Culture

"Feel-good films" are usually dismissed by film critics as being sentimental and without intellectual merit. But their popularity with audiences, who seek them out precisely because of their "feel-good" qualities, tells a more favorable story. Now, for the first time, this popular movie genre has been examined scientifically. A new study from the Max Planck Institute for Empirical Aesthetics investigates which feel-good films are considered by viewers to be prototypical and which factors constitute their feel-good effect.

Around 450 participants from Germany, Austria, and the German-speaking regions of Belgium and Switzerland took part in the study. Their responses point to romantic comedies as having a particularly high potential for emotional uplift. The feel-good films they identified as typical include Love Actually, Pretty Woman, Amélie, and The Intouchables. The study's findings provide clues as to which content-related and formal characteristics films must have in order for audiences to feel particularly good while watching them.

"In addition to an element of humor and the classic happy ending, feel-good films can be identified by certain recurring plot patterns and characters," explains study leader and first author Keyvan Sarkhosh. "Often these involve outsiders in search of true love, who have to prove themselves and fight against adverse circumstances, and who eventually find their role in the community."

But feel-good films are characterized not just by romance and humor, but also by moments of drama, which usually have a strong emotional effect on viewers. At the same time, these features are often embedded in a fairy-tale setting, which is another typical aspect of the genre and contributes considerably to its perceived lightness. Not least, the mixture of all these elements can be considered constitutive of the feel-good film.

The results of this study have just been published in the journal Projections. The article emphasizes the fact that many people watch feel-good films specifically to relax and lift their spirits. Many of the study participants agreed that while feel-good films may be sentimental, they were not kitschy, and that above all they were technically well made. In this respect, the positive use of the genre label by viewers differs considerably from the predominantly negative perspective brought to it by professional film critics.

Original Publication:

Original Publication:
Sarkhosh, K., und Menninghaus, W. (2021). The feel-good film: Genre features and emotional rewards. Projections, 15 (1), 55-92.
DOI:10.3167/proj.2021.150104

Journal

Projections

DOI

10.3167/proj.2021.150104

Muscle stem cells enable our muscle to build up and regenerate over a lifetime through exercise. But if certain muscle genes are mutated, the opposite occurs. In patients suffering from muscular dystrophy, the skeletal muscle already starts to weaken in childhood. Suddenly, these children are no longer able to run, play the piano or climb the stairs, and often they are dependent on a wheelchair by the age of 15. Currently, no therapy for this condition exists.

"Now, we are able to access these patients' gene mutations using CRISPR-Cas9 technology," explains Professor Simone Spuler, head of the Myology Lab at the Experimental and Clinical Research Center (ECRC), a joint institution of the Max Delbrück Center for Molecular Medicine in the Helmholtz Association and Charité - Universitätsmedizin Berlin. "We care for more than 2,000 patients at the Charité outpatient clinic for muscle disorders, and quickly recognized the potential of the new technology." The researchers immediately started working with some of the affected families, and have now presented their results in the journal JCI Insight. In the families studied, the parents were healthy and had no idea they possessed a mutated gene. The children all inherited a copy of the disease mutation from both parents.

Edited human muscle stem cells developed into muscle fibers in mice

The term "muscular dystrophy" is used to refer to some 50 different diseases. "They all take the same course, but differ due to the mutation of different genes," explains Spuler. "And even within the genes, different sites can be mutated." Following a genomic analysis of all patients, the researchers chose one family because of their particular form of the disease: Limb-girdle muscular dystrophy 2D/R3 is relatively common, progresses rapidly, and has a suitable docking site for the "genetic scissors" close to the mutation on the DNA.

For the study, the researchers took a sample of muscle tissue from a ten-year-old patient, isolated the stem cells, multiplied these in vitro, and used base editing to replace a base pair at the mutated site. They then injected the edited muscle stem cells into mouse muscles, which can tolerate foreign human cells. These multiplied in the rodent and most developed into muscle fibers. "With this, we were able to show for the first time that it is possible to replace diseased muscle cells with healthy ones," says Spuler. Following further tests, the repaired stem cells will be reintroduced to the patient.

Base editing - a sophisticated technique

Base editing is a newer and highly sophisticated variant of the CRISPR-Cas9 gene-editing tool. Whereas in the "classic" method, both strands of DNA are cut by these molecular scissors, the Cas enzymes used for base editing merely snip off the residual glucose from a particular base and attach a different one, thus creating a different base at the targeted site. "This tool works more like tweezers than scissors, and is perfect for carrying out targeted point mutations in a gene," says Dr. Helena Escobar, a molecular biologist in Spuler's team. "It is also a much safer method, because unwanted changes are extremely rare. In the genetically repaired muscle stem cells, we have not witnessed any misediting at unintended regions of the genome." Escobar is the study's lead author and the one who developed the technique for the muscle cells.

Autologous cell therapy - which involves removing a patient's own stem cells, editing them outside the body and then injecting them back into the muscle - will not enable sufferers who are already wheelchair-bound to walk again. "We cannot repair muscle that has already atrophied and been replaced by connective tissue," Spuler stresses. And the number of cells that can be edited in vitro is also limited. However, the study provides the first proof that a form of therapy may even be possible for a group of previously incurable diseases, and it could be used to repair small muscle defects, such as those in the finger flexor.

One step closer to a cure

But this is just the first step. "The next milestone will be to find a way to inject the base editor directly into the patient. Once inside the body, it would 'swim' around for a short while, edit all the muscle stem cells, and then quickly break down again." The team wants to start the first trials in a mouse model soon. If this also works, newborns could be tested for corresponding gene mutations in the future and the curative therapy could be initiated at a time when comparatively few cells would need to be edited.

So, what might an in vivo therapy for muscular dystrophy look like in concrete terms? This is something that scientists have been testing on animal models for some time using viral vectors. However, Helena Escobar explains that because these vectors remain in the body for too long, the risk of misediting and toxic effects is too high. "An alternative would be for mRNA molecules that contain the information for the editor to synthesize the tools in vivo," says the molecular biologist. "mRNA breaks down very quickly in the body, so the therapeutic enzymes can only remain in an active state for a short time." The therapy could probably also be repeated, if necessary. "We do not yet know whether this would need to be a therapy cycle involving several applications."

This therapeutic avenue would mean that, unlike with autologous cell therapy, not every patient would need to be treated individually. For each form of muscle therapy, one "tool" would be sufficient to cure muscle atrophy before major damage even occurred. But, for now, that is still a long way off.

DALLAS (SMU) - NASA has a long tradition of unexpected discoveries, and the space program's TESS mission is no different. SMU astrophysicist and her team have discovered a particularly bright gamma-ray burst using a NASA telescope designed to find exoplanets - those occurring outside our solar system - particularly those that might be able to support life.

It's the first time a gamma-ray burst has been found this way.

Gamma-ray bursts are the brightest explosions in the universe, typically associated with the collapse of a massive star and the birth of a black hole. They can produce as much radioactive energy as the sun will release during its entire 10-billion-year existence.

Krista Lynne Smith, an assistant professor of physics at Southern Methodist University, and her team confirmed the blast - called GRB 191016A - happened on Oct. 16 and also determined its location and duration. A study on the discovery has been published in The Astrophysical Journal.

"Our findings prove this TESS telescope is useful not just for finding new planets, but also for high-energy astrophysics," said Smith, who specializes in using satellites like TESS (Transiting Exoplanet Survey Satellite) to study supermassive black holes and gas that surrounds them. Such studies shed light on the behavior of matter in the deeply warped spacetime around black holes and the processes by which black holes emit powerful jets into their host galaxies.

Smith calculated that GRB 191016A had a peak magnitude of 15.1, which means it was 10,000 times fainter than the faintest stars we can see with the naked eyes.

That may sound quite dim, but the faintness has to do with how far away the burst occurred. It is estimated that light from GRB 191016A's galaxy had been travelling 11.7 billion years before becoming visible in the TESS telescope.

Most gamma ray bursts are dimmer - closer to 160,000 times fainter than the faintest stars.

The burst reached its peak brightness sometime between 1,000 and 2,600 seconds, then faded gradually until it fell below the ability of TESS to detect it some 7000 seconds after it first went off.

This gamma-ray burst was first detected by a NASA's satellite called Swift-BAT, which was built to find these bursts. But because GRB 191016A occurred too close to the moon, the Swift-BAT couldn't do the necessary follow-up it normally would have to learn more about it until hours later.

NASA's TESS happened to be looking at that same part of the sky. That was sheer luck, as TESS turns its attention to a new strip of the sky every month.

While exoplanet researchers at a ground-base for TESS could tell right away that a gamma-ray burst had happened, it would be months before they got any data from the TESS satellite on it. But since their focus was on new planets, these researchers asked if any other scientists at a TESS conference in Sydney, Australia were interested in doing more digging on the blast.

Smith was one of the few high-energy astrophysics specialists there at that time and quickly volunteered.

"The TESS satellite has a lot of potential for high-energy applications, and this was too good an example to pass up," she said. High-energy astrophysics studies the behavior of matter and energy in extreme environments, including the regions around black holes, powerful relativistic jets, and explosions like gamma-ray bursts.

TESS is an optical telescope that collects light curves on everything in its field of view, every half hour. Light curves are a graph of light intensity of a celestial object or region as a function of time. Smith analyzed three of these light curves to be able to determine how bright the burst was.

She also used data from ground-based observatories and the Swift gamma-ray satellite to determine the burst's distance and other qualities about it.

"Because the burst reached its peak brightness later and had a peak brightness that was higher than most bursts, it allowed the TESS telescope to make multiple observations before the burst faded below the telescope's detection limit," Smith said. "We've provided the only space-based optical follow-up on this exceptional burst."

Researchers from the Carl R. Woese Institute for Genomic Biology in collaboration with scientists at Oxford University have published a paper in Cell reporting the function of LanCL proteins. These proteins are found in eukaryotic cells but their function was previously unknown. The study is the first step towards understanding the importance of these ubiquitous proteins.

Bacteria contain enzymes called LanC that are capable of producing small proteins called lanthipeptides, which are characterized by the addition of a thiol group to a modified serine or threonine amino acid. Similar proteins--called LanC-like or LanCL--have been found in different eukaryotic cells for decades, but their function was unknown.

"LanCLs are found in nearly all higher organisms, including humans. Although scientists have worked on these proteins for over 20 years, we didn't know their function. We had several hypotheses, which we kept ruling out based on our experiments," said Wilfred van der Donk (MMG), a professor of chemistry and investigator of the Howard Hughes Medical Institute.

The first breakthrough came in 2015, when the Nair lab in the Department of Biochemistry solved the crystal structure of a LanC-containing protein in bacteria. The protein was bound to another enzyme called a kinase, which modifies proteins by adding a phosphate group. Inspired by this discovery, the researchers tested whether LanCL proteins were also binding to kinases in eukaryotic cells. "We saw that they were able to bind to many kinases, including AKT and mTOR, and all of a sudden the pieces of the puzzle started forming a picture," van der Donk said.

The next piece fell into place in collaboration with Benjamin Davis, a professor of chemistry at the University of Oxford. The Davis group showed that eliminating a particular phosphate group in kinases causes them to become activated. Scientists had assumed that such processed proteins would be inactive. Together, the Illinois and Oxford groups were able to show that LanCL adds glutathione to kinases with eliminated phosphate groups, after which the kinases became deactivated. "We realized that when the LanCL proteins are absent, the cell has a big problem because there are active proteins floating around that need to be turned off," van der Donk said.

The importance of these proteins became evident in mice that lacked them. "A third of the mice that lack these enzymes die when they are between four to six months old. They die suddenly without getting sick and we still don't understand why," said Jie Chen (GNDP), a professor of cell and developmental biology.

The researchers are interested in understanding the role of these proteins and making a complete list of all the possible targets of LanCLs. "When you have abnormal kinases, it can cause all kinds of problems, including cancer. LanCL proteins eliminate these damaged kinases and it is possible that they also affect other proteins that we are not aware of. We need to connect their cellular functions to the results we saw in the mice," Chen said.

"This study is just the tip of the iceberg. Since these proteins are found everywhere, you can also imagine their effects in feedstock and the future of farming," said Satish Nair (MME/MMG), Head of the Department of Biochemistry.

"This study was possible because of the persistence of our graduate students. Most of us would have given up long ago because the studies were initially going nowhere," Nair said. "It also shows the importance of exploratory research, where you're essentially just looking around. Although it is risky, it is great to see that there are rewards for students who stick it out," van der Donk said.

Scientists from several hospitals and research centers have shown what happens in individual cells of patients who died of COVID-19. In a study published in Nature, the researchers describe how infected cells from multiple organs exhibited a range of molecular and genomic changes. They also saw signs of multiple, unsuccessful attempts by the lungs to repair themselves in response to respiratory failure, which is the leading cause of death in COVID-19 patients.

"You really feel the tragedy of the disease when you see that result," said Aviv Regev, co-senior author of the study and a core institute member at the Broad Institute of MIT and Harvard when the study began. "The lung tries everything at its disposal, and it still can't fix itself. This was a very emotional study. We are grateful to the patients and families who agreed to donate tissue for COVID-19 research to help advance understanding of this devastating disease."

The researchers studied tissue obtained at autopsies of 17 individuals who succumbed to COVID-19 and were cared for at Beth Israel Deaconess Medical Center, Brigham and Women's Hospital, and Massachusetts General Hospital.

The team investigated how the SARS-CoV-2 virus interferes with the function of cells and their genetic programs. They used single-cell RNA sequencing data from tissue samples taken from 11 organ systems--including the lungs, heart, liver, and kidneys--to build a comprehensive "cell atlas" of hundreds of thousands of individual cells showing how COVID-19 can lead to organ failure and death.

"We knew people were passing away from COVID-related pneumonia and extrapulmonary complications," said Alexandra-Chloé Villani, an associate member of the Broad, a principal investigator at Mass General, an assistant professor of medicine at Harvard Medical School, and co-senior author on the study. "Before this study, we had limited knowledge of the cellular and molecular mechanisms that were involved in driving a patient's demise."

The study details the results of a collaboration of researchers from the Broad Institute, Mass General, the Ragon Institute of MGH, MIT and Harvard, MIT, Beth Israel Deaconess Medical Center, Brigham and Women's Hospital, Columbia University Irving Medical Center, and other institutions. A team led by the Columbia collaborators co-authored a companion study that is also published in Nature.

The team's cell atlas is freely and openly available for other scientists to explore. They also created a 420-specimen biobank from the autopsy samples that can be used for other COVID-19 studies. "We created a foundational resource for other researchers to use in the future to ask specific questions," said Orit Rozenblatt-Rosen, co-senior author and an institute scientist and the scientific director of the Klarman Cell Observatory at the Broad when the study began. "Hopefully our findings will allow people to find better therapeutics for COVID-19."

Novel techniques for a novel virus

To learn about cellular mechanisms underlying organ failure caused by COVID-19, the researchers knew they needed to study the organs themselves. For that, they would need samples from autopsies.

Working with autopsy samples is challenging under normal circumstances. To deal with samples that might carry a novel, highly contagious pathogen, the researchers developed new tissue collection and processing protocols compatible with requirements for a Biosafety Level 3 lab.

"We wanted to ensure we could learn and share as much as humanly possible to help prevent future deaths, while prioritizing the safety and well-being of all involved. This was no small feat, given COVID-related restrictions and all the surrounding uncertainties. It was amazing to see dozens of scientists and medical professionals from several institutes come together as a collaborative partnership to carefully design and coordinate our experimental and computational efforts," said institute member and co-senior author Alex K. Shalek, who is also a member of the Ragon Institute, and an associate professor of chemistry, a core member of the Institute for Medical Engineering and Science, and an extramural member of the Koch Institute for Integrative Cancer Research at MIT.

The team then profiled RNA from the individual cells and developed new methods to analyze and annotate the large amounts of sequence data. They compared gene expression signatures from different cells: COVID-19-damaged cells and uninfected cells from the COVID-19 patients, as well as cells from patients with other diseases and from healthy individuals.

Havoc in the lungs

The most extensive suite of findings were from the lungs. The scientists were astounded by the extent of the changes in genetic programs they found there. "The virus wreaks havoc in the lungs and we see it in the cells," Regev said.

One main cause of lung damage in COVID-19 is the destruction of AT1 cells, which enable breathing and gas transfer. The scientists found that as AT1 cells died, related lung cells called AT2 attempted to convert themselves into AT1 cells through a process called transdifferentiation. But this attempt halted mid-way through, leaving the cells in an intermediary state that is often seen in patients with other lung diseases such as pulmonary fibrosis.

In a last-ditch attempt at self-repair, the lungs tried to turn cells from higher up in the airways, known as intrapulmonary basal-like progenitor cells, into AT1 cells. This attempt at transdifferentiation had only previously been seen in mouse models.

The findings suggest that the lung failure in patients was caused by the inability of lung cells to outpace the damage caused by the virus as the cells tried to regenerate.

Changing programs

The paper also describes how the virus impacts other tissues outside of the lungs. One surprising finding was that while the heart sustained significant damage and showed evidence of altered genetic programs in many different cell types, there was very little viral RNA in the heart tissue itself. "Whether that means the virus had already been cleared, or that the heart was collateral damage is an area for further research," said Regev.

The researchers also looked at 27 different genes that previous genome-wide association studies have linked to severe COVID-19. They zeroed in on a handful that were highly expressed in key cell types in the new study, particularly those in infected lungs. This finding helps narrow down the list of potential genetic factors for severe disease and highlights the cell types that may be most relevant in severe COVID-19.

The team now plans to finish analyzing the other autopsied tissues, such as brain, spleen and trachea, to paint a more complete picture of COVID-19 pathology and provide a resource for future studies.

Jeremy Edwards, director of the Computational Genomics and Technology (CGaT) Laboratory at The University of New Mexico, and his colleagues at Centrillion Technologies in Palo Alto, Calif. and West Virginia University, have developed a chip that provides a simpler and more rapid method of genome sequencing for viruses like COVID-19.

Their research, titled, "Highly Accurate Chip-Based Resequencing of SARS-CoV-2 Clinical Samples" was published recently in the American Chemical Society's Langmuir. As part of the research, scientists created a tiled genome array they developed for rapid and inexpensive full viral genome resequencing and applied their SARS-CoV-2-specific genome tiling array to rapidly and accurately resequenced the viral genome from eight clinical samples acquired from patients in Wyoming that tested positive for SARS-CoV-2. Ultimately, they were able to sequence 95 percent of the genome of each sample with greater than 99.9 percent accuracy.

"This new technology allows for faster and more accurate tracing of COVID and other respiratory viruses, including the appearance of new variants," said Edwards, who is a professor in the UNM Department of Chemistry and Chemical Biology. "With this simple and rapid testing procedure, scientists will be able to more accurately track the progression and better prevent the onset of the next pandemic."

With more than 142 million people worldwide having contracted the virus, vigilant testing and contact tracing are the most effective ways to slow the spread of COVID-19. Traditional methods of clinical testing often produce false positives or negatives, and traditional methods of sequencing are time-consuming and expensive. This new technology will virtually eliminate all of these barriers.

"Since the submission of the paper, the technology has further evolved with improved accuracy and sensitivity," said Edwards. "The chip technology is the best available technology for large-scale viral genome surveillance and monitoring viral variants. This technology could not only help control this pandemic and also prevent future pandemics."

The mission of the Computational Genomics and Technology (CGaT) Laboratory is to provide training in bioinformatics research for undergraduate, master's and Ph.D. students, as well as postdoctoral fellows; provide collaborative research interactions to utilize bioinformatics computing tools for researchers at UNM, and to conduct state-of-the-art and innovative bioinformatics and genomics research within the center.

Researchers at Karolinska Institutet in Sweden have discovered a mechanism through which meningitis-causing bacteria can evade our immune system. In laboratory tests, they found that Streptococcus pneumoniae and Haemophilus influenzae respond to increasing temperatures by producing safeguards that keep them from getting killed. This may prime their defenses against our immune system and increase their chances of survival, the researchers say. The findings are published in the journal PLoS Pathogens.

"This discovery helps to increase our understanding of the mechanisms these bacteria use to evade our normal immune defenses," says co-corresponding author Edmund Loh, researcher in the Department of Microbiology, Tumor and Cell Biology at Karolinska Institutet. "It could be an important piece of the puzzle in examining what turns this usually harmless bacterium into a lethal killer."

Meningitis is an inflammation of the membranes surrounding the brain and the spinal cord. It can be caused by viruses, bacteria, fungi and parasites.

Bacterial meningitis is one of the most severe types and a major cause of death and disability in children worldwide. Several kinds of bacteria can cause the infection, including the respiratory pathogens Streptococcus pneumoniae and Haemophilus influenzae, which can be attributed to some 200,000 meningitis-caused deaths annually.

These two bacteria often reside in the nose and throat of healthy people without making them ill. In some cases they spread into the bloodstream and cause invasive diseases, but the reasons for this remain largely unknown.

In this study, the researchers set out to investigate the connection between temperature changes and survival of these bacteria in a laboratory setting. The experiments were prompted by another recent finding that linked the temperature sensing abilities of the bacterium N. meningitidis to invasive meningococcal disease.

One of the signs of an infection is elevated temperatures and fever, which typically boost our immune system's ability to fight illness. In this study, however, the researchers found that both S. pneumoniae and H. influenzae activated stronger immune protections when challenged with higher temperatures.

They did so through mechanisms involving four specific so-called RNA thermosensors (RNATs), which are temperature-sensitive non-coding RNA molecules. These RNATs helped boost the production of bigger protective capsules and immune modulatory Factor H binding proteins, both of which help shield these bacteria from immune system attacks.

"Our results indicate that these temperature sensing RNATs create an additional layer of protection that helps the bacteria colonize their normal habitat in the nose and throat," says the paper's first author Hannes Eichner, PhD student at the same department. "Interestingly, we saw that these RNATs do not possess any sequence similarity, but all retain the same thermosensing ability, which indicates that these RNATs have evolved independently to sense the same temperature cue in the nasopharynx to avoid immune killing."

More research is needed to understand exactly what triggers these pathogens to breach from the mucous membrane into the bloodstream and further into the brain. Future studies encompassing in vivo infection model are warranted to characterize the role of these RNATs during colonization and invasion, the researchers say.

WASHINGTON, D.C, (April 29, 2021) - An analysis of growth patterns in transcatheter aortic valve replacement (TAVR) programs across United States hospitals is being presented as late-breaking clinical science at the Society for Cardiovascular Angiography& Interventions (SCAI) 2021 Scientific Sessions. The findings indicate that TAVR hospital programs are predominately located in metropolitan areas serving patients with higher socioeconomic status, potentially contributing to the disparities in cardiac care.

TAVR is a minimally invasive procedure for patients in need of a valve repair or replacement and is an alternative to surgical aortic valve replacement (SAVR), a treatment option requiring open heart surgery. TAVR also provides eligible patients with quicker procedure times and a shorter recovery. Yet, despite the benefits of novel therapeutics such as TAVR, some patients are still referred to SAVR even if they are ideal candidates - prompting a deeper analysis of how the technology is disseminated in certain populations.

The study involved a cross-sectional analysis of Medicare claims data between January 1, 2012 to December 31, 2018. Linear regression models were used to compare socioeconomic characteristics of patients treated at hospitals that did and did not establish TAVR programs to determine the association between area-level markers of socioeconomic status and TAVR rates.

The findings reveal inequitable access to TAVR programs for non-metropolitan or lower income areas across the country. Between 2012 and 2018, 554 hospitals developed new TAVR programs including 543 (98.0%) in metropolitan areas, and 293 (52.9%) in metropolitan areas with pre-existing TAVR programs. Compared with hospitals that did not start TAVR programs, hospitals that did start TAVR programs treated patients with higher median household incomes (difference $1,305, 95% CI $134 to $12,477, p=0.03). Furthermore, TAVR rates per 100,000 Medicare beneficiaries were higher in areas with higher median income, despite adjusting for age and clinical comorbidities.

"TAVR has the potential to be an innovative and effective treatment option for heart valve patients, but can only work to its full potential if all patients have access to it. Our study results show a gap, and as clinicians, we know that these inequities can unfortunately translate into differing outcomes," said Ashwin Nathan MD, Fellow, Cardiovascular Medicine, Hospital of the University of Pennsylvania. "While this is just one example of health inequities, our hope is that these findings will activate a change in how we introduce high-tech solutions, so that all communities can access the care they need."

The authors also acknowledge that increasing access to TAVR and structural heart programs will require foresight into how clinical trials and approval for procedures and technologies at hospitals are distributed.

Improved Desalination Process Also Removes Toxic Metals to Produce Clean Water

-Adapted from UC Berkeley news release by Bob Sanders

Desalination - the removal of salt - is only one step in the process of producing drinkable water, or water for agriculture or industry, from ocean water or wastewater. Either before or after the removal of salt, the water often has to be treated to remove boron, which is toxic to plants, and heavy metals like arsenic and mercury, which are toxic to humans. Often, the process leaves behind a toxic brine that can be difficult to dispose of.

Now, a UC Berkeley-led research team in collaboration with Berkeley Lab has discovered a way to simplify the removal of toxic metals, like mercury and boron, during desalination to produce clean water, while at the same time potentially capturing valuable metals, such as gold. The study was recently published in the journal Science.

The new technique, which can easily be added to current membrane-based electrodialysis desalination processes, removes nearly 100% of these toxic metals, producing a pure brine along with pure water and isolating the valuable metals for later use or disposal.

Lead author Adam Uliana, a UC Berkeley graduate student, and senior author Jeffrey Long- a faculty scientist in Berkeley Lab's Materials Sciences Division and UC Berkeley chemistry professor, collaborated closely with Ngoc Bui, then a postdoctoral researcher in Berkeley Lab's Molecular Foundry and now an Assistant Professor at the University of Oklahoma, and Jeff Urban, director of the Molecular Foundry's Inorganic Nanostructures facility, to develop and implement the project.

"Virtually every element in the periodic table can be found in water, and being able to perform precise separations of critical elements is essential for achieving meaningful resource recovery," said Urban, who along with Bui pioneered a water-remediation technology called ZIOS that captures copper from wastewater with unprecedented atomic precision. "Performing remediation in concert with recovery would represent a huge step forward for water and energy technologies."

This work was supported by the National Science Foundation, and the Department of Energy's Office of Science and Laboratory Directed Research and Development (LDRD) Program.

Read the full UC Berkeley release here.

Infant-Warming Device Proven Effective and Safe in Reducing Neonatal Mortality

-By Kiran Julin

Newborn babies, particularly those born under-weight or preterm, are susceptible to hypothermia, since newborns are not yet able to maintain their own body heat. Hypothermia is recognized to be a significant contributor to newborn disease and death, particularly in low- and middle-income countries.

The World Health Organization and public health leaders have recommended best practices to prevent hypothermia in newborns. These include skin-to-skin contact with the mother, and if available, a supplemental external heat source. A new infant-warming device developed at Berkeley Lab and UC Berkeley offers a promising solution that does not require electricity, and is low-cost, convenient, and reusable.

A recent study in The Lancet found that the infant-warming device, known as the Dream Warmer, proved to be safe and effective at significantly lowering newborn mortality rates associated with hypothermia in Rwanda. The findings from a field trial led by Harvard Medical School showed that use of the infant warmer resulted in a drop in infant mortality from 2.8% to 0.9% in hospitals in Rwanda.

The Dream Warmer is a wrap-around pad containing a phase-change material, which is a substance that can absorb and release large amounts of thermal energy or heat when it melts or freezes. The Dream Warmer maintains a temperature of 98.6 degrees Fahrenheit, the average 020202boiling water and allowed to cool prior to use with newborn infants.

The technology was developed by Berkeley Lab scientists Ashok Gadgil and Vi Rapp, and builds upon an earlier design by Mike Elam, Jonathan Slack, and others at Berkeley Lab and UC Berkeley.

Gadgil and Rapp expected to see some effect on infant mortality but were thrilled to see the threefold drop. "That was a huge and quite unexpected result," said Gadgil.

"These results demonstrate the effectiveness and safety of the warmer, which will support its progression to an article of routine widespread use, first in Rwanda and then elsewhere," added Rapp.

The Harvard Medical School trial in Rwanda was conducted in collaboration with researchers at Berkeley Lab and UC Berkeley, and physicians at Partners in Health, Boston Children's Hospital, and the Rwanda Ministry of Health. The field research in Rwanda was funded by the Banyan Gates Foundation.

New Cuff-Based Technology Monitors Endothelial Function to Aid Prevention, Treatment of Heart Disease

-By Ruby Barcklay

Blood pressure monitors are a common at-home tool for monitoring heart health, but they don't look at the health of the endothelium, the lining of the blood vessels. And endothelial function is a powerful predictor of heart attack and stroke. It has also been linked to COVID-19 in a number of studies.

The trouble is, the current state-of-the-art method to monitor endothelial health, flow-mediated dilation (FMD), which measures the change in diameter in the brachial artery before and after shutting off blood flow, requires the use of an ultrasound scanner or expensive systems. The cost of these systems, and the technical skills needed to perform the measurement preclude frequent testing or continuous monitoring. And some FMD systems that are based on microvascular tone aren't always accurate, as they are sensitive to "sympathetic nervous activation," which can confound the results.

Berkeley Lab has developed a technology using cuffs, like those used for taking blood pressure, to monitor both endothelial function and endothelium-independent vasodilation. Studies on human subjects have verified that the cuff-based method is 37% more sensitive to arterial relaxation than brachial artery imaging. In addition, the apparatus costs one-fifteenth as much as an ultrasonic imager and eliminates the need for an ultrasound technician.

The lower cost and non-invasive method allows for routine detection and monitoring of endothelial health. That means earlier identification of cardiovascular disease and closer management of endothelial health.

"The cuffs are similar to the blood pressure devices many people already use," said bioscientist Jonathan Maltz, who developed the technology with fellow bioscientist Thomas Budinger. "With this technology, people can regularly monitor their endothelial health, in addition to their blood pressure, either at the doctor's office or in the comfort of their own homes."

Maltz also invented a way to calibrate the cuff-based measurements with those of ultrasound-based flow-mediated dilation. The calibrations allow health providers to monitor the effects of interventions such as exercise, smoking cessation, dietary modification, and cholesterol-lowering therapy, on patient health.

The Berkeley Lab technology is now available for licensing.

Meteorites Reveal Magnetic Record of Protoplanet Churn

-By Lori Tamura

If you stumble upon an unusual rock that could be a meteorite, do not place a magnet on it to see if it's magnetic - you'd end up erasing 4.5 billion years of magnetic history. Meteorites are remnants of our solar system's first protoplanets and, in some cases, retain a record of the magnetic fields they've experienced in the distant past.

"As planetary scientists, we're interested in understanding how protoplanets formed and evolved prior to the formation of the planets we know today," said Clara Maurel, a Ph.D. student at MIT's Department of Earth, Atmospheric, and Planetary Sciences. "There are many different areas of research that tackle these questions, and our angle of approach is to use magnetism."

In a recent paper published in the journal Geophysical Research Letters, Maurel and colleagues from MIT, Oxford, Arizona State, NASA's Jet Propulsion Laboratory, and Berkeley Lab detected the signatures of ancient magnetic fields imprinted in a meteorite's ferromagnetic grains at Berkeley Lab's Advanced Light Source (ALS).

The results revealed a bias in the magnetization directions found in different regions of the sample, indicating that the meteorite was exposed to a substantial, stable magnetic field that magnetized its ferromagnetic grains upon cooling. The team interpreted this as evidence for a dynamo-generated magnetic field powered by the parent body's churning, molten-metal core. A similar mechanism powers the Earth's magnetic field today.

Combined with earlier measurements of two other meteorites from the same parent and radioisotopic dating of the samples, the results support an extended time frame for the cooling of molten protoplanetary cores. Despite its small size compared to planets, this protoplanet did not cool quickly, but instead sustained a molten metallic core for tens of millions of years after the birth of the solar system.

"For people who are interested in modeling the evolution of protoplanets, experimental constraints like this are essential," said Maurel. "These data points represent an important first step toward a better understanding of the chronological activity of protoplanets, from their formation to the time they completely solidify and become inactive."

Lacticaseibacillus rhamnosus GG, or LGG, is the most studied probiotic bacterium in the world. However, its features are not perfect, as it is unable to utilise the milk carbohydrate lactose or break down the milk protein casein. This is why the bacterium grows poorly in milk and why it has to be separately added to probiotic dairy products.

In fact, attempts have been made to make L. rhamnosus GG better adjust to milk through genetic engineering. However, strict restrictions have prevented the use of such modified bacteria in human food.

Thanks to a recent breakthrough made at the University of Helsinki, Finland, with researchers from the National Institute for Biotechnology and Genetic Engineering, Pakistan, features have now been successfully added to the LGG probiotic without gene editing, making it thrive and grow in milk.

The method used is known as conjugation, which is a technique utilised by certain bacterial groups to transfer their traits to other bacteria. In the process, a bacterium produces a copy of its plasmid, a ring-shaped piece of DNA in the bacterium. Next, the bacterium transfers the plasmid to an adjacent bacterium. The spread of plasmids, which carry traits useful for bacteria, can be rapid among bacterial communities.

In the case of Lacticaseibacillus rhamnosus GG, the plasmid that provided the ability to make use of lactose and casein originated in a specific Lactococcus lactis bacterial strain grown in the same place.

"The new LGG strain is not genetically modified, which makes it possible to consume it and any products containing it without any permit procedures," says the project leader, Professor of Microbiology Per Saris from the Faculty of Agriculture and Forestry, University of Helsinki.

The new strain can be used as a starting point in the development of new dairy products where the probiotic concentration increases already in the production stage. In other words, the probiotic need not be separately added to the final product.

Furthermore, the new LGG strain can potentially be better equipped to grow, for example, in the infant gut where it would be able to utilise the lactose and casein found in breastmilk, producing more lactic acid than the original strain.

"Lactic acid lowers the pH of the surface of the intestine, reducing the viability of many gram-negative pathogenic bacteria, such as E. coli, Salmonella and Shigella, which threaten the health of infants. Moreover, in larger numbers the new LGG strain can potentially be more effective at protecting infants than the old strain. After all, LGG has previously been shown to alleviate infantile atopic dermatitis and boost the recovery of the gut microbiota after antibiotic therapies."

The researchers are in negotiations on the further application of their discovery.

A third of children and adolescents develop a mental health problem after a concussion, which could persist for several years post-injury, according to a new literature review.

The research, led by the Murdoch Children's Research Institute (MCRI) and published in the British Journal of Sports Medicine, found mental health should be evaluated as part of standard pediatric concussion assessment and management.

MCRI researcher and Monash University PhD candidate Alice Gornall said despite many post-concussion and mental health symptoms overlapping, the relationship between delayed recovery and mental health had remained poorly understood until this literature review.

The review of 69 articles published between 1980 to June 2020, involved almost 90,000 children, aged 0-18 years, from nine countries including Australia, US, Canada and New Zealand, who had a concussion. Falls (42.3 per cent) and sporting injuries (29.5 per cent) were the most common cause of injury, followed by car accidents (15.5 per cent).

It found up to 36.7 per cent experienced significantly high levels of internalising problems such as withdrawing, anxiety, depression and post-traumatic stress and 20 per cent externalising problems such as aggression, attention problems and hyperactivity after concussion compared with healthy children or children who sustained other injuries such as an arm fracture.

Pre-existing mental health problems were a strong predictor of post-concussion mental health issues. The review stated 29 per cent of children with a pre-injury mental health diagnoses received a new mental health diagnosis post-concussion. Up to 26 per cent without prior mental health problems went onto develop symptoms.

Ms Gornall said while significant improvements in mental health emerged between three and six months post-injury, a minority of children experienced persisting symptoms for several years afterwards.

The findings come after a recent study, led by MCRI and published in The Journal of Head Trauma Rehabilitation, found having a traumatic brain injury in early childhood was associated with lower IQ scores that persist up to seven years post-injury.

Ms Gornall said concussion was a growing public health concern with a third of children experiencing a head injury before 13 years of age.

"Despite the high incidence of concussion among children and adolescents, identifying those at risk of ongoing difficulties after concussion remains a prominent challenge for clinicians," she said.

"On top of this, children take twice as long to recover from concussion than adults, with one in four children experiencing symptoms beyond one-month post-injury."

Melbourne resident Emma, 17, has been seeking mental health support after suffering two concussions, a year apart.

In 2019 while playing netball she knocked her head on a goal post and last March she was hit with a ball in the back of the head.

Emma said after the second concussion she developed anxiety, headaches, a sense of hopelessness and had trouble concentrating.

"After my last concussion I found it very hard to be motivated for school and everyday life. Doing the simplest of tasks such as a walk was difficult for me, not being able to complete these tasks got me quite disheartened which impacted on my mental health," she said.

Emma's dad Bruce Henry said he welcomed the push for mental health to be part of paediatric concussion assessment and management as many cases would be going untreated.

"When a child has a concussion they might look fine but you can't see the underlying impact," he said. It's so important for mental health to form part of concussion management, which has been essential to Emma's recovery process."

MCRI researchers are also trialling an intervention, Concussion Essentials, to prevent children suffering long term post-concussion symptoms.

The eight session intervention combines physiotherapy and psychology treatments that target presenting symptoms with education around common concerns such as headache, fatigue and return to exercise, school and sports. Early data shows that the intervention is effective in accelerating recovery.

MCRI Professor Vicki Anderson said assessment, prevention and intervention of mental health difficulties after concussion should be integrated into standard concussion management.

"Mental health is central to concussion recovery. Concussion may both precipitate and exacerbate mental health difficulties, impacting delayed recovery and psychosocial outcomes," she said.

"Incorporating mental health risk into post-injury management represents an opportunity to engage children and adolescents with mental health services to either prevent unnecessary problems emerging or to treat already existing issues."

Developed by world-leading concussion experts at MCRI and The Royal Children's Hospital and in collaboration with the AFL, the HeadCheck app also helps parents, coaches and first aiders to recognise the signs of concussion and manage the child's safe return to school, play and organised sport.

A collaboration between experts and a Danish-based, global reaching patient organization has resulted in a groundbreaking medical publication, where guidelines are being presented on how to manage patients with unexplained low blood sugar.

Danielle Drachmann, founder of Ketotic Hypoglycemia International (KHI), spent years being dismissed by doctors due to the outdated perception that her children's dangerous low blood glucose (sugar) and high ketone levels were a normal variation.

Professor Henrik Christesen, Head of the Complex Hypoglycemia Center, Odense University Hospital, Denmark, could not identify the cause of the condition despite intense efforts, but recognized the severity of the children's condition and implemented strict monitoring and management guidelines to support the family.

Closing the gap: Uniting the patients and the experts

Henrik and Danielle shared frustrations due to the lack of knowledge of severe, unexplained ("idiopathic") ketotic hypoglycemia across the wider medical field.

This led Danielle to establish Ketotic Hypoglycemia International with Professor Christesen leading the Scientific Advisory Board.

The patient organization gathered leading experts from the fields of endocrinology and inborn errors of metabolism, uniting them with patient representatives from across the globe. The result is a shared publication in the international medical journal Orphanet Journal of Rare Diseases.

Low blood sugar in children is not just normal

For the first time since the term idiopathic ketotic hypoglycemia was coined in 1964, the the condition is now being divided in two, a physiological and a pathological (severe) form.

The key message is that pathological ketotic hypoglycemia of unknown cause is more than normal variation in small children. Pathological ketotic hypoglycemia should be diagnosed and treated as any other disease, according to the authors.

"The problem is that an old perception of ketotic hypoglycemia just being a normal variation of childhood has kept children from getting the medical investigations and help they need. The medical textbooks must be rewritten" Professor Christesen states.

Parents and experts are excited

With this paper, the severity-range of the condition has been recognized and family members are labeling the news of the upcoming paper as life changing;

"Multiple seizures and ER visits, and we are still being told that this is normal for children. The news of the paper gives me hope that Ketotic Hypoglycemia International has started a revolution. Hope for my child's future and hope that our voices are finally going to be heard," proclaims Victoria, a KHI group member from the United States.

Hypoglycemia expert Dr. David Weinstein, the former director of the Glycogen Storage Disease Program in the US and co-author of the paper, states;

"These children deserve to get answers and they deserve proper treatment. My one regret is that I never was able to get the medical field to take ketotic hypoglycemia seriously."

Be a part of the revolution

Ketotic hypoglycemia is placed somewhere between the two expert fields, pediatric endocrinology and inborn metabolic diseases, as a real orphan disease. The new patient organization has succeeded in bringing experts from the two different medical fields together in this publication.

On top of giving guidelines for diagnosis and treatment, the new patient organization, Ketotic Hypoglycemia International, is presented in the paper.

The organization urges all medical professionals to increase their knowledge and improve their clinical practice by reading this crucial publication about ketotic hypoglycemia,

The organization aims to help this misunderstood patient-group gain access to critical medical supplies, referrals to specialist providers and finally receive the professional validation that their symptoms warrant a full investigation.

"It's been a fantastic journey from feeling alone with two untreated children to become recognized together with hundreds of other families as having a real disease that deserves treatment", first author Danielle Drachmann says.

Facts about ketotic hypoglycemia

In ketotic hypoglycemia, the glucose metabolism works poorly, which is why the body switches to fat burning more quickly. The poor glucose metabolism results in low blood sugar (hypoglycemia) and the increased fat metabolism results in ketone bodies such as acetone. A patient can therefore directly smell of acetone if he or she has an attack of ketotic hypoglycemia. Both sugar and fat burning are enzymatic processes controlled by a number of hormones. In order to have unexplained (idiopathic) ketotic hypoglycemia, a number of enzyme defects in cell metabolism and a number of hormonal diseases must be ruled out. However, an explanation can be found in some of the patients if the cases are being investigated thoroughly, including major genetic analysis packages.

Over the past ten years, Henrik Christesen has met about 100 children with ketotic hypoglycemia and 15 parents who also had the condition in adulthood. Based on the new research, he estimates that 150 new children and adults annually need medical investigation due to hypoglycemia in Denmark alone.

Toxic pollution hits poorer populations hardest as firms experience more pollutant releases and spend less money on waste management in areas with lower average incomes.

Research from Lancaster University Management School and Texas Tech University, published in European Economic Review looked into the relationship between the location choices of potentially polluting firms and levels of local income to discover if firms made strategic decisions on site locations based on population demographics.

The team studied potentially polluting firms across Texas, and found a correlation between lower income locations and the probability of potentially polluting firms choosing to locate there. Their data, from the US Environment Agency's Toxic Release Inventory also showed the relative frequency of toxic releases decreased as household income rose.

"We looked both at whether firms made decisions on their location based on demographics - particularly income - of the local areas, and also whether firms made different choices on limiting the possibilities of toxic release through waste management based on those same statistics," said co-author Professor Dakshina De Silva, of Lancaster University's Department of Economics.

"Firms reduced their releases and increased spending on waste management in higher income areas - evidenced by a greater number of waste management services - while lower income areas were disproportionately subject to toxic releases.

"The patterns we observed lead us to conclude that, at least partially, potentially polluting firms seek to maximise their expected profits and recognise the financial risk associated with a release in different areas."

Releasing toxic chemicals in the environment is costly for firms because they will have to implement clean-up programmes, pay penalties and compensate local residents for damages. Higher incomes - and associated property values - increase the costs as damages are linked to reduced property values and lost income due to limitations on working.

"Potentially polluting firms seeking to maximise profits will be concerned with the liability of toxic releases and the threat such releases pose to their financial results," said co-author Dr Anita Schiller, of Lancaster University. "They will therefore take into account the demographics of an area when valuing the legal costs and compensation they would have to pay out in the event of a toxic release, and balance this with the cost of reducing the likelihood of such a release.

"In areas where there is a higher income and higher property prices, compensation levels will go up in the event of an incident, with the possibility of collective action by residents and businesses also increasing. Potentially polluting firms must also consider the financial risk of a release and the costs of managing such an incident's likelihood."

The researchers found that levels of toxic release had declined steadily since 2000 - by 34% between 2000 and 2006 and by a further 21% since 2006 - but suggested this drop was not uniform, with potentially polluting firms reducing releases through waste management where local opposition to their presence was the highest.

Co-author Dr Aurelie Slechten added: "Combined with our finding that economic activity and local income are linked with spending on waste management and with levels of toxic releases, this implies that the group most affected by releases will be poorer populations in industrial areas.

"Without further action, the disparity in exposure to toxic releases faced by certain groups will not be reduced by simply requiring that firms report their releases. Serious thought needs to be given to regulation on compensation schemes."

Coral reefs provide shelter, sustenance and stability to a range of organisms, but these vital ecosystems would not exist if not for the skeletal structure created by stony corals. Now, KAUST scientists together with an international team have revealed the underlying genetic story of how corals evolved from soft-bodied organisms to build the myriad calcified structures we see today.

"While the processes involved in coral calcification are well understood, it is less clear how corals' ability to grow calcium carbonate skeletons actually evolved," says Xin Wang, a former KAUST Ph.D. student who worked on the project under the supervision of Manual Aranda.

"How did a squishy anemone-like organism begin to build reefs?" asks Aranda. "Did the 'tools' already exist in their genetic code?"

There is a debate surrounding when calcified corals first began to emerge; the earliest fossils found to date are around 265 million years old, but their evolution began far earlier.

"We conducted a genomic search for conserved genes that might be involved in calcification," says Wang. "Our findings suggest that corals evolved to calcify somewhere between 308 and 265 million years ago."

The team compared the genomes of six different related species -- two evolutionary divergent reef-building corals, two of their closest noncalcifying relatives and two sea anemones. The complex analysis took two years using the KAUST supercomputer.

"We found that the necessary proteins to make coral skeletons were already present in the soft-bodied ancestor and that various existing proteins were recruited to boost the calcifying process. Essentially, we believe we've found the genetic toolkit for coral skeleton creation," says Wang.

To calcify, corals must draw in positively charged calcium ions from seawater. To make this process as efficient as possible, the coral proteins that help the calcium precipitate should be negatively charged and the pH balance of the calcifying fluid must be just right.

The team pinpointed the genes responsible for transporting calcium and removing protons in the soft-bodied organisms, and they showed that two of the three gene copies found in corals have been recruited to the calcifying tissue. The researchers then identified a gene encoding an acid-rich protein that was duplicated in corals twice and then recruited to precipitate and stabilize calcium carbonate in the initial stage of skeleton building. They also highlighted transmembrane proteins involved in bone matrix adhesion.

"This is a great example of how latent traits can evolve to become dominant given certain environmental pressures," says Aranda. "Next we hope to verify which of these components is critical to calcification and investigate how coral reefs might be influenced by the changing pH of future oceans."

LAWRENCE -- Researchers commonly work with the criminal justice system to implement reforms, bringing with them the latest science and data pointing to why a certain practice will help improve outcomes. New research from the University of Kansas shows if community corrections agencies are to sustain evidence-based reforms, they need to view them as legitimate.

Researchers worked with eight federal community corrections agencies to implement Contingency Management, an evidence-based practice used to help people convicted of drug offenses set and achieve goals to end addiction, avoid repeat offenses and increase pro-social behavior. Such evidence-based practices and reforms are frequently put in place across the criminal justice system.

Shannon Portillo"We've seen millions of dollars spent by institutions on evidence-based practices in community corrections settings, but there is very little research on if the reforms stick after researchers leave," said Shannon Portillo, associate professor of public affairs & administration at KU and co-author of the study. "We followed up after our original study with community corrections agencies, and we found reform only sticks when staff viewed the reform as legitimate. It is not enough to show that reforms are effective or efficient. Workers must view them as legitimate and aligned with their organization's goals."

The study, co-written with Danielle Rudes and Faye Taxman of George Mason University, was published in the British Journal of Criminology.

The researchers returned to the eight community corrections sites five years after implementing Contingency Management. While all sites saw the reformed practices as legitimate enough to initially consider adoption, two sites never adopted them, four sites experimented with reform, and two sites continued to use the reform after the study was over. The research team evaluated the legitimacy of the reform on three levels: Pragmatic, or if staff recognized that the practice could fit with their site routines and operations; moral, or if it was viewed as the right thing to do to help their clients; and cognitive, or if they could understand how this reform was different from current practices and was a shift in behaviors that could fit their agency.

Results showed that sites that sustained Contingency Management rated it moderately or strongly in all three areas but that it had to be viewed strongly in terms of cognitive legitimacy. Sites in which it was not sustained gave various reasons for scoring it lower; for example, one employee did not use the software provided to keep track of data, instead logging it manually and reporting it was additional work, resulting in a low score in pragmatic legitimacy. Leadership was key in implementing reforms but could not make others view them as legitimate simply by requiring staff to implement the new practice. In fact, leadership views of legitimacy, efficiency and effectiveness of the measure was not a key factor at all, compared to staff views of legitimacy.

"This shows it really had to be the workers who saw this change as worthwhile and saw how the reform was worth their time to change their behaviors and workplace practices," Portillo said.

In some of the sites where the evidence-based practice was not sustained, workers and management discussed the reform, but they indicated they were not sure exactly what it meant or how they could find a way to make it fit in their operations, meaning it did not score well in cognitive or pragmatic legitimacy. Contingency management works by helping individuals set goals for recovery, meet requirements set in terms of their probation or by courts and rewarding them with gift cards or points toward purchases when certain benchmarks are met.

"It sounds simple, but this is a huge shift in mindset for the criminal justice system, because the system is so punishment-oriented. So, it was not always viewed as legitimate," Portillo said.

Presenting such a fundamental change in operations shows that reform cannot be implemented or sustained without demonstrating to those tasked with carrying it out of its value. Demonstrating the efficacy or leadership simply telling workers it is something they have to do was not enough. While much effort and money have been invested in criminal justice reform, a deeper understanding of what reforms work as well as how to make them stick is vital to improving the criminal justice system and helping individuals successfully transition back to society.

"This is definitely an area that needs more research, as the federal government invests a lot, and individual organizations invest a lot of time and resources in reforms and evidence-based practices," Portillo said. "We need to know more about how reform can be successful and how it is sustained for the long term."