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The increases in homicides were particularly stark among Black and Hispanic men, while suicides involving firearms rose among all adults.Homicides and suicides involving guns, which soared in 2020, the first year of the pandemic, continued rising in 2021, reaching the highest rates in three decades, the Centers for Disease Control and Prevention reported on Thursday.Firearms caused 47,286 homicide and suicide deaths in 2021, up from 43,675 in 2020, according to the agency’s research, which is based on provisional data. Rates of gun-related homicide and suicide each rose by 8.3 percent last year.Including unintentional deaths and those related to law enforcement activities, the total number of gun-related deaths in the United States was 48,832 in 2021, according to a separate analysis by the Johns Hopkins Center for Gun Violence Solutions.“Everyone is talking about the rise in homicides, but it is largely driven by guns,” said Ari Davis, a policy adviser at the center.Yet gun suicides also drove an overall rise in suicides. “An 8 percent increase in gun suicides over one year is a really large increase,” Mr. Davis said. “It’s very worrisome.”From 2019 to 2021, homicides involving guns increased by 45 percent, while murders that did not involve firearms increased by only 6 percent, according to a preliminary analysis by the Johns Hopkins center.While gun-related suicides increased by 10 percent over the two-year period, suicides by other means decreased by about 8 percent, according to the analysis.Read More on the Coronavirus PandemicAn ‘Anti-Vax’ Capital No More: Vaccine skeptics once found a home in Marin County Calif. Now, the pandemic has made them unwelcome, as Covid vaccine rates soar there.New Boosters: The updated shots were authorized at the end of August, but nearly half of U.S. adults had heard little or nothing about it by mid- to late September, according to a new report.A Persistent Variant: Ten months have passed since Omicron’s debut. Since then it has displayed a remarkable capacity to evolve new tricks.A Blunted Response: Major data gaps, the result of decades of underinvestment in public health, have undercut the U.S. government’s response to Covid — and now to monkeypox.Although the C.D.C. research does not address the underlying causes, the increase in firearm deaths parallels a spike in gun purchases during the pandemic, including an increase in first-time owners.Americans went on a gun-buying spree in 2020 that continued into 2021, when in a single week the Federal Bureau of Investigation reported a record 1.2 million background checks.Purchasers often turn to handguns for self-protection, but research has shown that having a firearm in the home dramatically raises the risk of gun death, including both homicides and suicides.Other disruptive aspects of the pandemic may also have contributed to increased violence, said Thomas Simon, the lead author of the C.D.C. research.“There have been changes and disruptions in services, in education, increased mental stress and isolation, and economic stressors, all related to Covid,” Dr. Simon said.He added: “We also had concerns in a lot of communities about law enforcement’s use of lethal force, and tension and distrust of law enforcement. So there may have been an impact on the community’s willingness to engage with law enforcement.”Domestic violence may also have increased during the pandemic, Dr. Simon said.Gun deaths rose among both men and women in 2021, though men still made up the majority of gun-related victims and suicides. Young adults ages 25 to 44 were the most likely to be killed with a firearm.And while there were increases in gun homicides among all racial and ethnic groups last year, the rise was primarily concentrated in Black and Hispanic communities. Black people continued to experience the highest gun homicide rates in every age group.The racial disparity is particularly acute among youngsters and young adults ages 10 to 24.The firearm homicide rate among Black youngsters and young adults in 2020 was already 20 times higher than among white young people. In 2021, the gap widened as gun homicides among white youngsters decreased slightly, and the rate of firearm homicides among Black young people is now almost 25 times as high.“This is an example of an unacceptable disparity that has continue to go in the wrong direction,” Dr. Simon said. “It’s possible the stressors associated with the pandemic, which we know hit racial and ethnic communities harder in many areas, could be contributing to these inequities.”Over all, Black and Hispanic Americans were 13.7 and 2.4 times, respectively, as likely to die in a gun homicide as white people in 2021 — the largest such difference in over a decade, according to the Johns Hopkins analysis.Suicides involving firearms increased by only 1 percent during the first year of the pandemic but soared in 2021, increasing from 24,292 in 2020 to 26,320 in 2021, the highest one-year increase reported by the C.D.C. and a record high, according to Mr. Davis.The increase occurred among both men and women, and in most age, racial and ethnic groups.Gun-related suicides have long been more common among older white men, and in 2021 more than 80 percent of all gun suicides were among white Americans. Those age 45 and older had the highest gun suicide rates.But Black and Hispanic Americans accounted for the greatest increases in gun suicide rates overall from 2020 to 2021, and Native American and Alaska Native people had the highest gun-related suicide rate among adults under 45 years of age.Sarah Burd Sharps, senior director of research at Everytown for Gun Safety, called on gun owners to keep firearms locked, unloaded and separate from ammunition and for the implementation of so-called red flag laws that enable the temporary removal of firearms from individuals who are in crisis.“The pandemic continues to cause huge dislocations in everyone’s lives — economic uncertainty, social upheaval, anxiety about our health, loss of routines affecting everyone — and it’s had a particular toll on young people,” Ms. Sharps said.She added, “And there have been years of policy decisions where gun laws are being loosened in some states, and continued underinvestment in Black and Latinx communities.”

Three babies have been born after receiving the world’s first spina bifida treatment combining surgery with stem cells. This was made possible by a landmark clinical trial at UC Davis Health.
The one-of-a-kind treatment, delivered while a fetus is still developing in the mother’s womb, could improve outcomes for children with this birth defect.
Launched in the spring of 2021, the clinical trial is known formally as the “CuRe Trial: Cellular Therapy for In Utero Repair of Myelomeningocele.” Thirty-five patients will be treated in total.
The three babies from the trial that have been born so far will be monitored by the research team until 30 months of age to fully assess the procedure’s safety and effectiveness.
The first phase of the trial is funded by a $9 million state grant from the state’s stem cell agency, the California Institute for Regenerative Medicine (CIRM).
“This clinical trial could enhance the quality of life for so many patients to come,” said Emily, the first clinical trial participant who traveled from Austin, Tex. to participate. Her daughter Robbie was born last October. “We didn’t know about spina bifida until the diagnosis. We are so thankful that we got to be a part of this. We are giving our daughter the very best chance at a bright future.”
Spina bifida, also known as myelomeningocele, occurs when spinal tissue fails to fuse properly during the early stages of pregnancy. The birth defect can lead to a range of lifelong cognitive, mobility, urinary and bowel disabilities. It affects 1,500 to 2,000 children in the U.S. every year. It is often diagnosed through ultrasound.

Scientists at the UNC School of Medicine have made a significant advance in the promising field of cellular reprogramming and organ regeneration, and the discovery could play a major role in future medicines to heal damaged hearts.
In a study published in the journal Cell Stem Cell, scientists at the University of North Carolina at Chapel Hill discovered a more streamlined and efficient method for reprogramming scar tissue cells (fibroblasts) to become healthy heart muscle cells (cardiomyocytes). Fibroblasts produce the fibrous, stiff tissue that contributes to heart failure after a heart attack or because of heart disease. Turning fibroblasts into cardiomyocytes is being investigated as a potential future strategy for treating or even someday curing this common and deadly condition.
Surprisingly, the key to the new cardiomyocyte-making technique turned out to be a gene activity-controlling protein called Ascl1, which is known to be a crucial protein involved in turning fibroblasts into neurons. Researchers had thought Ascl1 was neuron-specific.
“It’s an outside-the-box finding, and we expect it to be useful in developing future cardiac therapies and potentially other kinds of therapeutic cellular reprogramming,” said study senior author Li Qian, PhD, associate professor in the UNC Department of Pathology and Lab Medicine and associate director of the McAllister Heart Institute at UNC School of Medicine.
Scientists over the last 15 years have developed various techniques to reprogram adult cells to become stem cells, then to induce those stem cells to become adult cells of some other type. More recently, scientists have been finding ways to do this reprogramming more directly — straight from one mature cell type to another. The hope has been that when these methods are made maximally safe, effective, and efficient, doctors will be able to use a simple injection into patients to reprogram harm-causing cells into beneficial ones.
“Reprogramming fibroblasts has long been one of the important goals in the field,” Qian said. “Fibroblast over-activity underlies many major diseases and conditions including heart failure, chronic obstructive pulmonary disease, liver disease, kidney disease, and the scar-like brain damage that occurs after strokes.”
In the new study, Qian’s team, including co-first-authors Haofei Wang, PhD, a postdoctoral researcher, and MD/PhD student Benjamin Keepers, used three existing techniques to reprogram mouse fibroblasts into cardiomyocytes, liver cells, and neurons. Their aim was to catalogue and compare the changes in cells’ gene activity patterns and gene-activity regulation factors during these three distinct reprogrammings.

Cancer is in Switzerland the second leading cause of death. Among the different types of cancers, non-small cell lung cancer (NSCLC) kills the most patients and remains largely incurable. Unfortunately, even newly approved therapies can extend the life of patients only by a few months and only few survive the metastatic stadium long-term. Thus, new treatments which attack the cancer in novel ways are sought. In a recently published study in the Journal Cell Genomics, researchers of the University of Bern and the Insel Hospital determined new targets for drug development for this cancer type.
The Dark Matter of the genome
For new targets, they looked at the poorly-understood class of genes called “long noncoding RNAs (Ribonucleic acids)” (lncRNAs). LncRNAs exist in abundance in the so-called “Dark Matter” or non-protein-coding DNA that constitutes the vast majority of our genome. The human genome contains around 20,000 “classical” protein-coding genes, but this number is dwarfed by 100,000 lncRNAs. Of 99% of lncRNAs the biological functions are unknown.
As the name long noncoding RNAs implies, unlike messenger RNAs (mRNAs), they do not encode the construction plans for proteins. Like for mRNAs, the building instructions for lncRNAs are contained in the cell’s DNA.
New tool determines potential targets
To study the role of lncRNAs in NSCLC, the researchers started by analyzing publicly available datasets to see which lncRNAs are present in NSCLC. This analysis led to a list of over 800 lnRNAs, whose importance for NSCLC cells the researchers wished to investigate. For this investigation, they developed a screening system which prevents the production of the selected lncRNAs by deleting part of their construction instructions in the DNA.

A team of researchers working with the CHILD Cohort Study (CHILD) has developed a simple new symptom-based screening tool that detects asthma risk in children as young as two years of age.
The efficacy of the tool — the CHILDhood Asthma Risk Tool, or CHART — is detailed in a study published in the highly influential Journal of the American Medical Association (JAMA).
“Asthma affects nearly 330 million people worldwide, carries a heavy healthcare cost, and is the leading cause of hospitalization among kids in Canada — especially kids under five,” comments co-senior author Dr. Padmaja Subbarao, who is a respirologist and CRC Tier 1 Chair in Pediatric Asthma and Lung health at The Hospital for Sick Children (SickKids) and the Director of CHILD. She also a Professor in the Department of Pediatrics at the University of Toronto and an Adjunct Professor in Respirology and Medicine at McMaster University.
“Earlier detection of this condition will allow doctors to treat kids sooner, so they will suffer less and avoid going to the hospital, thus also lowering costs to the healthcare system.”
“One reason asthma often goes undetected in young children is because most conventional asthma tests are difficult to perform in children, time consuming and invasive, involving skin pricks and blood-taking, so many patients and doctors choose to avoid them,” notes the study’s co-first author, Myrtha E Reyna-Vargas, who is an M.Sc. and a biostatistician at SickKids. “Other conventional tests can also require appointments with specialists and the use of specialized equipment to test lung function, with associated costs.”
CHART categorizes children’s risk of future asthma and persistent symptoms as ‘High,’ ‘Moderate’ or ‘Low,’ based on information reported before age three. The tool recommends follow-up actions for each group.

Systemic sclerosis — or scleroderma that affects the skin and internal organs -, is one of the rarest autoimmune diseases, affecting roughly 100,000 people (primarily women) in the United States.,However, systemic sclerosis is devastating — it has the highest mortality rate among rheumatic diseases, according to Dinesh Khanna M.B.B.S., M.Sc., director of the Michigan Medicine Scleroderma Program.
And with no licensed treatments available for this subset of scleroderma patients, rheumatology researchers are constantly searching for opportunities to use resources and technology that have proven beneficial in treating other autoimmune and rheumatic diseases.
One resource that clinicians at Michigan Medicine and the University of Pittsburgh recently explored in early-stage systemic sclerosis was an FDA-approved rheumatoid arthritis drug, tofacitinib. Their goals for the study included finding out if the drug was safe in patients and to understand how the drug would mechanically work at the cellular level in the disease.
“We wanted to understand first, if there was any clinical benefit of tofacitinib to patients, but we were also asking, what are the differences in the cells of healthy skin versus systemic sclerosis cells…how does the drug work?” said Khanna.
In their new study published in JCI Insight, researchers found that tofacitinib was well tolerated among patients with early systemic sclerosis, and discovered the drug primarily affected the protein, interferon, both in fibroblasts and keratinocytes cells.
The study sample size consisted of 15 patients with early diffuse cutaneous systemic sclerosis — patients with skin hardening and issues with organs. Of the total participants, 10 patients received 5 milligrams of tofacitinib twice a day, and the remaining received placebo in a double-blind randomized placebo-controlled trial.

Loss of myelin — a protective insulating layer around neurons — is a key contributor to many neurological diseases including multiple sclerosis, traumatic brain and spinal cord injuries, stroke, and dementia; however, there are currently no imaging tests to accurately identify such demyelination and distinguish it from other pathological processes that occur in these conditions.
Investigators at Massachusetts General Hospital (MGH) have now developed such a test: a radioactive demyelination tracer that can be detected by positron emission tomography (PET) scans. They evaluated its use in humans in a study published in the European Journal of Nuclear Medicine and Molecular Imaging.
“Having an imaging tool that it is specific to demyelination can help to better understand the contribution of demyelination to different diseases and better monitor a disease or the response to therapy — for example, a remyelinating therapy,” says co-lead author Pedro Brugarolas, PhD, an investigator at the Gordon Center for Imaging at MGH and an assistant professor of radiology at Harvard Medical School.
In healthy volunteers, Brugarolas and his colleagues investigated the safety of their new PET tracer — called [18F]3F4AP — and looked to see what happens to it after it’s injected intravenously into the body. This was the first time the tracer was given to humans, following studies that were conducted in monkeys.
The tracer distributed widely throughout the body, including into the brain, the organ of interest. In addition, the team calculated the volunteers’ radiation exposure from the tracer and they performed basic safety assessments. “As expected for PET tracers, the radiation dose was within normal limits and we didn’t see signs that could indicate that the tracer wasn’t safe,” says co-lead author Moses Wilks, PhD, an assistant in physics at MGH and an instructor at Harvard Medical School. One unexpected finding was that the tracer cleared from circulation faster than expected, which they plan to investigate further.
The scientists hope that their findings will help advance research related to diseases involving demyelination.
“Giving a new tracer to humans is a big deal as it requires being able to make the tracer in a sterile environment, demonstrating to the U.S. Food and Drug Administration that the trace meets a very strict quality control and getting permission from the agency to administer it to humans,” says senior author Georges El Fakhri, PhD, director of the Gordon Center for Medical Imaging at MGH and a professor of radiology at Harvard Medical School. “Once a tracer has been in humans for the first time and it has been shown to be safe — which is what this study shows — it is easier for other researchers to use it.”
Additional co-authors include Jacqueline Noel, Julia-Ann Kaiser, Danielle R. Vesper, Karla M. Ramos-Torres, Nicolas J. Guehl, Marina T. Macdonald-Soccorso, Yang Sun, Peter A. Rice, Daniel L. Yokell, Ruth Lim, and Marc D. Normandin.
This work was supported by the National Institutes of Health.
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A research team led by a University of Massachusetts Amherst scientist has made a significant genetic discovery that sheds light on the use of the drug caspofungin to treat a deadly fungal infection, Aspergillus fumigatus, which kills some 100,000 severely immunocompromised people each year.
Typically, healthy people inhale about 50 to 100 spores of A. fumigatus every day when outdoors. “Our body does a great job of identifying them and destroying them,” says UMass Amherst associate professor of food science John Gibbons, whose microbial genomics lab studies the fungus.
But in people with compromised immune systems from cancer treatment, organ transplants, HIV, COVID-19 and other conditions, A. fumigatus can cause “a really nasty infection, invasive pulmonary aspergillosis, with a 50% mortality rate,” Gibbons says. “And there’s a limited way to treat these infections.”
To complicate matters, when given in high concentrations as a treatment for an A. fumigatus infection, the anti-fungal drug sometimes creates a “caspofungin paradoxical effect” [CPE], which increases the fungal growth rather than eradicating it.
In research published in the journal Microbiology Spectrum, senior author Gibbons, Shu Zhao, a former graduate student in the Gibbons lab, and colleagues describe a first important step in the effort to understand when and why treatment with caspofungin could be more harmful than beneficial. The team, including scientists from Vanderbilt University, the University of Tennessee Science Health Center and the University of São Paolo in Brazil, completed the first genomic and molecular identification of two genes that contribute to the paradoxical effect in A. fumigatus.
“This is one of the first studies to apply genome-wide association (GWA) analysis to identify genes involved in an Aspergillus fumigatus phenotype,” the paper states.
The team sequenced the genome of 67 clinical samples, about half of which had CPE, spotting genetic differences between the groups and then using GWA, a statistical method, to determine how these genetic variants are associated with growth patterns at high concentrations of caspofungin. “We identified a few candidate genes that we thought might contribute to this paradoxical effect,” Gibbons says.
The scientists then used the genetic engineering technology, CRISPR, to delete those candidate genes from the genome, creating gene-deletion mutants and enabling the researchers to determine that two of the genes were involved in the paradoxical effect.
“It looks like there are many genes and many genetic variants that contribute to this phenotype,” Gibbons says. “We aren’t done yet. One idea is that we could potentially generate new drug targets if we find the full collection of genes. We don’t understand the mechanisms yet.”
Ultimately the team hopes they can use DNA sequencing to understand the genetic basis of different phenotypes in general and to predict for clinical benefits if a patient sample of A. fumigatus has a genotype that is associated with the paradoxical effect.
“That would be an important tool that could really improve treatment,” Gibbons says.
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In a rare disease called mucolipidosis type II, people’s hearts and abdomens swell, and their bones grow malformed.
A lysosomal storage disorder, mucolipidosis type II causes edema of the internal organs and skeletal dysplasia. Children diagnosed with the genetic disease often die before they reach age 7. Now, University of Michigan researchers have identified a new gene implicated in the disease, TMEM251, which is necessary for lysosomes to function correctly.
Lysosomes are organelles within all cells of the body — except red blood cells — responsible for taking in and recycling the garbage your cells produce. When the lysosome can’t function properly, it fails to recycle this garbage and instead simply stockpiles them in the organelle.
The team, led by Ming Li, assistant professor of molecular, cellular and developmental biology, discovered that if TMEM251 is defective, it fails to encode the pathway for the enzymes necessary for the correct function of lysosomes to travel inside the lysosome. The study is published in Nature Communications.
There are about 50 to 60 enzymes inside the lysosomes that digest worn-out cellular parts as well as waste from outside the cell. The lysosome also recycles this waste — proteins, nucleic acid, carbohydrates and lipids — back into usable material. But for these enzymes to travel inside the lysosome, they need a signal called the mannose-6-phosphate biosynthetic pathway, or M6P.
“It’s like a postage stamp. The enzymes have to have this signal in order to go inside the lysosome. If they don’t have M6P, they aren’t able to go into the lysosome,” Li said. “So consequently, you still have lysosomes, but not a single one of them would be functional because they lack these enzymes.”
Li’s lab studies the lysosome, and in particular, the composition of lysosome membrane proteins. The lysosome has the ability to regulate its own membrane protein by triggering the degradation of these proteins through a process called ubiquitination. This process allows proteins to travel from the membrane of the lysosome inside the organelle for degradation. The researchers also wanted to understand which genes were responsible for lysosome function and what happens when those genes are defective.