New collaborative research from the Woods Hole Oceanographic Institution and five partner institutions (University of Arizona, University of Washington, Pennsylvania State University, Desert Research Institute and University of Bergen), published today in Nature Geoscience, reveals that during past periods glaciers and ice caps in coastal west Greenland experienced climate conditions much different than the interior of Greenland. Over the past 2,000 years, these ice caps endured periods of warming during which they grew larger rather than shrinking.

This novel study breaks down the climate history displayed in a core taken from an ice cap off Greenland’s western coast. According to the study’s researchers, while ice core drilling has been ongoing in Greenland since the mid-20^th century, coastal ice core studies remain extremely limited, and these new findings are providing a new perspective on climate change compared to what scientists previously understood by using ice cores from the interior portions of the Greenland ice sheet alone.

“Glaciers and ice caps are unique high-resolution repositories of Earth’s climate history, and ice core analysis allows scientists to examine how environmental changes — like shifts in precipitation patterns and global warming — affect rates of snowfall, melting, and in turn influence ice cap growth and retreat,” said Sarah Das, Associate Scientist of Geology and Geophysics at WHOI. “Looking at differences in climate change recorded across several ice core records allows us to compare and contrast the climate history and ice response across different regions of the Arctic.” However, during the course of this study, it also became clear that many of these coastal ice caps are now melting so substantially that these incredible archives are in great peril of disappearing forever.

Due to the challenging nature of studying and accessing these ice caps, this team was the first to do such work, centering their study, which began in 2015, around a core collected from the Nuussuaq Peninsula in Greenland. This single core offers insight into how coastal climate conditions and ice cap changes covaried during the last 2,000 years, due to tracked changes in its chemical composition and the amount of snowfall archived year after year in the core. Through their analysis, investigators found that during periods of past warming, ice caps were growing rather than melting, contradicting what we see in the present day.

“Currently, we know Greenland’s ice caps are melting due to warming, further contributing to sea level rise. But, we have yet to explore how these ice caps have changed in the past due to changes in climate,” said Matthew Osman, postdoctoral research associate at the University of Arizona and a 2019 graduate of the MIT-WHOI Joint program. “The findings of this study were a surprise because we see that there is an ongoing shift in the fundamental response of these ice caps to climate: today, they’re disappearing, but in the past, within small degrees of warming, they actually tended to grow.”

According to Das and Osman, this phenomenon happens because of a “tug-of-war” between what causes an ice cap to grow (increased precipitation) or recede (increased melting) during periods of warming. Today, scientists observe melting rates that are outpacing the rate of annual snowfall atop ice caps. However, in past centuries these ice caps would expand due to increased levels of precipitation brought about by warmer temperatures. The difference between the past and present is the severity of modern anthropogenic warming.

The team gathered this data by drilling through an ice cap on top of one of the higher peaks of the Nuussuaq Peninsula. The entire core, about 140 meters in length, took about a week to retrieve. They then brought the meter-long pieces of core to the National Science Foundation Ice Core Facility in Denver, Colorado, and stored at -20 degrees Celsius. The core pieces were then analyzed by their layers for melt features and trace chemistry at the Desert Research Institute in Reno, Nevada. By looking at different properties of the core’s chemical content, such as parts per billion of lead and sulfur, investigators were able to accurately date the core by combining these measurements with a model of past glacier flow.

“These model estimates of ice cap flow, coupled with the actual ages that we have from this high precision chemistry, help us outline changes in ice cap growth over time. This method provides a new way of understanding past ice cap changes and how that is correlated with climate,” said Das. “Because we’re collecting a climate record from the coast, we’re able to document for the first time that there were these large shifts in temperature, snowfall and melt over the last 2,000 years, showing much more variability than is observed in records from the interior of Greenland,” Das added.

“Our findings should urge researchers to return to these remaining ice caps and collect new climate records while they still exist,” added Osman.

The process, detailed recently in the American Chemical Society journal ACS Sustainable Chemical Engineering, turns hydrogen sulfide — more commonly called “sewer gas” — into hydrogen fuel. Hydrogen sulfide is emitted from manure piles and sewer pipes and is a key byproduct of industrial activities including refining oil and gas, producing paper and mining.

The process detailed in this study uses relatively little energy and a relatively cheap material — the chemical iron sulfide with a trace amount of molybdenum as an additive.

In addition to smelling like rotten eggs, hydrogen sulfide is highly toxic, corroding pipes and harming the health of people who encounter it.

“Hydrogen sulfide is one of the most harmful gases in industry and to the environment,” said Lang Qin, a co-author on the study and a research associate in chemical and biomolecular engineering at The Ohio State University. “And because the gas is so harmful, a number of researchers want to turn hydrogen sulfide into something that is not so harmful, preferably valuable.”

The study is built on previous work by the same research group using a process called chemical looping, which involves adding metal oxide particles in high-pressure reactors to burn fuels without direct contact between air and fuel. The team first used chemical looping on coal and shale gas to convert fossil fuels into electricity without emitting carbon dioxide into the atmosphere. The initial process used iron oxide to break down the fossil fuels.

The researchers later applied the concept to hydrogen sulfide and invented the SULGEN process, which converts hydrogen sulfide into hydrogen. The researchers found that the pure chemical, iron sulfide, didn’t perform well at the large scales needed for industrial use, Qin said. The research team has been trying to identify other inexpensive chemicals that could catalyze that transformation in higher quantities. This study shows that introducing a trace amount of molybdenum into iron sulfide might be an attractive option.

That material is relatively inexpensive and easy to acquire, making it an attractive option for larger-scale operations.

Transforming this toxic gas into hydrogen fuel creates an alternative oil and gas, which are major contributors to climate change, the researchers said.

“It is too soon to tell if our research can replace any of the hydrogen fuel production technologies that are out there,” said Kalyani Jangam, lead author of the study and a graduate student in Ohio State’s Clean Energy Research Laboratory. “But what we are doing is adjusting this decomposition process and making a valuable product from that.”

For this most recent study, the researchers found that molybdenum improves the breakdown of hydrogen sulfide, splitting it into two parts — hydrogen fuel and sulfur.

This work is early in the scientific process — the researchers showed that the process worked in the lab; tests at the industrial level are forthcoming.

“The big picture is we want to solve the harmful gas issue, and we thought that our chemical looping process would allow that,” Qin said. “And here, we have found a way to do it in the lab that creates this value-added hydrogen fuel.”

The senior author on this paper is Liang-Shih Fan, professor of chemical and biomolecular engineering at Ohio State. Yu-Yen Chen, a former doctoral student in Fan’s laboratory, also contributed.

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Materials provided by Ohio State University. Original written by Laura Arenschield. Note: Content may be edited for style and length.

This is a common situation after a traumatic brain injury — many people experience bad side effects months or years later. These long-term effects can last a few days or the rest of a person’s life.

“No therapies currently exist to prevent the disabilities that can develop after a brain trauma,” says Jeanne Paz, PhD, associate investigator at Gladstone Institutes. “So, understanding how the traumatic brain injury affects the brain, especially in the long term, is a really important gap in research that could help develop new and better treatment options.”

In a new study published in the journal Science, Paz and her team helped close that gap. They identified a specific molecule in a part of the brain called the thalamus that plays a key role in secondary effects of brain injury, such as sleep disruption, epileptic activity, and inflammation. In collaboration with scientists at Annexon Biosciences, a clinical-stage biopharmaceutical company, they also showed that an antibody treatment could prevent the development of these negative outcomes.

A Vulnerable Brain Region

Traumatic brain injuries, which range from a mild concussion to a severe injury, can be the result of a fall, sports injury, gunshot injury, blow to the head, explosion, or domestic violence. Often, soldiers returning from war also suffer head injuries, which commonly lead to the development of epilepsy. Traumatic brain injury affects 69 million people around the world annually, and is the leading cause of death in children and a major source of disability in adults.

“These injuries are frequent and can happen to anyone,” says Paz, who is also an associate professor of neurology at UC San Francisco (UCSF) and a member of the Kavli Institute for Fundamental Neuroscience. “The goal of our study was to understand how the brain changes after traumatic brain injuries and how those changes can lead to chronic problems, such as the development of epilepsy, sleep disruption, and difficulty with sensory processing.”

To do so, Paz and her team recorded the activity of different cells and circuits in the brain of mice after brain injury. The researchers monitored the mice continually and wirelessly, meaning the mice could go about their normal activities without being disrupted.

“We collected so much data, from the time of injury and over the next several months, that it actually crashed our computers,” says Paz. “But it was important to capture all the different stages of sleep and wakefulness to get the whole picture.”

During a trauma to the head, the region of the brain called the cerebral cortex is often the primary site of injury, because it sits directly beneath the skull.

But at later time points, the researchers discovered that another region — the thalamus — was even more disrupted than the cortex. In particular, they found that a molecule called C1q was present at abnormally high levels in the thalamus for months after the initial injury, and these high levels were associated with inflammation, dysfunctional brain circuits, and the death of neurons.

“The thalamus seems particularly vulnerable, even after a mild traumatic brain injury,” says Stephanie Holden, PhD, first author of the study and former graduate student in Paz’s lab at Gladstone. “This doesn’t mean the cortex isn’t affected, but simply that it might have the necessary tools to recover over time. Our findings suggest that the higher levels of C1q in the thalamus could contribute to several long-term effects of brain injury.”

The Paz Lab collaborated with Eleonora Aronica, MD, PhD, a neuropathologist at the University of Amsterdam, to validate their findings in human brain tissues obtained from autopsies, in which they found high levels of the C1q molecule in the thalamus 8 days after people had sustained a traumatic brain injury. In addition, by working with fellow Gladstone Assistant Investigator Ryan Corces, PhD, they determined that C1q in the thalamus likely came from microglia, the immune cells in the brain.

“Our study answered some very big questions in the field about where and how changes are happening in the brain after a trauma, and which ones are actually important for causing deficits,” says Paz.

The Right Window to Treat Chronic Effects After Traumatic Brain Injury

The C1q molecule, which is part of an immune pathway, has well-documented roles in brain development and normal brain functions. For instance, it protects the central nervous system from infection and helps the brain forget memories — a process needed to store new memories. The accumulation of C1q in the brain has also been studied in various neurological and psychiatric disorders and is associated, for example, with Alzheimer’s disease and schizophrenia.

“C1q can be both good and bad,” says Paz. “We wanted to find a way to prevent this molecule’s detrimental effect, but without impacting its beneficial role. This is an example of what makes neuroscience a really hard field these days, but it’s also what makes it exciting.”

She and her group decided to leverage the “latent phase” after a traumatic brain injury, during which changes are occurring in the brain but before long-term symptoms appear.

“My cousin, for example, was hit in the head when he was 10 years old, and the impact broke his skull and damaged his brain,” says Paz. “But it wasn’t until he was 20 that he developed epilepsy. This latent phase presents a window of opportunity for us to intervene in hopes of modifying the disease and preventing any complications.”

Paz reached out to her collaborators at Annexon Biosciences, who produce a clinical antibody that can block the activity of the C1q molecule. Then, her team treated the mice who sustained brain injury with this antibody to see if it might have beneficial effects.

When the researchers studied mice genetically engineered to lack C1q at the time of the trauma, the brain injury appeared much worse. However, when they selectively blocked C1q with the antibody during the latent phase, they prevented chronic inflammation and the loss of neurons in the thalamus.

“This indicates that the C1q molecule shouldn’t be blocked at the time of injury, because it’s likely very important at this stage for protecting the brain and helping prevent cell death,” says Holden. “But at later time points, blocking C1q can actually reduce harmful inflammatory responses. It’s a way of telling the brain, ‘It’s okay, you’ve done the protective part and you can now turn off the inflammation.'”

“There is a paucity of treatments for patients who have suffered from an acute brain injury,” says Ted Yednock, PhD, executive vice president and chief scientific officer at Annexon Biosciences, and an author of the study. “This result is exciting because it suggests that we could treat patients in the hours to days after an acute injury like traumatic brain injury to protect against secondary neuronal damage and provide significant functional benefit.”

Path to a Potential Treatment

In addition to chronic inflammation, Paz and her team also uncovered abnormal brain activity in the mice with traumatic brain injury.

First, the researchers noticed disruptions in sleep spindles, which are normal brain rhythms that occur during sleep. These are important for memory consolidation, among other things. The scientists also found epileptic spikes, or abnormal fluctuations in brain activity. These spikes can be disruptive to cognition and normal behavior, and are also indicative of a greater susceptibility to seizures.

The scientists observed that the anti-C1q antibody treatment not only helped restore the sleep spindles, but also prevented the development of epileptic activities.

“Overall, our study indicates that targeting the C1q molecule after injury could avoid some of the most devastating, long-term consequences of traumatic brain injury,” says Holden. “We hope this could eventually lead to the development of treatments for traumatic brain injury.”

Annexon’s anti-C1q inhibitors are designed to treat multiple autoimmune and neurological disorders, and are already being examined in clinical trials, including for an autoimmune disorder known as Guillain-Barré syndrome, where the drug has been shown to be safe in humans.

“The fact that the drug is already in clinical trials may speed the pace at which a treatment could eventually be made available to patients,” says Yednock. “We already understand doses of drug that are safe and effective in patients for blocking C1q in the brain, and could move directly into studies that ameliorate the chronic effects after traumatic brain injury.”

For Holden, who previously worked with individuals who experienced brain injury and heard many of their personal stories, the impact of this study is particularly meaningful.

“Brain injury is a hidden disability for many of the people I met,” she says. “The side effects they experience can be difficult to diagnose and their physicians often can’t provide any medical treatment. Being able to contribute to finding ways to treat the detrimental consequences of the injury after it happens is really inspiring.”

Paz and her lab are continuing to expand their understanding of what happens in the brain after injury. Next, they will focus on studying whether they can help prevent convulsive seizures, which are often reported by people with severe traumatic brain injuries.

“The holy grail would be to have a treatment that could be offered to a patient after a trauma and that would prevent chronic inflammation in the brain, sleep disruption, and seizures,” she adds. “Wouldn’t it be wonderful if our study helped make that a reality?”

Protons (H⁺) and hydronium ions (H₃O⁺) in free aqueous solutions seem to migrate faster than other ions due to the the Grotthuss-mechanism. Individual protons do not really migrate at all. Instead, bonds of the hydronium ions are broken and new bonds to other water molecules are formed, so that the individual proton does not migrate. Rather charges are transported directly from one water molecule to the next. This process is quicker than the diffusion of an ion through the solution.

Behavior in Confined Spaces Unexplored

So far, many studies have investigated the transport of protons in free aqueous solution. “In real life such conditions are relatively rare,” says Professor Martina Havenith, speaker of RESOLV and an author of the study. “Most protons transport processes actually occur in confined spaces or in nanopores.” Hydronium ions are involved in defining the pH value. Up to now, the effect the of confinement has not yet been completely understood.

To change that, researchers from Bochum and Berkeley combined theoretical and experimental methods. They created tiny water pools, whose size could be precisely controlled. As soon as the diameter of the droplets became smaller than two nanometers, the proton transport mechanism in the experiment and simulations changed abruptly. “Under two nanometers the proton migration is restricted by confinement effects. This effect is reduced when the water pool is enlarged,” explains Martina Havenith. “Suprisingly we found that above two nanometres, where the formation of hydronium ions is possible, there is a proton traffic jam.” The proton is stuck in an oscillatory state, where it bounces back and forth along the surface of the water pool, but makes no progress forward, resulting in the conductivity not increasing further — as originally expected.

Short-Circuit in the Hydrogen-Bonding Network

In addition to the size of the pools, the acid concentration also influences the proton migration behavior. When the research team increased the acid content, they created a type of short-circuit in the hydrogen bonding network of the droplet, so that the proton no longer migrated from its position, but rather paused in oscillatory bouncing state. “That has consequences for every system that relies on proton transport, because the size of the system or the proton concentration can lead to a traffic jam and for example disrupt the signaling process,” concludes Havenith.

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Materials provided by Ruhr-University Bochum. Note: Content may be edited for style and length.