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Published3 hours agoShareclose panelShare pageCopy linkAbout sharingImage source, Getty ImagesBy Azadeh MoshiriBBC NewsUtah has become the first US state to require social media firms get parental consent for children to use their apps and verify users are at least 18.The governor said he signed the two sweeping measures to protect young people in the state.The bills will give parents full access to their children’s online accounts, including posts and private messages.The move comes amidst heightened concern over the impact of social media on children’s mental health. Under the measures enacted on Thursday, a parent or guardian’s explicit consent will be needed before children can create accounts on apps such Instagram, Facebook and TikTok.Parents powerless over kids’ social media – WinsletThe bills also impose a social media curfew that blocks children’s access between 22:30 and 06:30, unless adjusted by their parents.Under the legislation, social media companies will no longer be able to collect a child’s data or be targeted for advertising. The two bills – which are also designed to make it easier to take legal action against social media companies – will take effect on March 1, 2024.Governor Spencer Cox, a Republican, wrote on Twitter: “We’re no longer willing to let social media companies continue to harm the mental health of our youth.”As leaders, and parents, we have a responsibility to protect our young people.”Children’s advocacy group Commons Sense Media welcomed the governor’s move to curtail some of social media’s most addictive features, calling it a “huge victory for kids and families in Utah”. “It adds momentum for other states to hold social media companies accountable to ensure kids across the country are protected online,” said Jim Steyer, Common Sense Media’s founder and CEO.Similar regulations are being considered in four other Republican-led states – Arkansas, Texas, Ohio and Louisiana – and Democratic-led New Jersey.But Common Sense Media and other advocacy groups warned some parts of the new legislation could put children at risk.Ari Z Cohn, a free speech lawyer for TechFreedom, said the bill posed “significant free speech problems”.”There are so many children who might be in abusive households,” he told the BBC, “who might be LGBT, who could be cut-off from social media entirely.”In response, Meta, Facebook’s parent company, said it has robust tools to keep children safe.A spokesperson told the BBC: “We’ve developed more than 30 tools to support teens and families, including tools that let parents and teens work together to limit the amount of time teens spend on Instagram, and age verification technology that helps teens have age-appropriate experiences.”There has been other US bipartisan support for social media legislation aimed at protecting children.President Joe Biden’s State of the Union address in February called for laws banning tech companies from collecting data on children.Last year, California state lawmakers passed their own child data law. Among other measures, the California Age-Appropriate Design Code Act requires digital platforms to make the highest privacy features for under-18 users a default setting.The passage of the Utah bills coincides with a bruising congressional hearing for TikTok CEO Shou Zi Chew. Five key moments in TikTok CEO’s Congress grilling

They have become the new frontier in the US battle over abortion access. Now, a lawsuit in Texas threatens to pull mifepristone off shelves nationwide. The drug is one of two pills used for medication abortion, which account for half of all abortions in the country. The BBC’s Nomia Iqbal explains.Video by Joyce Liu and Angélica Casas

Metabolic pathways consist of a series of biochemical reactions in cells that convert a starting component into other products. There is growing evidence that metabolic pathways coupled with external stress factors influence the health of cells and tissues. Many human diseases, including retinal or neurodegenerative diseases, are associated with imbalances in metabolic pathways.
Elisabeth Knust leads a team of researchers from the Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG) in Dresden, Germany, who describe an essential role for one such metabolic pathway in maintaining retinal health under conditions of stress. They studied the classic Drosophila genes cinnabar, cardinal, white, and scarlet, originally characterized decades ago and named due to their role in eye color pigmentation, in particular the formation of the brown pigment of the fly eye. These genes encode components of the kynurenine pathway, whose activity converts the amino acid tryptophan by various steps into other products. In this study, the authors have highlighted the function of this metabolic pathway in retinal health, independent of its role in pigment formation.
The Kynurenine pathway is an evolutionary conserved metabolic pathway that regulates a variety of biological processes. Its disruption can result in the buildup of either toxic or protective biomolecules or metabolites, which can worsen or improve, respectively, the health of the brain, including the retina. Knowledge on this important metabolic pathway was recently extended by the research team, led by Elisabeth Knust, Director Emerita at the MPI-CBG, in their publication in the journal Plos Genetics. Being aware of the remarkable conservation of this metabolic pathway and the genes that regulate it, they used flies as a model system to unravel the role of individual metabolites in retinal health. The researchers looked at four genes — cinnabar, cardinal, white, and scarlet – named after abnormal eye colors following their loss in flies. “Since the Kynurenine pathway is conserved from flies to humans, we asked whether these genes regulate retinal health independent of their role in pigment formation,” says Sarita Hebbar, one of the lead authors of the study.
To find this out, the scientists used a combination of genetics, dietary changes, and biochemical analysis of metabolites to study different mutations of the fruit fly, Drosophila melanogaster. Sofia Traikov, a co-author, developed a method for the biochemical analysis of the metabolites of the Kynurenine pathway. This allowed the researchers to link different metabolite levels to the health state of the retina. They found that one metabolite, 3-hydroxykynurenine (3OH-K), is damaging to the retina. More importantly, they could show that the degree of degeneration is influenced by the balance between toxic 3OH-K and protective metabolites, such as Kynurenic Acid (KYNA), and not just by their absolute amounts. Sarita continues: “We also fed two of these metabolites to normal (non-mutant) flies and found that 3OH-K enhanced stress-induced retinal damage, whereas KYNA protected the retina from stress-related damage.” This means that retinal health in certain conditions can be improved by altering the ratio of metabolites of the Kynurenine pathway.
Furthermore, by targeting these four genes and therefore four distinct steps within the pathway, the researchers were able to demonstrate that not only the accumulation of 3OH-K as such, but also its location in the cell and hence its availability in further reactions, is important for retinal health.
“This work shows that the Kynurenine pathway is important not only in pigment formation but that the level of individual metabolites fulfills important roles in maintaining retinal health,” says Elisabeth Knust, who supervised the study. She concludes, “In the future, the ratio of the various metabolites and the specific sites of their accumulation and activity should be taken into account in therapeutic strategies for diseases with impaired Kynurenine pathway function, observed in various neurodegenerative conditions.”

The medicinal secrets of the Chilean soapbark tree have been laid bare, unlocking a future of more potent, affordable, and sustainably sought vaccines.
The evergreen species, Quillaja saponaria has, for decades, been highly prized for producing molecules called QS saponins, which are used in the food and drinks industry as foaming agents.
More recently an important new function has emerged with saponins obtained from the tree’s bark used as potent adjuvants in the production of vaccines. Adjuvants play a critical role in some vaccines, working to boost the potency of a vaccine by enhancing the host immune response.
Molecules extracted from soapbark tree are used as adjuvants in vaccines protecting people against COVID-19, shingles, and malaria.
QS saponins are sourced directly from the tree and although this is at a much smaller scale than the food and drink industry, vaccine manufacturers are actively working to reduce the environmental impact and improve sustainability of sourcing these important resources.
Researchers at the John Innes Centre have taken a major step forward in addressing this problem, by using a combination of genome mining and bioengineering techniques to produce saponin-based vaccine adjuvants in the laboratory without harvesting material directly from trees.

Dr James Reed, first author of the study and postdoctoral researcher at the John Innes Centre says: “These are complex molecules that have thwarted attempts to synthesize them at scale using chemistry in the lab. After many twists and turns, we have now discovered the core set of genes responsible for the biosynthesis of QS saponins.”
In research which appears in Science, the Osbourn group at the John Innes Centre first sequenced the genome of Quillaja saponaria. Then they used powerful computational gene-mining tools to predict which among the ~30,000 genes that make up its genome were responsible for saponin biosynthesis.
This led to the identification of a biosynthetic pathway of 16 genes which together produce the enzymes which are nature’s building blocks for saponin production. Together these newly discovered genes and enzymes act as an instruction manual for future adjuvant bioengineering, say the team.
Identification of a further three enzymes resulted in a complete biosynthetic pathway to the saponin QS-7, a saponin that is included in a vaccine adjuvant with proven clinical efficacy, but that is notoriously difficult to purify from soapbark tree.
The pathway to these molecules was reconstructed in a plant called Nicotiana benthamiana, using a rapid and powerful technique called transient combinatorial expression.
This dwarf wild relative of tobacco is well known as an amenable host for the bioproduction of therapeutic proteins and pharmaceuticals.

The team is already using this instruction manual to attempt to produce other valuable saponins including QS-21, a potent adjuvant and key component in human vaccines.
The levels of saponins produced in this study equate to amounts normally obtained from the leaves of the soapbark tree rather than its bark.
The team have partnered with Plant Bioscience Limited (PBL, Norwich UK), who are leading on the commercialisation of the research and are now looking to work with commercial and academic partners to scale up these quantities further.
Professor Anne Osbourn, the lead of the study, and a group leader at the John Innes Centre said: “The COVID-19 pandemic has demonstrated the huge demand for lifesaving vaccines. By assembling the genome sequence of Quillaja saponaria we now have the instruction manual which has enabled us to decode how the tree makes these potent medicinal molecules. This opens the possibility of producing known and new-to-nature saponin-based vaccine adjuvants optimized for immunostimulant activity and suitable for human applications in our rapid transient plant expression system.”
Elucidation of the pathway for biosynthesis of saponin adjuvants from the soapbark tree appears in Science.
Vaccine Adjuvants — a brief timeline
Described as hidden helpers, vaccine adjuvants are immunostimulatory substances that are added to some vaccines to boost the immune response, doing so by inducing strong antibody and T-cell responses.
Until recently the only adjuvants in clinical use were insoluble aluminium salts or oil in water emulsions containing squalene, an organic compound obtained from shark liver.
As natural surfactants, saponins have been used in veterinary medicine for a century. But these adjuvants have been unsuitable for human use due to poor tolerability. A vaccine containing a saponin-based adjuvant has been approved for use in humans.
QS-7 and QS-21 are included in a complex mix of saponins formulated as Matrix-M adjuvant in the Novavax COVID 19 vaccine. Approval of this vaccine in countries worldwide is increasing the interest for saponin-based adjuvants and alternative methods of production.
Knowledge of the biosynthetic pathway will enable researchers to develop bespoke saponin-based adjuvants with a diverse spectrum of immune-stimulating properties.

Nearly 16 million operations were performed on inpatients in German hospitals in 2021. In Switzerland, the figure is around 1.1 million. Even if the actual operation goes well, it is not uncommon for a wound infection to occur afterwards, which can have dramatic consequences for those affected. In extreme cases, such infections are fatal.
A new study now shows: In most cases, the causative agents of these infections are bacteria from the patient’s own intestine. For this, the intestine does not even have to be injured during the operation. Even so, these pathogens overcome the intestinal barrier postoperatively and spread throughout the body via the bloodstream and lymphatic vessels. They can be stopped by special immune cells, which patrol all organs, including the liver.
A better understanding of side infections
This study was published in the current issue of the journal Cell Reports. Jointly responsible for this are Professor Guido Beldi, Chief of Visceral Surgery at the University Hospital for Visceral Surgery and Medicine at Inselspital in Bern, and Dr. Mercedes Gomez de Agüero, head of a junior research group at the Institute of Systems Immunology at Julius-Maximilians-Universität Würzburg (JMU).
“It has long been known that side infections increase mortality during invasive procedures. For this reason, extensive hygiene and asepsis measures are implemented to eliminate microorganisms in the surgical field,” explains Guido Beldi. As it now turns out, however, the danger comes from a completely different corner: the patient’s intestine.
100 trillion microorganisms live in the intestine
“Several hundred strains of different bacteria with around one hundred trillion microorganisms live in the human intestine. They form the natural intestinal flora, also called the microbiome,” Gomez de Agüero explains. Their existence is beneficial to humans: they help with digestion, eliminate pathogens and train the immune system. However, this only applies as long as these bacteria do not overcome the so-called intestinal barrier and spread throughout the body.

However, this is exactly what can happen after a surgical procedure: “In our study, we analyzed the microorganisms that caused side infections in almost 4,000 patients after a major surgical procedure,” explains Guido Beldi. It showed that in virtually all cases, the infectious agents were bacteria from the patient’s intestine, such as Enterococcus, Escherichia coli and Clostridium.
They most frequently caused infections after operations on the liver, pancreas and bile ducts, as well as during operations on the small and large intestine. In particular, patients who underwent major liver resection — the removal of large parts of the liver — suffered such infections, which significantly delayed the healing process.
Important players are located in the liver
The researchers were able to demonstrate in the mouse model that the liver actually plays a special role in this infection process: “We know that special cells of the immune system that reside in the liver are responsible for controlling these spreading bacteria and for the healing process after major surgery,” says Gomez de Agüero. They are a group of lymphocytes called innate lymphoid cells (ILCs), which are important players in the innate immune system.
If bacteria from the intestine enter the liver via the bloodstream, these ILCs are activated and release special messenger substances, such as interleukin 22, a protein that can trigger and regulate immune reactions. In this way, they stimulate liver cells to produce antimicrobial substances. “In this way, innate lymphoid cells residing in the liver control the systemic spread of intestinal bacteria and effectively combat side infections after surgery.

“Boosting immunity thus represents a useful prophylactic and therapeutic alternative strategy to standard antimicrobial therapies to prevent concomitant infections after surgery,” suggests Guido Beldi. At least until it has been clarified which factors are responsible for the intestinal barrier no longer preventing intestinal bacteria from invading the interior of the body after a surgical intervention. The research team now wants to investigate these questions.
The Insel Group
The Insel Group is Switzerland’s leading hospital group for university and integrated medicine. It offers people comprehensive healthcare by means of pioneering quality, research, innovation and education: in all phases of life, around the clock and in the right place. The Insel Group provides over 900,000 outpatient consultations annually and treats around 62,000 inpatients using the latest therapeutic methods. The Insel Group is a training center for a variety of professions and an important institution for the continuing education of young physicians. More than 12,000 employees (including apprentices) work at the Insel Group.
The Institute of Systems Immunology
The Institute of Systems Immunology has its roots in the Max Planck Research Group for Systems Immunology — a joint initiative of the University of Würzburg and the Max Planck Society with the aim of promoting excellent immunological research. It is headed by Professors Wolfgang Kastenmüller, holder of the Chair of Systems Immunology I, and Georg Gasteiger, holder of the Chair of Systems Immunology II.
About 50 scientists from more than 20 countries are now working at the Institute of Systems Immunology. The common goal is to understand the fundamentals of a successful immune response against infectious agents, chronic inflammatory diseases and tumors in order to develop new concepts and strategies for vaccines and immunotherapies.

Type 2 diabetes is a chronic disease in which the body does not produce enough insulin, or does not use it efficiently. It is caused by the combination of a genetic predisposition to obesity, sedentarism and an unhealthy diet, and it affects millions of people around the world. Now, researchers of the University of Barcelona (UB), the Institute for Research in Biomedicine (IRB) and the Diabetes and Associated Metabolic Diseases Networking Biomedical Centre (CIBERDEM), have identified a molecular mechanism involved in the development of this disease.
The study, published in the journal Redox Biology, has described — in patients and animal model samples of type 2 diabetes — a decrease in mitochondrial proteins that synthesize complex subunits of the respiratory chain. This decrease in proteins is associated with an increase in intracellular nitric oxide which, according to the researchers, could be a method for diagnosing the disease.
Mitochondria are the organelles that produce cell energy, and there is evidence relating dysfunctions in its functioning with insulin resistance, typical of type 2 diabetes. The aim of the study was to determine whether there were alterations in the complex subunits of the mitochondrial respiratory chain that could be associated with this mitochondrial dysfunction. Then, the researchers wanted to explore whether nitric oxide — a present molecule in mitochondria that acts as a cell messenger in several physiological and pathological processes — is involved in these alterations.
To do so, the researchers analyzed muscular samples of obese patients with type 2 diabetes (it usually appears around the age of 55), obese patients with early diabetes (around the age of 25), and samples of model animals with diabetes. “In this study, conducted in collaboration with clinical doctors from Dublin City University and the Trinity College Dublin’s St James’s Hospital (Ireland) and researchers from IRB Barcelona, we found that mtRNA synthetases (proteins that synthetize the mitochondrial complexes) play a relevant role in the defects observed in mitochondrial respiration, since its decrease involves the decrease in synthesis of specific subunits of the respiratory chain complexes and, therefore, a mitochondrial dysfunction associated with a larger production of reactive oxygen species (ROS), and specifically, nitric oxide,” notes Maribel Hernández-Alvarez, researcher at the Faculty of Biology of the UB, the Institute of Biomedicine of the UB (IBUB) and CIBERDEM, who led the study together with Antonio Zorzano (UB-IRB-CIBERDEM).
These results open the door to more research into the effects of nitric oxide-producing enzymes and how they affect the abundance of mtRNA synthetases and their relationship to mitochondrial protein synthesis.

Researchers have used pluripotent stem cells to make thymus organoids that support the development of patient-specific T-cells, researchers report March 23rd in the journal Stem Cell Reports. The proof-of-concept work provides the basis for studying human thymus function, T-cell development, and transplant immunity.
“We have established the framework for further basic science and translational research interrogating human thymus development and function in vitro, and in a patient-specific manner,” says senior author Holger Russ, of the University of Florida. “We anticipate our work provides important conceptual and technical advances for the field.”
The thymus is required for the development of a functional immune system, facilitating the generation of self-tolerant T cells that can respond to foreign substances. But the aging process results in a decrease in thymus function and T cell output, leading to increased autoimmunity and disease risk.
In the new study, Russ and his collaborators generated functional, patient-specific, stem cell-derived thymic organoids, which supported the development of thymic epithelial cells and T cells derived from human pluripotent stem cells (hPSCs). The organoids consisted of thymic epithelial progenitors, hematopoietic progenitor cells, and mesenchymal cells, differentiated from the same hPSC line. Russ says the generation of functional hPSC-derived hymic epithelial cells in the lab had never before been achieved.
The generation of a functional human thymus from human pluripotent stem cells is an attractive regenerative strategy. “An experimental model system to interrogate the mechanisms of thymic insufficiency and function is necessary and could serve to further the development of cell-based treatments for thymic defects,” Russ says.

Research from Johns Hopkins Kimmel Cancer Center experts revealed a type of RNA, previously considered to be “junk,” that may help doctors distinguish and treat a subgroup of patients with medulloblastoma.
Medulloblastoma is the most common malignant brain tumor in children, accounting for about 20% of all pediatric brain cancers. Four groups of medulloblastomas have been identified, and one is named sonic hedgehog (SHH) because of the spiky, hedgehog-like appearance of fruit flies missing the gene.
“We have identified a new molecule that is specific for the sonic hedgehog group of medulloblastomas. We believe that this molecule is important for early detection, and we would like to use this molecule marker as a therapeutic target,” says senior study author Ranjan Perera, Ph.D., director of the Center for RNA Biology and senior scientist at the Cancer & Blood Disorders Institute at Johns Hopkins All Children’s Hospital.
The findings are reported in the journal Acta Neuropathologica Communications.
The ability to better distinguish between subtypes of medulloblastomas has important implications for developing treatments and improving survival.
SHH medulloblastoma is the most common form in patients younger than 3 years old and accounts for around 30% of all medulloblastomas.

“This research identifies a new and novel target to teat medulloblastoma, a much-needed advance for this aggressive pediatric cancer,” says Chetan Bettegowda, M.D., Ph.D., Jennison and Novak Families Professor of Neurosurgery.
RNA plays a part in how genes work and what they do. Noncoding RNA, which doesn’t produce proteins, was called “junk RNA” for many years. Scientists are now unraveling what role noncoding RNA plays in the body.
Circular RNA (circRNA) is a type of noncoding RNA that is thought to play a role in the development of different types of cancers, making them good targets for cancer drug development. In addition, circRNAs are abundant in the brains of mammals, which makes them potential biomarkers of medulloblastoma and its subtypes.
The researchers started by merging a group of publicly available genetic data for 175 samples of medulloblastoma tissue from each of the four classification groups. These included group 3, the most aggressive; group 4, the most common; and Wnt and SHH, named for the genetic signaling pathways thought to play prominent roles in the development and progression of the cancer.
“We were trying to identify the most significantly expressed circRNAs in these four groups. We identified a couple of circRNAs that are highly enriched in sonic hedgehog and decided to go after these,” says Perera, who is also an associate professor of oncology and neurosurgery at the Johns Hopkins University School of Medicine.

From this group, they found that only circ_63706 showed much higher expression in the SHH subgroup compared with the other three groups, so the researchers selected circ_63706 for additional investigation.
Next, they transplanted the brains of mice with medulloblastoma cells that were programmed not to carry out the instructions of circ_63706 and control cells to see how it impacted tumor growth. Mice without functioning circ_63706 had significantly smaller tumors than those transplanted with control cells.
Mice without functioning circ_63706 tumor cells were found to have reduced cell proliferation and significantly prolonged survival compared with the control group, demonstrating that circ_63706 regulates tumor growth and may function as a type of gene that has the potential to cause cancer.
Exploring the mechanisms circ_63706 uses to promote cancer cell growth, Perera and colleagues uncovered a link to lipid metabolism (fat burning), which is already known to be a key factor in tumor cell proliferation and growth. They found when circ_63706 is turned off, fat metabolism increases, and this action, known as lipid oxidation, is toxic to cancer, ultimately leading to cell death.
The researchers say these findings point to a potential for a targeted therapy, using a drug or drugs to block circ_63706 and cause tumor cells to die.
“We are showing in our preliminary study that when you implant circ_63706 knockout cells into mice you get reduced tumor growth,” says Perera. “This supports it as a therapeutic target.”
Next, this group will be studying the mechanistic role of this molecule, including but not limited to, in interacting protein partners to develop potential therapeutics.
“Although tremendous improvements have occurred in therapies and supportive care, there is more work to be done on the subclassifications and how these subgroups can be managed uniquely by improved molecular diagnostics and targeted therapies,” says Stacie Stapleton, M.D., director of pediatric neuro-oncology and member of the Cancer & Blood Disorders Institute at Johns Hopkins All Children’s Hospital. “The discovery of this circular RNA in SHH medulloblastoma is promising to help with diagnostics and therapeutics to help the children we see in clinic.”
Other researchers include Keisuke Katsushima, Rudramani Pokhrel, Iqbal Mahmud, Menglang Yuan, Prabin Baral, Rui Zhou, Prem Chapagain, Timothy Garrett, George Jallo, Rabi Murad, Eric Raab, Robert J. Wechsler-Reya and Charles Eberhart.
The research was supported by Schamroth Project, Ian’s Friends Foundation, the Hough Foundation, the Johns Hopkins Kimmel Cancer Center Support Grant CA006973, and National Cancer Institute grant 5P30CA030199.

Why do some people with a genetic mutation associated with leukemia remain healthy, while others with the same mutation develop the blood cancer? In a new study published in Blood, scientists from the USC Stem Cell laboratory of Rong Lu discovered a mechanism that linked a leukemic mutation to varying potentials for disease development — a discovery which could eventually lead to a way to identify patients with the mutation who are most at risk.
To explore this paradox, first author Charles Bramlett and his colleagues labeled and tracked individual blood stem cells in mice with a mutation in a gene called TET2, which is prevalent in patients with myeloid leukemia. The scientists found that a subset of blood stem cells and their progeny — known as clones — made an outsized contribution to the overall population of blood and immune cells. The over-contributing clones tended to produce a lot of “myeloid” cells including immune cells called granulocytes, which may potentially lead to myeloid leukemia.
There were also notable differences in the gene activity of the over-contributing clones, compared to the rest of the clones. The over-contributing clones showed reduced activity in several genes known to suppress the development of leukemia and other cancers. They also showed reduced activity in genes that are involved in “RNA splicing,” the process of removing non-coding sequences from the RNA that carries messages from the DNA to the cell’s protein-making machinery.
One of these RNA splicing genes, Rbm25, showed a particularly dramatic reduction in its activity in the over-contributing clones. To explore the effect of Rbm25, the scientists used CRISPR/Cas9 gene editing to manipulate the activity of Rbm25 in cells with TET2 mutations. They found that increasing Rbm25 activity slowed the cells’ proliferation. In contrast, reducing Rbm25 activity made the cells multiply more quickly, and also caused changes in RNA splicing of the gene Bcl2l1, which regulates programmed cell death, also known as apoptosis. The natural process of apoptosis is critical for ridding the body of aberrant cells, such as pre-cancerous cells that multiply too aggressively and accumulate dangerous mutations that can lead to disease.
In accordance with these new discoveries in mice, Rbm25 activity is also negatively correlated with white blood cell counts that mark poor survival in human patients with myeloid leukemia.
“Our study suggests that a leukemia-associated genetic mutation could trigger different amounts of myeloid cell production, which may be modulated by other risk factors such as RNA splicing regulators,” said Lu, an associate professor of stem cell biology and regenerative medicine, biomedical engineering, medicine, and gerontology at USC, and a Leukemia & Lymphoma Society Scholar. “These findings could be used to better stratify which patients are at the highest risk, and also present intriguing possibilities for developing future therapies that target aberrant RNA splicing in preleukemia phases.”
Additional co-authors include Jiya Eerdeng, Du Jiang, Yeachan Lee, Ivon Garcia, Mary Vergel-Rodriguez, Patrick Condie, and Anna Nogalska from the Lu Lab.
Around 90 percent of this project was supported by federal funding from the National Heart, Lung, and Blood Institute (grants R35HL150826, R01HL138225, R01HL135292, K99/R00HL113104, 1F31HL149278-01A1) and the National Cancer Institute (grant P30CA014089). Additional support came from the California Institute for Regenerative Medicine (grants EDUC4-12756 and EDUC2-12607), the Leukemia & Lymphoma Society (grant LLS-1370-20), and a Richard N. Merkin Assistant Professorship.

A study co-authored by Southwest Research Institute Senior Research Scientist Dr. Jason Hofgartner explains the unusual radar signatures of icy satellites orbiting Jupiter and Saturn. Their radar signatures, which differ significantly from those of rocky worlds and most ice on Earth, have long been a vexing question for the scientific community.
“Six different models have been published in an attempt to explain the radar signatures of the icy moons that orbit Jupiter and Saturn,” said Hofgartner, first author of the study, which was published this month in Nature Astronomy. “The way these objects scatter radar is drastically different than that of the rocky worlds, such as Mars and Earth, as well as smaller bodies such as asteroids and comets.”
The objects are also extremely bright, even in areas where they should be darker.
“When we look up at Earth’s moon it looks like a circular disk, even though we know it’s a sphere. Planets and other moons similarly look like disks through telescopes,” Hofgartner said. “While making radar observations, the center of the disk is very bright and the edges much darker. The change from center to edge is very different for these icy satellites than for rocky worlds.”
In collaboration with Dr. Kevin Hand of NASA’s Jet Propulsion Laboratory, Hofgartner argues that the extraordinary radar properties of these satellites, such as their reflectiveness and polarization (the orientation of light waves as they propagate through space) is very likely to be explained by the coherent backscatter opposition effect (CBOE).
“When you’re at opposition, the Sun is positioned directly behind you on the line between you and an object, the surface appears much brighter than it would otherwise,” Hofgartner said. “This is known as the opposition effect. In the case of radar, a transmitter stands in for the Sun and a receiver for your eyes.”
An icy surface, Hofgartner explained, has an even stronger opposition effect than normal. For every scattering path of light bouncing through the ice, at opposition there is a path in the exact opposite direction. Because the two paths have precisely the same length, they combine coherently, resulting in further brightening.
In the 1990s, studies were published stating that the CBOE was one explanation for the anomalous radar signatures of icy satellites, but other explanations could explain the data equally well. Hofgartner and Hand improved the polarization description of the CBOE model and also showed that their modified CBOE model is the only published model that can explain all of the icy satellite radar properties.
“I think that tells us that the surfaces of these objects and their subsurfaces down to many meters are very tortured,” Hofgartner said. “They’re not very uniform. Icy rocks dominate the landscape, perhaps looking somewhat like the chaotic mess after a landslide. That would explain why the light is bouncing in so many different directions, giving us these unusual polarization signatures.”
The radar observations Hofgartner and Hand used were from the Arecibo Observatory, which was one of only two telescopes making radar observations of icy satellites until it was severely damaged by the collapse of its support structure, antenna and dome assembly and subsequently decommissioned. The researchers hope to make follow-up observations when possible and plan to study additional archival data that may shed even more light on icy satellites and the CBOE, as well as radar studies of ice at the poles of Mercury, the Moon, and Mars.