Culture

Even as studies have shown that the uneven distribution of urban heat islands, urban tree canopy cover, and urban environmental hazards, for example, are strongly dictated by structural racism and classism in cities, relatively few studies have addressed the varied contributions of social factors like race to ecological heterogeneity in cities. Here, Christopher J. Schell and colleagues integrate findings from ecology, evolution, and the social sciences to underscore such relationships. Their findings, they say, are necessary to conserve biodiversity, improve human health, and promote justice in nature and society. They start with a well-known hypothesis called the luxury effect - which suggests that urban biodiversity, and plant diversity in particular, is positively correlated with neighborhood wealth. A direct effect of the luxury effect is that poorer-income neighborhoods usually have less tree cover - and thus more heat. These neighborhoods are also typically located closer to pollution sources. "Work on heat islands and pollution support the idea that inequality in neighborhood wealth leads not only to a diversity of environmental hazards," the authors say, "but that these hazards compound to create unique, challenging environmental patches." They also cite research that has shown that neighborhood racial composition can be a stronger predictor of urban socio-ecological patterns than wealth. Neighborhoods that were "redlined" decades ago - by a policy that segregated urban residential neighborhoods principally by race - have on average 21 percent less tree canopy, for example. Knowing where these cities are could help to identify and predict geographic regions with compounding anthropogenic disturbances that require more sustained stewardship, the authors say. "Our capacity to understand urban ecosystems and non-human organisms necessitates a more thorough integration of the natural and social parameters of our cities," Schell and colleagues write. "We cannot generalize human behavior in urban ecosystems without dealing with systemic racism and other inequities."

WASHINGTON (Aug. 13, 2020) -- Fingolimod, an FDA-approved immunosuppressive drug used to treat multiple sclerosis flare-ups, may be used to block HIV infection and reduce the latent reservoir. Researchers at the George Washington University (GW) published their novel findings in PLOS Pathogens.

"While antiretroviral drugs have been effective in treating HIV thus far, drug resistance, negative side effects of antiretroviral therapy, and its varying efficacy underscore the need to develop alternative treatment and prevention options," said Alberto Bosque, PhD, MBA, assistant professor of microbiology, immunology, and tropical medicine at the GW School of Medicine and Health Sciences. "For the first time, our research team found that by targeting the receptors to the signaling molecule Sphingosine-1-phosphate (S1P), we could effectively block HIV infection and cell-to-cell transmission of the virus and consequently reduce the seeding of the latent virus in the test tube."

Treatment for HIV is lifelong, due to a latent reservoir of HIV-infected cells that may reactivate at any time. In addition to other drawbacks, current antiretroviral therapies do not specifically target latent infection. Finding ways to not only target infection, but also reduce the latent reservoir would have a great impact on the nearly 40 million people living with HIV worldwide.

Fingolimod, known also as Gilenya, works by acting as a functional antagonist of S1P receptors. By observing human immune cells, Bosque and his research team found that HIV infection was blocked by targeting S1P receptors with Fingolimod. The team discovered that the HIV life cycle was impacted at multiple levels. First, the drug reduced the surface density of the HIV receptor in T-cells, inhibiting viral binding and fusion. Secondly, Fingolimod activated the antiviral restriction factor SAMHD1, leading to a reduction in levels of total and integrated HIV.

"We believe this compound may be a promising novel therapy for HIV treatment and prevention," said Bosque.

"Fingolimod inhibits multiple stages of the HIV-1 life cycle," was published in PLOS Pathogens and is available at https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1008679.

Mitochondria are small organelles that provide the energy critical for each cell in our body, in particular in the high fuel-consuming brain. In this week's edition of Science, a Belgian team of researchers led by Pierre Vanderhaeghen (VIB-KU Leuven, ULB) finds that mitochondria also regulate a key event during brain development: how neural stem cells become nerve cells. Mitochondria influence this cell fate switch during a precise period that is twice as long in humans compared to mice. The seminal findings highlight an unexpected function for mitochondria that may help explain how humans developed a bigger brain during evolution, and how mitochondrial defects lead to neurodevelopmental diseases.

Our brains are made up of billions of incredibly diverse neurons. They first arise in the developing brain when stem cells stop self-renewing and differentiate into a particular type of neuron. This process, called neurogenesis, is precisely regulated to give rise to the enormous complex structure that is our brain. It is thought that small differences in the way neural stem cells generate neurons are at the origin of the dramatic increase in the size and complexity of our brain.

To gain insight in this complex process, prof. Pierre Vanderhaeghen (VIB-KU Leuven, ULB) and his colleagues examined the mitochondria, small organelles that provide energy in every cell in the body, including the developing brain.

"Diseases caused by defects in mitochondria lead to developmental problems in many organs, in particular the brain," explains Vanderhaeghen, a specialist in stem cell and developmental neurobiology. "We used to think that this was related to the crucial function of mitochondria to provide energy to the cells, but this is only part of the story: recent work in stem cells suggests that mitochondria have a direct influence on organ development. We have tested whether and how this could be the case in the brain."

Fission and fusion

Together with his team, he explored whether and how mitochondrial remodeling is coupled with neuronal fate commitment during neurogenesis. "Mitochondria are highly dynamic organelles, that can join together (fusion) or split up (fission), and we know these dynamics are associated with fate changes in various types of stem cells," says Vanderhaeghen.

Ryohei Iwata, a postdoctoral researcher in the Vanderhaeghen lab, developed a new method to watch mitochondria in great detail as the neural stem cells are 'caught in the act' to become neurons. "We found that shortly after stem cells divide, the mitochondria in daughter cells destined to self-renew will fuse, while those in daughter cells that become neurons show high levels of fission instead," says Ryohei Iwata.

But this was not just a coincidence: indeed, the researchers could show that increased mitochondrial fission in fact promotes differentiation to a neuronal fate, while mitochondrial fusion after mitosis redirects daughter cells towards self-renewal.

Time window

So mitochondrial dynamics are important to become a neuron--but there is more.

"We found that the influence of mitochondrial dynamics on cell fate choice is limited to a very specific time window, right after cell division," says Pierre Casimir, a PhD student in Vanderhaeghen's lab. "Interestingly, the restricted time window is twice as long in humans compared to mice."

"Previous findings were primarily focused on fate decision of neural stem cells before they divide, but our data reveal that cell fate can be influenced for a much longer period, even after neural stem cell division," says Vanderhaeghen. This may have interesting implications in the emerging field of cell reprogramming, where scientists try to convert non-neuronal cells directly in neuronal cells for therapeutic purposes for instance.

"Since this period of plasticity is much longer in human cells compared to mouse cells, it is tempting to speculate that it contributes to the increased self-renewal capacity of human progenitor cells, and thus to the uniquely developed brain and cognitive abilities of our species. It is fascinating to think that mitochondria, small organelles that have evolved in cells more than a billion years ago, might have contributed to the recent evolution of the human brain."

What The Study Did: Excess deaths in New York during the peak of the 1918 influenza pandemic were compared with those during the initial period of the COVID-19 outbreak in this study.

Authors: Jeremy S. Faust, M.D., M.S., of Brigham and Women's Hospital and Harvard Medical School in Boston, is the corresponding author.

To access the embargoed study: Visit our For The Media website at this link https://media.jamanetwork.com/

(doi:10.1001/jamanetworkopen.2020.17527)

Editor's Note: The article includes conflict of interest disclosures. Please see the article for additional information, including other authors, author contributions and affiliations, conflict of interest and financial disclosures, and funding and support.

What The Study Did: COVID-19-related outcomes in French nursing homes that implemented voluntary staff confinement with residents are investigated in this study.

Authors: Joel Belmin, M.D., Ph.D., of the Hopital Charles Foix in  Ivry-sur-Seine, France, is the corresponding author.

To access the embargoed study: Visit our For The Media website at this link https://media.jamanetwork.com/

(doi:10.1001/jamanetworkopen.2020.17533)

Editor's Note: Please see the article for additional information, including other authors, author contributions and affiliations, conflict of interest and financial disclosures, and funding and support.

What The Study Did: National Cancer Database data from 2004 to 2014 were used to examine the association between overall survival and timing of radiotherapy relative to androgen deprivation therapy in patients with prostate cancer.

Authors: Vinayak Muralidhar, M.D., M.Sc., of the Dana-Farber Cancer Institute/Brigham and Women's Hospital and Harvard Medical School in Boston is the corresponding author.

To access the embargoed study: Visit our For The Media website at this link https://media.jamanetwork.com/ 

(doi:10.1001/jamaoncol.2020.3545)

Editor's Note: The article includes conflicts of interest and funding/support disclosures. Please see the article for additional information, including other authors, author contributions and affiliations, conflict of interest and financial disclosures, and funding and support.

What The Viewpoint Says: This Viewpoint calls for greater attention to racial and socioeconomic health disparities affecting patients with cancer in the setting of COVID-19.

Authors: Onyinye D. Balogun, M.D., of Weill Cornell Medicine in New York, is the corresponding author.

To access the embargoed study: Visit our For The Media website at this link https://media.jamanetwork.com/ 

(doi:10.1001/jamaoncol.2020.3327)

Editor's Note: The article includes conflicts of interest and funding/support disclosures. Please see the article for additional information, including other authors, author contributions and affiliations, conflict of interest and financial disclosures, and funding and support.

What The Study Did: The association between receipt of the bradykinin 2 (B2) receptor antagonist icatibant and improved oxygenation in patients with COVID-19 is investigated in this study.

Authors: Frank L. van de Veerdonk, M.D., Ph.D., of the Radboud University Medical Center in Nijmegen, the Netherlands, is the corresponding author.

To access the embargoed study: Visit our For The Media website at this link https://media.jamanetwork.com/

(doi:10.1001/jamanetworkopen.2020.17708)

Editor's Note: The article includes conflict of interest disclosures. Please see the article for additional information, including other authors, author contributions and affiliations, conflict of interest and financial disclosures, and funding and support.

Syphilis is a sexually transmitted disease - and while commonly dismissed due to the availability of modern treatments, it is in fact spreading at an alarming rate: Over the last decades, more than 10 million people around the world have been infected with the syphilis subspecies pallidum of the Treponema pallidum bacteria. Other treponematoses, such as yaws and bejel, are caused by other subspecies of Treponema pallidum. The origins of syphilis, which wreaked havoc in Europe from the late 15th to the 18th century, are still unclear. The most popular hypothesis so far holds Christopher Columbus and his sailors liable for bringing the disease to Europe from the New World.

Yaws already widespread in Europe

The new study indicates a fair possibility that Treponema pallidum already existed in Europe before Columbus ever set sails to America. The researchers found treponematoses in archaeological human remains from Finland, Estonia and the Netherlands. Both molecular dating of the ancient bacterial genomes and traditional radiocarbon dating of the samples were used to estimate the age of the pathogens causing these diseases. The results indicate that the genomes dated back to between the early 15th and 18th century.

In addition to the syphilis cases, the researchers found yaws in one of the individuals. Like syphilis, yaws is transmitted via skin contact, although rarely through sexual intercourse. Today, the disease is only found in tropical and subtropical regions. "Our data indicates that yaws was spread through all of Europe. It was not limited to the tropics, as it is today," says last author Verena Schünemann, professor of paleogenetics at the Institute of Evolutionary Medicine of the University of Zurich.

Genome of a previously unknown pathogen discovered

The research team also discovered something else: The skeleton found in the Netherlands contained a pathogen belonging to a new, unknown and basal treponemal lineage. This lineage evolved in parallel to syphilis and yaws but is no longer present as a modern-day disease. "This unforeseen discovery is particularly exciting for us, because this lineage is genetically similar to all present treponemal subspecies, but also has unique qualities that differ from them," says first author Kerttu Majander from UZH.

Because several closely related subspecies of Treponema pallidum existed throughout Europe, it is possible that the diseases persisted in overlapping regions, and sometimes infected the same patient. The spatial distribution in the northern periphery of Europe also suggests that endemic treponematoses had already spread widely in Europe in the early modern period.

Not just Columbus

"Using our ancient genomes, it is now possible for the first time to apply a more reliable dating to the treponema family tree," says Schünemann. The genetic analyses conducted in this study suggest that the predecessor of all modern Treponema pallidum subspecies likely evolved at least 2,500 years ago. For venereal syphilis in particular, the latest common ancestor existed between the 12th and 16th century.

According to the newly discovered diversity of treponematoses in early modern Europe, syphilis may have either originated or perhaps further developed in the Old World. "It seems that the first known syphilis breakout cannot be solely attributed to Columbus' voyages to America," concludes Schünemann. "The strains of treponematoses may have co-evolved and interchanged genetic material before and during the intercontinental contacts. We may yet have to revise our theories about the origins of syphilis and other treponemal diseases".

Researchers have shed fresh light on the evolution and function of the shapes we see in nature - using as a model the heart shaped fruits of the Capsella genus.

The natural world is full of diverse shapes from organs to whole organisms that are fitted by evolution to perform and reproduce optimally in their environment.

The Capsella seed pods with their distinctive heart-shaped shoulders offer an anatomical novelty and an excellent study system for understanding the diversity of shapes.

Earlier studies have shown that the expression of key regulatory genes is a primary driver in controlling shape evolution in organs. This new study carried out by John Innes Centre researchers adds another critical step in this pathway by revealing a modification of protein activity that is critical for organ-shape formation.

They show that the SUMO-protease HEARTBREAK (HTB) from Capsella rubella controls the activity of the key regulator of fruit development INDEHISCENT via a process called de-SUMOylation.

Only via this de-SUMOylation - a kind of molecular trimming activity - is a pathway activated which allows biosynthesis of the plant hormone auxin which in turn facilitates anisotropic cell expansion to form the heart-shaped Capsella fruit.

Professor Lars Østergaard a programme leader at the John Innes Centre and corresponding author of the paper explains the significance: "We know that the diversity in shape we observe in nature frequently is caused by changes in the position and timing of key regulatory genes: that is how a lot of variation occurs.

"What we have found is that there is this post translational effect, beyond the gene expression. This protein modification is at the basis of this type of diversity of fruit shape - and goes a long way to explain the difference for example between the fruits of Capsella and those from the related model plant Arabidopsis. This is about a modification of protein activity at a different stage than we have seen before."

Researchers used forward genetic screening - a technique to study a range of traits - which identified a mutant with compromised development of the heart-shaped fruit. The mutant was therefore named, heartbreak. They used time-lapse 3D imaging and molecular genetics to characterise the heartbreak phenotype at the cellular and molecular level.

First author Dr Yang Dong added: "We now have an entire pathway based on gene expression, hormone dynamics and post translational modification of proteins in such detail that we can test to what extent these kinds of pathways with these components are shared much wider across kingdoms and not just within the plant kingdom."

One of the next steps for the researchers is to is to translate this fundamental discovery from the research plant Capsella to the related commercial crop oilseed rape.

The research answers a key question about how these shapes appear.

But why does nature come up with such an unusual shape as the heart-shaped pods of Capsella? What is the function behind this form? The reason is still debatable, explains Professor Østergaard.

"Previously we thought these shapes might be a good functional design for seed dispersal because the shape could allow the wind to catch the seed pod walls, but our assays comparing them with Arabidopsis and oilseed rape do not reveal any great advantage of the Capsella fruit in seed dispersal. So, we don't think that can be a major factor.

"It is possible they could act like solar panels. In other words, maybe they function to capture sunlight and increase photosynthetic capacity. We know that the photosynthetic capacity of the seed pod walls can have a strong effect on seed development inside the pod and therefore on yields. So, by understanding this mechanism it does give us tools to perhaps be able to manipulate the seed pod walls in crops like oilseed rape."

Social inequalities, specifically racism and classism, are impacting the biodiversity, evolutionary shifts and ecological health of plants and animals in our cities.

That's the main finding of a review paper led by the University of Washington, with co-authors at the University of California, Berkeley, and University of Michigan, which examined more than 170 published studies and analyzed the influence of systemic inequalities on ecology and evolution. Published Aug. 13 in Science, it calls on the scientific community to focus on environmental justice and anti-racism practices to transform biological research and conservation.

"Racism is destroying our planet, and how we treat each other is essentially structural violence against our natural world," said lead author Christopher Schell, an assistant professor of urban ecology at the University of Washington Tacoma. "Rather than just changing the conversation about how we treat each other, this paper will hopefully change the conversation about how we treat the natural world."

The paper cites other studies that have found racism and other inequalities are reducing biodiversity, increasing urban heat island effects and augmenting impacts of climate crises across the United States.

For example, several studies the authors included found fewer trees in low-income and racially minoritized neighborhoods in major cities across the U.S. Less tree cover means hotter temperatures and fewer plant and animal species. Additionally, these areas tend to be closer to industrial waste or dumping sites than wealthier, predominantly white areas -- a reality that was put in place intentionally through policies like redlining, the authors explain.

Fewer trees, over decades, has led to pockets of neighborhoods that are hotter, more polluted, and have more disease-carrying pests such as rodents and mosquitoes that can survive in harsh environments. These ecological differences inevitably affect human health and well-being, the authors said.

The main purpose of the paper is to show the scientific community that fundamental practices in science are based on systems that support white supremacy and perpetuate systemic racism, the authors said. They hope their colleagues in science fields will begin to dig into the history of the various laws and practices that built present-day inequalities -- such as redlining and Jim Crow laws -- and then start to reevaluate how they run their labs and conduct their research.

"I hope this paper will shine the light and create a paradigm shift in science," Schell said. "That means fundamentally changing how researchers do their science, which questions they ask, and realizing that their usual set of questions might be incomplete."

For example, Schell said he has seen numerous papers comparing biodiversity in urban and rural areas. However, organisms in cities were often only measured in wealthier areas, negating the possibility for differences among urban neighborhoods of different income levels. That type of science, even if done unknowingly, is negligent, he said.

The authors also hope this paper paves the way for younger scientists entering the field, especially people of color, to have legitimacy in pushing for science that is centered around anti-racism and environmental justice.

"I hope many of my senior colleagues would start to rethink how they do their science," Schell said. "And for those scientists coming up, that this gives them the platform to say: 'No, this is a legitimate question: How do we reduce, minimize, abolish racism in America?'"

Ultimately, the authors said, environmental issues should be recast to encompass societal issues, which departs from what traditional, mostly white environmentalists advocate.

For example, creating affordable housing should be on every environmentalist's agenda, they explained. More secure housing, with less turnover and fewer vacant lots or construction areas, promotes ecological stability for people, animals and plants. Additionally, more equitable access to parks and greenways within cities also promotes more animal and plant biodiversity. And better public transportation to and from well-paid jobs cuts carbon emissions and reduces animal-vehicle collisions.

Notably, each of these actions benefits humans as well as plants and animals -- and all are not included in traditional definitions of environmentalism.

Schell also led a recent paper, in Nature Ecology and Evolution, that lays out tangible actions scientists can take to fight racism and white supremacy. For Schell, this includes paying everyone who works in his lab, making sure people of color are treated equitably, and advocating for women of color to hold leadership positions in professional societies and organizations. He encourages colleagues to do the same.

"I'm hopeful things are going to happen, because I have to be," he said. "We have the power to be activists in our own ways, in our own sectors, and we have the ability to motivate others to do the same."

University of Otago researchers have learnt more about how viruses operate and can evade the immune system and are now using their discovery to help learn more about COVID-19.

The recent research, led by Dr Mihnea Bostina and PhD student Sai Velamoor from the Department of Microbiology and Immunology and Otago Micro and Nano Imaging, Electron Microscopy, specifically looked at the Oryctes rhinoceros nudivirus (OrNV) virus, an important biocontrol agent against the coconut rhinoceros beetle, a devastating pest for coconut and oil palm trees in Southeast Asia and the Pacific Islands.

The Otago scientists found the virus used a "decoy" strategy to evade the immune system. Dr Bostina explains the findings are a small step in the bid to better understand infectious disease.

The research team is now using the same technique to investigate changes in cells infected with SARS-CoV-2, the coronavirus that causes COVID-19.

"We have used the same technique to investigate changes in cells infected with SARS-CoV-2 and are continuing work in this area."

Dr Bostina explains that viruses that replicate and assemble inside the nucleus have evolved special approaches to modify the nuclear landscape for their advantage. The research team used electron microscopy to investigate cellular changes occurring during nudivirus infection and found a unique mechanism for how the virus works.

"Our study revealed that the virus acquires a membrane inside the nucleus of the infected cell and it gets fully equipped to infect new cells at this precise location. This is in contrast with other enveloped viruses - like coronavirus, which is also an enveloped virus - which derive their membranes from other cellular compartments.

"After it gets fully assembled, the virus uses a clever tactic of passing through different environments, packed inside various membrane structures until it gets released at the cellular membrane."

Ms Velamoor says this strategy implies that many of the viruses released by the infected cells will be enclosed in a cellular membrane while travelling inside the infected organism.

"This means they will be missed by the immune system and they can use this membrane decoy to penetrate any other type of cells, without the need of a virus specific receptor.

"It shows for the very first time a clever strategy available to insect viruses. It will be interesting to find in what measure other types of viruses - like the ones infecting humans - are also capable of carrying out a similar process."

Dr Bostina says the research demonstrates another manner in which viruses are capable of hijacking infected cells and alerts scientists to the novel mechanism of viral transmission.

"Viruses will never cease to amaze us with their indefatigable arsenal of tricks. Only by studying them can we be prepared to adequately respond when they infect us."

New research by Dr Camilla Whittington and her team at the University of Sydney has found male seahorses transport nutrients to their developing babies during pregnancy. This discovery provides an opportunity for further comparative evolutionary research.

Seahorses and their relatives are the only vertebrates that have male pregnancy. The expectant fathers incubate developing babies inside a pocket called a “brood pouch”. We know a male seahorse can have more than a thousand embryos in the pouch at once but until now, researchers had limited understanding of how the babies are fed.

“This work adds to the growing evidence that male pregnancy in seahorses could be as complex as female pregnancy in other animals, including ourselves,” said Dr Whittington, from the School of Life and Environmental Sciences. “We now know that seahorse dads can transport nutrients to the babies during pregnancy, and we think they do this via a placenta. It’s not exactly like a human placenta though - they don’t have an umbilical cord, for example. We need to do further histological work to confirm this.”

Seahorses are emerging as important model species for understanding the evolution of live-bearing reproduction, said Dr Whittington.

“We can draw some parallels between seahorse pregnancy and human pregnancy,” she said. “Seahorse dads seem to do some of the same things that human mums do, including transporting nutrients and oxygen to developing embryos, and immune modulation to protect the babies from infection.”

The research published in Journal of Comparative Physiology B was led by University of Sydney Honours student Zoe Skalkos in collaboration with Dr James Van Dyke at La Trobe University.

The study builds on previous genetic evidence suggesting that male seahorses might transport nutrients to developing embryos. This new study confirms, in the first experimental evidence of ‘patrotrophy’ (nutrient transport from dad to babies). It also identified one of the classes of nutrients being transported: energy-rich fats.

“My team is using a range of techniques to investigate the biology of seahorse pregnancy,” Dr Whittington said. “We want to understand more about the seahorse pouch and the ways it protects and supports the baby seahorses.”

Honours student Zoe Skalkos, who led the research, said: “It’s really exciting because it’s a big step in understanding the relationship between dad and baby in male pregnancy.”

Key Points:

Seahorses and their relatives are the only vertebrates that have male pregnancy. Dads incubate developing babies inside a pocket called a "brood pouch".

Male seahorses transport nutrients, including fats, to developing babies during pregnancy. The babies use these energy-rich fats for growth and development.

The new results raise the question of whether seahorse embryos can influence how much nutrition they can get from dad while they are in the brood pouch.

Scientists from Nanyang Technological University, Singapore (NTU Singapore) have developed an Artificial Intelligence (AI) system that recognises hand gestures by combining skin-like electronics with computer vision.

The recognition of human hand gestures by AI systems has been a valuable development over the last decade and has been adopted in high-precision surgical robots, health monitoring equipment and in gaming systems.

AI gesture recognition systems that were initially visual-only have been improved upon by integrating inputs from wearable sensors, an approach known as 'data fusion'. The wearable sensors recreate the skin's sensing ability, one of which is known as 'somatosensory'.

However, gesture recognition precision is still hampered by the low quality of data arriving from wearable sensors, typically due to their bulkiness and poor contact with the user, and the effects of visually blocked objects and poor lighting. Further challenges arise from the integration of visual and sensory data as they represent mismatched datasets that must be processed separately and then merged at the end, which is inefficient and leads to slower response times.

To tackle these challenges, the NTU team created a 'bioinspired' data fusion system that uses skin-like stretchable strain sensors made from single-walled carbon nanotubes, and an AI approach that resembles the way that the skin senses and vision are handled together in the brain.

The NTU scientists developed their bio-inspired AI system by combining three neural network approaches in one system: they used a 'convolutional neural network', which is a machine learning method for early visual processing, a multilayer neural network for early somatosensory information processing, and a 'sparse neural network' to 'fuse' the visual and somatosensory information together.

The result is a system that can recognise human gestures more accurately and efficiently than existing methods.

Lead author of the study, Professor Chen Xiaodong, from the School of Materials Science and Engineering at NTU, said, "Our data fusion architecture has its own unique bioinspired features which include a man-made system resembling the somatosensory-visual fusion hierarchy in the brain. We believe such features make our architecture unique to existing approaches."

"Compared to rigid wearable sensors that do not form an intimate enough contact with the user for accurate data collection, our innovation uses stretchable strain sensors that comfortably attaches onto the human skin. This allows for high-quality signal acquisition, which is vital to high-precision recognition tasks," added Prof Chen, who is also Director of the Innovative Centre for Flexible Devices (iFLEX) at NTU.

The team comprising scientists from NTU Singapore and the University of Technology Sydney (UTS) published their findings in the scientific journal Nature Electronics in June.

High recognition accuracy even in poor environmental conditions

To capture reliable sensory data from hand gestures, the research team fabricated a transparent, stretchable strain sensor that adheres to the skin but cannot be seen in camera images.

As a proof of concept, the team tested their bio-inspired AI system using a robot controlled through hand gestures and guided it through a maze.

Results showed that hand gesture recognition powered by the bio-inspired AI system was able to guide the robot through the maze with zero errors, compared to six recognition errors made by a visual-based recognition system.

High accuracy was also maintained when the new AI system was tested under poor conditions including noise and unfavourable lighting. The AI system worked effectively in the dark, achieving a recognition accuracy of over 96.7 per cent.

First author of the study, Dr Wang Ming from the School of Materials Science & Engineering at NTU Singapore, said, "The secret behind the high accuracy in our architecture lies in the fact that the visual and somatosensory information can interact and complement each other at an early stage before carrying out complex interpretation. As a result, the system can rationally collect coherent information with less redundant data and less perceptual ambiguity, resulting in better accuracy".

Providing an independent view, Professor Markus Antonietti, Director of Max Planck Institute of Colloids and Interfaces in Germany said, "The findings from this paper bring us another step forward to a smarter and more machine-supported world. Much like the invention of the smartphone which has revolutionised society, this work gives us hope that we could one day physically control all of our surrounding world with great reliability and precision through a gesture."

"There are simply endless applications for such technology in the marketplace to support this future. For example, from a remote robot control over smart workplaces to exoskeletons for the elderly."

The NTU research team is now looking to build a VR and AR system based on the AI system developed, for use in areas where high-precision recognition and control are desired, such as entertainment technologies and rehabilitation in the home.

This news release is a revision of one originally published on July 31, 2020.

Using state-of-the-art 3D microscopy and mathematics, Dr Hermes Gadêlha from the University of Bristol, Dr Gabriel Corkidi and Dr Alberto Darszon from the Universidad Nacional Autonoma de Mexico, have reconstructed the movement of the sperm tail in 3D with high-precision.

Using a high-speed camera capable of recording over 8,000 frames in one second, and a microscope stage with a piezoelectric device to move the sample up and down at an incredibly high rate, they were able to scan the sperm swimming freely in 3D.

"Human sperm roll as they swim, much like playful otters corkscrewing through water to swim forwards," said Dr Gadelha, head of the Polymaths Laboratory at Bristol's Department of Engineering Mathematics and an expert in the mathematics of fertility.

"The otter-like spinning of human sperm is however complex: the sperms' rapid and highly synchronised spinning causes the to tail rotate around the swimming direction, drilling into the fluid with helical waves."

"The centreline of the 3D tail shows travelling waves of changes in chirality, known in mathematics as perversion. This is similar to changes in spiralling direction we see in plant tendrils. We now know that these perversion waves are correlated to the spinning movement of the sperm's head."

Computer-assisted semen analysis systems in use today, both in clinics and for research, still use 2D views to look at sperm movement. We can now see that 2D projections of sperm swimming can introduce inaccuracies in how we see the tail's movement. Novel use of 3D microscope technology combined with mathematics, may provide fresh avenues for unlocking the secrets of human sperm swimming.

"With over half of infertility caused by male factors, understanding how the human sperm tail moves is fundamental to developing future diagnostic tools to identify unhealthy sperm," adds Dr Gadelha, whose work has previously revealed the biomechanics of sperm bendiness and the precise rhythmic tendencies that characterise how a sperm moves forward.