different mechanical stimuli.

It also identifies for the first time the presence of specialised ion channels involved in the transmission of pain signals throughout these sensory nerves; and how pharmacological modulation of these ion channels alters pain signalling and ultimately regulates vaginal pain sensitivity in vivo.

"These findings contribute towards the understanding of how mechanical stimuli is detected and transmitted from female reproductive organs and uncover potential molecular targets to investigate as novel therapeutics to relieve painful intercourse," says Dr Castro Kraftchenko.

"With this, we hope to ultimately improve the quality of life of patients with endometriosis and vulvodynia."

New tools and methods have been described by WEHI researchers to study an unusual protein modification and gain fresh insights into its roles in human health and disease.

The study - about how certain sugars modify proteins - was published today in Nature Chemical Biology. Led by WEHI researcher Associate Professor Ethan Goddard-Borger, this work lays a foundation for better understanding diseases like muscular dystrophy and cancer.

At a glance

WEHI researchers have developed new tools and methods to determine how 'tryptophan C-mannosylation', an unusual protein modification, impacts the stability and function of disease-relevant proteins.

These tools have been used to map the prevalence of this protein modification in healthy tissue.

This work lays the foundation for future studies into the role this protein modification plays in diseases as diverse as muscular dystrophy and cancer.

The 'dark matter' of biology

Glycosylation is the process by which proteins are modified with sugars. About 90 per cent of proteins on the surface of human cells - and half of the cells' total proteins - are modified with sugars. These modifications can range from the addition of a single sugar, to long complex polymer chains. They've been described as the 'dark matter' of biology because their distribution, variability and biological functions are, for the most part, not well understood.

Associate Professor Goddard-Borger said his team, and the glycobiology field more generally, are making concerted efforts to build a better understanding of the roles that glycosylation plays in health and disease.

"There are a whole range of diseases that feature aberrant cellular glycosylation - a change in 'normal' glycosylation patterns," he said.

"These changes may yield new therapeutic strategies, however a better understanding of what constitutes 'normal' glycosylation is required before we can further develop drugs targeting protein glycosylation."

"It's a scenario that is akin to the 'dark matter' of the universe: we know that all of this protein glycosylation exists in the body, but we don't fully appreciate its composition and function."

Shedding light on a sweet process

Glycosylation usually occurs on the nitrogen or oxygen atoms of a protein. However, it can also occur on carbon atoms through the process of 'tryptophan C-mannosylation'. This latter protein modification is particularly poorly understood and so the WEHI team set out to develop tools and methods to shed light on this aspect of the biological 'dark matter'.

"We've developed methods that will enable researchers to easily install this unusual modification on nearly any protein they want, allowing them to investigate its effect on protein stability and function," Associate Professor Goddard-Borger said.

"In this work, we've shown that a common feature of tryptophan C-mannosylation is that it stabilises proteins. Diverse, unrelated proteins all appear to be more stable once modified. However, we've also demonstrated for the first time that some proteins' functions can be modulated by tryptophan C-mannosylation'. There is clearly much left to learn about this process and now we have the means to perform these studies."

Mapping the prevalence of tryptophan C-mannosylation

Associate Professor Goddard-Borger said the tools developed by his team also enable the abundance of this poorly understood protein modification to be determined in healthy and diseased tissues, which will fortify efforts by scientists around the world to map and understand protein glycosylation in health and disease.

"The methods we describe combine state-of-the-art mass spectrometry techniques with recombinant antibody tools generated at WEHI," he said.

"We've reported some really unexpected results regarding the prevalence of this modification in healthy brain tissue. At present, we are extending this to map the modification across most tissues in the body to better understand the biology of this weird and wonderful form of protein glycosylation, as well as its role in cancer and muscular dystrophies."

In order to produce tiny electronic memories or sensors in future, it is essential to be able to arrange individual metal atoms on an insulating layer. Scientists at Bielefeld University's Faculty of Chemistry have now demonstrated that this is possible at room temperature: molecules of the metal-containing compound molybdenum acetate form an ordered structure on the insulator calcite without jumping to other positions or rotating. Their findings have been presented in the Nature Communications journal. The work was done in cooperation with researchers from the universities of Kaiserslautern, Lincoln (UK) and Mainz.

'Until now, it has been difficult to arrange metal atoms on an insulator surface. It's easier on a metal surface, but that's not of much benefit for use in electronic components,' says Professor Dr Angelika Kühnle, who heads the Physical Chemistry I working group at the Faculty of Chemistry. 'That's what's special about our study: we've found a way to arrange metal atoms on insulators in a lattice-like structure.' Insulators are materials in which electrons cannot move freely and are therefore very poor conductors of electricity.

The difficulty is in robustly anchoring metal atoms even at room temperature - without them attracting each other, jumping to other positions or rotating. Until now, scientists have been able to arrange small molecules on insulators at very low temperatures, but at room temperature they were too mobile. Larger molecules solved the problem of mobility, but quickly formed clusters.

For their research, Kühnle and her working group used molybdenum acetate, a compound that contains two atoms each of the metal molybdenum. The fact that this compound shows interesting structural properties on a gold surface had previously been discovered by a research team from the Technical University of Kaiserslautern. 'If molybdenum acetate is now applied to a calcite surface, the molecules form an ordered structure. This means that the molybdenum atoms are also arranged in an ordered array,' says Dr Simon Aeschlimann, who conducted research in Kühnle's group and is lead author of the published study. 'By means of various experiments and simulations, we were able to show that the molybdenum acetate molecules neither jump nor rotate, nor do they form clusters. They are firmly anchored on the calcite surface.'

The scientists conducted the experiments with the aid of an atomic force microscope. 'In atomic force microscopy, a tiny needle scans the surface of materials - like a record player, except that the needle does not touch the surface directly, but is deflected by atomic forces. This then creates an image of the surface structure,' says Aeschlimann. The scientists examined, for example, where the molybdenum acetate molecules are located on the calcite surface and in which direction they align themselves.

The ordered structure is created because the molybdenum acetate molecules align themselves precisely with the charge distribution on the calcite surface. Calcite consists of calcium and carbonate building blocks that form a regular lattice structure. 'Each molybdenum acetate molecule fits only in a very specific place on the calcite surface and at the same time does not interact with its neighbouring molybdenum acetate molecules. That means it is firmly anchored,' says Kühnle.

As a scientist engaged in pure research, Kühnle is interested in the question of how molecular structures form on surfaces or interfaces. But the results are also relevant for electronic applications: if, for example, magnetic metals can be arranged according to the same principle, this could be used in nanotechnology to produce data storage - i.e. memories that are only a few millionths of a millimetre in size. Other possible areas of application include optical or chemical sensors.

Cardiac patients who also have diabetes will be able to do their rehabilitation exercises more safely, thanks to the world's first guidance on the subject, which has been published by international experts including a Swansea University academic.

The guidance will be a crucial resource for healthcare professionals, so they can help the growing number of cardiac rehabilitation patients who also have diabetes.

The guidance, approved by international diabetes organisations, was drawn up by a team including Dr. Richard Bracken of the School of Sports and Exercise Sciences, College of Engineering and the Diabetes Research group, located in the Medical School at Swansea University.

Physical exercise and improving activity levels are central parts of cardiac rehabilitation, which aims to boost the health and fitness of people with heart problems.

At present, around 25% of participants attending cardiac rehabilitation in Europe, North America and Australia also have diabetes. This figure is increasing, largely because there are some common risk factors for both cardiovascular disease and diabetes, especially obesity and sedentary lifestyles.

While being more active is crucial for cardiac rehabilitation patients, a major obstacle is that many worry that the exercise itself will put them at risk.

For those patients who also have diabetes, however, there are additional worries, especially about falling blood sugar levels leading to hypoglycaemia. Fear of having a "hypo", which can lead to dizziness, disorientation, anxiety and many other symptoms, is one of the main barriers stopping people with diabetes from incorporating exercise into daily life.

This helps explain why cardiac patients who also have diabetes have are less likely to take up and continue a cardiac rehabilitation programme than those without diabetes.

This is where the new guidance can make a difference. It focuses on managing levels of blood sugar during rehabilitation activities, to reduce the risk of acute glycaemic problems during exercise. The aim is to give more confidence to patients with diabetes, making them more likely to do the rehabilitation exercises and keep at it, improving their overall health.

The new guidance gives health professionals clear advice covering areas such as:

-The interactions that can occur between medicines that patients with both cardiovascular disease and diabetes may be using

-The best types of exercise for these patients, the ideal intensity level, and the safest times of day

-The different requirements for patients with Type 1 and Type 2 diabetes

The guidance, contained in a position statement, was approved by the British and Canadian Associations of Cardiovascular Prevention and Rehabilitation, the International Council for Cardiovascular Prevention and Rehabilitation and the British Association of Sport and Exercise Sciences.

Dr Richard Bracken, one of the authors, and a diabetes expert from the A-STEM research team in Swansea University School of Sports and Exercise Sciences and the Lifestyle research group lead in the Diabetes Research Group, Medical School, said:

"Exercising safely is essential to improve the health of patients with cardiovascular problems.

A rising number of these patients also have diabetes, so it's essential that cardiac rehabilitation programmes meet their needs.

This expert guidance will mean health professionals can design cardiac rehabilitation to give patients with diabetes the reassurance they need to start and stick with the programme, boosting their overall health."

The guidance was published in the British Journal of Sports Medicine doi: 10.1136/bjsports-2020-102446

Between chemistry classes, gemstones, and electronics, the idea of crystals, substances with an ordered and periodic arrangement of atoms is quite common. But about 40 years ago, a strange particle was discovered by scientists that hasn't become commonplace in our world yet: quasicrystals. These are structures with curious atomic arrangements, which, while superficially similar to crystals, lack periodicity despite being ordered. Because of their structures, quasicrystals exhibit symmetries forbidden to crystals and are endowed with interesting properties that crystals cannot show, such as high resistance to heat flow, current flow, and corrosion.

Since their discovery, quasicrystals have been researched extensively by materials scientists around the world. Due to their rarity, scientists have often resorted to studying models mimicking them, called approximants. Recently, in a class of gold-based approximants, called "Tsai-type approximants", the presence of magnetic order was detected whose type can be controlled by the composition of the approximants--an exciting possibility for material scientists to explore.

In such approximants of increasing complexity, such as that composed of gold (Au), aluminum (Al), and terbium (Tb), the magnetic order was found to be antiferromagnetic, where each ion in the crystal acts as a small magnets with its poles opposite to those of its neighbors. In a new study published in Physical Review B, Prof. Ryuji Tamura from the Tokyo University of Science (TUS), Japan, along with his colleagues Sam Coates of TUS, and Hem Raj Sharma and Ronan McGrath of the University of Liverpool, explored the atomic structure of the antiferromagnetic surface this Tsai-type approximant. Prof. Tamura, who led the study, says: "Au-based Tsai approximants are under-researched compared to their silver (Ag)-based counterparts, particularly in the field of surface science. Understanding the structures of these Tsai-type materials will allow for in-depth interpretations of their specific properties, such as magnetic transitions, electronic features, and superconductivity." Their study yielded unexpected results.

The building blocks of Tsai-type approximants are "Tsai-type clusters", polyhedral shells whose number of sides depends on the variant of the approximant. In their study, Prof. Tamura's team chose a 1/1 variant of the Au-Al-Tb approximant in which a tetrahedral unit was enclosed within a dodecahedron, icosahedron, icosidodecahedron, and rhombic triacontahedron. The Tb atoms occupied the vertices of the icosahedron while the Au/Al atoms occupied the vertices of the remaining shells.

The scientists looked into a specific surface of a single crystal of the 1/1 Au-Al-Tb using a scanning tunneling microscope (STM) and backed up their observations with density functional theory (DFT) calculations.

They found that the surface had a peculiar step-terrace-like structure with the terraces ending at planes containing Tb atoms and a step height that, interestingly, appeared to minimize the number of incomplete icosahedrons. Furthermore, they found that the terrace structure depended on the sign of the biasing voltage applied to the sample. While at positive bias, the Tb atoms showed a rhombohedral or hexagonal arrangement, negative bias revealed the Au/Al atoms to be arranged in a linear row-like structure, a kind of switching not observed in a Tsai-type material before. "As this is the first Tsai-type material to show such a scheme, we need to further investigate Au-based Tsai types to assess whether chemical composition has a role to play in surface structure," comments Prof. Tamura. The observations were consistent with DFT calculations.

While quasicrystals have found several applications, ranging from surgical instruments, LEDs to non-stick frying pans, they are far from being well understood and the recent findings in quasicrystal-like structures serve to hint at the untapped exotic possibilities they harbor. "The unique structure of the Tsai-type surface suggests that quasicrystals could be used as a template for molecular adsorption in the creation of organic semiconducting thin films," Prof. Tamura says. "Understanding of how the structure change corresponds to the magnetism can open doors to new applications," he adds.

One thing's for sure: the quasicrystal is a little clearer!

In order to fight pathogens, mast cells regulate inflammatory reactions of the immune system. Both mast cells and neutrophils are white blood cells and are critical for the body's immune defense. A team of scientists around the immunologist Prof. Dr. Anne Dudeck and the bioengineer Jan Dudeck has discovered a crucial aspect of the communication between mast cells and neutrophils. These new findings may allow for developing innovative, targeted therapeutic strategies to dampen allergic responses and inflammatory reactions. The results have been published in the renowned journal "Immunity".

Neutrophils are rapidly recruited to sites of inflammation or infection. Consequently, they are the first mobile line of defense of our body against infections. In contrast, mast cells are tissue-resident cells that act as sentinels, responding to pathogens or tissue damage by attracting additional immune cells. For a long time, mast cells had a rather bad reputation, because they are also key cells of unwanted allergic reactions. Mast cell-released histamine causes the well-known symptoms that afflict persons with allergies: hay fever, itching, hives or even shortness of breath. But that is just one side of the coin. On the flip side, mast cells are essential for a fast immune response against pathogens, because they orchestrate the arrival of neutrophils at sites of inflammation or infection.

The team surrounding first author Jan Dudeck has analysed, how mast cells influence this recruitment of neutrophils. Scientists already established in the last couple of years that mast cells are involved in this process but up to now the exact molecular mechanisms remained elusive. Mast cells store a whole range of inflammatory mediators, including the messenger tumor necrosis factor (TNF), inside small secretory reservoirs, the granula.

The authors could show that against their expectation, the mast cell-derived TNF is dispensable for the activation of endothelial cells lining the blood vessel. Instead, the neutrophils circulating in the blood stream were directly activated in order to migrate into the inflamed tissues.

But how is the TNF of tissue-resident mast cells delivered to neutrophils circulating inside blood vessels? The Magdeburg scientists employed high-resolution 2-Photon-Microscopy to show in fascinating pictures that the mast cells use a surprising trick. They position themselves, guardian-like, directly around the blood vessel and even insert protrusions into the vessel lumen. In case of emergency, granula containing TNF are released directionally from these protrusions. Thereby the TNF immediately is present where the neutrophils can "see" it - in the bloodstream, circulating through the vessels. The TNF activates surface proteins on the neutrophils. Thereby the cells become stickier, can attach themselves at the vessel wall and then migrate into the surrounding tissue.

Prof. Dr. Anne Dudeck explains the significance of these results: "The capacity of mast cells to degranulate directionally into the blood stream might explain why local allergen encounter can trigger a systemic anaphylactic shock. Next, we want to understand the exact mechanisms mast cells use to insert these protrusions into the vessel wall. Targeting these might reveal therapeutic strategies to dampen allergic shock or cytokine storm syndromes. At the same time, it might also enable us to harness the ability of mast cells to stimulate the immune response, notably the recruitment of neutrophils, during infections."

The immunologist is leading the group Immunoregulation at the Institute for Molecular and Clinical Immunology at the Otto-von-Guericke University Magdeburg. Since many years, her research contributes to improving the reputation of mast cells. In previous studies, she already demonstrated that mast cells play a critical role during immune reactions, particularly contributing to adaptive, i.e. long-lived and highly specific immune responses against pathogens.

Treating equine donor stem cells with a growth factor called TGF-β2 may allow them to avoid "tripping" the immune response in recipients, according to new research from North Carolina State University. The work could simplify the stem cell treatment process for ligament and tendon injuries in horses, and may also have implications for human stem cell therapies.

Mesenchymal stem cell therapy is a promising avenue for treating musculoskeletal injuries - particularly tendon and ligament injuries - in horses. Mesenchymal stem cells are adult stem cells found in bone marrow that act as repair directors, producing secretions that recruit paracrine, or healing, factors to the site of injury.

Just as blood cells have "types," depending upon which antigens are on the blood cell's surface, mesenchymal stem cells have differing sets of major histocompatibility complex molecules, or MHCs, on their surfaces. If the MHCs of donor and recipient aren't a match, the donor's stem cells cause an immune response. In organ transplants, MHCs are carefully matched to prevent rejection.

"These treatments aren't like a bone marrow transplant or an organ transplant," says Lauren Schnabel, associate professor of equine orthopedic surgery at NC State and corresponding author of the work. "Since the mesenchymal stem cells are being used temporarily to treat localized injury, researchers once thought that they didn't need to be matched - that they wouldn't cause an immune response. Unfortunately, that isn't the case."

Schnabel and Alix Berglund, a research scholar at NC State and lead author of the paper describing the work, wanted to find a way to utilize mesenchymal stem cell therapy without the time, effort and additional cost of donor/recipient matching.

"Since these cells don't have to be in the body as long as an organ does, 'hiding' them from the immune system long enough for them to secrete their paracrine factors could be a way around donor/recipient matching," Berglund says. "Downregulating expression of the MHC molecules could be one way to do this."

The researchers cultured stem cells and lymphocytes, or T cells, from eight horses, cross-pairing them in vitro so that the stem cells and lymphocytes had differing MHC haplotypes. In one group, stem cells had been treated with transforming growth factor beta (TGF-β2) prior to being added to the lymphocytes in the culture media; the other group was untreated. TGF-β2 is a cell-signaling molecule produced by white blood cells that blocks immune responses.

Cultures with treated stem cells had a 50% higher stem cell survival rate than untreated cultures.

"We use mesenchymal stem cells to treat musculoskeletal injuries - particularly tendon injuries - in horses very effectively," Schnabel says. "And while you can extract the secretions from the stem cells, you get better results with the cells themselves. Stem cells aren't just a reservoir of secretions, they're a communications hub that tells other cells what they should be doing. So finding a way to utilize these cells without stimulating immune response gives us better treatment options."

"This is a promising pilot study," Berglund says. "Our next steps will be to further explore the immune response in vivo, and to look at human cells in vitro, as this work has excellent potential to help humans with these injuries as well."

The research appears in Frontiers in Cell and Developmental Biology, and was supported by the National Institutes of Health (grants K08AR060875 and K01OD027037) and the Morris Animal Foundation (grants D16EQ-405 and D18EQ-055). Research specialist Julie Long and statistician James Robertson, both of NC State, also contributed to the work.

Floating sea macro-litter is a threat to the conservation of marine ecosystems worldwide. The largest density of floating litter is in the great ocean gyres -systems of circular currents that spin and catch litter- but the polluting waste is abundant in coastal waters and semi closed seas such as the Mediterranean.

MARLIT, an open access web app based on an algorithm designed with deep learning techniques, will enable the detection and quantification of floating plastics in the sea with a reliability over 80%, according to a study published in the journal Environmental Pollution and carried out by experts of the Faculty of Biology and the Biodiversity Research Institute of the University of Barcelona (IRBio).

This methodology results from the analysis through artificial intelligence techniques of more than 3,800 aerial images of the Mediterranean coast in Catalonia, and it will allow researchers to make progress in the assessment of the presence, density and distribution of the plastic pollutants in the seas and oceans worldwide. Among the participants in the study, published in the journal Environmental Pollution, are the experts of the Consolidated Research Group on Large Marine Vertebrates of the UB and IRBio, and the Research Group on Biostatistics and Bioinformatics (GRBIO) of the UB, integrated in the Bioinformatics Barcelona platform (BIB).

Litter that floats and pollutes the ocean

Historically, direct observations (boats, planes, etc.) are the base for the common methodology to assess the impact of floating marine macro-litter (FMML). However, the great ocean area and the volume of data make it hard for the researchers to advance with the monitoring studies.

"Automatic aerial photography techniques combined with analytical algorithms are more efficient protocols for the control and study of this kind of pollutants", notes Odei Garcia-Garin, first author of the article and member of the CRG on Large Marine Mammals, led by Professor Àlex Aguilar.

"However, -he continues-, automated remote sensing of these materials is at an early stage. There are several factors in the ocean (waves, wind, clouds, etc.) that harden the detection of floating litter automatically with the aerial images of the marine surface. This is why there are only a few studies that made the effort to work on algorithms to apply to this new research context".

The experts designed a new algorithm to automate the quantification of floating plastics in the sea through aerial photographs by applying the deep learning techniques, automatic learning methodology with artificial neuronal networks able to learn and take the learning to higher levels.

"The great amount of images of the marine surface obtained by drones and planes in monitoring campaigns on marine litter -also in experimental studies with known floating objects- enabled us to develop and test a new algorithm that reaches a 80% of precision in the remote sensing of floating marine macro-litter", notes Garcia-Garin, member of the Department of Evolutionary Biology, Ecology and Environmental Sciences of the UB and IRBio.

Preservation of the oceans with deep learning techniques

The new algorithm has been implemented to MARLIT, an open access web app described in the article and which is available to all managers and professionals in the study of the detection and quantification of floating marine macro-litter with aerial images. In particular, this is a proof of concept based on an R Shiny package, a methodological innovation with great interest to speed up the monitoring procedures of floating marine macro-litter.

MARLIT enables the analysis of images individually, as well as to divide them into several segments -according to the user's guidelines-, identify the presence of floating litter in each certain area and estimate their density with the image metadata (height, resolution). In the future, it is expected to adapt the app to a remote sensor (for instance, a drone) to automate the remote sensing process.

At a European level, the EU Marine Strategy Framework Directive indicates the application of FMML monitoring techniques to fulfil the continuous assessment of the environmental state of the marine environment. "Therefore, the automatization of monitoring processes and the use of apps such as MARLIT would ease the member states' fulfilment of the directive", conclude the authors of the study.

A new study led by the University of Kent's Durrell Institute of Conservation and Ecology (DICE) has found that elephants living around the world-famous Masai Mara National Reserve, Kenya, are crop-raiding closer to the protected area, more frequently and throughout the year but are causing less damage when doing so.

Findings show that the direct economic impact of this crop-raiding in the Trans Mara region has dropped, yet farmers have to spend more time protecting their fields, further reducing support for conservation in communities who currently receive few benefits from living with wildlife.

The research published by Biological Conservation demonstrates the effects that climate change, agricultural expansion and increased cattle grazing within the reserve have had on elephant crop-raiding trends in the region.

The team of conservationists, led by Professor Bob Smith and DICE alumna Dr Lydia Tiller (Research and Science Manager, Save the Elephants), investigated the seasonal, temporal and spatial trends of elephant crop-raiding in the Trans Mara, Kenya during 2014-2015, comparing results to a previous DICE study from 1999 to 2000.

The number of crop-raiding incidents increased by 49% over the 15 years, but crop damage per incident dropped by 83%. This could be because farmers are better prepared to frighten off elephants. It could also be because landcover change makes it harder for elephants to hide in forest patches, and this spread of farmland and loss of forest to illegal charcoal clearing means that more of the crop-raiding incidents are taking place closer to the protected area.

Professor Smith said: 'Landcover change has had a major impact on where human-elephant conflict takes place. Better land-use planning and support for farmers would help reduce crop-raiding as well as people's tolerance of elephants.'

Lydia Tiller said: 'The change in crop-raiding trends going from being highly seasonal during 1999-2000 when maize crops are ripe, to year-round during 2014-2015, is yet another demonstration of how climate change is affecting nature. With less natural vegetation available for elephants to eat in the Masai Mara, this is not surprising. Restoring elephants' feeding habitat in the park is vital to reducing human-elephant conflict in the area.'

In a new perspective piece published in the Feb. 5 issue of Science, pharmacologist Namandje Bumpus, Ph.D. -- who recently became the first African American woman to head a Johns Hopkins University School of Medicine department, and is the only African American woman leading a pharmacology department in the country -- outlines the molecular origins for differences in how well certain drugs work among distinct populations. She also lays out a four-part plan to improve the equity of drug development.

"Human beings are more similar than we are different," says Bumpus. "Yet, the slightest variations in our genetic material can cause big differences in how well drugs work in our bodies. This is not a new idea."

Genetic variants can be more likely to occur in some ethnic groups versus others, and, as a champion for diversity in science, Bumpus advocates that these differences make it even more important to increase diversity in clinical trials of new drugs and therapies. Yet, many clinical trials continue without diverse participation, potentially leading to poor outcomes for people of color and less access to emerging therapies.

Some medicines available today, such as warfarin, used for blood thinning, have been found to be less effective in people of African origins; and, according to previous studies, one in five new drugs approved by the FDA showed differences in effectiveness across ethnic groups.

Now, as new treatments and vaccines sweep us toward a critical turning point in a pandemic that has disproportionately affected people of color, the need for better standards for diversity in clinical trials is greater than ever, says Bumpus, the E.K. Marshall and Thomas H. Maren Professor and Director of the Department of Pharmacology and Molecular Sciences at the Johns Hopkins University School of Medicine.

But simply increasing the number of underrepresented minorities in clinical trials is not enough to solve the systemic problems, she adds.

Bumpus' framework for better drug development includes a four-part plan involving the laboratory research of cellular and animal models to study genetic variability; better hiring practices to diversify the scientific workforce; diversity requirements for funding agencies; and diversity reporting requirements on clinical trial demographics in articles published in scientific journals.

By implementing diversity requirements that demand diversity among clinical trial participants and in study design, funding agencies would ensure accountability -- and scientific journals would increase transparency for their audiences, says Bumpus. At the level of research institutions, biotechnology and pharmaceutical companies, Bumpus advocates for hiring practices to build a more diverse workforce. With a diverse workforce comes diversity in thought, she says, and a higher likelihood that researchers will be more attuned to build genetic variation into their studies.

She notes that animal models can be genetically engineered to reflect the variations that occur across ethnic groups, potentially to "bolster predictability of drug outcomes and provide a mechanistic foundation for understanding disparities."

Genetic variations related to drug response are often associated with a family of enzymes vital to drug metabolism, known as cytochromes P450. This family of enzymes in humans processes about 75% of clinically available drugs.

Still, subtle genetic differences can alter the enzyme in people and some gene variants are more prevalent in specific ethnic groups. The altered enzyme could affect how medicines are processed and used by the body, so that what works for one person could be ineffective or toxic for another.

Because most clinical trials of these drugs included people of European descent and few people of African descent, disparities in drug effectiveness are often not immediately known.

Bumpus says the framework may compel the drug development field to take steps toward a future where "treatments are most likely to work for all people" and "existing health disparities are not further exacerbated."

CHAMPAIGN, Ill. -- Chemical manufacturers frequently use toxic solvents such as alcohols and benzene to make products like pharmaceuticals and plastics. Researchers are examining a previously overlooked and misunderstood phenomenon in the chemical reactions used to make these products. This discovery brings a new fundamental understanding of catalytic chemistry and a steppingstone to practical applications that could someday make chemical manufacturing less wasteful and more environmentally sound.

The study led by University of Illinois Urbana-Champaign researcher David Flaherty, University of Minnesota, Twin Cities researcher Matthew Neurock and Virginia Tech researcher Ayman Karim is published in the journal Science.

Combining solvents and metal nanoparticles accelerates many chemical reactions and helps maximize yield and profit margins for the chemical industry. However, many solvents are toxic and difficult to safely dispose, the researchers said. Water works, too, but it is not nearly as efficient or reliable as organic solvents. The reason for the difference was thought to be the limited solubility of some reactants in water. However, multiple irregularities in experimental data have led the team to realize the reasons for these differences were not fully understood.

To better understand the process, the team ran experiments to analyze the reduction of oxygen to hydrogen peroxide - one set using water, another with methanol, and others with water and methanol mixtures. All experiments used palladium nanoparticles.

"In experiments with methanol, we observed spontaneous decomposition of the solvent that leaves an organic residue, or scum, on the surface of the nanoparticles," said Flaherty, a professor of chemical and biomolecular engineering at Illinois. "In some cases, the scumlike residue clings to the nanoparticles and increases reaction rates and the amount of hydrogen peroxide formed instead of hampering the reaction. This observation made us wonder how it could be helping."

The team found that the residue, or surface redox mediator, holds oxygen-containing species, including a key component hydroxymethyl. It accumulates on the palladium nanoparticles' surface and opens new chemical reaction pathways, the study reports.

"Once formed, the residue becomes part of the catalytic cycle and is likely responsible for some of the different efficiencies among solvents reported over the past 40 years of work on this reaction," Flaherty said. "Our work provides strong evidence that these surface redox mediators form in alcohol solvents and that they may explain many past mysteries for this chemistry."

By working with multiple types of experiments and computational simulations, the team learned that these redox mediators effectively transfer both protons and electrons to reactants, whereas reactions in pure water transfer protons easily, but not electrons. These mediators also alter the nanoparticles' surface in a way that lowers the energy barrier to be overcome for proton and electron transfer, the study reports.

"We show that the alcohol solvents as well as organic additives can react to form metal-bound surface mediators that act much in the same way that the enzymatic cofactors in our bodies do in catalyzing oxidation and reduction reactions," Neurock said.

Additionally, this work may have implications for reducing the amounts of solvent used and waste generated in the chemical industry.

"Our research suggests that for some situations, chemical producers could form the surface redox mediators by adding small amounts of an additive to pure water instead of pumping thousands of gallons of organic solvents through these reactors," Flaherty said.