Culture

A group of researchers from four countries, including Brazil, have worked out exactly how a pollen tube, the plant cell that emerges from a grain of pollen, grows up to a thousand-fold to reach an ovule deep inside the flower. The key to this growth is an inflow and outflow of protons that creates electrical activity at the cell membrane and makes the cell grow. The results of the study will help scientists understand an array of related phenomena, such as seed production, the growth of fungi, and even how neurons develop.

The study was supported by FAPESP. The findings are described in a paper authored by researchers affiliated with institutions in Brazil, Denmark, Portugal and the United States and published in Nature Communications.

“A grain of pollen consists of a single cell. When it comes into contact with the female sex organ on the surface of a flower, it grows at a very high speed, forming what we call a pollen tube, until it reaches the base of the flower’s ovary and discharges the sperm cells. How this happens was very poorly understood until now” according to Maria Teresa Portes, who conducted the research during a postdoctoral fellowship at the University of Maryland in the US.

Scientists have long been intrigued by the exceptionally fast pace of pollen tube growth, which is the fastest type of cell growth observed among all living organisms. Its elongation originates at the tip of the tube and is termed tip growth. The species used in the study was Arabidopsis thaliana (thale cress), a small flowering plant native to Eurasia and Africa. It belongs to the mustard family (Brassicaceae) and is widely chosen as a model organism because of its usefulness for genetic experiments. Its pollen tube grows as much as 3 mm per day.

The researchers produced mutant varieties of the plant in the laboratory in which some genes were modified. They discovered that inactivating three AHA genes inhibited pollen tube growth. AHA refers to the autoinhibited H+-ATPase gene family.

In the mutant plants, only the eggs closest to the surface were fertilized. As a result, the plants produced only 5% of the normal number of seeds.

In a series of experiments, the researchers found that the proteins expressed from these genes acted as proton pumps, injecting protons from the environment to make the pollen tube cell more acidic and promote faster growth.

Proton pumps regulate the electrochemical gradient that energizes the nutrient uptake system and acid growth mechanism of plant cells.

“We wanted to understand how the cell organizes this growth process. Proton distribution in the ion gradient was found to be non-uniform, with protons bunching at the tip of the tube, and there are also gradients of molecules such as calcium and actin,” said Daniel Santa Cruz Damineli, another coauthor of the study who is currently a postdoctoral fellow in the University of São Paulo’s Medical School (FM-USP) in Brazil with a scholarship from FAPESP.

From seeds to neurons

Among several potential developments arising from the study’s findings is a deeper understanding of how seeds are produced, so that they can, in theory, be used to create improved varieties of food crops such as legumes and cereals.

“We don’t know everything about how the pollen tube is guided and how a plant’s male and female organs communicate,” Portes said. “This is a major research interest and could culminate in seed production. Plant growth necessarily involves this mechanism, which we’re just starting to understand more deeply.”

This knowledge should also help scientists understand tip-growth in other cells or organisms, such as that of fungal hyphae, neurons and cancer cells.

“Biologically speaking, how tip growth is orchestrated is poorly understood. Now we can study it further,” Damineli said.

Researchers from Skoltech, Lomonosov Moscow State University, and the Kharkevich Institute for Information Transmission Problems have studied the genomes of some 200 strains of bacteria to determine which proteins in the ribosome, part of the key cell machinery, can be safely lost and why. The paper was published in the journal Molecular Biology and Evolution.

The ribosome is a universal cellular machine, present in all eukaryotes and prokaryotes, that builds proteins in a process called translation. The two major components of the ribosome, the so-called small and large ribosomal subunits, consist of ribosomal RNA (rRNA) molecules and ribosomal proteins.

The composition of these fundamental 'protein factories' is fairly consistent across cells, but there is evidence that some bacteria function without a complete set of ribosomal proteins, so researchers have been looking to determine which of the proteins are truly essential for a working ribosome.

Skoltech professor and vice president for biomedical research Mikhail Gelfand and his colleagues analyzed ribosomal protein composition in 214 relatively small bacterial genomes. They identified a set of frequently lost proteins and showed that only nine ribosomal proteins were completely conserved, while each of the remaining 48 was lost in at least one strain from the dataset.

"Tiny genomes are characteristic of endosymbionts, bacteria that live within other bacteria or eukaryotic cells. In this non-changing environment and under weak selection they tend to lose non-essential (even if necessary for free-living bacteria) genes -- similar to multicellular parasites that often miss entire organs. The ribosome has been assumed to be the most conserved organelle with a standard set of proteins; but if you have only 121 genes -- the present bacterial record for simplicity -- you cannot encode all fifty-something ribosomal proteins, so some of them have to be lost. We have demonstrated that the patterns of this loss are not random," Professor Gelfand says.

Apparently, ribosomal proteins of the small subunit were more likely to be retained than the large subunit proteins, and most frequently lost proteins were located on the ribosome surface, where they formed fewer contacts with other ribosome components. They were also incorporated in the ribosome late in evolution, so it seems that bacteria tend to practice the 'last in, first out' approach when it comes to dropping ribosomal proteins.

The researchers also found that the three bacteria with the shortest genomes in the group lost the largest number of proteins; there was a correlation between genome size and a number of retained ribosomal proteins. Yet since ribosomal proteins are in the cell's essential toolkit, they are generally among the last to leave a 'downsizing' bacterial genome.

A career in professional football may yield an array of health benefits that extend beyond playing years: NFL players engage in vigorous training, tend to be more educated than other men in the U.S. and have higher median incomes than most fellow Americans--all factors associated with better overall health.

But new research from Harvard Medical School and the Harvard T.H. Chan School of Public Health suggests that even these advantages may not be enough to neutralize persistent gaps in health outcomes among Black, white and players of other racial backgrounds.

The analysis, based on self-reports among former NFL players, found that Black players were significantly more likely than white players to experience diminished quality of life due to impaired physical function, pain, cognitive troubles, depression and anxiety. In four of five health outcomes, the gaps were greatest between Black and white former players.

The findings, published on August 4 in Annals of Epidemiology, are based on a survey of 3,794 former NFL players, ages 24 to 89, conducted as part of the ongoing Football Players Health Study at Harvard University, a research initiative that encompasses a constellation of studies designed to evaluate various aspects of players' health across the lifespan.

The researchers categorized former players into three groups based on self-identified race: Black (1,423), white (2,215) and Hawaiian and other races (109)--a group that included American Indian/Alaskan Native, Native Hawaiian/Pacific Islander and Asian, among others.

Next, the researchers compared self-reported symptoms in five categories: physical functioning, pain, cognitive function, depression and anxiety.

The analysis showed that Black former NFL players were 50 percent more likely than white former players to have pain that interfered with daily activities, as well as depression and anxiety. Black former players were 36 percent more likely to have cognitive symptoms--including memory deficits and attention problems--that impacted their quality of life. Black former players were also nearly 90 percent more likely to report impaired physical functioning, compared with their white peers.

The study found that other nonwhite players, including Native Hawaiians, had a higher risk for all categories of adverse health outcomes, except impaired physical functioning.

"Our analysis points to persistent and dramatic gaps in health outcomes among former NFL players that are particularly pronounced among Black athletes and also present among other Hawaiians, Native Americans and Asian players," said study lead author Andrea Roberts, senior research scientist at the Harvard T.H. Chan School of Public Health.

"Our findings underscore the urgent need to develop public health interventions and policies that address underlying systemic factors that give rise to such disparities both among former athletes and in the general population," Roberts added.

To examine the role of other factors that may affect health outcomes, the researchers also looked at number of seasons played in the NFL, position played, concussion symptoms, surgeries, body-mass index, use of performance-enhancing drugs, lifestyle habits including drinking and smoking, as well as pain medication use. The differences persisted even when the researchers accounted for the possible influence of these factors.

Next, the researchers examined whether differences in health varied by a player's age, as a surrogate marker for diversity and equity in the era that they played in. Although younger nonwhite players were in the NFL during a period marked by greater diversity and greater equity, their risk for adverse health outcomes remained the same as that of older players.

The researchers suggested that factors such as discrimination prior to, during, or following a player's time in the NFL could account for the disparities. Systemic and structural racism has been linked with worse mental and physical health and higher mortality. Additionally, past research indicates that nonwhites are more likely to receive lower quality health care than whites.

"We tend to think that elite athletes may be shielded from health inequities, but our findings counter that notion and reveal important differences in quality of life among former athletes," said study senior author Marc Weisskopf, professor of environmental epidemiology and physiology at the Harvard Chan School. "These gaps echo well-documented health disparities in the general population and demand both short-term interventions and long-term solutions."

"As we begin to unpack the complexities around these health disparities between white and nonwhite players, we can begin to see the confluence of challenges that extend beyond the socioeconomic benefits of playing in the NFL," said study co-author Herman Taylor, a co-investigator of the Football Players Health Study and director of the Cardiovascular Research Institute at the Morehouse School of Medicine. "Meaningful solutions to systemic inequities that fuel health disparities will not emerge overnight. In the meantime, we urge players to consult their physicians about the health concerns we've outlined in this study that might impact their quality of life."

A new study published today demonstrates that a technology developed at the University of Central Florida could serve as a more reliable clinically-based model of amyotrophic lateral sclerosis (ALS) and a better screening tool for novel therapies than currently use preclinical models.

The Human-on-a-Chip®technology was developed by UCF Professor James J. Hickman in his Hybrid Systems Lab at UCF. It has been licensed to Hesperos, Inc., a company founded by Hickman and Michael L. Shuler, Ph.D.

"This study supports the ability of our Human-on-a-Chip system to more accurately and rapidly assess new treatments for ALS, and potentially speed up the overall drug development process," says Hickman, co-author of the paper, titled "A Human-Based Functional NMJ System for Personalized ALS Modeling and Drug Testing," published in the journal Advanced Therapeutics . "This is also the first data to demonstrate the efficacy of the Deanna protocol for the treatment of ALS, utilizing a clinically relevant assay system."

ALS is a progressive disease that damages nerves and over time causes the loss of muscle control and eventual death. Between 12,000-15,000 people in the nation are diagnosed with ALS with about 5,000 new cases every year, according to the Centers for Disease Control and Prevention. Also known as Lou Gerhig's disease, there is no cure.

In the new journal article, researchers from UCF and Cornell University describe a functional neuromuscular junction (NMJ) disease model comprising motoneurons derived from induced pluripotent stem cells (iPSCs) of ALS patients and wild type primary human muscle fibers housed in a compartmentalized chambered system. Most importantly, the functional system was able to reproduce assays used in the clinic to assess ALS deficits where a patient is given a task to do with increased speed to detect spasticity or loss of muscle strength. This was reproduced by stimulating the motoneurons at increasing frequency and monitoring the muscle to record "skips" as well as accelerated fatigue.

The iPSCs were derived from three separate ALS lines, two expressing SOD1 mutations and one expressing the FUS mutation. Compared to healthy controls, each of the three cell lines of ALS motoneurons exhibited mutant-specific pathological phenotypes at varying degrees of severity, including increased axonal varicosities, reduced axon branching and elongation, and increased excitability.

When ALS motoneurons were incubated in the dual chamber system with muscle tissue, functional NMJs were formed without cell death from axons transported through tiny tunnels to the muscle chamber. However, there were significant impairments in NMJ formation, electrical activity transmission, and muscle contraction with increasing stimulation frequency. These data suggest that the system is a valid model that recapitulates the morphological and functional deficits in ALS.

"To our knowledge, this is the first study to demonstrate that while different ALS mutations display various phenotypes, all have the common point-of-origin deficit at the NMJ for each mutation, which is useful for not only the familial form of the disease but potentially sporadic as well" said Hickman.

The Deanna protocol is a regimen of holistic, supplements that contains five components targeting various cellular mechanisms known to be pathologically altered in ALS and this over-the-counter ALS treatment is commercially available. While this strategy has been anecdotally reported to successfully treat ALS, there was previously no scientific evidence in a human functional model that support its therapeutic use.

In the study, upon treatment with the Deanna protocol the NMJ functional deficits were reversed. Specifically, treatment led to significant improvements in NMJ formation, electrical activity transmission and muscle contractions, even at higher frequencies of stimulation.

"Hesperos is looking forward to exploring how this interconnected multi-organ platform could be used to reveal additional patient-specific phenotypes in ALS and for high-content screening of drug candidates," said Michael L. Shuler, Ph.D., Chief Executive Officer of Hesperos.

STONY BROOK, NY, August 11, 2020 - Human networking involves every field and includes small groups of people to large, coordinated systems working together toward a goal, be it traffic management in an urban area, economic systems or epidemic control. A new study published in Nature Communications suggests by using a model of violin synchronization in a network of violin players, there are ways to drown out distractions and miscommunications that could be used as a model for human networks in society.

Titled "The Synchronization of Complex Human Networks," the study was conceived by Elad Shniderman, a graduate student in the Department of Music in the College of Arts and Sciences at Stony Brook University, and scientist Moti Fridman, PhD, at the Institute of Nanotechnology and Advanced Materials at Bar-llan University. He co-authored the paper with Daniel Weymouth, PhD, Associate Professor of Composition and Theory in the Department of Music and scientists at Bar-llan and the Weizmann Institute of Science in Israel. The collaboration was initiated at the Fetter Museum of Nanoscience and Art.

The research team devised an experiment involving 16 violinists with electric violins connected to a computer system. Each of the violinists had sound-canceling headphones, hearing only the sound received from the computer. All violinists played a simple repeating musical phrase and tried to synchronize with other violinists according to what they heard in their headphones.

According to Shniderman, Weymouth and their fellow authors: "Research on network links or coupling has focused predominantly on all-to-do coupling, whereas current social networks and human interactions are often based on complex coupling configurations.

This study of synchronization between violin players in complex networks with full control over network connectivity, coupling strength and delay, revealed that players can tune their playing period and delete connections by ignoring frustrating signals to find a stable solution. These controlled and new degrees of freedom enable new strategies and yield better solutions potentially applicable for other human networking models."

"Society in its complexity is recognizing how human networks affect a broad range of crucial issues, including economic inequality, stock market crashes, political polarization and the spread of disease," says Weymouth. "We believe there are a lot of important, real-world applications to the results of this experiment and ongoing work."

CAMBRIDGE, MA - New research from Harvard's Growth Lab finds a direct link between a country's incoming business travel and the growth of new and existing industries. The findings, published in the journal Nature Human Behaviour, support a Growth Lab hypothesis that moving knowhow, the tacit knowledge accumulated and transferred from brain to brain through a long process of imitation, repetition, and feedback, is critical to economic growth, and business travel plays a key part in that process. The research also raises new concerns about the economic implications of the international travel restrictions imposed to combat COVID-19.

Researchers Michele Coscia and Frank Neffke, working with Growth Lab Director Ricardo Hausmann, used anonymous transaction insights provided by Mastercard to map the flow of global business travel. This research is part of a collaboration between the Mastercard Center for Inclusive Growth and the Growth Lab at the Center for International Development at Harvard Kennedy School to understand the flow and accumulation of business 'knowhow,' a key driver for inclusive economic growth. Through this network, they created a Knowhow Index which ranks countries on incoming and outgoing knowhow. Germany, Canada, the US, UK, and Korea are the top sources of knowhow flows, while Austria, Ireland, Switzerland, Denmark, and Belgium received the most knowhow.

"We've been puzzled by the fact that business travel has been growing faster than world GDP, despite the widespread adoption of alternatives like Skype, FaceTime, email, etc.," said Hausmann, Rafik Hariri Professor of the Practice of International Political Economy at Harvard Kennedy School. "We posited that maybe there is a difference between moving information and moving brains. We obviously never imagined a complete shutdown of business travel, but the paper allows us to delve into the consequences."

The team created an interactive visualization that shows the effects of the disappearance of business travelers originating from a specific country. For example, if German businesspeople stopped traveling, the research estimates that Austria, South Africa, Switzerland, Nigeria, Czechia, and Turkey would be most affected, and global GDP would decrease by 4.8%.

"According to our study, the world is benefiting enormously by mobilizing the knowhow in brains through business travel. A permanent shutdown of this channel would probably imply a double-digit loss in global GDP," said Hausmann.

The research also suggests that business travel represents another development divide. "Obstacles to business travel, such as cumbersome visa regimes and long connections, constrain access to knowhow and limit growth opportunities, especially in developing countries," said Frank Neffke, research director at the Growth Lab.

An international team of scientists, including a researcher from Sechenov University, reviewed scientific articles on proteins (and genes encoding them) that help cancer cells enter the brain. An understanding of the processes that facilitate the formation of metastases in the brain will allow scientists to create new methods for cancer diagnosis and treatment. Details of the study can be found in the journal Trends in Cancer.

Brain tissues are very sensitive to changes in the levels of many substances and to the penetration of microorganisms and immune cells, but they need a large amount of nutrients and oxygen. Satisfying the needs of the brain requires a dense network of thin blood vessels, covered with a special shell that lets in essential substances and blocks all other compounds and cells. This shell, consisting of adjacent endothelial cells tightly connected to each other by special proteins, forms the blood-brain barrier (BBB), which prevents the free exchange of substances between blood vessels and brain tissues.

BBB works very well (letting in less than 2% of the molecules), but it is still not perfect: cancer cells sometimes manage to slip through it and trigger the development of metastases; since many drugs cannot get into the brain, this significantly complicates cancer treatment and worsens the prognosis for patients with metastases. The authors of the article decided to find out which genes give cancer cells such a 'superpower'.

'Metastasis formation is controlled by proteins and genes encoding these proteins. The purpose of this work was to systematise experimentally or clinically proven findings about the proteins and microRNAs that allow migration of tumour cells to the brain. It turned out that their production is typical for a number of metastases, while most of the cell molecules described in literature are unique for a particular type of tumour. Thus, the possibility of regulating genes that stimulate the migration of tumour cells to the brain may be a challenge faced by doctors in reducing the formation of intracerebral metastases in the future,' said Ilya Ulasov, one of the authors, a leading researcher at the Institute of Regenerative Medicine, Sechenov University.

Tumour cells are known to enter the brain both through dense contacts between the cells of the tunicae (layers of the blood vessels) and through these cells themselves. In the first case, cancer cells use enzymes and/or microRNAs to disrupt the structure of the dense contacts and increase the permeability of the BBB.

One of these enzymes is cathepsin C: it destroys the proteins of the dense contacts, and its inhibitors (substances that slow down its action) can suppress the growth of metastases in breast cancer. Two other enzymes - seprase and urokinase-type plasminogen activator - have shown similar effects in melanoma, and some metalloproteinases may be possible targets for anti-cancer therapy. Another protein, placental growth factor, triggers a chain of reactions to facilitate the development of metastases in lung, gastric or colorectal cancer.

MicroRNAs enable communication between cancer cells and their environment, including BBB cells and proteins. For example, miR-105 affects ZO-1 protein, contributing to the formation of metastases in breast cancer, while miR-143-3p can enhance BBB permeability in lung cancer.

The second way - penetration of cancer cells through BBB cells - is possible due to proteins of the cell wall, integrins, and certain groups of enzymes. In several types of cancer, metastasis cells showed an increased content of integrins avβ3 and avβ8. It is possible that they are involved in the formation of metastases in the brain and can serve as a biomarker of the disease. Another integrin, VLA-4, is produced in the metastases of most melanoma patients and promotes the binding of cancer cells and BBB cells, which opens the way to the brain.

In total, the authors reviewed 44 proteins, described the mechanism of their influence on the formation of metastases and listed the genes encoding them. The study will help scientists work out new ways to prevent and treat cancer, stroke and Alzheimer's disease, which also affect BBB integrity.

Researchers at Michigan Tech, TÜV SÜD UK National Engineering Laboratory and University of Edinburgh call for increased research on virus surface stability and interaction in "Surface Chemistry Can Unlock Drivers of Surface Stability of SARS-CoV-2 in Variety of Environmental Conditions" in the Cell Press journal Chem. They highlight the need to understand the different environmental conditions that affect the surface chemistry of viruses like SARS-CoV-2, the virus that causes the disease COVID-19.

Creating an Unfriendly Surface for Viruses

We're told to wash our hands with soap for 20 seconds to kill viruses. Why? Because the soap interacts with the surface chemistry of a virus, particularly the lipid, or fatty, casing around it, and essentially makes the virus explode.

Handwashing is a clear example of why understanding how viruses interact with surface environments is important. Increased research will better equip us to diminish how long viruses survive on surfaces or in the air, an important way to stop the spread.

"If the surface is not friendly, it's easier for the virus to fall apart. Where the virus has more friendly interactions with the surface, it's more likely to stay infectious," said Caryn Heldt, professor of chemical engineering and director of the Health Research Institute at Michigan Technological University.

"Viruses have unique ways of interacting with surfaces. The surface chemistry of the virus will change how the virus interacts with water," Heldt said. "If water such as humidity, which is common in your breath and in the air, gets between the virus and a surface, it can really change the way the virus interacts with that surface. The virus surface and the environment: you can't separate them out."

More Than One Way to Skin a Cat... Or a Virus

Part of the reason the scientific community's understanding of the SARS-CoV-2 virus continues to evolve is because there are only a few techniques available to measure the small amounts of virus particles required to infect a person as compared to other types of biomolecules, such as proteins.

"We need to understand how viruses interact with surfaces with and without water present, but the traditional ways we think of studying surface chemistry cannot detect these low levels of virus," Heldt said.

Heldt and coauthors said their article provides a broad overview of different ways researchers could learn more about these surface interactions on a chemical level.

Unlike the viruses that cause influenza, SARS-CoV-2 is mainly transmitted through aerosols, or particles that travel through and stay suspended in the air when people talk, sing, cough or sneeze.

The flu is transmitted by large droplets you breathe out, which fall to and stay infectious on surfaces. Heldt said surfaces have not been ruled out as a mode of transmission, but that the most common form of transition seems to be aerosol inhalation. "It's about how close you are to someone and for how long," she said.

Temperature and humidity in particular seem to have greater effects on the SARS-CoV-2 virus' virility.

"For the first time, we highlight potential mechanisms of the novel SARS-CoV-2 surface stability in various environmental conditions including temperature and relative humidity," said Aliakbar Hassanpouryouzband, a postdoctoral research associate at the University of Edinburgh.

While viruses are typically more stable when it's colder, which explains why flu season hits during the winter, that doesn't seem to be the case for the virus that causes COVID-19. However, researchers can infer from what heat does to molecules -- it increases their energy, causing them to move and vibrate more quickly -- that increased vibrations of virus molecules causes them to explode and no longer be infectious.

When it comes to humidity, viruses need to bind some water to their surfaces. But dehydrating a virus molecule isn't a cut-and-dried solution -- it can actually make some molecules more stable.

Along with further research into the effects of humidity, temperature and other environmental conditions, there's a need to explore the effects of pH balance and protein casings on the virus. The work to better understand the surface chemistry of SARS-CoV-2 will help scientists around the world design vaccines for this pandemic and those of the future.

"We hope that this article will assist experimental scientists worldwide in their investigations for unravelling the molecular drivers implicated in this new coronavirus transmission from the surfaces as well as in vaccine development and antiviral drug design," said Edris Joonaki, fluid properties expert at TÜV SÜD UK National Engineering Laboratory.

WASHINGTON, August 11, 2020 -- As we use resources, such as coal, oil, natural gas, copper, silicon and aluminum, to power massive computer farms and process digital information, our technological progress is redistributing Earth's matter from physical atoms to digital information -- the fifth state of matter, alongside liquid, solid, gas and plasma.

Eventually, we will reach a point of full saturation, a period in our evolution in which digital bits will outnumber atoms on Earth, a world "mostly computer simulated and dominated by digital bits and computer code," according to an article published in AIP Advances, by AIP Publishing.

It is just a matter of time.

"We are literally changing the planet bit by bit, and it is an invisible crisis," author Melvin Vopson said.

Vopson examines the factors driving this digital evolution. He said the impending limit on the number of bits, the energy to produce them, and the distribution of physical and digital mass will overwhelm the planet soon.

For example, using current data storage densities, the number of bits produced per year and the size of a bit compared to the size of an atom, at a rate of 50% annual growth, the number of bits would equal the number of atoms on Earth in approximately 150 years.

It would be approximately 130 years until the power needed to sustain digital information creation would equal all the power currently produced on planet Earth, and by 2245, half of Earth's mass would be converted to digital information mass.

"The growth of digital information seems truly unstoppable," Vopson said. "According to IBM and other big data research sources, 90% of the world's data today has been created in the last 10 years alone. In some ways, the current COVID-19 pandemic has accelerated this process as more digital content is used and produced than ever before."

Vopson draws on the mass-energy equivalence in Einstein's theory of general relativity; the work of Rolf Landauer, who applied the laws of thermodynamics to information; and the work of Claude Shannon, the inventor of the digital bit.

In 2019, Vopson formulated a principle that postulates that information moves between states of mass and energy just like other matter.

"The mass-energy-information equivalence principle builds on these concepts and opens up a huge range of new physics, especially in cosmology," he said. "When one brings information content into existing physical theories, it is almost like an extra dimension to everything in physics."

It's commonly known that gun sales go up after a mass shooting, but two competing hypotheses have been put forth to explain why that's the case: is it because people fear more violence and want to protect themselves, or is it because mass shootings trigger discussions about tighter gun regulations, which sends people out to stock up? In a new study appearing August 11 in the journal Patterns, investigators used data science to study this phenomenon. By working with spatio-temporal data from all the states in the US, they determined that the increase in firearm purchases after mass shootings is driven by a concern about regulations rather than a perceived need for protection.

"It's been well documented that mass shootings are linked to increases in firearm purchases, but the motivation behind this connection has been understudied," says first author Maurizio Porfiri, Institute Professor at the New York University Tandon School of Engineering, who is currently on research sabbatical at the Technical University of Cartagena in Spain. "Previous research on this topic has been done mostly from the perspective of social science. We instead used a data-science approach."

Porfiri and his colleagues employed a statistical method called transfer entropy analysis, which is used to study large, complex systems like financial markets and climate-change models. With this approach, two variables are defined, and then computational techniques are used to determine if the future of one of them can be predicted by the past of the other. "This is a step above studying correlation," Porfiri explains. "It's actually looking at causation. Unique to this study is the analysis of spatio-temporal data, by examining the behavior of all the US states"

The data that were put into consideration came from several sources: FBI background checks, which enabled the approximation of monthly gun sales by state; a Washington Post database on mass shootings; and news coverage about mass shooting from five major newspapers around the country. The news stories were put in two categories: those that mentioned gun regulations and those that didn't. In all, the study used data related to 87 mass shootings that occurred in the United States between 1999 and 2017.

The researchers also rated individual states by how restrictive their gun laws are. "We expected to find that gun sales increased in states that have more permissive gun laws, but it was less expected in states with restrictive laws. We saw it in both," Porfiri says. "Also, when we looked at particular geographic areas, we didn't find any evidence that gun sales increased when mass shootings happened nearby."

He adds that one limitation of the data is that news coverage may not fully capture public sentiment at a given time. In addition, although the study was successful in determining causal links among states, more work is needed to study the nature of these relationships, especially when one has laws that are much more restrictive than another

Porfiri usually uses computational systems to study topics related to engineering, including ionic polymer metal composites and underwater robots. His reason for studying mass shootings is personal: he received his PhD in 2006 from Virginia Tech, which, the following year, was the site where--at that time--the deadliest mass shooting in the country took place. One member of his PhD committee was killed in the shooting, and he knew many others who were deeply affected.

For him, this project is part of a larger effort to study gun violence. "Mass shootings are a small part of death from guns," Porfiri says. "Suicide and homicide are much more common. But mass shootings are an important catalyst for a larger discussion. I plan to look at the wider role of guns in the future."

What The Study Did: Nationally representative survey data were used to examine changes over nearly two decades in daily use of high-dose biotin supplements, which are marketed as stimulating growth of hair and nails.

Authors: Danni Li, Ph.D., of the University of Minnesota in Minneapolis, 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/jama.2020.8144)

Editor's Note: The article includes conflict 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.

WASHINGTON, August 11, 2020 -- In severe cases of COVID-19, damage can spread beyond the lungs and into other organs, such as the heart, liver, kidney and parts of the neurological system. Beyond these specific sets of organs, however, the virus seems to lack impact.

Ernesto Estrada, from the University of Zaragoza and Agencia Aragonesa para la Investigación Foundation in Spain, aimed to uncover an explanation as to how it is possible for these damages to propagate selectively rather than affecting the entire body. He discusses his findings in the journal Chaos, from AIP Publishing.

In order to enter human cells, the coronavirus relies on interactions with an abundant protein called angiotensin-converting enzyme 2.

"This receptor is ubiquitous in most human organs, such that if the virus is circulating in the body, it can also enter into other organs and affect them," Estrada said. "However, the virus affects some organs selectively and not all, as expected from these potential mechanisms."

Once inside a human cell, the virus's proteins interact with those in the body, allowing for its effects to cultivate. COVID-19 damages only a subset of organs, signaling to Estrada that there must be a different pathway for its transmission. To uncover a plausible route, he considered the displacements of proteins prevalent in the lungs and how they interact with proteins in other organs.

"For two proteins to find each other and form an interaction complex, they need to move inside the cell in a subdiffusive way," Estrada said.

He described this subdiffusive motion as resembling a drunkard walking on a crowded street. The crowd presents obstacles to the drunkard, stunting displacement and making it difficult to reach the destination.

Similarly, proteins in a cell face several crowded obstacles they must overcome in order to interact. Adding to the complexity of the process, some proteins exist within the same cell or organ, but others do not.

Taking these into account, Estrada developed a mathematical model that allowed him to find a group of 59 proteins within the lungs that act as the primary activators affecting other human organs. A chain of interactions, beginning with this set, triggers changes in proteins down the line, ultimately impacting their health.

"Targeting some of these proteins in the lungs with existing drugs will prevent the perturbation of the proteins expressed in organs other than the lungs, avoiding multiorgan failure, which, in many cases, conduces the death of the patient," Estrada said.

How the affected proteins travel between organs remains an open question that Estrada is dedicating for future studies.

Scientists have discovered that the larynx, or voice box, of primates is significantly larger relative to body size, has greater variation, and is under faster rates of evolution than in other mammals.

Published in the journal PLOS Biology and led by academics from Anglia Ruskin University (ARU), Stanford University, and the University of Vienna, the research is the first large-scale study into the evolution of the larynx.

The larynx has three main functions: protecting the airway during feeding, regulating the supply of air to the lungs, and vocal communication. Because of its important role in facilitating social behaviour, through vocalisation, it has long been believed that the larynx is a key area of evolution, particularly in species with highly developed vocal communication systems.

The researchers made CT-scans of specimens from 55 different species, and produced 3D computer models of their larynges. These were studied alongside detailed measurements, including body length and body mass.

The primates ranged in size from a pygmy marmoset (Cebuella pygmaea) weighing just 110g, to a Western gorilla (Gorilla gorilla) weighing approximately 120kg. The carnivorans spanned from a 280g common dwarf mongoose (Helogale parvula) to a 180kg tiger (Panthera tigris).

The study found that, for a given body length, primate larynges are on average 38% larger than those of carnivorans, and that the rate of larynx evolution is faster in these species.

There is also more variation in larynx size relative to body size among primates, indicating that primates have greater flexibility to evolve in different ways. Carnivorans follow more of a fixed larynx-size to body-size ratio.

Larynx size was also found to be a good predictor of the call frequency of a species, which demonstrates the relevance for vocal communication of the observed size variations.

Co-lead author Dr Jacob Dunn, Reader in Evolutionary Biology at Anglia Ruskin University (ARU), said: "This study demonstrates clear differences in the evolution of the larynx between groups of mammals.

"Specifically, we have shown for the first time that the primate larynx is larger, less closely linked to body size, and under faster rates of evolution than the carnivoran larynx, which is a well-matched comparison group, indicating fundamental differences in the evolution of the vocal organ across species."

Co-lead author Dr Daniel Bowling, Instructor in Psychiatry and Behavioral Sciences at Stanford University, added: "Our study also shows that differences in larynx size predict changes in voice pitch, highlighting the larynx's crucial role in vocal communication. This is demonstrated by the rich and varied calls produced by many primate species.

"The results imply fundamental differences between primates and carnivorans in the forces constraining larynx size, as well as highlighting an evolutionary flexibility in primates that may help explain why they have developed complex and diverse uses of the vocal organ for communication. This provides an exciting avenue for future studies examining variation among other mammalian groups."

What The Viewpoint Says: This Viewpoint advises parents on how to assess virtual schooling options for their children for the fall semester during the COVID-19 pandemic.

Authors: Lindsay A. Thompson, M.D., M.S., of the University of Florida in Gainesville, 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/jamapediatrics.2020.3800)

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.

Weary working parents aren't the only ones eager for their children to return to school in a few weeks. Many teachers, staff and administrators also want those classroom doors to reopen. Most importantly, kids are craving the clamor of school hallways and interaction with their friends.

The American Academy of Pediatrics recently highlighted the importance of students' returning to the classroom in its COVID-19 return-to-school guidance. Jason Wang, MD, PhD, of Stanford Health Policy also believes it's time for kids in the United States to get back to school. But he believes school districts could better protect their 55 million K-12 students by adhering to an additional set of strict measures.

"Prolonged school closures can exacerbate socioeconomic disparities, causing negative education and health outcomes, and amplifying existing educational inequalities," said Wang, a pediatrician and director of the Center for Policy, Outcomes and Prevention in the Stanford School of Medicine. "School closure may also aggravate food insecurity, domestic violence and mental health disorders. Many children from low-income households obtain food through the National School Lunch Program, and estimates suggest that 1 in 4 children may face hunger this year due to COVID-19."

But serious precautions must first be put into place, Wang said, starting with each school district establishing a COVID-19 task force composed of the superintendent, members of the school board, teachers, parents and health care professionals to develop policies and procedures.

"To implement and evaluate specific measures, the task force should create and oversee a command center for the school district, composed of data analysts and health experts who can liaise with the local health department," Wang writes in a JAMA Pediatrics article with co-author Henry Bair, a medical student at the Stanford School of Medicine who is also working on an MBA at the university's graduate school of business. The article will be published Aug. 11.

Three-pronged testing approach

The academy's guidance does not include ways schools can test for the virus, so the authors recommend that school districts collaborate with local hospitals to:

Test all students with symptoms.

Devise a schedule to randomly select a proportion of students and staffers for COVID-19 testing to identify asymptomatic individuals. The researchers note that a pooled testing strategy can significantly reduce costs.

Offer more frequent testing to students from high-risk households in ZIP codes with socioeconomic challenges.

In addition, the authors recommend that district task forces:

Work with its local health department to provide educational materials and training for students, parents and school staff on the basics of COVID-19 prevention.

Provide school staff with thermometers and train them to screen for COVID-19 symptoms.

Build temporary modular buildings if schools cannot maintain 6 feet of physical distance among students and teachers.

Expand the district's fleet of school buses or develop different pickup schedules.

Increase budgets to boost disinfection efforts of all teaching spaces, common areas and high-touch surfaces such as doorknobs, computers and desks.

Place transparent plastic shields in front of and along the sides of student desks.

Provide hand sanitizers and protective equipment, such as disposable surgical masks, reusable cloth masks or reusable face shields.

Wang concedes these are expensive measures. But as the Centers for Disease Control and Prevention noted in its July 24 telebriefing on new resources and tools to support opening schools: The 5.6 million parents who haven't been able to work due to school closures have collectively lost an estimated $232 billion in earnings.

Stricter measures mean bigger budgets

Some low-resource communities might find these guidelines difficult to adopt. Those transparent desk barriers, for example, range from $100 to $200 per desk; COVID-19 tests run between $50 and $200 per individual.

Wang said that's why additional federal funding and state subsidies are crucial for the low-income communities already hit by the double whammy of having more parents as essential workers and some of the highest hospitalization and fatality rates from the pandemic.

"Low-income communities are suffering most from shelter-in-place policies because parents who are essential workers are out of the home and not able to help with online learning," Wang said. "And many children in these communities also live in crowded conditions that are not conducive to learning at home."

Wang and Bair note the academy's guidelines emphasize the importance of identifying symptoms and signs of COVID-19, but don't go far enough in recommending operational approaches.

"To address this, we recommend that schools implement multilevel screening for students and staff," they write. Each morning parents should report any fever or COVID-19 symptoms to an online or an automated telephone-based program maintained by the school or district. Any students with symptoms should stay home.

Even with all the precautions in place, COVID-19 outbreaks within schools are still likely, the authors said. Schools should prepare for temporary closures and be ready to transition back to full-time online education by investing in remote education platforms and training.

"Schools will need to ensure equitable implementation of online education among students, especially those with limited knowledge of or access to technological resources and consider subsidizing educational technologies for these students," the authors write.