Earth

The world expects some teenagers to become criminals. These "troublemakers" are taken away from everything and everyone they know. The State places them in children's homes, often far from family and friends.

"Care-leavers from children's homes live with more layers of vulnerability. They can be more vulnerable than youth growing up in poor families", says Prof Adrian van Breda. He is a researcher at the Department of Social Work, University of Johannesburg, South Africa.

He authored the study Patterns of criminal activity among residential care-leavers in South Africa.

"For most, the children's home is the very 'last stop'. Their grandmothers are not providing foster care, they are not placed in foster care with other families, and not adopted. Some are moved from one foster placement to the next. Often, behavioural issues contributed to them being placed in a children's home."

Fragile statistics

In Australia, for example, 27% of care-leavers reported contact with police and 11% had been found guilty of a crime since turning 18 (Note 1). And in Sweden, 37% of male care-leavers went on to serious crime, compared to 5% of the general population (Note 2).

"Often, youth in children's homes lack healthy family connections. This may make them more vulnerable than poor teenagers. A poor teenager can still have healthy relationships with their parents, siblings and extended family. Family connections are a potent form of 'social capital'," adds Van Breda.

"The young person who grows up in care in this study, entered care on average at age 12. Most of them do have family, but their relationships with family became fragmented and thin. Sometimes, they were moved into care to protect them from their family.

"When care-leavers move out of a children's home, they often do not have the networks and skills to help them navigate into employment. A child who grows up in a poor community with their family may have far more social capital," he says.

Kieren, year 1 after leaving the children's home

Kieren (not his real name) lives with his parents. He got caught with drugs and had a fight with his mom. She called the police. After spending a few days in jail, he stopped dealing cannabis. He says that he "can just be triggered", "like a ticking timebomb". He agrees that he never learnt to deal with his anger at the children's home.

Kieren was interviewed five times during the study, at yearly intervals.

Unusual results from South Africa

Contrary to what we might expect, the majority of care-leavers in Van Breda's South African study do not engage in criminal activities. Instead, about three quarters (73%) say that they didn't engage in any criminal activities. They each took part in two or more annual interviews up to 5 years after leaving a children's home.

This encouraging result is despite a sudden stop in State support when the care-leaver turns 18. To them, this means no further housing and no further support for training and education. It is also despite a 55.2% unemployment rate among 15-24 year olds in 2019, according to Statistics SA.

The small study engaged with 100 young people leaving the children's homes in three South African provinces. They represent the racial diversity of the country.

They were recruited into the study just before leaving the children's home, between 2012 and 2016. By the end of 2018, 51 young people had given two or more in-depth annual interviews to research field workers. In total the study included 163 interviews with these 51 care-leavers.

The hungry, sleepy 10%

The second group in the study is the 10% who say that they engaged in one minor incident of crime after leaving care. This group stays out of serious trouble with the law.

"Some of these incidents were people who were hungry and stole food. Or they stole money to buy food. Others did not have a place to live. They would go to sleep at a vacant site or house because they needed shelter. They would be found and arrested for trespassing. These incidents of criminal activity are often survival-driven," says Van Breda.

Kieren, year 2 after leaving the children's home

Kieren spent nine months in juvenile prison after the previous interview. In prison, he saw a gang member "trying to hit on this guy. I know this guy from a long time. And I could not let him down like that."

So he stabbed the gang member in the neck. The gang member was in hospital for about a week. The police beat Kieren up "very badly".

The more violent 17%

The third group is the 17% who self-report more serious incidents of criminal activity in two or more years after leaving care.

These incidents are more frequent and more violent than the second group. They are more likely than the second group to come into conflict with the law and to spend at least one day in jail.

It is this third group that Kieren (not his real name) belongs to in the study. He is an unusual interviewee in the study, because he is the only one to serve a long prison sentence.

"This group told us about significantly more incidents of violence. They were usually unarmed, though, and the victims seldom needed medical care. The violent incidents decrease slightly over time," says Van Breda.

"They were holding and selling stolen goods and doing it more frequently as time went on. Most said that they dealt in drugs and used every year. Some stole, but a bit less frequently over time, and the monetary value was usually low."

Kieren, Year 3

Kieren is still living with his caregivers. He got into an argument and reflects "because I have a short temper I just switched." He went to prison for assault and was released two months later. He is still smoking cigarettes and cannabis, but not drinking, not stealing. He is holding and dealing stolen electronics and drugs.

Kieren, Year 4

The research field worker interviews Kieren in prison where he on trial for murder. He lived with a relative, until he assaulted a man and was charged with attempted murder.

Kieren, Year 5

The research field worker interviews Kieren in jail through a glass screen via a phone. He is serving a life sentence for the murder of the relative he had lived with.

What happens to care-leavers in Africa?

Globally, little research exists about crime committed by care-leavers. In Africa, little research has been done about care-leavers in general, says Van Breda.

"Statistics about crime committed by care-leavers in the global north exists. But often we don't know what is actually happening. What criminal activities do the care leavers engage in? How often do these happen? Is it a once-off exploratory thing that any young person might do, or is it continuous over time and increasing in frequency or severity? This study offers more insight on what is going on in this area, by collecting both numerical and narrative data.

"We think is it important to understand how to help care-leavers find their way successfully into young adulthood. Understanding this very vulnerable group can teach us how to better support other vulnerable young people transitioning into adulthood," says Van Breda.

Van Breda is a founding member of the Africa Network of Care-Leaving Researchers (ANCR). The researchers in ANCR collaborate online to research how young people in Africa transition out of alternative care.

Vulnerability across generations

"It is now more than 20 years after democracy in South Africa, a developing country that was colonised by the global north. Vulnerability and trauma in families continues to run along race and gender lines. This includes access to quality health care and education, access to social security, opportunities to learn a trade and find jobs.

"Black African youth and women are significantly more vulnerable than other young people. Existing State interventions do not fully address these vulnerable groups."

Van Breda concludes: "Young people under 30 is a fast-growing section of the South African population. Because of this, we need to understand how to better support care-leavers from children's homes and foster care. Juveniles need that support before they have to make their own way into the world."

The American College of Cardiology has released the 2020 Clinical Competencies for Nurse Practitioners and Physician Assistants in Adult Cardiovascular Medicine, identifying the knowledge and skills that are important for nurse practitioners (NPs) and physician assistants (PAs) working in general cardiovascular medicine and cardiovascular medicine subspecialty areas. This is the first competency statement issued for non-physician members of the cardiovascular care team.

"Model cardiovascular care teams include NPs and PAs as integral members to manage and treat patients," said George P. Rodgers, MD, FACC, chair of the clinical competency statement. "Through clinical competencies we are promoting enhanced collaborative, high-quality and patient-centered care teams. The goal is for NPs and PAs to practice at their highest levels of education, training and experience to provide patients with optimal care."

As part of its strategic vision, the College is ensuring that all types of cardiovascular professionals have access to the education and knowledge they need to advance their careers and provide optimal patient care. The overarching goal in competency statements is to provide a framework by which educational initiatives and clinical competencies can be coordinated to improve the overall delivery of care to cardiovascular patients.

"When NPs and PAs are practicing at the full scope of education, training and licensure, they improve access to care, provide comprehensive clinical care, increase physician efficiency and enhance patient satisfaction, extending the capabilities of the general or subspecialty cardiologist and the entire cardiovascular team," said Jane A. Linderbaum, MS, CNP-BC, AACC, NP co-chair of the writing committee.

The competency framework includes core competencies for systems-based practice, practice-based learning and improvement, interpersonal and communication skills, and professionalism, as well as competencies that encompass medical knowledge and patient care and procedural skill related to 11 specific clinical areas.

"This document assists NPs and PAs in identifying learning needs and opportunities for professional growth, creates a foundation for writing competency-based education curriculum, and assists NPs and PAs in transitioning from one practice type in cardiovascular medicine to another," said Dorothy D. Pearson, PA-C, AACC, PA co-chair of the writing committee.

The writing committee addressed more than 1,200 comments from cardiologists, NPs, PAs and others to finalize the document. Thirteen organizations participated in the review process, resulting in endorsement from the American Academy of Physician Assistants, American Association of Heart Failure Nurses, American Association of Nurse Practitioners, American Heart Association, Association of Physician Assistants in Cardiology, Heart Rhythm Society, Physician Assistant Education Association, Preventive Cardiovascular Nurses Association, the Society of Cardiovascular Angiography and Interventions and The National Organization of Nurse Practitioners Faculties.

The 2020 Clinical Competencies for Nurse Practitioners and Physician Assistants in Adult Cardiovascular Medicine will be published in the Journal of the American College of Cardiology.

A new method to accurately record brain activity at scale has been developed by researchers at the Crick, Stanford University and UCL. The technique could lead to new medical devices to help amputees, people with paralysis or people with neurological conditions such as motor neurone disease.

The research in mice, published in Science Advances, developed an accurate and scalable method to record brain activity across large areas, including on the surface and in deeper regions simultaneously.

Using the latest in electronics and engineering techniques, the new device combines silicon chip technology with super-slim microwires, up to 15-times thinner than a human hair. The wires are so thin they can be placed deep in the brain without causing significant damage. Alongside its ability to accurately monitor brain activity, the device could also be used to inject electrical signals into precise areas of the brain.

"This technology provides the basis for lots of exciting future developments beyond neuroscience research. It could lead to tech that can pass a signal from the brain to a machine, for example helping those with amputations to control a prosthetic limb to shake a hand or stand up. It could also be used to create electrical signals in the brain when neurons are damaged and aren't firing themselves, such as in motor neurone disease," says Andreas Schaefer, group leader in the neurophysiology of behaviour laboratory at the Crick and professor of neuroscience at UCL.

When the device is connected to a brain, electrical signals from active neurons travel up the nearby microwires to a silicon chip, where the data is processed and analysed showing which areas of the brain are active.

The researchers ensured the design of the device allows it to be easily scaled depending on the size of the animal, with a few hundred wires for a mouse to over 100,000 for larger mammals. This is a key feature of the device as it means it holds potential, in the future, to be scaled for use with humans.

Mihaly Kollo, co-lead author, postdoc at the Crick's neurophysiology of behaviour laboratory and senior research associate at UCL, says: "One of the great challenges in recording brain activity, especially in deeper regions, is how to get the wires, called electrodes, in position without causing a lot of tissue damage or bleeding. Our method overcomes this by using electrodes that are sufficiently thin.

"Another challenge is recording the activity of many neurons that are that are distributed in layers with complex shapes in the three-dimensional space. Again, our method provides a solution as the wires can be readily arranged into any 3D shape."

The technology described in the study is also the basis for a fully integrated brain computer interface system that is being developed by Paradromics, a company founded by Matthew Angle, one of the authors of this paper. The Texas-based company is working to develop a medical device platform that will improve the lives of people with critical diseases, including paralysis, sensory impairment and drug resistant neuropsychiatric diseases.

Former Tropical Cyclone Herold is now a fading area of low-pressure in the Southern Indian Ocean and NASA's Aqua satellite provided forecasters with a visible image.

On Mar. 19 at 4 p.m. EDT (2100 UTC), the Joint Typhoon Warning Center issued their final bulletin on Herold. At that time, Herold's center was located near latitude 26.6 degrees south and longitude 73.0 degrees east, approximately 948 nautical miles east-southeast of Port Louis, Mauritius. Herold's maximum sustained winds at the time were near 30 knots (34.5 mph/55.5 kph) making it a tropical depression. It has since weakened.

On Mar. 20, the Moderate Resolution Imaging Spectroradiometer or MODIS instrument that flies aboard NASA's Aqua satellite provided a visible image of the clouds circling Herold's center. The clouds appeared wispy and devoid of heavy rainfall. The storm showed no strong convection (rising air that forms the thunderstorms that make up a tropical cyclone). Herold has moved over cooler waters which have sapped thunderstorm development.

Herold is expected to dissipate later in the day on Mar. 20.

NASA's Aqua satellite is one in a fleet of NASA satellites that provide data for hurricane research.

Tropical cyclones/hurricanes are the most powerful weather events on Earth. NASA's expertise in space and scientific exploration contributes to essential services provided to the American people by other federal agencies, such as hurricane weather forecasting.

Egyptian blue is one of the oldest manmade colour pigments. It adorns, for instance, the crown of the world famous bust of Nefertiti. But the pigment can do even more. An international research team led by Dr Sebastian Kruss from the Institute of Physical Chemistry at the University of Göttingen has produced a new nanomaterial based on the Egyptian blue pigment, which is ideally suited for applications in imaging using near infrared spectroscopy and microscopy. The results have been published in the journal Nature Communications.

Microscopy and optical imaging are important tools in basic research and biomedicine. They use substances that can release light when excited. Known as "fluorophores", these substances are used to stain very small structures in samples, enabling clear resolution using modern microscopes. Most fluorophores shine in the range of light visible to humans. When using light in the near infrared spectrum, with a wavelength starting at 800 nanometres, light penetrates even deeper into tissue and there are fewer distortions to the image. So far, however, there are only a few known fluorophores that work in the near infrared spectrum.

The research team has now succeeded in exfoliating extremely thin layers from grains of calcium copper silicate, also known as Egyptian blue. These nanosheets are 100,000 times thinner than a human hair and fluoresce in the near infrared range. "We were able to show that even the smallest nanosheets are extremely stable, shine brightly and do not bleach," says Dr Sebastian Kruss, "making them ideal for optical imaging."

The scientists tested their idea for microscopy in animals and plants. For example, they followed the movement of individual nanosheets in order to visualise mechanical processes and the structure of the tissue around cell nuclei in the fruit fly. In addition, they integrated the nanosheets into plants and were able to identify them even without a microscope, which promises future applications in the agricultural industry. "The potential for state-of-the-art microscopy from this material means that new findings in biomedical research can be expected in the future," says Kruss.

Teams around the world are working hard to develop active substances against SARS-CoV-2. The structural analysis of functional proteins of the virus is very helpful for this goal. The function of a protein is closely related to its 3D architecture. If this 3D architecture is known, it is possible to identify specific points of attack for active substances.

A special protein is responsible for the reproduction of the viruses: the viral main protease (Mpro or also 3CLpro). A team led by Prof. Dr. Rolf Hilgenfeld, University of Lübeck, has now decoded the 3D architecture of the main protease of SARS-CoV-2. The researchers have used the high-intensity X-ray light from the BESSY II facility of the Helmholtz-Zentrum Berlin.

"For such issues of highest relevance, we can offer fast track access to our instruments", says Dr. Manfred Weiss, who heads the Research Group Macromolecular Crystallography (MX) at HZB. At the so-called MX instruments tiny protein crystals can be analysed with highly brilliant X-ray light. The images contain information about the 3D architecture of the protein molecules. The complex shape of the protein molecule and its electron density is then calculated by computer algorithms.

The 3D architecture provides concrete starting points for developing active substances or inhibitors. These drugs could dock specifically to target points of the macromolecule and impede its function. Rolf Hilgenfeld is a world-renowned expert in the field of virology and already developed an inhibitor against the SARS-virus during the 2002/2003 SARS pandemic. In 2016, he succeeded in deciphering an enzyme of the Zika virus.

A novel serotype 2 oral poliovirus vaccine - and complete removal of the current formulation (OPV2) - is urgently needed, a new statistical modeling study suggests. Its results demonstrate that, despite the withdrawal of OPV2 in 2016, the aftereffects of its administration continue to contribute to the highest number of vaccine-derived poliovirus outbreaks and transmission rates to date. The novel OPV2 will be more genetically stable than the last and is currently in phase II clinical trials, but in case the formulation takes too long or lacks efficacy, back-up strategies are necessary, the authors add. The re-emergence of paralytic polio caused by mutated poliovirus derived from the OPV2 has been a major obstacle to achieving polio eradication across the world, leading to the withdrawal of OPV2 in April 2016 - commonly referred to as "the Switch." However, cases of vaccine-derived poliovirus have since been reported across several continents, posing a threat to unvaccinated children born after the Switch. For now, vaccination with OPV2 is the only available method to induce immunity and prevent transmission. But further use of OPV2 risks seeding more of the mutated poliovirus. What's more, Grace Macklin and colleagues now show the probability of new vaccine-derived poliovirus outbreaks and person-to-person transmission is increasing over time. They ran statistical models on data from acute polio paralysis cases obtained through the Global Polio Laboratory Network (GPLN). They determined the rate of viral mutation (one nucleotide change observed after approximately 35 days) and estimated that the vaccine-derived virus emerged between May 2016 and November 2019. Between these dates, GPLN had detected 859 isolates of the vaccine-derived virus across 26 countries - of which 65.5% were most likely seeded after the Switch, the researchers calculated. They identified 62 post-Switch transmittable vaccine-derived poliovirus events and 41 outbreaks in various African and Asian countries. Shortly after the first outbreaks, OPV2 was rolled out again, causing 21 of the total 41 outbreaks between 2016 and 2019. Based on their findings, it's clear OPV2 removal is essential to seize the spread of paralytic polio, the authors say.

Stanford researchers have developed a technique that reprograms cells to use synthetic materials, provided by the scientists, to build artificial structures able to carry out functions inside the body.

"We turned cells into chemical engineers of a sort, that use materials we provide to construct functional polymers that change their behaviors in specific ways," said Karl Deisseroth, professor of bioengineering and of psychiatry and behavioral sciences, who co-led the work.

In the March 20 edition of Science, the researchers explain how they developed genetically targeted chemical assembly, or GTCA, and used the new method to build artificial structures on mammalian brain cells and on neurons in the tiny worm called C. elegans. The structures were made using two different biocompatible materials, each with a different electronic property. One material was an insulator, the other a conductor.

Study co-leader Zhenan Bao, professor and chair of chemical engineering, said that while the current experiments focused mainly on brain cells or neurons, GTCA should also work with other cell types. "We've developed a technology platform that can tap into the biochemical processes of cells throughout the body," Bao said.

The researchers began by genetically reprogramming the cells they wanted to affect. They did this by using standard bioengineering techniques to deliver instructions for adding an enzyme, called APEX2, into specific neurons.

Next, the scientists immersed the worms and other experimental tissues in a solution with two active ingredients - an extremely low, non-lethal dose of hydrogen peroxide, and billions of molecules of the raw material they wanted the cells to use for their building projects.

Contact between the hydrogen peroxide and the neurons with the APEX2 enzyme triggered a series of chemical reactions that fused the raw-material molecules together into a chain known as a polymer to form a mesh-like material. In this way, the researchers were able to weave artificial nets with either insulative or conductive properties around only the neurons they wanted.

The polymers changed the properties of the neurons. Depending on which polymer was formed, the neurons fired faster or slower, and when these polymers were created in cells of C. elegans, the worms' crawling movements were altered in opposite ways.

In the mammalian cell experiments, the researchers ran similar polymer-forming experiments on living slices from mouse brains and on cultured neurons from rat brains, and verified the conducting or insulating properties of the synthesized polymers. Finally, they injected a low-concentration hydrogen peroxide solution along with millions of the raw-material molecules into the brains of live mice to verify that these elements were not toxic together.

Rather than a medical application, Deisseroth says, "what we have are tools for exploration." But these tools could be used to study how multiple sclerosis, caused by the fraying of myelin insulation around nerves, might respond if diseased cells could be induced to form insulating polymers as replacements. Researchers might also explore whether forming conductive polymers atop misfiring neurons in autism or epilepsy might modify those conditions.

Going forward, the researchers would like to explore variants of their cell-targeted technology. GTCA could be used to produce a wide range of functional materials, implemented by diverse chemical signals. "We're imagining a whole world of possibilities at this new interface of chemistry and biology," Deisseroth said.

Researchers at Baylor College of Medicine and the Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital have improved our understanding of how tremor -- the most common movement disorder -- happens, opening the possibility of novel therapies for this condition.

Working with animal models, the researchers discovered that a particular brain cell type, known as the Purkinje cell, triggers tremor when its pattern of signaling to other neurons changes from a regular pattern to signaling in bursts. The altered signaling pattern returned to normal and the tremor stopped when the animals were treated with deep-brain stimulation directed at a group of cerebellar neurons that communicate with Purkinje cells. The study appears in the journal eLife.

"Tremor is an involuntary, rhythmic shaking movement in one or more parts of the body. Available treatments are not always effective and the development of novel therapies to help people with this condition has been limited in part by not knowing what cell types are involved," said first author Amanda M. Brown, graduate student in the lab of Dr. Roy Sillitoe at Baylor. "In this study, we looked at the underlying brain activity that is associated with this condition in animal models and discovered that Purkinje cells in the cerebellum can trigger and propagate the signals for tremor."

There are different categories of tremor. Some can be intermittent or constant and occur sporadically, or some can be associated with many other neurological disorders, such as Parkinson's disease, ataxia or dystonia. Although tremor as a condition is not life-threatening, it can be disabling or make essential daily tasks, such as eating, drinking and walking, difficult.

Purkinje cells play an active role in tremor

Previous studies had hinted that having defective Purkinje cells in the cerebellum, a brain area involved in movement, balance and coordination and other functions, seemed to contribute to the generation of tremor. These findings led Brown and her colleagues to directly test this possibility.

First, they genetically removed the Purkinje cells' ability to communicate with other cells in the mouse models, expecting that these mice would develop tremor.

"Surprisingly, we saw no tremor," Brown said. "This told us that the activity, rather than loss of activity, of Purkinje cells was important for causing tremor. Purkinje cells had to be able to signal other brain cells for tremor to occur."

But, what type of signal would trigger tremor?

To answer this question, Brown and her colleagues placed electrodes into the brain of mice and recorded the activity of Purkinje cells during tremor and at normal state.

"We found that at normal state, the signals Purkinje cells send to other brain cells follow a regular pattern of activity, but during tremor, the signals come in bursts," Brown said.

Further experiments showed that it was this burst-like activity that triggered tremor. The experiments used a technique called optogenetics, which allows scientists to control brain activity with light. Brown and colleagues designed their optogenetics method to purposely make Purkinje cells signal in bursts. When the researchers triggered a burst-like activity, the animals had a tremor.

"By varying the frequency of the signal produced by Purkinje cells, we were able to vary the frequency of the tremor," Brown said. "This suggests that the cerebellum may be involved in many different kinds of tremor disorders."

Stopping tremor with deep brain stimulation

Currently, for individuals who have tremor that is not responding to drug treatment, deep-brain stimulation usually is recommended and typically directed to a brain region called the thalamus, which receives input from the cerebellum among other places. This treatment usually is helpful, Brown explained, but over time it can become less effective. The researchers were hoping to identify a new target location for treatment that could add benefits and potentially last longer.

The researchers set up an experimental system that enabled them to begin deep brain stimulation only when a mouse had a tremor. The results were exciting and encouraging. They showed that deep-brain stimulation of the cerebellum can successfully reduce tremor severity to normal levels.

"It was very exciting to see that cerebellar deep brain stimulation can stop the most severe tremors in mice," said Sillitoe, corresponding author and associate professor of pathology and immunology and of neuroscience at Baylor and Texas Children's. Sillitoe also is the co-director of the Development, Disease Models and Therapeutics Graduate Program at Baylor. "Although these findings are promising, there is still much work to do before we can bring this approach to the clinic."

Chestnut Hill, Mass. (3/19/2020) - Using a single atom-thick sheet of graphene to track the electronic signals inherent in biological structures, a team led by Boston College researchers has developed a platform to selectively identify deadly strains of bacteria, an advance that could lead to more accurate targeting of infections with appropriate antibiotics, the team reported in the journal Biosensors and Bioelectronics.

The prototype demonstrates the first selective, rapid, and inexpensive electrical detection of the pathogenic bacterial species Staphylococcus aureus and antibiotic resistant Acinetobacter baumannii on a single platform, said Boston College Professor of Physics Kenneth Burch, a lead co-author of the paper.

The rapid increase in antibiotic resistant pathogenic bacteria has become a global threat, in large part because of the over prescription of antibiotics. This is driven largely by the lack of fast, cheap, scalable, and accurate diagnostics, according to co-author and Boston College Associate Professor of Biology Tim van Opijnen.

Particularly crucial is identifying the bacterial species and whether it is resistant to antibiotics, and to do so in a platform which can be easily operated at the majority of points of care. Currently such diagnostics are relatively slow - taking from hours to days - require extensive expertise, and very expensive equipment.

The BC researchers, working with colleagues from Boston University, developed a sensor, known as a graphene field effect transistor (G-FET), that can overcome critical shortcomings of prior detection efforts since it is a highly scalable platform that employs peptides, chains of multiple linked amino acids, which are inexpensive and easy-to-use chemical agents, according to co-author and BC Professor of Chemistry Jianmin Gao.

The team set out to show it could construct a device that can "rapidly detect the presence of specific bacterial strains and species, exploiting the large amount of electric charge on their surface and ability to capture them with synthetic peptides of our own design," said Burch.

The initiative built upon the earlier research of van Opijnen and Gao, who previously found peptides were highly selective, but at that time required expensive fluorescence microscopes for their detection. In addition to Burch, Gao, and van Opijnen, the lead co-authors of the paper included Boston University Assistant Professor of Chemistry Xi Ling.

The team modified existing peptides to allow them to attach to graphene, a single atomic layer of carbon. The peptides were designed to bind to specific bacteria, rejecting all others. In essence, the G-FET is able to monitor the electric charge on the graphene, while exposing it to various biological agents.

Due to the selectivity of the peptides, the researchers were able to pinpoint their attachment to the desired bacterial strain, the team reported in the article "Dielectrophoresis assisted rapid, selective and single cell detection of antibiotic resistant bacteria with G-FETs." By electrically monitoring the resistance and, ultimately, charge on the device, the presence of bacteria attached to graphene could be resolved, even for just a single cell.

To enable greater speed and high sensitivity, an electrical field was placed on the liquid to drive the bacteria to the device, again exploiting the charge on the bacteria, the team reported. This process, known as dielectrocphoresis, had never previously been applied to graphene-based sensors and could potentially open the door to dramatically improving efforts in that field to employ graphene for biosensing, the team reported.

"We were surprised how well the bacteria were electrically guided to the devices," said Burch. "We thought it would somewhat reduce the required time and needed concentration. Instead, it worked so well that the electric field was able to bring needed concentration of bacteria down by a factor of 1000, and reduce the time to detection to five minutes."

Irvine, Calif. - March 19, 2020 - A team of University of California, Irvine researchers have published the first comprehensive overview of the major changes that occur in mammalian skin cells as they prepare to heal wounds. Results from the study provide a blueprint for future investigation into pathological conditions associated with poor wound healing, such as in diabetic patients.

"This study is the first comprehensive dissection of the major changes in cellular heterogeneity from a normal state to wound healing in skin," said Xing Dai, PhD, a professor of biological chemistry and dermatology in the UCI School of Medicine, and senior author. "This work also showcases the collaborative efforts between biologists, mathematician and physicists at UCI, with support from the National Institute of Arthritis & Musculoskeletal & Skin Diseases-funded UCI Skin Biology Resource-based Center and the NSF-Simons Center for Multiscale Cell Fate Research.

The study, titled, "Defining epidermal basal cell states during skin homeostasis and wound healing using single-cell transcriptomics," was published this week in Cell Reports.

"Our research uncovered at least four distinct transcriptional states in the epidermal basal layer as part of a 'hierarchical-lineage' model of the epidermal homeostasis, or stable state of the skin, clarifying a long-term debate in the skin stem cell field," said Dai.

Using single-cell RNA sequencing coupled with RNAScope and fluorescence lifetime imaging, the team identified three non-proliferative and one proliferative basal cell state in homeostatic skin that differ in metabolic preference and become spatially partitioned during wound re-epithelialization, which is the process by which the skin and mucous membranes replace superficial epithelial cells damaged or lost in a wound.

Epithelial tissue maintenance is driven by resident stem cells, the proliferation and differentiation dynamics of which need to be tailored to the tissue's homeostatic and regenerative needs. However, our understanding of tissue-specific cellular dynamics in vivo at single-cell and tissue scales is often very limited.

"Our study lays a foundation for future investigation into the adult epidermis, specifically how the skin is maintained and how it can robustly regenerate itself upon injury," said Dai.

Opening plastic packaging, such as plastic bags and bottles may contribute to the generation of small amounts of microplastics -- small plastic particles less than 5 mm long -- during daily tasks, according to a study published in Scientific Reports.

Microplastics are generally believed to originate directly from industry, for example as cosmetic exfoliates, or indirectly from the breakdown of larger plastic items over time. However, the contribution of daily tasks such as cutting, tearing or twisting open plastic packaging and containers has not been fully understood.

Cheng Fang and colleagues monitored the generation of microplastics during the tearing open of chocolate packaging, cutting of sealing tapes and opening of plastic bottle caps. The generation of microplastics during these processes was confirmed using chemical tests and microscopy.

The authors found that different shapes and sizes of microplastics were generated during tearing or cutting. These included fibers, fragments or triangles, ranging from nanometers to millimeters in size. Fragments and fibers were generated most often. The authors estimated that ten to 30 nanograms (0.00001-0.00003 milligrams) of microplastics may be generated per 300 centimetres of plastic during cutting or twisting, depending on the opening approach and conditions of the plastic, such as stiffness, thickness or density.

The results suggest that everyday activities such as opening plastic bags and bottles could be additional sources of small quantities of microplastics; however, their risk, possible toxicity and how they may be ingested are not yet resolved and further research into human exposure is needed.

A new study by an international team of scientists has revealed the developmental and evolutionary mechanisms underlying the origin of a major phylum.

The Cambrian Explosion was a pivotal event in the history of life half a billion years ago with the sudden appearance of dozens of distinctive animal body plans. After this initial burst of innovation, the appearance of new body plans slowed to a halt. This pattern has puzzled and intrigued scientists and led to hypotheses regarding the ecological and developmental influences on animal evolution.

The study investigates the questions of whether this pattern resulted from abundant ecological opportunity early in the history of life, which became dampened with competition through time, or from evolutionary shifts in growth and development that limit evolutionary innovation through time.

Bradley Deline--lead author in the study, from the University of West Georgia (USA)--assembled a team of experts to address this question by compiling the vast anatomical features found within echinoderms.

This phylum that includes sea stars and sea urchins, was ideal for this study because it contains an incredible richness of forms and features, especially early in its evolutionary history.

"With this information, we can trace the evolution of complex forms and address fundamental questions regarding the mechanisms that govern the overall appearance of animals through time," Deline said.

Scientists have argued that features defining animal body plans have become increasingly elaborate through time such that they become burdened by their own complexity. This burden could prevent change and would explain the lack of new phyla since the Cambrian Explosion.

Recent studies in modern animals show genetic interactions that mirror this hypothesis in which the genes and gene interactions that govern complex features are conserved through time. However, modern animals are 500 million years removed from the origin of their phylum, such that these questions can only be answered with the fossil record.

Colin Sumrall from the University of Tennessee (USA), worked to integrate this wealth of information with a new and expansive evolutionary tree of early echinoderms. This showed the steady exploration of body plans through time that ultimately became distinctive with the extinction of transitional forms.

However, body plans' distinctiveness was subsequently diminished with animals independently converging on similar forms.

"This highlights the amazing complexity within echinoderms with so many groups arriving on similar solutions to become successful," Sumrall explained. "There are many examples of echinoderms continuing to change dramatically long after the Cambrian Explosion."

Co-author Jeffrey Thompson, from University College London (UK), suggested testing developmental mechanisms by comparing the evolutionary stability of both complex and simple features within echinoderms.

"We see no difference in the stability or evolutionary patterns in simple and complex features," Thompson exclaimed. "Large-scale characters are flexible allowing echinoderms to routinely break through constraints allowing for continued evolutionary innovation."

Therefore, based on the results of this study, the major factor limiting this vast potential for evolutionary change seems to be ecological opportunity rather than rigidly constrained developmental processes.

This study, along with work on modern animals, clarifies evolution and development during the Cambrian Explosion and beyond in which complex and burdened features retain flexibility enabling continued change and anatomical innovation in an ever-changing world.

When parents eat low-protein or high-fat diets it can lead to metabolic disorders in their adult offspring. Now, an international team led by researchers at the RIKEN Cluster for Pioneering Research (CPR) have identified a key player and the molecular events underlying this phenomenon in mice.

The Developmental Origins of Health and Disease is a school of thought that focuses on how prenatal factors such as stress and diet impact the development of diseases when children reach adulthood. Experimental evidence indicates that environmental factors that affect parents do play a role in reprogramming the health of their offspring throughout their lifespan. In particular, parental low-protein diets are known to be related to metabolic disorders in their children, such as diabetes.

This phenomenon is thought to be regulated through epigenetics--heritable changes in which genes are turned on and off without actually changing an individual's DNA. However, until now, the details of this process were unknown. In their study published in Molecular Cell, a team led by Keisuke Yoshida and Shunsuke Ishii at RIKEN CPR tackled this question in a mouse model and discovered that a protein called ATF7 is essential for the intergenerational effect. ATF7 is a transcription factor, meaning that it regulates when genes are turned on and off.

The researchers fed male and female mice on normal diets or low protein diets and then allowed them to mate. They compared gene expression--which genes were turned on--in adult offspring of male mice who had been on the two different diets and found that expression differed for hundreds of genes in the liver, many of which are involved in cholesterol metabolism. However, when they used genetically engineered male mice that lacked one copy of the ATF7 gene, gene expression in the offspring did not differ from the expression in offspring whose parents ate normal diets.

This result means that a male mouse's diet can influence the health of future children. As male mice cannot affect offspring in pregnant females, the researchers concluded that the most likely scenario was that the epigenetic changes occurred in the male's sperm before conception, and that ATF7 has a critical function in this process.

Based on this logic, the team searched for and found genes in sperm cells that are controlled by ATF7, including those for fat metabolism in the liver and cholesterol production. Experiments revealed that when fathers-to-be ate low protein diets, ATF7 came loose and no longer bound to these genes. This in turn reduced a particular modification to histone proteins, with a net effect that these sperm-cell genes were turned on, rather than the normal situation of being turned off. "The most surprising and exciting discovery was that the epigenetic change induced by paternal low protein diet is maintained in mature sperm during spermatogenesis and transmitted to the next generation," Ishii says.

Using a mouse model, this study helps explain the molecular details underlying the Developmental Origins of Health and Disease theory, and the kinds of nutritional conditions that could lead to lifestyle-related diseases in children, such as diabetes. In addition, it should now be possible to predict metabolic changes in the next generation by measuring epigenetic changes in the identified genes of paternal sperm cells. "We hope that people, especially those who have poor nutrition by choice, will pay more attention to their diet when planning for the next generation. Our results indicate that diets with more protein and less fat are healthier not just for everyone's own body, but also for sperm and the health of potential children."

Sugar-rich diets have a negative impact on health independent of obesity reports a new study led by the MRC London Institute of Medical Sciences, UK.

Researchers discovered that the shortened survival of fruit flies fed a sugar-rich diet is not the result of their diabetic-like metabolic issues.

The findings, published in the journal Cell Metabolism, instead suggest that early death from excess sugar is related to the build-up of a natural waste product, uric acid.

We all know that consuming too much sugar is unhealthy. It increases our risk of developing metabolic disorders, such as obesity and diabetes, and can shorten our life expectancy by several years. While this reduction in lifespan is widely believed to be caused by metabolic defects, this new study in fruit flies reveals that this may not be the case.

"Just like humans, flies fed a high-sugar diet show many hallmarks of metabolic disease - for instance, they become fat and insulin resistant", says Dr Helena Cochemé, the principal investigator of the study. "Obesity and diabetes are known to increase mortality in humans, and so people always assumed that this was how excess sugar is damaging for survival in flies".

However, like salt, sugar also causes dehydration. In fact, thirst is an early symptom of high blood sugar and diabetes. Dr Cochemé continues: "Water is vital for our health, yet its importance is often overlooked in metabolic studies. Therefore, we were surprised that flies fed a high-sugar diet did not show a reduced lifespan, simply by providing them with an extra source of water to drink. Unexpectedly, we found that these flies still exhibited the typical metabolic defects associated with high dietary sugar".

Based on this water effect, the team decided to focus on the fly renal system. They showed that excess dietary sugar caused the flies to accumulate a molecule called uric acid. Uric acid is an end-product from the breakdown of purines, which are important building blocks in our DNA. But uric acid is also prone to crystallise, giving rise to kidney stones in the fly. Researchers could prevent these stones, either by diluting their formation with drinking water or by blocking the production of uric acid with a drug. In turn, this protected against the shortened survival associated with a sugar-rich diet.

So, does this mean we can eat all the sugary treats we want, as long as we drink plenty of tea? "Unfortunately not," says Dr Cochemé, "the sugar-fed flies may live longer when we give them access to water, but they are still unhealthy. And in humans, for instance, obesity increases the risk of heart disease. But our study suggests that disruption of the purine pathway is the limiting factor for survival in high-sugar-fed flies. This means that early death by sugar is not necessarily a direct consequence of obesity itself".

To understand the impact of dietary sugars on human health, collaborators from Kiel University in Germany explored the influence of diet in healthy volunteers. "Strikingly, just like flies, we found that dietary sugar intake in humans was associated with worse kidney function and higher purine levels in the blood", says Prof. Christoph Kaleta, co-author of the study.

Accumulation of uric acid is a known direct cause of kidney stones in humans, as well as gout, a form of inflammatory arthritis. Uric acid levels also tend to increase with age, and can predict the onset of metabolic diseases such as diabetes. "It will be very interesting to explore how our results from the fly translate to humans, and whether the purine pathway also contributes to regulating human survival", concludes Dr Cochemé. "There is substantial evidence that what we eat influences our life expectancy and our risk for age-related diseases. By focusing on the purine pathway, our group hopes to find new therapeutic targets and strategies that promote healthy ageing".