Hand gestures constitute another important mode of human communication that could be adopted for human-computer interactions. Recent progress in camera systems, image analysis, and machine learning have made optical-based gesture recognition a more attractive option in most contexts than approaches relying on wearable sensors or data gloves, as used by Anderton in Minority Report. However, current methods are hindered by a variety of limitations, including high computational complexity, low speed, poor accuracy, or a low number of recognizable gestures. To tackle these issues, a team led by Zhiyi Yu of Sun Yat-sen University, China, recently developed a new hand gesture recognition algorithm that strikes a good balance between complexity, accuracy, and applicability. As detailed in their paper, which was published in the Journal of Electronic Imaging, the team adopted innovative strategies to overcome key challenges and realize an algorithm that can be easily applied in consumer-level devices.

One of the main features of the algorithm is adaptability to different hand types. The algorithm first tries to classify the hand type of the user as either slim, normal, or broad based on three measurements accounting for relationships between palm width, palm length, and finger length. If this classification is successful, subsequent steps in the hand gesture recognition process only compare the input gesture with stored samples of the same hand type. “Traditional simple algorithms tend to suffer from low recognition rates because they cannot cope with different hand types. By first classifying the input gesture by hand type and then using sample libraries that match this type, we can improve the overall recognition rate with almost negligible resource consumption,” explains Yu.

Another key aspect of the team’s method is the use of a “shortcut feature” to perform a prerecognition step. While the recognition algorithm is capable of identifying an input gesture out of nine possible gestures, comparing all the features of the input gesture with those of the stored samples for all possible gestures would be very time consuming. To solve this problem, the prerecognition step calculates a ratio of the area of the hand to select the three most likely gestures of the possible nine. This simple feature is enough to narrow down the number of candidate gestures to three, out of which the final gesture is decided using a much more complex and high-precision feature extraction based on “Hu invariant moments.” Yu says, “The gesture prerecognition step not only reduces the number of calculations and hardware resources required but also improves recognition speed without compromising accuracy.”

The team tested their algorithm both in a commercial PC processor and an FPGA platform using an USB camera. They had 40 volunteers make the nine hand gestures multiple times to build up the sample library, and another 40 volunteers to determine the accuracy of the system. Overall, the results showed that the proposed approach could recognize hand gestures in real time with an accuracy exceeding 93%, even if the input gesture images were rotated, translated, or scaled. According to the researchers, future work will focus on improving the performance of the algorithm under poor lightning conditions and increasing the number of possible gestures.

Gesture recognition has many promising fields of application and could pave the way to new ways of controlling electronic devices. A revolution in human-computer interaction might be close at hand!

Story Source:

Materials provided by SPIE–International Society for Optics and Photonics. Note: Content may be edited for style and length.

Researchers investigated how neutrophils are able to differentiate between bacteria to be destroyed and other compounds in the bloodstream, such as cholesterol particles. They tested a library consisting of 23 different protein-based nanoparticles in mice with ALI which revealed a set of “rules” that predict uptake by neutrophils. Neutrophils don’t take up symmetrical, rigid particles, such as viruses, but they do take up particles that exhibited “protein clumping,” which the researchers call nanoparticles with agglutinated protein (NAPs).

“We want to utilize the existing function of neutrophils that identifies and eliminates invaders to inform how to design a ‘Trojan horse’ nanoparticle that overactive neutrophils will intake and deliver treatment to alleviate ALI and ARDS,” said study lead author Jacob Myerson, PhD, a postdoctoral research fellow in the Department of Systems Pharmacology and Translational Therapeutics. “In order to build this ‘Trojan horse’ delivery system, though, we had to determine how neutrophils identify which particles in the blood to take up.”

ALI and ARDS are life-threatening forms of respiratory failure with high morbidity and mortality rates. Prior to COVID-19, there were 190,000 annual cases of ARDS in the U.S. and 75,000 deaths, with the ARDS being caused by pneumonia, sepsis, and trauma. However, COVID has increased ARDS cases into the millions. When ALI or ARDS occurs, the lung’s air sacs recruit neutrophils to the lungs in order to eliminate circulating microbes. This process causes neutrophils to release compounds that further aggravate lung injury and damage the air sacs, so patients develop low blood oxygen levels. Unfortunately, despite the severity of ALI/ARDS, there is no effective drug to control it, and treatment currently focuses on supporting patients while the lungs naturally, but slowly, heal.

To address ARDS and other medical problems, researchers at Penn and elsewhere have been using nanoparticles to concentrate drugs in injured or diseased organs. Such nanoparticles are also being used for gene therapy and immunotherapy.

The researchers note that while the development of viable therapies for ALI/ARDS using nanoparticles to deliver treatments via neutrophils are a long way off, this research represents a significant step in understanding the condition and function of the immune system.

“Now that we have determined that neutrophils patrol for nanoparticles with agglutinated protein, our next step is to understand how and why other microbes, like viruses, which are rigid and symmetrical, evolved to evade neutrophils,” said senior author Jacob Brenner, MD, PhD, an associate professor of Pulmonary Medicine in the Division of Pulmonary, Allergy, and Critical Care. “With this knowledge, we can continue to utilize this unique combination of material science and engineering, to create disease-specific therapies that target more advanced and complicated pathologies.”

The research was funded by the National Institutes of Health (R01 HL125462).

The discovery published in Disease Models and Mechanisms has prompted further examination of the link as a fundamental, early driver of Alzheimer’s disease in humans.

In the study, the researchers analysed the young adult brains of zebrafish with gene mutations associated with early-onset Alzheimer’s disease. Zebrafish were chosen for the study because they produce very large families, which makes it easier to detect subtle effects.

The team used cutting-edge gene technology and mathematical analysis to compare gene activity and detect subtle differences between the normal fish and those with the mutations.

While the researchers found different mutations in different genes have many different effects on brain cell function, they also found Alzheimer’s disease mutations affect one very important cell function in common — the use of oxygen within cells to produce energy.

Lead researcher Dr Karissa Barthelson from the University of Adelaide’s Alzheimer’s Disease Genetics Laboratory said: “This is very interesting because we know when Alzheimer’s disease eventually develops, people’s brains become severely deficient in energy production.

“When we realised this common link we took our research one step further and re-analysed data from another research group that had studied an important Alzheimer’s disease gene in mice.

“We could see a similar effect, and this reinforces our confidence that we have found a fundamental, early driver of Alzheimer’s disease in humans.”

Brains are made up of many different types of cells that have complicated ways of producing and sharing energy. The Adelaide research group now wants to examine how Alzheimer’s disease mutations affect those different cell types.

“It is very satisfying to have found this important common, early factor driving the development of Alzheimer’s disease.

The researchers say the costs of Alzheimer’s disease to society are huge, not only in caring for those who cannot care for themselves but also in lost relationships with loved ones as memories and cognition fade.

“Energy production is the most fundamentally important cellular activity supporting all other functions, particularly in highly active organs such as brains,” said Dr Barthelson.

“If we can understand in detail what is going wrong with oxygen use and energy production, we may see ways of stopping the disease before it starts — and that would enormously benefit our ageing population.”

Story Source:

Materials provided by University of Adelaide. Original written by Kelly Brown. Note: Content may be edited for style and length.

In a new study published in Geophysical Research Letters, a research team led by the University of Tsukuba used seismic data generated by a magnitude 7.3 earthquake that occurred off the northeasternmost tip of New Zealand’s North Island on March 4, 2021, detected by seismometers around the world, to investigate the particularly unusual geometry and stress states of the subducted slab deep below the surface in this region.

“The 2021 East Cape earthquake showed a complex rupture process, likely because of its location at the boundary between the Kermadec Trench to the north and the Hikurangi Margin to the south,” lead author of the study Assistant Professor Ryo Okuwaki explains. “To investigate the geometry of the stress field and earthquake rupture process, we used a novel finite-fault inversion technique that required no pre-existing knowledge of the area’s faults.”

This investigation revealed multiple episodes of rupture, generated by both compression and extension in the subsurface at different depths. These episodes included shallow (~30 km) rupture due to extension perpendicular to the trench as would typically be expected in a subduction zone. Unexpectedly, however, the deep (~70 km) rupture occurred with compression parallel to the subduction trench.

“Two alternative or inter-related factors may explain the unique rupture geometry of the 2021 East Cape earthquake,” senior author Professor Yuji Yagi explains. “First, subduction of a seamount or multiple seamounts along with the subducted slab could contort the slab and create local changes in the stress field. Second, the transition from the Kermadec Trench to the Hikurangi Margin, where the subducted oceanic crust is considerably thicker, could create the local conditions responsible for the unusual faulting pattern.”

Because of the rarity of deep intraslab earthquakes in this region, distinguishing between these two possibilities is currently challenging, and indeed both factors might play significant roles in creating the complex stress field revealed by the East Cape earthquake. Additional earthquakes off the northeast coast of New Zealand in the future may shed further light on this deep tectonic mystery.

This work was supported by the Grant-in-Aid for Scientific Research (C) 19K04030.

Story Source:

Materials provided by University of Tsukuba. Note: Content may be edited for style and length.

Sometimes radioactive damage cannot be great enough — especially when it comes to destroying tumour tissue with ionizing radiation. In radiation therapy, substances that specifically enhance the damage of the radiation in the tumour tissue are used. “The intermolecular Coulombic decay we found could help make such sensitizers more effective,” says Alexander Dorn, who heads a research group at the Max Planck Institute for Nuclear Physics and was instrumental in the current study. His team’s observations could also improve our understanding of how artificial or natural ionizing radiation damages the genetic material of healthy tissue.

Excess energy leads to a Coulomb explosion

The DNA double helix of the genome resembles a rope ladder with rungs of nucleic base pairs. “Because experiments with the free nucleic bases are difficult, we initially studied pairs of benzene molecules as a model system,” explains Dorn. These hydrocarbon rings are connected in a similar way to the nucleic bases stacked on top of each other in a strand of DNA. The researchers bombarded the benzene pairs with electrons, thereby imitating radioactive radiation to a certain extent. When an electron hit a benzene molecule, it was ionized and charged with a lot of energy. The team has now observed that the molecule transferred some of this energy to its partner molecule. This energy boost was enough to ionize the second molecule as well. Both molecules were thus positively charged. Of course, that didn’t last long. The two molecular ions repelled each other and flew apart in a Coulomb explosion.

Until now, scientists had assumed that ionizing radiation damages biomolecules mainly indirectly. The high-energy radiation also ionizes the water of which a cell is largely composed and which surrounds biomolecules such as DNA. The ionized water molecules — especially hydroxide ions — then attack the DNA. And if an electron of the beta radiation or a gamma quantum does hit a DNA molecule directly, the excess energy normally is dissipated by processes in the molecule itself. It thus remains intact. Or at least that was the assumption up to now. In any case, the weak bonds between different molecules or different parts of the molecule — as they exist in DNA and proteins — should not be affected by this either. However, in their reaction microscope, the researchers observed that radioactive radiation can indeed break such bonds. This instrument allows them not only to detect the two separating benzene molecules and measure their energy but also to characterize the electrons emitted.

Fatal consequences of multiple DNA breaks

“It is not yet clear how the intermolecular Coulombic decay affects the DNA strand,” says Dorn. If a single strand in the DNA ladder breaks, the consequences should not be too serious. However, the mechanism observed also releases several electrons that can “blow up” further pairs of molecules. And if both strands of DNA are broken in the immediate vicinity, this could have fatal consequences.

In order to better assess the effect of the radiation on the genetic material, Dorn’s team will now also bombard pairs of nucleic acids with electrons under the reaction microscope. “This is experimentally challenging because we have to heat the nucleic bases in order to vaporize them,” explains Dorn. “But they must not get too hot either — so that they are not destroyed.” Nuclear doctors can also follow the trail to more effective sensitizers that the Heidelberg team has blazed with the observation of intermolecular Coulombic decay. The mechanism could therefore be relevant for both cases of radiation damage: those that need to be avoided as far as possible and those that should be as great as possible.

Story Source:

Materials provided by Max-Planck-Gesellschaft. Note: Content may be edited for style and length.

A team led by DESY’s Andreas Stierle has laid the foundations for an alternative method: storing hydrogen in tiny nanoparticles made of the precious metal palladium, just 1.2 nanometres in diameter. The fact that palladium can absorb hydrogen like a sponge has been known for some time. “However, until now getting the hydrogen out of the material again has posed a problem,” Stierle explains. “That’s why we are trying palladium particles that are only about one nanometre across.” A nanometre is a millionth of a millimetre.

To ensure that the tiny particles are sufficiently sturdy, they are stabilised by a core made of the rare precious metal iridium. In addition, they are attached to a graphene support, an extremely thin layer of carbon. “We are able to attach the palladium particles to the graphene at intervals of just two and a half nanometres,” reports Stierle, who is the head of the DESY NanoLab. “This results in a regular, periodic structure.” The team, which also includes researchers from the Universities of Cologne and Hamburg, published its findings in the American Chemical Society (ACS) journal ACS Nano.

DESY’s X-ray source PETRA III was used to observe what happens when the palladium particles come into contact with hydrogen: essentially, the hydrogen sticks to the nanoparticles’ surfaces, with hardly any of it penetrating inside. The nanoparticles can be pictured as resembling chocolates: an iridium nut at the centre, enveloped in a layer of palladium, rather than marzipan, and chocolate-coated on the outside by the hydrogen. All it takes to recover the stored hydrogen is for a small amount of heat to be added; the hydrogen is rapidly released from the surface of the particles, because the gas molecules don’t have to push their way out from inside the cluster.

“Next, we want to find out what storage densities can be achieved using this new method,” says Stierle. However, some challenges still need to be overcome before proceeding to practical applications. For example, other forms of carbon structures might be a more suitable carrier than graphene — the experts are considering using carbon sponges, containing tiny pores. Substantial amounts of the palladium nanoparticles should fit inside these.

Story Source:

Materials provided by Deutsches Elektronen-Synchrotron DESY. Note: Content may be edited for style and length.

As the fetus grows, it needs to communicate its increasing needs for food to the mother. It receives its nourishment via blood vessels in the placenta, a specialised organ that contains cells from both baby and mother.

Between 10% and 15% of babies grow poorly in the womb, often showing reduced growth of blood vessels in the placenta. In humans, these blood vessels expand dramatically between mid and late gestation, reaching a total length of approximately 320 kilometres at term.

In a study published today in Developmental Cell, a team led by scientists at the University of Cambridge used genetically engineered mice to show how the fetus produces a signal to encourage growth of blood vessels within the placenta. This signal also causes modifications to other cells of the placenta to allow for more nutrients from the mother to go through to the fetus.

Dr Ionel Sandovici, the paper’s first author, said: “As it grows in the womb, the fetus needs food from its mum, and healthy blood vessels in the placenta are essential to help it get the correct amount of nutrients it needs.

“We’ve identified one way that the fetus uses to communicate with the placenta to prompt the correct expansion of these blood vessels. When this communication breaks down, the blood vessels don’t develop properly and the baby will struggle to get all the food it needs.”

The team found that the fetus sends a signal known as IGF2 that reaches the placenta through the umbilical cord. In humans, levels of IGF2 in the umbilical cord progressively increase between 29 weeks of gestation and term: too much IGF2 is associated with too much growth, while not enough IGF2 is associated with too little growth. Babies that are too large or too small are more likely to suffer or even die at birth, and have a higher risk to develop diabetes and heart problems as adults.

Dr Sandovici added: “We’ve known for some time that IGF2 promotes the growth of the organs where it is produced. In this study, we’ve shown that IGF2 also acts like a classical hormone — it’s produced by the fetus, goes into the fetal blood, through the umbilical cord and to the placenta, where it acts.”

Particularly interesting is what their findings reveal about the tussle taking place in the womb.

In mice, the response to IGF2 in the blood vessels of the placenta is mediated by another protein, called IGF2R. The two genes that produce IGF2 and IGF2R are ‘imprinted’ — a process by which molecular switches on the genes identify their parental origin and can turn the genes on or off. In this case, only the copy of the igf2 gene inherited from the father is active, while only the copy of igf2r inherited from the mother is active.

Lead author Dr Miguel Constância, said: “One theory about imprinted genes is that paternally-expressed genes are greedy and selfish. They want to extract the most resources as possible from the mother. But maternally-expressed genes act as countermeasures to balance these demands.”

“In our study, the father’s gene drives the fetus’s demands for larger blood vessels and more nutrients, while the mother’s gene in the placenta tries to control how much nourishment she provides. There’s a tug-of-war taking place, a battle of the sexes at the level of the genome.”

The team say their findings will allow a better understanding of how the fetus, placenta and mother communicate with each other during pregnancy. This in turn could lead to ways of measuring levels of IGF2 in the fetus and finding ways to use medication to normalise these levels or promote normal development of placental vasculature.

The researchers used mice, as it is possible to manipulate their genes to mimic different developmental conditions. This enables them to study in detail the different mechanisms taking place. The physiology and biology of mice have many similarities with those of humans, allowing researchers to model human pregnancy, in order to understand it better.

The lead researchers are based at the Department of Obstetrics and Gynaecology, the Medical Research Council Metabolic Diseases Unit, part of the Wellcome-MRC Institute of Metabolic Science, and the Centre for Trophoblast Research, all at the University of Cambridge.

The research was largely funded by the Biotechnology and Biological Sciences Research Council, Medical Research Council, Wellcome Trust and Centre for Trophoblast Research.