The event took place aboard a collaborative cruise in Puerto Rico between February and March, 2022. The group responsible for the core collection was led by Prof. Steven D’Hondt and Dr. Robert Pockalny from the University of Rhode Island’s Graduate School of Oceanography and included researchers and technicians from WHOI, University of Rhode Island, University of California San Diego, Oregon State University, University of Washington, University of Puerto Rico Mayagüez, and University of Munich.

Long sediment cores are generally collected by allowing a core pipe with a lead weight on top to fall through the water and into soft sediment that collects on the seafloor over long periods of time. When the pipe is pulled out of the seafloor and back up to the ship, the recovered sediment inside can be used to study Earth’s environmental conditions and climate dating back tens or hundreds of thousands, or even millions, of years ago.

Scientists are also interested in understanding genetic traits that enable microscopic organisms to survive within seafloor sediments. The main objective of this expedition was to better understand how microbes at different depths below the seafloor have adapted to vastly different environmental conditions present across the entire depth range of the trench. Over the course of three weeks at sea, the team collected cores from a water depth of about 50 meters (165 feet) to the trench’s maximum depth of about 8,385 meters (27,510 feet).

“We took these cores to learn how microbes that live beneath the seafloor respond to pressure,” said D’Hondt. “Our ultimate objective is to improve understanding of how organisms in extreme environments engage in the world around them. “Our team’s success in extracting this core from the deepest part of the Atlantic Ocean will enable us to make a tremendous advance in our understanding of this little-known part of life on Earth.”

The core collections were made possible by the long core system originally developed at WHOI in 2007 by then-research specialist Jim Broda for the research vessel Knorr. After the ship’s retirement, the system was adapted to fit the slightly shorter vessel Neil Armstrong. After this expedition, the long corer will be transferred to the OSU Marine Sediment Sampling Group, which is funded by the U.S. National Science Foundation and supports coring operations throughout the U.S. academic research fleet, so it can be made available to the entire oceanographic community.

“This achievement was only possible thanks to phenomenal teamwork by everyone involved, including those who helped develop the long corer nearly 20 years ago,” said Rick Murray, WHOI Deputy Director and Vice President of Science and Engineering. “The fact that the long corer will move to the capable hands of our friends and colleagues at Oregon State University means it will have many more years of use by the ocean science community to help advance knowledge about our planet.”

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Materials provided by Woods Hole Oceanographic Institution. Note: Content may be edited for style and length.

All ship channels must be regularly cleared of sand, debris settled on the bottom (called shoal) and miscellaneous trash. That means ship channel management regularly faces the mighty task of dredging. How do they make the wisest decisions with the best timing?

“The quandary involves weighing factors for the optimal decision of channel dredging and disposal activities,” said Zheyong Bian, assistant professor of construction management at the University of Houston College of Technology and the lead author of a study published in the journal Transportation Research Part E: Logistics and Transportation Review. “Some factors are static, like geographical features of navigation channels and confined disposal facilities. Others vary substantially, such as navigability condition deterioration (shoaling), traffic, economic values, annual budget and more.”

Bian, then a doctoral student at Rutgers University, The State University of New Jersey, collaborated with project leader Yun Bai from the Center for Advanced Infrastructure and Transportation (CAIT) at Rutgers, to develop a dredging planning optimization model (DPOM) and a dynamic prioritization planning (DPP) algorithm that factor in known variables, such as the volume of debris expected and availability of nearby confined disposal facilities. It also considers grouping phases of the project and how costs can be affected by interest rates and inflation.

But — this is a key advantage, Bian stressed — the algorithm also holds the flexibility that weighs input from local professionals. In other words, it values boots-on-the-ground opinions and learns from experience.

Once all factors are included, the algorithm suggests timing, prioritization and the grouping of projects. It also projects costs, with interest and inflation included, as well as monies likely to be recouped (through repurposing of sand, for example).

In these days of tightened budgets, public funds are deployed with ever more care. The new DPOM model and DPP algorithm could strengthen cost efficiencies at ship channels around the world. The New Jersey Department of Transportation Office of Maritime Resources provided funding and data to support this study.

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Materials provided by University of Houston. Original written by Sally Strong. Note: Content may be edited for style and length.

Neuroscientists believed that, in the aftermath of a stroke, calming overexcited neurons might prevent them from releasing a toxic molecule that can kill neurons already damaged by lack of oxygen. This idea was supported by studies in cells and animals, but it lost favor in the early 2000s after numerous clinical trials failed to improve outcomes for stroke patients.

But a fresh approach has yielded evidence that the idea may have been discarded too hastily. The new findings are available online in the journal Brain.

By scanning the whole genomes of nearly 6,000 people who had experienced strokes, researchers at Washington University School of Medicine in St. Louis identified two genes associated with recovery within the pivotal first 24 hours after stroke. Events — good or bad — that occur in the first day set stroke patients on their courses toward long-term recovery. Both genes turned out to be involved in regulating neuronal excitability, providing evidence that overstimulated neurons influence stroke outcomes.

“There’s been this lingering question about whether excitotoxicity really matters for stroke recovery in people,” said co-senior author Jin-Moo Lee, MD, PhD, the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology. “We can cure stroke in a mouse using blockers of excitotoxicity. But in humans we performed numerous clinical trials, and we couldn’t move the needle. Every last one of them was negative. In this study, out of 20,000 genes, the top two genetic hits point to mechanisms involving neuronal excitation. That’s pretty remarkable. This is the first genetic evidence that shows excitotoxicity matters in people and not just in mice.”

Every year nearly 800,000 people in the U.S. have ischemic strokes, the most common kind of stroke. Ischemic strokes occur when a clot blocks a blood vessel and cuts off oxygen to part of the brain, triggering sudden numbness, weakness, confusion, difficulty speaking or other symptoms. Over the next 24 hours, some people’s symptoms continue to worsen while others’ stabilize or improve.

In the 1990s, Dennis Choi, MD, PhD, then head of the Department of Neurology at Washington University, performed groundbreaking research on excitotoxicity in stroke. He and others showed that stroke can cause neurons to release large amounts of glutamate, a molecule that transmits excitatory messages between neurons. Glutamate is constantly being released by neurons as part of the normal functioning of the nervous system, but too much all at once can be toxic. Efforts to translate this basic research into therapies for people did not pan out, and eventually pharmaceutical companies let their anti-excitotoxic drug development programs lapse.

But Lee, who formerly worked on excitotoxicity with Choi, did not give up. He teamed up with genetics researcher and co-senior author Carlos Cruchaga, PhD, the Barbara Burton and Reuben M. Morriss III Professor of Neurology and a professor of psychiatry; first author Laura Ibañez, PhD, an assistant professor of psychiatry; and co-author Laura Heitsch, MD, an assistant professor of emergency medicine and of neurology, to tackle the question of what drives post-stroke brain injury. The team identified people who had experienced strokes, and they looked for genetic differences between those who naturally recovered substantial function in the first day and those who did not.

As members of the International Stroke Genetics Consortium, the research team was able to study 5,876 ischemic stroke patients from seven countries: Spain, Finland, Poland, the United States, Costa Rica, Mexico and South Korea. They measured each person’s recovery or deterioration over the first day using the difference between their scores on the National Institutes of Health (NIH) Stroke Scale at six and 24 hours after symptoms first appeared. The scale gauges a person’s degree of neurological impairment based on measures such as the ability to answer basic questions such as “How old are you?”; to perform movements such as holding up the arm or leg; and to feel sensation when touched.

The researchers performed a genomewide association study by scanning the participants’ DNA for genetic variations related to the change in their NIH stroke scale scores. The top two hits were genes that coded for the proteins ADAM23 and GluR1. Both are related to sending excitatory messages between neurons. ADAM23 forms bridges between two neurons so that signaling molecules such as glutamate can be passed from one to the other. GluR1 is a receptor for glutamate.

“We started with no hypotheses about the mechanism of neuronal injury,” Cruchaga said. “We started with the assumption that some genetic variants are associated with stroke recovery, but which ones they are, we did not guess. We tested every single gene and genetic region. So the fact that an unbiased analysis yielded two genes involved in excitotoxicity tells us that it must be important.”

In the years since anti-excitotoxic drug development was abandoned, clot-busting drugs have become the standard of care for ischemic stroke. Such drugs aim to restore blood flow so that oxygen — and anything else in the bloodstream, including medication — can reach affected brain tissue. Consequently, experimental neuroprotective therapies that failed in the past might be more effective now that they have a better chance of reaching the affected area.

“We know that that first 24-hour period has the greatest impact on outcomes,” Lee said. “Beyond 24 hours, there’s diminishing returns in terms of influence on long-term recovery. Right now, we don’t have any neuroprotective agents for that first 24 hours. Many of the original studies with anti-excitotoxic agents were performed at a time when we weren’t sure about the best trial design. We’ve learned a lot about stroke in the last few decades. I think it’s time for a re-examination.”

A new study puts a number on how dangerous such chronic tiredness can be, at least in regard to driving. For every eight additional breathing interruptions per hour, the odds of making a dangerous driving move such as speeding, braking hard or accelerating suddenly increase by 27%, according to a study by researchers at Washington University School of Medicine in St. Louis.

Older adults are more likely to develop sleep apnea. They also are more likely to be seriously injured or killed in a car accident. The findings, available online in the journal Sleep, suggest that screening older adults for sleep apnea and for treatment, if needed, may help older people continue driving safely for longer.

“The percentage of older adults with mild sleep apnea is 30% to 50%, but if such adults don’t have daytime sleepiness or other evidence of impairment, they may not come to medical attention,” said co-senior author Brendan Lucey, MD, an associate professor of neurology and director of Washington University’s Sleep Medicine Center. “However, these findings suggest that we might want a lower threshold to evaluate older adults for sleep apnea and track their breathing interruptions. If their conditions worsen by just eight interruptions an hour, that could have significant adverse effects on their driving and their risk of suffering serious injury.”

People 65 and over are the most responsible drivers on the road. They obey speed limits. They drive defensively. They avoid driving at night, in bad weather and in unfamiliar places. But the changes that often come with advancing age — such as deteriorating vision, slower reflexes and, yes, difficulty sleeping — can undermine even the safest habits.

Lucey teamed up with driving researcher Ganesh M. Babulal, PhD, OTD, an assistant professor of neurology and the paper’s co-senior author, to investigate the relationship between sleep apnea and risky driving behaviors. Participants were recruited from ongoing studies at Washington University’s Charles F. and Joanne Knight Alzheimer Disease Research Center (Knight ADRC).

Babulal and Lucey monitored the driving and sleep habits of 96 older adults under real-world conditions. They used a commercially available take-home test to identify people with sleep apnea and measure its severity. Less than five breathing interruptions per hour is considered normal, five to 15 is mild sleep apnea, 15 to 30 is moderate, and greater than 30 is severe.

To assess driving habits, the researchers installed a chip developed by Babulal and colleagues into participants’ personal vehicles and monitored their driving for a year, focusing on episodes of hard braking, sudden acceleration and speeding. In total, they collected data on more than 100,000 trips. Participants also were evaluated by researchers at the Knight ADRC for cognitive impairments and molecular signs of early Alzheimer’s disease.

Even though all participants were cognitively normal, about a third had brain changes indicative of early Alzheimer’s disease. The researchers found that the frequency with which drivers made dangerous moves behind the wheel rose in parallel with the frequency with which their sleep was interrupted at night, regardless of whether their brains bore the marks of early Alzheimer’s.

“We didn’t have cameras in the vehicles, so we don’t know exactly what happened that caused someone to, say, brake hard suddenly,” Babulal said. “But it could be something like a stoplight that they didn’t realize was red until they got close and had to stomp on the brakes. The more tired you are, the less attention you have to deploy to the task at hand, especially if it is novel and constantly changing.”

The study helps untangle the ways aging-associated risk factors such as poor sleep and Alzheimer’s disease put older adults in danger while driving, and could aid efforts to find ways to maximize years of safe driving, the researchers said.

“Driving always carries the risk of crashing, and older adults are at risk of more severe injury than younger adults if they experience a crash,” Babulal said. “But we can’t just tell them to give up their keys. When older people stop driving, they lose a lot of their independence and mobility, which is often associated with negative health and social outcomes. What we want to understand is what puts them at a higher risk so we can intervene and help them stay behind the wheel, safely, for as long as possible.”

These nerve cells are often generated far from where they will eventually reside and function in the new brain, a migration that, while much investigated in animal models using chemical or biological tracers, has never been studied directly in humans. Until now.

In a new paper, published online April 20, 2022 in Nature, scientists at University of California San Diego School of Medicine and Rady Children’s Institute of Genomic Medicine describe novel methods for inferring the movement of human brain cells during fetal development by studying healthy adult individuals who have recently passed away from natural causes.

“Every time a cell divides into two daughter cells, by chance, there arise one or more new mutations, which leave a trail of breadcrumbs that can be read out by modern DNA sequencers,” said senior author Joseph Gleeson, MD, Rady Professor of Neuroscience at UC San Diego School of Medicine and director of neuroscience research at the Rady Children’s Institute for Genomic Medicine.

“By developing methods to read these mutations across the brain, we are able to reveal key insights into how the human brain forms, in comparison with other species.”

Although there are 3 billion DNA bases — and more than 30 trillion cells in the human body — Gleeson and colleagues focused their efforts on just a few hundred DNA mutations that likely arose during the first few cell divisions after fertilization of the embryo or during early development of the brain. By tracking these mutations throughout the brain in deceased individuals, they were able to reconstruct development of the human brain for the first time.

To understand the type of cells displaying these breadcrumb mutations, they developed methods to isolate each of the major cell types in the brain. For instance, by profiling the mutations in excitatory neurons compared with inhibitory neurons, they confirmed the long-held suspicion that these two cell types are generated in different germinal zones of the brain, and then later mix together in the cerebral cortex, the outermost layer of the organ.

However, they also discovered that the mutations found in the left and right sides of the brain were different from one another, suggesting that — at least in humans — the two cerebral hemispheres separate during development much earlier than previously suspected.

The results have implications for certain human diseases, like intractable epilepsies, where patients show spontaneous convulsive seizures and require surgery to remove an epileptic brain focus, said Martin W. Breuss, PhD, former project scientist at UC San Diego and now an assistant professor at the University of Colorado School of Medicine.

Breuss is co-first author with Xiaoxu Yang, PhD, postdoctoral scholar and Johannes C. M. Schlachetzki, MD, project scientist, both at UC San Diego; and Danny Antaki, PhD, a former postdoctoral scholar at UC San Diego, now at Twist Biosciences.

“This study,” the authors said, “solves the mystery as to why these foci are almost always restricted to one hemisphere of the brain. Applying these results to other neurological conditions could help scientists understand more mysteries of the brain.”

Co-authors include: Xin Xu, Changuk Chung, Guoliang Chai, Valentina Stanley, Qiong Song, Traci F. Newmeyer, An Nguyen, Beibei Cao, Jennifer McEvoy-Venneri and Brett R. Copeland, all at UC San Diego and Rady Children’s Institute for Genomic Medicine; Addison J. Lana, Sydney O’Brien, Marten A. Hoeksema, Alexi Nott, Martina P. Pasilla, Scott T. Barton, and Christopher K. Glass, all at UC San Diego; Shareef Nahas, Lucitia Van Der Kraan and Yan Ding, Rady Children’s Institute for Genomic Medicine and the NIMH Brain Somatic Mosaicism Network.

Funding for this research came, in part, from the Howard Hughes Medical Institute, the National Institute of Mental Health (grants MH108898, RO1 MH124890, R21 AG070462), the National Institute on Aging (grants RF1 AGO6106-02, R01 AGO56511-02, R01 NS096170-04) and the UC San Diego IGM Genomics Center (S10 OD026929).

Video: https://youtu.be/WfrvSYi9M6A

The results, published April 20 in Nature, may aid the development of a new generation of more effective neurological and psychiatric therapies with fewer side effects.

The new research takes a close look at glutamate, the most prevalent neurotransmitter in the brain. Glutamate binds to receptors on brain cells, which opens a channel into the cell, allowing ions to pass through to propagate an electrical signal.

“The way the brain works is through communication between neurons, and these are the main receptors which allow this communication,” says Alexander Sobolevsky, PhD, associate professor of biochemistry and molecular biophysics at Columbia and senior author on the paper.

Each receptor can bind up to four molecules of glutamate and produce four different levels of conductivity. Previous studies had linked binding to conductivity in a simple stepwise fashion, in which binding each additional glutamate molecule increased the conductivity another step.

While that explanation made sense, nobody had looked closely enough to confirm it. In the new work, the investigators combined a technique called cryo-electron microscopy with sophisticated data analysis to reveal the first detailed pictures of glutamate binding to its receptors.

“We actually carried out experiments in the conditions where we see all these intermediates, one glutamate and then two glutamates, three glutamates, and then it binds all four,” says Sobolevsky.

These images reveal that glutamate binds to the subunits of its receptor only in specific patterns. That overturns the prevailing view that each subunit binds glutamate independently and points toward new levels of complexity in neuronal signaling and drug responses.

Instead of straightforward stepwise transitions, Sobolevsky and his colleagues found that a glutamate molecule must bind to one of two specific receptor subunits before any glutamates can bind to the other two subunits. In addition, the conductivity levels of the receptor didn’t correlate directly to the number of glutamates bound to it; a receptor could have two or more glutamates attached but still only reach the first level of conductivity.

The results open an entirely new line of investigation, and the team is now probing how different accessory molecules on neurons affect the interaction. Learning more about the glutamate receptors’ specific activation states may aid the development of better drugs for conditions that involve glutamate receptors, such as depression, dementia, Parkinson’s disease, epilepsy, and stroke.

Video: https://youtu.be/IeQZTFMz5ek

The study was supported by the National Institutes of Health (R01 CA206573, R01 NS083660, R01 NS107253, R01 AR078814, R01 GM128195, and R01 AG065594) and the National Science Foundation (1818086, 1818213, and 1563291).