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R.S.V. has probably peaked, but flu is still surging and Covid-19 cases are rising. Scientists are hopeful next winter will be better.It has become wearyingly routine: Americans are embarking upon yet another holiday travel season in the midst of a viral onslaught.New, immune evasive versions of the Omicron variant are spreading, and Covid-19 cases, hospitalizations and deaths are once again rising, although the figures remain far below last winter’s peak. But this year the coronavirus has company: Common seasonal viruses, which lay low for the last two winters, have come roaring back.“And as it turns out, they have some makeup work to do,” said Peter Graven, who directs the office of advanced analytics at Oregon Health & Science University.In particular, influenza and R.S.V., or respiratory syncytial virus, hit early and hard this fall, causing major outbreaks that are now overlapping with a resurgent coronavirus. This viral pileup — what some are calling a “tripledemic” — has already set off an exhausting season of sickness, triggering sky-high demand for pain and fever relievers and pushing children’s hospitals to the brink.But each of these three viruses is on a slightly different trajectory. Although there is considerable geographic variation, in most parts of the country R.S.V. has probably already peaked, while flu is now surging, experts said. And Covid is still ramping up, with cases likely to continue rising.That means that more difficult, fever-filled weeks still lie ahead. “A lot of sniffly kids,” said Andrew Lover, an infectious disease epidemiologist at the UMass Amherst School of Public Health and Health Sciences. “There’ll be a lot of respiratory illness floating around from all these different sources.”It is not too late to get a Covid booster or a flu shot, which appears to be well-matched to the influenza strains circulating this year, scientists said. And experts repeated their now-common exhortations to take basic precautions, such as wearing masks in crowded indoor spaces, using rapid Covid tests before visiting vulnerable people and staying home when feeling unwell.“I know people are kind of tired of hearing some of that stuff,” Dr. Graven said. “We’re not saying people need to change your life forever. Right now, for the next some number of weeks, we’re in not a great spot.”Scientists are hopeful that next winter will be better, noting that this brutal season is an unfortunate, and not entirely unexpected, byproduct of several years of pandemic precautions, such as masking and social distancing. These measures shielded many people from routine winter infections and may have spared overburdened health care systems from even bigger surges.But many children and adults also missed out on the opportunity to build or bolster their immune defenses against flu and R.S.V., leaving the viruses with an unusually vulnerable population this fall.“There was a bit of a buildup of susceptibility at the population level,” said Virginia Pitzer, an infectious disease epidemiologist at the Yale School of Public Health. “It’s a worse than normal winter, but one that hopefully will not be repeated next year.”A viral comebackR.S.V. typically peaks in December or January, but this year, cases of R.S.V. began rising steeply in September.Centers for Disease Control and Prevention, via Associated PressThe first virus to surge this fall was R.S.V., which usually causes mild illness but can be severe, or even fatal, in older adults and young children. By the time children in the United States are two years old, almost all have been exposed to the virus.The virus typically peaks in December or January. But this year, cases of R.S.V. began rising steeply in September, and by mid-November, pediatric hospitalization rates had hit the highest level since tracking began in 2018. Hospitalization rates for older adults have surged, too.Flu took off in October, about six weeks ahead of schedule, and has already caused at least 150,000 hospitalizations and 9,300 deaths, according to estimates from the Centers for Disease Control and Prevention. The cumulative hospitalization rate is higher for this time of year than it has been in more than a decade.“We had a huge pool of people, compared to what we normally do, who could be infected by R.S.V. and could be infected by flu because we’ve basically missed two seasons of it,” said Jeffrey Shaman, an infectious disease epidemiologist at Columbia University. As a result, he said, the viruses were “able to go to work early and infect a lot of people. And that’s why we’re seeing these very large, marked outbreaks early on.”There have also been reports that cases of invasive infections of group A Streptococcus bacteria, or strep A, may be on the rise in the United States and Europe. Although these cases remain rare, they may be related to the recent surges in flu and R.S.V., which can leave people more vulnerable to invasive strep, officials have said.However, some encouraging signs have recently emerged, especially regarding R.S.V. Nationally, hospitalization rates and R.S.V. detections have fallen since mid-November, according to C.D.C. data.“I think it’s likely that the R.S.V. season has peaked in most parts of the country,” Dr. Pitzer said. “I think that there is a light at the end of the tunnel.”The trajectory of the flu surge is more difficult to discern, scientists said. Levels of the virus are still very high, and some locations may be seeing their flu peaks now. “It still looks really serious most everywhere,” Dr. Lover said.But there are hints that conditions may be beginning to improve in some areas of the country, including in parts of the South and the Mid-Atlantic States. According to the C.D.C.’s latest influenza report, during the week that ended on Dec. 10, the percentage of laboratory samples testing positive for flu held steady, nationally, and the number of hospital admissions declined, compared with that of the previous week.Several experts expressed hope that this year’s early-starting flu season might also end early, with cases plummeting quickly as the virus finds fewer people to infect. “It burns through all the people who are susceptible to disease or to infection and doesn’t have as much fuel during the traditional season,” said Justin Lessler, an infectious disease epidemiologist at the University of North Carolina at Chapel Hill.Earlier this year, for instance, Australia saw a severe, early flu season, with cases rising precipitously and then “crashing down pretty quickly,” Dr. Shaman noted.Alternatively, flu cases could plateau for a while. In a number of California communities, the amount of influenza present in the wastewater has stopped rising but remains high, said Alexandria Boehm, an environmental engineer at Stanford University and a lead investigator for WastewaterSCAN, a national sewage surveillance initiative. “That suggests that there are still quite a few infections,” she said.Even if the current outbreak abates, another flu bump could occur later in the season, scientists said.“The optimistic view is that we had an early, severe season, and that hopefully what will happen over the next couple of weeks is that all of the numbers will start going down,” said Dr. Helen Chu, an infectious-disease physician and epidemiologist at the University of Washington. “But the pessimistic view is that this is just the beginning, and then we’ll see a couple of later waves.”Covid, againExperts stress that it’s not too late to get a Covid booster or a flu shot, which appears to be well-matched to the influenza strains circulating this year. Rogelio V. Solis/Associated PressCovid-19, on the other hand, appears to be on the upswing. At many of WastewaterSCAN’s sites, coronavirus levels began increasing in early November and surged around Thanksgiving, Dr. Boehm said. Levels are still trending upward at most sites, she said; at some, they are even approaching last winter’s peaks.Officially recorded Covid cases, which remain a significant underestimate, have increased 24 percent over the past two weeks, while hospitalizations are up nine percent. There are more than 400 Covid-related deaths a day, on average, a 41 percent jump from two weeks ago.Those figures are likely to rise further in the coming weeks, experts predicted, fueled by a combination of holiday travel, indoor gatherings, waning immunity and the spread of BQ.1 and BQ.1.1, two new, highly immune-evasive versions of Omicron. (So far, these subvariants do not appear to be causing more severe disease than earlier forms of Omicron did, scientists said.)The precise timing and size of a new Covid wave is difficult to predict, with experts forecasting that cases might peak nationally anytime between the end of December and early February. Most predicted that high levels of pre-existing immunity — from vaccination, infection or both — would likely keep the overall toll lower than during previous winter surges.“We’re going to get a noticeable and meaningful peak in hospitalizations and deaths but nothing that looks like what we saw the past two winters,” Dr. Lessler said.The emergence of new variants remains a wild card. The explosion of cases in China could theoretically increase that risk; the more the virus spreads, the more opportunities it has to mutate and evolve. But new variants can emerge anywhere, and given how widespread the virus already is around the world, China’s current outbreak may not have “an appreciable impact on the rate at which new variants are emerging,” Dr. Lessler said.It remains too early to say whether flu and R.S.V. will return to their typical rhythms next year. But not every winter will be this bad, scientists predicted. “We are sort of making up for the immunity gap that existed during these last two years,” Dr. Chu said. “Things will probably get better.” (An R.S.V. vaccine might be available by next winter, too, she noted.)Still, even before the pandemic, the flu burden varied widely from year to year — a bad season can cause more than 50,000 deaths and overwhelm hospitals — and Covid is likely to remain part of the winter mix.“That’s going to run up the numbers every year, in terms of how many people have severe respiratory disease,” Dr. Lessler said. “I wouldn’t be surprised if just the overall burden from severe respiratory disease is going to be higher in the coming decade than it was in the decade leading up to 2020.”

Ten young children born without functioning immune systems and lacking the ability to fight infections are on track for healthier lives thanks to a new gene therapy treatment pioneered at UC San Francisco, reports a Dec. 22 study in the New England Journal of Medicine.
The children have Artemis-SCID, a very rare genetic disorder that is typically treated with a bone marrow transplant from a healthy donor, ideally a matched brother or sister. The new gene therapy allows researchers to treat newly diagnosed babies with their own cells — adding a healthy copy of the Artemis gene to the baby’s harvested marrow stem cells, then infusing the corrected stem cells back into their bodies — in hopes of avoiding many of the short- and long-term complications of the standard treatment, including death.
The children in the trial — all under the age of 5 — are living at home with their families, attending daycare and preschool, playing outside, and living normal lives, said Mort Cowan, MD, UCSF pediatrics professor and the trial’s lead investigator.
“Already, the course of their illness is so much better than with the typical treatment,” said Cowan, who has treated more than 30 children with Artemis-SCID using standard bone marrow transplants. “I’ve never seen results like this in any of the other kids. It’s amazing.”
Gene correction has been used before in patients with other genetic forms of SCID, but its use in Artemis-SCID is significant because these patients usually respond more poorly to standard bone marrow transplants. Complications can include rejecting the marrow graft, graft-vs.-host disease — in which the donor T cells attack the recipient’s tissues — chronic infections leading to organ damage, stunted growth, and premature death.
Signs of Stronger Immunity
The first outcome of the Phase I/II trial involved the safe transfusion of gene-corrected cells that would differentiate into white blood cells by 42 days after infusion. Researchers theorized patients would need less chemotherapy to prepare their marrow for transfusion when their own cells were being used; thus only 25% of a full dose of busulfan was administered. The second outcome was T-cell reconstitution at 12 months, a measurement of the strength of the immune system.

Researchers at the BC Cancer Research Institute have made an advancement in genetic testing that allows for more accurate prediction of which parent’s genes led to an individual’s increased cancer risk. This improves the efficiency of familial testing strategies and could eliminate concern for patients at high risk of cancer caused by genes inherited from a parent.
The approach was spearheaded by Vahid Akbari and Dr. Steven Jones at Canada’s Michael Smith Genome Sciences Centre (GSC) at BC Cancer, and by Vincent Hanlon and Dr. Peter Lansdorp at the BC Cancer Research Institute’s Terry Fox Laboratory. The new test confirms whether a cancer predisposing gene variant is present in a patient, and can determine whether the variant was inherited from the mother or the father — an understanding that was not possible until now.
“Being able to assign the parent of origin to cancer variants allows us to rapidly identify other family members who may be at risk,” says Dr. Kasmintan Schrader, co-medical director of the Provincial Hereditary Cancer Program at BC Cancer, assistant professor of medical genetics at the University of British Columbia (UBC) and a co-author of the study. “Allowing us to focus on one side of the family will help save lives by concentrating on prevention efforts. This new approach will eliminate the unnecessary psychological burden of needing to test family members on the other side who are not at an increased risk, reduce the need for clinical counselling and focus resources on identifying and supporting those truly at risk.”
Dr. Steven Jones, co-director of the Genome Sciences Centre and professor of medical genetics at UBC adds, “The approach has been enabled by new long-read sequencing technology which can sequence not only DNA but also determine subtle functional alterations to DNA.” Unlike other DNA sequencing approaches, this approach uses thousands of microscopically small pores to determine the sequence of DNA as it travels through them.
“All of our chromosomes have marks that are indicative of whether the chromosome came from our mother or our father,” says Dr. Louis Lefebvre, associate professor of medical genetics at UBC and co-author of the paper. “The challenge is that over the three billion base pairs that represent our genome, only approximately 190 tiny regions contain these parental marks.” Technology developed by Dr. Lansdorp provided the final missing piece, allowing these tiny regions to be linked to entire chromosomes.
For certain patients the promise of this test might be more profound. Those bearing damaging variants of the SDHD or SDHAF2 genes are at very high risk of developing certain cancers over their lifetime, but only if the defective gene is inherited from their father. If it is inherited from the mother, the patient has no increased risk. For those at risk, they face a lifetime of regular screening and testing to identify tumours early. For some individuals with the variant, though, family members are not around to help identify from which parent the variant was inherited. For half of the approximately three hundred patients in Canada in this position and many more around the world, this new test could eliminate a lifetime of unnecessary hospital visits and the psychological burden of increased cancer risk.
Quick Facts: The Hereditary Cancer Program provides genetic counselling and genetic testing for BC/Yukon residents who may have inherited an increased risk for specific types of cancer. Hereditary cancer is not common. Less than 10 per cent of all cancer is hereditary. Self-referrals to the Hereditary Cancer Program are accepted if a relative has shared details about their hereditary cancer gene mutation or if you are concerned about cancer in your family and do not currently have a family doctor or nurse practitioner. As a research institute at UBC and PHSA, the BC Cancer Research Institute (BCCRI) is as a hub for cancer research activity across the province, advancing cancer research discoveries and transformational technologies and treatments.
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In people with active secondary progressive multiple sclerosis (MS), hematopoietic stem cell transplants may delay disability longer than some other MS medications, according to a study published in the December 21, 2022, online issue of Neurology®, the medical journal of the American Academy of Neurology. The study involved autologous hematopoietic stem cell transplants, which use healthy blood stem cells from a person’s own body to replace diseased cells.
While most people with MS are first diagnosed with relapsing-remitting MS, marked by symptom flare-ups followed by periods of remission, many people with relapsing-remitting MS eventually transition to secondary progressive MS, which does not have wide swings in symptoms but instead a slow, steady worsening of the disease.
“Hematopoietic stem cell transplants have been previously found to delay disability in people with relapsing-remitting MS, but less is known about whether such transplants could help delay disability during the more advanced stage of the disease,” said study author Matilde Inglese, MD, PhD, of the University of Genoa in Italy and a member of the American Academy of Neurology. “Our results are encouraging, because while current treatments for secondary progressive MS have modest or small benefits, our study found stem cell transplants may not only delay disability longer than many other MS medications, they may also provide a slight improvement in symptoms.”
The retrospective study included 79 people with active secondary progressive MS who received stem cell transplants and 1,975 people from the Italian MS registry who were treated with MS drugs. All received treatment after being diagnosed with active secondary progressive MS. The two groups were matched for age, sex and level of disability. Drugs included beta-interferons, azathioprine, glatiramer acetate, mitoxantrone, fingolimod, natalizumab, methotrexate, teriflunomide, cyclophosphamide, dimethyl fumarate and alemtuzumab.
Participants’ level of disability was measured on the Expanded Disability Status Scale, a common method to quantify disability with scores ranging from 0, no symptoms, to 10 points, death due to MS. Participants were assessed at various time points over 10 years.
At the beginning of the study, participants had a median score of 6.5 for both those who received transplants and those receiving the medications. Scores of 6.0 are defined as needing to use a cane or brace intermittently or on one side to walk about 100 meters with or without resting. Scores of 6.5 are defined as needing to use a cane or brace constantly on both sides to walk about 20 meters without resting.
Five years into the study, researchers found 62% of the people who had stem cell transplants experienced no worsening of their MS disability compared to 46% of those who took medications.
Also, at five years, researchers found people who received stem cell transplants were more likely to see sustained improvements over time, with 19% experiencing less disability than at the start of the study, compared to just 4% of people taking medications.
Over 10 years, the disability score for people who had stem cell transplants decreased by an average of 0.01 points per year, signifying less disability, while the average score for people taking medications increased by 0.16 points per year, an increase in disability.
“Our study shows that hematopoietic stem cell transplants were associated with a slowing of disability progression and a higher likelihood of disability improvement compared to other therapies,” said Inglese. “While these results are encouraging, they are not applicable to patients with secondary progressive MS who do not have signs of inflammatory disease activity; more research is needed in larger groups of people to confirm our findings.”
A limitation of the study is that it was retrospective and observational, and does not prove cause and effect. It only suggests an association. The study also did not include people taking the MS drugs siponimod, cladribine, ocrelizumab, ofatumumab, or rituximab.
The study was funded by the Italian Multiple Sclerosis Foundation.

While cluster headache is more common in men than in women, a new study suggests that the disorder may be more severe for women. The study is published in the December 21, 2022, online issue of Neurology®, the medical journal of the American Academy of Neurology.
Cluster headaches are short but extremely painful headaches that can occur many days, or even weeks, in a row. The headaches can last anywhere from 15 minutes to three hours.
“Cluster headache is still often misdiagnosed in women, perhaps because some aspects can be similar to migraine,” said study author Andrea C. Belin, PhD, of the Karolinska Institutet in Stockholm, Sweden. “It is important for physicians to be aware of how the disorder manifests differently in men and women so the most effective treatment can be given as fast as possible.”
The study involved 874 people diagnosed with cluster headache, with 66% male and 34% female.
Participants answered a detailed questionnaire about their symptoms, medications, headache triggers and lifestyle habits.
Women were more likely to be diagnosed with chronic cluster headache than men. Chronic cluster headache is defined as recurring cluster headache attacks for one year or more without interruption, or with short intermissions with no symptoms that last less than three months. Eighteen percent of women were diagnosed with chronic cluster headache, compared to 9% of men.
Attacks also lasted longer for women than for men. For example, 8% of women said headache bouts lasted an average of four to seven months, compared to 5% of men, while 26% of women said bouts on average lasted less than one month, compared to 30% of men.
Women were also more likely to report that their attacks occurred at various times throughout the day than men, 74% to 63%. Women were more likely to have a family member with a history of cluster headache, 15% to 7%.
“While the ratio of men to women with cluster headache has been shifting over the years, it is still considered mainly a disorder of men, making it more difficult for women with milder symptoms to be diagnosed with cluster headache than men,” Belin said. “It’s possible this could contribute to the higher rate of chronic cluster headache in women.”
A limitation of the study was that information was reported by the participants, so they may not have remembered everything correctly.
The study was supported by the Swedish Brain Foundation, Mellby Gård Foundation, Swedish Research Council, Region Stockholm and Karolinska Institutet.
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A new study, published in Science Translational Medicine by researchers at the University of Oxford has identified that Talarozole, a drug that is known to increase retinoic acid, was able to prevent osteoarthritis (OA) in disease models.
Tonia Vincent, Professor of Musculoskeletal Biology & Honorary Rheumatologist at Oxford’s Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences (NDORMS), said: ‘Hand osteoarthritis is a common and debilitating medical condition that affects mainly women, especially around the time of the menopause. We currently have no effective treatments that modify their disease.’
The researchers started by investigating a common gene variant that had been linked to severe hand OA. Using patient samples collected at the time of routine hand surgery, as well as a number of experimental models, they were able to identify a key molecule that was especially low in ‘at risk’ individuals, called retinoic acid.
More than 40% of individuals will develop osteoarthritis (OA) during their lifetime. Hand (OA) is an extremely common form of OA and there are currently no disease modifying treatments that effectively relieve symptoms or stop deformity and stiffness of the joints.
Professor Vincent added: ‘This project was only possible because of the multi-disciplinary approach that we took; working with our hand surgical colleagues, geneticists, data scientists and biologists.’
As talarozole has an acceptable safety profile in human subjects, a small proof of concept clinical study is underway to see whether this drug might represent a new disease modifying treatment in patients.
Dr Neha Issar-Brown, Director of Research and Health Intelligence at the charity Versus Arthritis, which funded the research, said: ‘Around 8.5 million people in the UK live with OA. Despite often being dismissed as just a few aches and pains, OA can have a profound and far-reaching impact on life, affecting people’s ability to work, care for a family, or live independently.
‘There is an urgent need for disease-modifying treatments designed to prevent or reverse the painful symptoms of OA. This study reveals a new understanding of the causes of hand osteoarthritis, which could lead to identifying new biological targets for intervention in hand OA.
‘This research is still at an early stage, but with these encouraging findings we are a big step closer in being able to develop a new class of disease-modifying drugs to treat osteoarthritis, prevent chronic pain, and enable people to live well with the condition,’ Dr Issar-Brown concludes.
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In a new study published in the Journal of Cellular and Molecular Medicine, a team at Lawson Health Research Institute have discovered unique patterns of blood plasma proteins in critically ill patients that may help develop a more personalized approach to treating severe COVID-19.
Called the plasma proteome, the proteins being studied are released by cells that often play an important role in the body’s immune response to viruses. The research team studied how they adapt and change to a COVID-19 infection.
As part of the study, blood samples were taken from 30 subjects in three patient groups at London Health Sciences Centre (LHSC). One group had patients with COVID-19, another group had patients with severe infection but were negative for COVID-19, and the third was a healthy control group. Blood samples were drawn on the day of critical care admission and again on days three, seven and ten in hospital.
“We collected plasma from these patients and measured well over a thousand proteins with great accuracy using new technology that combines immunology and genomics,” says Dr. Douglas Fraser, Lawson Scientist, Critical Care Physician at Children’s Hospital at LHSC and Professor at Western University’s Schulich School of Medicine & Dentistry. “With the use of this advanced technology, we were able to better analyze the protein patterns and better understand what is happening with COVID-19, especially in critically ill patients.”
The research team found that COVID-19 patients demonstrated changes in immunosuppression pathways, which typically keeps the immune system balanced. In critically ill patients, the changes were heightened. Analyses of the plasma proteome helped researchers determine which cells in the body are active during the disease state and which signaling pathways were activated.
“In-depth analysis of the human plasma proteome helps us capture tissue proteins that can provide us with information regarding organ integrity during infection,” says Cristiana Iosef, Lawson Research Associate. “This is important because it will allow us to search for new blood biomarkers that are specific for COVID-19 patients.”
This research, which used state-of the-art analysis technology, was enabled by existing expertise and technologies through Children’s Health Research Institute (CHRI), a program of Lawson.
“This study has allowed us to understand the progression of the disease processes in very sick patients, providing us clues on the body’s immune system and other systems that were reacting to the severe disease,” says Dr. Victor Han, Lawson Scientist, Director of CHRI and Professor at Schulich Medicine & Dentistry. “We hope that this knowledge will allow us to identify the patients who will become severely ill and develop new therapies to counteract the changes occurring within their bodies.”
Dr. Fraser, who is also a scientist at CHRI, adds that the team can now examine potential new drug therapies with the hopes of improving outcomes for these patients.
The next steps for the research team will be to use this technology to examine plasma biomarkers in long COVID patients to determine why some develop prolonged disease after a COVID-19 infection.
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The evidence-based health benefits of walking continue to accumulate, according to ongoing research by a University of Massachusetts Amherst physical activity epidemiologist, who leads an international consortium known as the Steps for Health Collaborative.
Findings from the latest study led by Amanda Paluch, assistant professor of kinesiology in the School of Public Health and Health Sciences, show that older adults who walked between 6,000 and 9,000 steps per day had a 40-50% reduced risk of a cardiovascular event, such as a heart attack or stroke, compared to those who walked 2,000 steps per day.
“We found for adults over 60, there was a strikingly lower risk of a cardiovascular event or disease over an average follow-up of six years,” says Paluch, whose team’s research was published this week in the journal Circulation. “When accumulating more steps per day, there was a progressively lower risk.”
Earlier this year, research by Paluch and the Steps for Health Collaborative showed that more movement, even below the highly touted but unscientific “10,000 steps per day,” was associated with longevity benefits. The meta-analysis of 15 studies involving nearly 50,000 people from four continents found that walking between 6,000 and 8,000 steps per day was linked with a lower risk of death from all causes among older adults.
Following those findings, Paluch and team wanted to tackle the less-charted territory of steps per day and cardiovascular disease. The results were similar, in terms of the most beneficial range of steps.
While there appears to be a continual additional benefit for those who walk more than 6,000 steps, Paluch says, encouraging the least-active older adults to take more steps is perhaps the most important public health message.
“The people who are the least active have the most to gain,” she says. “For those who are at 2,000 or 3,000 steps a day, doing a little bit more can mean a lot for their heart health. If you’re at 6,000 steps, getting to 7,000 and then to 8,000 also is beneficial, it’s just a smaller, incremental improvement.”
The meta-analysis of eight studies involved more than 20,000 people from the U.S. and 42 other countries. For younger adults, no link between steps per day and cardiovascular risk was detected.
“This is because cardiovascular disease is a disease of aging and often doesn’t come to fruition until we’re at older ages,” says Paluch, whose project was supported by the Centers for Disease Control and Prevention (CDC). “You’re not going to see many people develop cardiovascular disease after six years of follow-up in young to middle adulthood.”
Future research involving younger adults and steps per day would focus on the precursors of cardiovascular disease, including high blood pressure, obesity and type 2 diabetes. “Those conditions develop in younger adults and are important for early prevention,” Paluch says.
Four of the eight studies the researchers analyzed included data about walking intensity, or how fast the steps were taken. “We’re interpreting these results with caution, but we did not find any striking association with walking intensity,” she says. “There was no additional benefit with how fast you’re walking, beyond the total number of steps that you accumulated.”
Paluch is among the researchers working to build a firm evidence base to guide public health recommendations for simple, accessible physical activity, such as walking.

The reason some people fail to recover their sense of smell after COVID-19 is linked to an ongoing immune assault on olfactory nerve cells and an associated decline in the number of those cells, a team of scientists led by Duke Health report.
The finding, publishing online Dec. 21 in the journal Science Translational Medicine, provides an important insight into a vexing problem that has plagued millions who have not fully recovered their sense of smell after COVID-19.
While focusing on the loss smell, the finding also sheds light on the possible underlying causes of other long COVID-19 symptoms — including generalized fatigue, shortness of breath, and brain fog — that might be triggered by similar biological mechanisms.
“One of the first symptoms that has typically been associated with COVID-19 infection is loss of smell,” said senior author Bradley Goldstein, M.D., Ph.D., associate professor in Duke’s Department of Head and Neck Surgery and Communication Sciences and the Department of Neurobiology.
“Fortunately, many people who have an altered sense of smell during the acute phase of viral infection will recover smell within the next one to two weeks, but some do not,” Goldstein said. “We need to better understand why this subset of people will go on to have persistent smell loss for months to years after being infected with SARS-CoV2.”
In the study, Goldstein and colleagues at Duke, Harvard and the University of California-San Diego analyzed olfactory epithelial samples collected from 24 biopsies, including nine patients suffering from long-term smell loss following COVID-19.

What keeps bones able to remodel themselves and stay healthy? A team from Charité Berlin has discovered clues to the key function of non-collagen protein compounds and how they help bone cells react to external load. The scientists used fish models to examine bone samples with and without bone cells to elucidate differences in microstructures and the incorporation of water. Using 3D neutron tomography at the Berlin research reactor BER II, they succeeded for the first time in precisely measuring the water diffusion across bone material — with a surprising result.
Around 500 million years ago, early vertebrates in the seas became fish, adopting an inner skeleton and a flexible spine based on a nanocmposite of fibers and mineral, known as bone material. This “invention” of evolution was so successful that the basic structure was also adopted for later vertebrates that lived on land. However, while the bones of all terrestrial vertebrates are basically equipped with bone cells (osteocytes), certain fish species continued to evolve and finally managed to create a more energy efficient material: bone lacking bone cells, found today for example in fish such as salmon, medaka or tilapia.
Samples with and without bone cells
“We asked ourselves how bone samples with and without bone cells actually differ in their microstructures and properties,” says Prof. Paul Zaslansky, who heads a research group at Charité Berlin and specializes in mineralized biomaterials including teeth and bones. Together with PhD student Andreia Silvera and international partners, they have now compared bone samples from zebrafish and medaka. Both fish species are of similar size and live in similar conditions, so their skeletons must withstand similar stresses. However, while zebrafish have bone cells, the skeleton of medaka do not.
“The background to the question is that the function of bone cells in bone and how they change with age is of great interest to the aging population,” Silvera explains. Bone cells can respond to physical stress by sending biochemical signals that lead to the formation or resorption of bone tissue, adapting to load. But with age or in diseases such as osteoporosis, this mechanism no longer seems to work. “With our basic research, we want to find out how bones with and without bone cells differ and cope with the challenges of external stress,” Zaslansky says.
Strength and elasticity
Bones have a complex structure: they comprise nanofibers of collagen and nanoparticles of mineral but also other minor ingredients. Certain protein compounds, so called Proteoglycans (PGs), are embedded in a tissue of collagen fibers and nanocrystals and play important roles in tissue formation and maintenance. “PGs may be compared to salt in the soup. Too little or too much of it is not good,” Zaslansky says. The PGs can retain water, and there are plenty of PGs in healthy cartilage, making it as elastic as a sponge. Together, these components form an extracellular matrix (ECM), a 3D structure that provides strength and elasticity, ensuring function for many years. In bones, an open network (Lacunar Channel Network or LCN) of channels and pores with diameters ranging from a few hundred nanometers to micrometers is created in this 3D structure. This LCN hosts the bone osteocytes, cells that sense load and orchestrate bone remodeling. In the LCN and within the nanocomposite, bone contains up to 20% of its volume in water, with many functions including toughening and adaptation to mechanical stress.