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After a year of virtual gathering, getting back to real-life relationships can be intimidating. These eight simple exercises can help.As we move through the spring of The Great Vaccination, many of us are feeling cautious optimism, and also its flip side: creeping dread.Maybe you have a sense of ambivalence about how to interact with others again. If you used to work in an office, you might be worried about returning to work — but eager to see people again. Or you find yourself having to confront a neighbor about a longstanding problem — but you’re out of practice with conflict resolution. (I’m not sure I remember how to talk to another human anymore, let alone one I disagree with.)Whatever the specifics, “there will be new forms of social anxiety, said Dacher Keltner, a professor of psychology and the director of the Social Interaction Lab at the University of California, Berkeley.“People are really anxious about being out in restaurants with friends, or about dancing with a big sweaty group of people — or even about sharing a yoga mat,” he said. “It’s always good to remember individual differences — there’s a lot of variability. But there will be a lasting societal legacy around intimacy, the noise that comes with returning to school, the complexity of the playground and of work.”Dr. Keltner has studied human behavior and the biological and evolutionary underpinnings of emotions for decades, with a focus on “pro-social” states — behavior that strengthens connections between individuals — that are especially good for society.“We’re hyper-social mammals — it’s our most signature strength,” said Dr. Keltner, a co-founder of the Greater Good Science Center who was also a scientific consultant on emotions for the Pixar film “Inside Out.” “It’s what sets us apart from other primates: We help, we laugh, we collaborate, we assist.”Lately, we’ve been living our lives siloed away online, missing many of the essential face-to-face experiences that are key to human interaction. It’s notable that Dr. Vivek Murthy, the newly reappointed U.S. Surgeon General, has talked not only about the physical and economic toll of the pandemic, but also of “the social recession.”Before Covid, this kind of post-isolation anxiety was most often suffered by people who re-enter the civilian world after prison, wartime deployment, humanitarian aid work or remote expeditions. The challenge now is that so many more of us will be experiencing some aspect of this all at once, and coming back to social situations with others who likely have their own fears too. It is stalled social development, on a societal level.Debra Kaysen, a clinical psychologist and a professor of psychiatry and behavioral sciences at Stanford University, said that coming back to so-called “civilian life” can be disorienting, surreal and difficult — and not just for combat veterans. Her clinical and research work focuses on anxiety disorders and trauma, and she has worked on developing coping strategies for health care workers dealing with mental health concerns during the pandemic.Now, everyone is trying to navigate conflicting threat levels in a way that used to be specific to those populations, she said. Cues that used to be neutral or positive, like being around other people (I love my friends and family!) are now associated with threat (my friends and family might infect me with Covid!). And we are confronting the challenge of how to turn off that alarm. “What’s a true alarm and what’s a false alarm has gotten more confusing for all of us,” Dr. Kaysen said.So how do we relearn how to be together?Give yourself permission to set small, achievable goals. And accept that other people are going to have different responses than you — the friend or family member who wants to eat inside the restaurant when you don’t, for example, or who is ready to get on a plane and take a vacation.Accept that certain activities may feel tough for awhile. Driving an hour to a meeting. Flying a red-eye to a conference. Attending a family reunion, say, or four pandemic-postponed weddings in one month.All of this can prompt you to ask, of your family or your boss or even yourself: “Is it really worth the time?” and “Now that I know things can be different, do I want to go back to my old life?”Recovering doesn’t mean you go back to the way you were before, Dr. Kaysen said, using kintsugi, the Japanese technique of repairing broken pottery with gold, as an analogy for coming out of hard times with awareness of the change, and stronger than before. “It’s that you create a new normal, one that’s functional and beautiful — and different.”Dr. Keltner agreed that we may need to “re-educate ourselves” — “like, how do we hug again?” Your timing might be off for a hug, or a joke or even a compliment. “How do you look someone in the eye so that it’s not intrusive? How do you compliment someone? You might not have done it for a year.”Rather than be overwhelmed by everything at once — for example, going to a party where you have to adjust to greeting acquaintances, eating with others and attempting to make small talk — all at the same time — why not take things step by step? This moment can be an opportunity.8 Exercises to Strengthen Your Social MusclesHere are eight small, science-based exercises Dr. Keltner recommends to help ease back into your community. Go at your own pace.Share food with someone.Eating a meal together boosts mood and is a potent antidote for loneliness — aiming for in-person interaction around the ritual of eating is a great goal, even if you don’t meet it every single day. An outdoor picnic or a distanced backyard happy hour is a great and safe option for reconnecting with friends and family.Tell someone a joke in person.You may be out of practice and have to work on your timing. But making eye contact and laughing together is essential to feeling connected to someone else — even if the joke falls flat, being silly together will feel really good.Ask someone what they’re listening to or reading right now.Music and literature can be a community-building gift. Listen to music together; exchange books and have an in-person discussion afterward. This is a social exercise, but also one that will give you a much-needed hit of novelty along with the insight.Reach out to someone you’ve lost touch with.Make a phone call, send a meaningful text, write an email. It’s time to start rebuilding the larger social infrastructure outside our immediate circles.Strike up a conversation with a stranger.Pick someone with whom you have passing contact: a fellow dog-walker, the cashier at a grocery store, a delivery person on your doorstep. Make eye contact; talk to each of them as a person rather than as a function. It’s so easy to ignore the human behind a mask. Make the effort to ask something outside the normal transaction — what’s changed since the last time you saw each other, what they’re looking forward to.Move with someone.Dance, walk, run, swim, bike — or even do the dishes and fold the laundry together. Physical synchronicity is one of the most important ways we have to connect with someone else.Sit quietly with someone …and remember how to comfortably be, without talking, in companionable silence, with someone else. Let the other person know it’s OK to not always fill the air. Nonverbal communication is important to practice — and it’s a way to deepen your relationship.Make a date for the future.Think of something fun to do with someone you love — it could be a summer beach weekend, or maybe a ski trip next winter. Having something to look forward to is essential for well-being. Practice optimism, in anticipation of normalcy. Plan with hope.Bonnie Tsui’s books include “Why We Swim” and “The Uncertain Sea.”

Modern humans are fundamentally different from our closest living relatives, the great apes: We live on the ground, walk on two legs and have much larger brains. The first populations of the genus Homo emerged in Africa about 2.5 million years ago. They already walked upright, but their brains were only about half the size of today’s humans. These earliest Homo populations in Africa had primitive ape-like brains — just like their extinct ancestors, the australopithecines. So when and where did the typical human brain evolve?
CT comparisons of skulls reveal modern brain structures
An international team led by Christoph Zollikofer and Marcia Ponce de León from the Department of Anthropology at the University of Zurich (UZH) has now succeeded in answering these questions. “Our analyses suggest that modern human brain structures emerged only 1.5 to 1.7 million years ago in African Homo populations,” Zollikofer says. The researchers used computed tomography to examine the skulls of Homo fossils that lived in Africa and Asia 1 to 2 million years ago. They then compared the fossil data with reference data from great apes and humans.
Apart from the size, the human brain differs from that of the great apes particularly in the location and organization of individual brain regions. “The features typical to humans are primarily those regions in the frontal lobe that are responsible for planning and executing complex patterns of thought and action, and ultimately also for language,” notes first author Marcia Ponce de León. Since these areas are significantly larger in the human brain, the adjacent brain regions shifted further back.
Typical human brain spread rapidly from Africa to Asia
The first Homo populations outside Africa — in Dmanisi in what is now Georgia — had brains that were just as primitive as their African relatives. It follows, therefore, that the brains of early humans did not become particularly large or particularly modern until around 1.7 million years ago. However, these early humans were quite capable of making numerous tools, adapting to the new environmental conditions of Eurasia, developing animal food sources, and caring for group members in need of help.
During this period, the cultures in Africa became more complex and diverse, as evidenced by the discovery of various types of stone tools. The researchers think that biological and cultural evolution are probably interdependent. “It is likely that the earliest forms of human language also developed during this period,” says anthropologist Ponce de León. Fossils found on Java provide evidence that the new populations were extremely successful: Shortly after their first appearance in Africa, they had already spread to Southeast Asia.
Brain imprints in fossil skulls reveal evolution of humans
Previous theories had little to support them because of the lack of reliable data. “The problem is that the brains of our ancestors were not preserved as fossils. Their brain structures can only be deduced from impressions left by the folds and furrows on the inner surfaces of fossil skulls,” says study leader Zollikofer. Because these imprints vary considerably from individual to individual, until now it was not possible to clearly determine whether a particular Homo fossil had a more ape-like or a more human-like brain. Using computed tomography analyses of a range of fossil skulls, the researchers have now been able to close this gap for the first time.
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The millions of people who have chronic sinusitis deal not only with stuffy noses and headaches, they also commonly struggle to focus, and experience depression and other symptoms that implicate the brain’s involvement in their illness.
New research links sinus inflammation with alterations in brain activity, specifically with the neural networks that modulate cognition, introspection and response to external stimuli.
The paper was published today in JAMA Otolaryngology-Head & Neck Surgery.
“This is the first study that links chronic sinus inflammation with a neurobiological change,” said lead author Dr. Aria Jafari, a surgeon and assistant professor of Otolaryngology-Head & Neck Surgery at the University of Washington School of Medicine.
“We know from previous studies that patients who have sinusitis often decide to seek medical care not because they have a runny nose and sinus pressure, but because the disease is affecting how they interact with the world: They can’t be productive, thinking is difficult, sleep is lousy. It broadly impacts their quality of life. Now we have a prospective mechanism for what we observe clinically.”
Chronic rhinosinusitis affects about 11% of U.S. adults, according to the Centers for Disease Control and Prevention. The condition can necessitate treatment over a span of years, typically involving antibiotics. Repeated cycles of inflammation and repair thicken sinus tissues, much like calloused skin. Surgery may resolve the issue, but symptoms also can recur.

New research has uncovered a surprising role for so-called “jumping” genes that are a source of genetic mutations responsible for a number of human diseases. In the new study from Children’s Medical Center Research Institute at UT Southwestern (CRI), scientists made the unexpected discovery that these DNA sequences, also known as transposons, can protect against certain blood cancers.
These findings, published in Nature Genetics, led scientists to identify a new biomarker that could help predict how patients will respond to cancer therapies and find new therapeutic targets for acute myeloid leukemia (AML), the deadliest type of blood cancer in adults and children.
Transposons are DNA sequences that can move, or jump, from one location in the genome to another when activated. Though many different classes of transposons exist, scientists in the Xu laboratory focused on a type known as long interspersed element-1 (L1) retrotransposons. L1 sequences work by copying and then pasting themselves into different locations in the genome, which often leads to mutations that can cause diseases such as cancer. Nearly half of all cancers contain mutations caused by L1 insertion into other genes, particularly lung, colorectal, and head-and-neck cancers. The incidence of L1 mutations in blood cancers such as AML is extremely low, but the reasons why are poorly understood.
When researchers screened human AML cells to identify genes essential for cancer cell survival, they found MPP8, a known regulator of L1, to be selectively required by AML cells. Curious to understand the underlying basis of this connection, scientists in the Xu lab studied how L1 sequences were regulated in human and mouse leukemia cells. They made two key discoveries. The first was that MPP8 blocked the copying of L1 sequences in the cells that initiate AML. The second was that when the activity of L1 was turned on, it could impair the growth or survival of AML cells.
“Our initial finding was a surprise because it’s been long thought that activated transposons promote cancer development by generating genetic mutations. We found it was the opposite for blood cancers, and that decreased L1 activity was associated with worse clinical outcomes and therapy resistance in patients,” says Jian Xu, Ph.D., associate professor in CRI and senior author of the study.
MPP8 thus suppressed L1 in order to safeguard the cancer cell genome and allow AML-initiating cells to survive and proliferate. Cancer cells, just like healthy cells, need to maintain a stable genome to replicate. Too many mutations, like those created by L1 activity, can impair the replication of cancer cells. Researchers found L1 activation led to genome instability, which in turn activated a DNA damage response that triggered cell death or eliminated the cell’s ability to replicate itself. Xu believes this discovery may provide a mechanistic explanation for the unusual sensitivity of myeloid leukemia cells to DNA damage-inducing therapies that are currently used to treat patients.
“Our discovery that L1 activation can suppress the survival of certain blood cancers opens up the possibility of using it as a prognostic biomarker, and possibly leveraging its activity to target cancer cells without affecting normal cells,” says Xu.
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Researchers at the Francis Crick Institute have found that blocking a specific protein could increase tumour sensitivity to treatment with PARP inhibitors. Their work published in Science , suggests combining treatments could lead to improved therapy for patients with inheritable breast cancers.
Some cancers, including certain breast, ovarian and prostate tumours, are caused by a fault in the BRCA1 or BRCA2 genes, which are important for DNA repair. Treatment for these cancers has greatly improved thanks to the discovery of PARP inhibitors, drugs which capitalise on this weakness in the cancer as they block a back-up repair mechanism. This means the cancer cells cannot repair breaks in their DNA, which stops the tumour from growing.
However, in many cases, the cancer eventually develops resistance to this treatment and the tumour starts to regrow aggressively. Finding new ways to effectively kill cancer cells before this resistance develops, or re-sensitise them to treatment, is crucial to offer patients an improved chance of survival.
In their study, the research team used human cells to screen for proteins that affect their sensitivity to PARP inhibitor drugs. They found that blocking a protein, DNPH1, sensitised BRCA-defective cancer cells to treatment with the PARP inhibitor, leading to cell death in the laboratory.
Importantly, cells that had acquired resistance to the PARP inhibitor were killed when this protein was also blocked. And, as the combination did not affect healthy cells, this discovery suggests that DNPH1 is a promising target for future drug development.
Stephen West, lead author and group leader of the DNA Recombination and Repair Laboratory at the Crick says: “PARP inhibitors were a great breakthrough in the treatment of certain cancers, extending the lives of many people. However, patients have to take these drugs for the rest of their lives which sadly gives most tumours time to mutate and eventually develop resistance.
“We want to improve treatments for these patients by finding a way to strengthen PARP inhibitors so they completely kill the cancer. While more work needs to be done, in the lab and then in clinical trials, we’ve found a really promising potential treatment combination.”
In further experiments, the researchers characterised the role of the DNPH1 protein. It acts as a ‘scavenger’, removing faulty nucleotides from the pool of nucleotides which are used to build DNA. Without this process, this nucleotide ‘junk’ is incorporated into strands of DNA. The incorporation of faulty nucleotides is the key determinant that makes the cells more susceptible to the effects of PARP inhibitors.
Kasper Fugger, lead author and postdoc in the DNA Recombination and Repair Laboratory at the Crick says: “By investigating the function of DNPH1 and finding the molecules it interacts with, we have a good understanding of how the protein works in cells. This knowledge should help us to more effectively kill cancer cells by developing an inhibitor drug, which is specific enough to be used safely in people.”
The researchers are now collaborating with pharmaceutical companies to develop an inhibitor of the DNPH1 protein which, if shown to be safe and effective in clinical trials, could be used alongside PARP inhibitors as a cancer treatment.
The topic of DNA repair in cancer was the focus of a virtual conference, Medicine at the Crick, held in February. The event was part of a series which showcases major advances in biomedical science and brings together lab-based scientists together and clinicians to consider the potential impact on patient treatment.
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Two studies published in the open-access journal PLOS Pathogens provide new evidence supporting an important role for the immune system in shaping the evolution of SARS-CoV-2, the virus that causes COVID-19. These findings — and the novel technology behind them — improve understanding of how new SARS-CoV-2 strains arise, which could help guide treatment and vaccination efforts.
For the first study, Rachel Eguia of Fred Hutchinson Cancer Research Center in Seattle, Washington, and colleagues sought to better understand SARS-CoV-2 by investigating a closely related virus that has circulated widely for a far longer period of time: the common-cold virus 229E.
229E and SARS-CoV-2 are both in the coronavirus family, which features a “spike protein” that enables infection of human cells. A person who is infected with 229E develops an immune response against the spike protein that protects them from reinfection, but only for a few years. Whether reinfection then occurs because the immune response wears off or because 229E evolves to escape it has been unclear.
Eguia and colleagues addressed this question by testing the activity of serum samples collected from patients in the 1980s-90s against spike proteins from both old 229E strains and strains that evolved later on. They found that the old spike proteins were vulnerable to the older sera. However, modern spike proteins were able to evade older sera while remaining vulnerable to sera from modern patients.
This analysis suggests that modern strains of 229E have accumulated spike protein mutations that enable them to evade older sera. These findings raise the possibility that SARS-CoV-2 and other coronaviruses could undergo similar evolution, and that COVID-19 vaccines may require periodic updates to remain effective against new strains.
The authors add, “The human common-cold coronavirus evolves over the span of years to decades to erode neutralization by human polyclonal serum antibodies. This work suggests that human coronaviruses undergo significant antigenic evolution that may contribute to eventual re-infections.”
For the second study, Sung Hee Ko of the National Institute of Allergy and Infectious Diseases in Bethesda, Maryland, and colleagues developed new technology for genetic sequencing of the SARS-CoV-2 spike protein, enabling detection of multiple SARS-CoV-2 strains that may be present at the same time within a single infected patient.
Previous studies have used standard sequencing methods to produce a single genetic sequence from an individual patient, obscuring the potential presence of multiple SARS-CoV-2 strains. By contrast, the new technology highlights virus diversity within each patient and enables tracking of the evolution of new SARS-CoV-2 strains during acute infection.
Indeed, when the researchers applied the new method to human respiratory samples, they found new SARS-CoV-2 variants arising within the same patient over the course of acute infection. The precise mutations in these variants suggest that they arose in response to selective pressure from the immune system.
Future application of the new technology could improve understanding of how the evolution of new SARS-CoV-2 variants within a single patient impacts their outcomes. The findings also suggest that patients might see greater benefits from early treatment with antiviral drugs capable of targeting multiple strains, than from delayed treatment with a single antiviral drug.
The authors add, “We used new technology to show that coronavirus variants with mutated spike proteins can arise early in the course of infection. Our results suggest more virus evolution in each person than previously thought, with potential implications for clinical outcomes and for the emergence of transmissible variant strains.”
Together, these two studies deepen understanding of how new SARS-CoV-2 strains arise in response to immune system activity, potentially paving the way for additional research and improved treatment.
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A rare and controversial mutation in the phospholipase D3 (PLD3) protein — previously linked to Alzheimer’s disease — interferes with PLD3’s vital recycling function inside neurons. Matthew Schrag of Vanderbilt University Medical Center and colleagues report these new findings in a paper published April 8th in PLOS Genetics.
About 1 percent of people with Alzheimer’s disease carry a specific mutation in their PLD3 gene. The question of whether or not this mutation leads to Alzheimer’s disease has remained controversial, however, due to its rarity and because the protein’s function was previously unknown. In the new study, Schrag’s team delved deeper into the function of this gene and its link to the disease. The researchers found that PLD3 is located in lysosomes inside neurons. Lysosomes are highly acidic sacs of enzymes that act as the recycling system of the cell. PLD3 produces an important component of the membrane of these acidic organelles, and this function is lost in the mutant form. In the brains of people with Alzheimer’s disease, PLD3 occurred near buildups of toxic proteins called β-amyloid plaques. Furthermore, people with high levels of PLD3 had fewer β-amyloid plaques and less cognitive decline, suggesting that normal PLD3 helps protect against the disease.
Together, these discoveries establish the PLD3 mutation places a person at higher risk of developing Alzheimer’s disease, most likely by disrupting its role in the lysosome. The researchers propose that future studies should focus on investigating whether boosting PLD3 can have a protective effect that reduces the effects of the disease. Ultimately, these findings may yield new drug targets for Alzheimer’s disease therapies and improve our understanding of the role of the lysosome in this common and burdensome disease.
“The discovery of Phospholipase D3 as a genetic risk factor for Alzheimer’s disease points to the critically important role of the lysosome in dementia,” the authors add. “Targeting experimental therapies to these lysosomes could lead us to new approaches to treat this disease.”
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Six years ago, Michael Niederweis, Ph.D., described the first toxin ever found for the deadly pathogen Mycobacterium tuberculosis. This toxin, tuberculosis necrotizing toxin, or TNT, became the founding member of a novel class of previously unrecognized toxins present in more than 600 bacterial and fungal species, as determined by protein sequence similarity. The toxin is released as M. tuberculosis bacteria survive and grow inside their human macrophage host, killing the macrophage and allowing the escape and spread of the bacteria.
For 132 years, the lack of an identified toxin in M. tuberculosis had contrasted with nearly all other pathogenic bacteria whose toxins contribute to illness or death. M. tuberculosis infects 9 million people a year and kills more than 1 million.
Now, in another groundbreaking work, the University of Alabama at Birmingham researcher and colleagues describe how two small ESX proteins made by the M. tuberculosis bacteria mediate secretion of TNT by pore formation in the membranes that envelop the bacteria. This finding may have broad application because a distinctive three-amino acid motif found on EsxE and EsxF — tryptophan/any-amino-acid/glycine, known in shorthand as WXG — is also found on many other small mycobacterium proteins and on the large WXG100 superfamily of bacterial proteins that resemble EsxE and EsxF.
“Here, we show for the first time that small Esx proteins of the WXG100 family have an important molecular function inside the Mtb cell by mediating toxin secretion,” said Niederweis, a professor in the UAB Department of Microbiology. “Our results suggest a dynamic mechanism of pore formation by small Esx proteins that might be applicable to other members of the large WXG100 protein family. Thus, our study not only represents a major advancement in our understanding of secretion of TNT and likely of other proteins in M. tuberculosis, but also describes a biological function for Esx-paralogs in M. tuberculosis and their homologs in the large WXG100 protein family in Gram-positive bacteria.”
TNT is one of two domains in the M. tuberculosis outer membrane protein CpnT; activity of the TNT domain of CpnT in the cytosol of the macrophage induces macrophage death by hydrolyzing NAD+. M. tuberculosis has an inner membrane and an outer membrane, and a protein needs to get through each layer to be secreted outside of the bacterium. How CpnT gets to the outer membrane was unknown.
EsxE and EsxF are part of the same gene segment as CpnT, and the UAB researchers hypothesized that the two small proteins might be involved in secretion of the toxin.

Alzheimer’s disease is known for its slow attack on neurons crucial to memory and cognition. But why are these particular neurons in aging brains so susceptible to the disease’s ravages, while others remain resilient?
A new study led by researchers at the Yale School of Medicine has found that susceptible neurons in the prefrontal cortex develop a “leak” in calcium storage with advancing age, they report April 8 in the journal Alzheimer’s & Dementia, The Journal of the Alzheimer’s Association. This disruption of calcium storage in turns leads to accumulation of phosphorylated, or modified, tau proteins which cause the neurofibrillary tangles in the brain that are a hallmark of Alzheimer’s.
These changes occur slowly, building over many years, and can be seen within neurons in the brains of very old monkeys, the researchers report.
“Altered calcium signaling with advancing age is linked to early-stage tau pathology in the neurons that subserve higher cognition,” said corresponding author Amy Arnsten, the Albert E. Kent Professor of Neuroscience and professor of psychology and member of the Kavli Institute of Neuroscience at Yale University.
These vulnerable neurons face another problem. As they age, they tend to lose a key regulator of calcium signaling, a protein called calbindin, which protects neurons from calcium overload, and is abundant in the neurons of younger individuals.
“With age, these neurons face a double whammy, with an excessive calcium leak that initiates toxic actions, as well as diminished levels of the protectant, calbindin,” said Arnsten.
Neurons in the prefrontal cortex require relatively high levels of calcium to perform their cognitive operations, but the calcium must be tightly regulated. However, as regulation is lost with increasing age, neurons become susceptible to tau pathology and degeneration. Essentially, neurons “eat” themselves from within.
“Understanding these early pathological changes may provide strategies to slow or prevent disease progression,” Arnsten said.
The study is a collaboration between the labs of Arnsten and Angus Nairn at Yale; Dibyadeep Datta and Shannon N. Leslie are co-first authors of the research.
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Materials provided by Yale University. Original written by Bill Hathaway. Note: Content may be edited for style and length.

When you think of ways to treat opioid use disorder, you might think methadone clinics and Narcotics Anonymous meetings. You probably don’t imagine stretches and strengthening exercises.
But Anne Swisher — professor at the West Virginia University School of Medicine — is working to address opioid misuse in an unconventional way: through physical therapy. She and her colleagues have enhanced physical therapy instruction at WVU to emphasize the profession’s role in preventing and treating opioid use disorder.
“Students have different interests and passions within the profession, and they find their niche,” said Swisher, a researcher and director of scholarship in the Division of Physical Therapy. “No matter what their passion is, there is a way they can make a difference, whether it’s by preventing people from starting down the road of opioids — by minimizing pain medication and doing movement interventions — or whether it’s by helping people in the recovery process become healthier overall.”
Swisher and her team devised a model to show doctor of physical therapy students how key topics in their curriculum — such as women’s health, pediatric care and sports therapy — could all address opioid use disorder in various ways.
Their model — which was published in rehabilitation journal Physical Therapy — is innovative because it goes beyond musculoskeletal issues and addresses how physical therapists can assist people across the lifespan, from neonatal to hospice settings. It also illustrates how physical therapists can help improve human movement across what Swisher calls the “whole addiction spectrum.”
“In our curriculum, our students learn about all of these different aspects — what to do with somebody who’s critically ill, the appropriate developmental milestones for children, how to help older people stay active — but it was really just a matter of connecting it all together,” she said.