Publisher Health

Pregnant and breastfeeding women respond to the first dose of the coronavirus vaccines more slowly than other women, and mount a less potent defense against the virus, according to a new study. After the second dose, however, their response looks almost normal. The results, published this month in the journal Science Translational Medicine, suggest that pregnant and breastfeeding women remain susceptible to the virus for longer after vaccination. The study underscores the importance of giving these women the second dose in time, and monitoring them closely in the meantime for signs of infection.During pregnancy, the immune system is modified to tolerate the fetus — effectively a foreign entity — leaving pregnant women particularly susceptible to pathogens like the coronavirus. Because of this, pregnant women are more likely to become severely ill and to die from Covid than other women of the same age.Earlier research had suggested that pregnancy might also dampen the response to vaccines. But the initial trials of Covid vaccines did not include pregnant and breastfeeding women because of safety concerns, so there has been limited information about how well they respond to the inoculations.The researchers analyzed the antibodies produced by 84 pregnant women, 31 breastfeeding women and 16 nonpregnant women of the same ages, immunized with the coronavirus vaccines made by Pfizer-BioNTech or Moderna.After the first dose, pregnant and breastfeeding women had fewer antibodies than other women of the same age. And the antibodies were less effective at recruiting other parts of the immune system to fight the virus.Two to six weeks after the second dose, pregnant and breastfeeding women had about as many antibodies as other women their age, consistent with results from other studies, and the qualitative differences also narrowed.Breastfeeding women boosted their response more effectively than pregnant women after the second dose, and the quality of their immune response more closely resembled that of nonpregnant women.The women in the study were immunized at different times during pregnancy. Future studies should analyze the optimal time during pregnancy to deliver the vaccines, the researchers said.

Humans carry around with them, often abundantly so, at least two kinds of fat tissue: white and brown. White fat cells are essentially inert containers for energy stored in the form of a single large, oily droplet. Brown fat cells are more complex, containing multiple, smaller droplets intermixed with dark-colored mitochondria — cellular organelles that give them their color and are the “engines” that convert the lipid droplets into heat and energy.
Some people also have “beige” fat cells, brown-like cells residing within white fat that can be activated to burn energy.
In recent years, there has been much effort to find ways to increase brown or beige fat cell activity, to induce fat cells, known as adipocytes, to burn energy and generate heat in a process called thermogenesis as a means to treat obesity, type 2 diabetes and other conditions.
But the therapeutic potential of brown fat — and perhaps beige fat cells — has been stymied by the complexity of the processes involved. It wasn’t until 2009 that the existence of active brown fat cells in healthy adults was confirmed; previously it was believed they were common only in newborns.
In a new study, published online October 27, 2021 in Nature, an international team of researchers led by senior author Alan Saltiel, PhD, director of the Institute for Diabetes and Metabolic Health at University of California San Diego School of Medicine, describe how energy expenditure and heat production are regulated in obesity through a previously unknown cellular pathway.
The human body breaks down consumed carbohydrates into a type of sugar called glucose, which is the main source of fuel for cells. Unneeded glucose is packaged and stored as glycogen in liver and skeletal muscle cells, where it can be extracted and quickly used for sudden energy needs or to maintain blood sugar levels.
Unlike in muscle and liver, the role of glycogen in fat has been a mystery. The researchers discovered that glycogen does much more than simply store energy in fat cells. It provides a signal that produces a major shift in how energy is handled.
In this “surprise discovery,” Saltiel and colleagues report that the browning of fat cells depends on their ability to both make and then degrade glycogen. The turnover of glycogen sends a signal that it is safe for the cell to “uncouple” the production of ATP, the molecule that provides the energy that fuels most cellular processes.
“Uncoupling is a way to generate heat, and in the process help balance energy. This pathway thus ensures that only the fat cells with enough energy stores to fuel the generation of heat are allowed to do so,” said Saltiel.
The dramatic increase in worldwide obesity — 650 million people or 13 percent, a tripling since 1975 — has underscored the importance of understanding how the human body balances energy intake and expenditure.
Glycogen regulates and promotes fat metabolism: the higher the levels, the more robust the metabolic processes, essentially burning fat quicker with resulting weight loss in obese mice. In humans, the genes involved in these complex processes were found to be lower in patients who were obese or prone to weight gain, suggesting that the glycogen pathway is needed in fat cells to burn off excess weight. The new findings, wrote the authors, suggest that modulating glycogen metabolism in fat cells might provide new approaches for weight loss and overall improvement in metabolic health.
Co-authors include: Omer Keinan, Joseph M. Valentine, Shannon M. Reilly, Mohammad Abu-Odeh, Julia H. Deluca, Benyamin Dadpey, Leslie Cho and Austin Pan, all at UC San Diego; Haopeng Xiao and Edward T. Chouchani, Dana-Farber Cancer Institute and Harvard University; Sushil K. Mahata, VA San Diego Healthcare System and UC San Diego; Ruth T. Yu, Yang Dai, Michael Downes and Ronald M. Evans, Salk Institute; Christopher Liddle, University of Sydney, Australia; Aldons J. Lusis, UCLA; Markku Laakso, University of Eastern Finland; and Mikael Ryde’n, Karolinska Institutet.

The world’s most common form of arthritis, knee osteoarthritis, causes sufferers pain and hurts their quality of life. Total knee replacement is the only option for people with severe knee osteoarthritis, but even that invasive surgery still leaves up to a third of patients with chronic knee pain. Many people who undergo total knee replacement surgery go on to become chronic opioid users.
“Osteoarthritis is one of the most common conditions for which opioids are prescribed [in the United States],” says Kosaku Aoyagi, a physical therapist and researcher at Boston University. “With the aging of the population and rising prevalence of osteoarthritis, the number of total knee replacement procedures is expected to rise exponentially over the next decade.”
Now, Aoyagi and a team of Boston University researchers have discovered at least one promising way to reduce a patient’s risk of opioid addiction: Participate in physical therapy either before or after total knee replacement surgery.
In the largest study of its kind, published Wednesday in JAMA Network Open, Deepak Kumar, a BU College of Health & Rehabilitation Sciences: Sargent College assistant professor of physical therapy, and collaborators analyzed more than 67,000 patient records, and discovered that even low levels of physical therapy were associated with lower risk of chronic opioid use after total knee replacement.
Specifically, they found that participation in physical therapy within 90 days before or after total knee replacement was associated with lower risk of chronic opioid use. Going further, they found that six or more sessions of physical therapy post-surgery was linked to reduced chance of chronic opioid use, as were instances when physical therapy was initiated within 30 days of surgery.
Kumar, a physical therapist by training, says their analysis revealed that the longer a patient waits to start physical therapy, the greater their odds of chronic opioid use.

No two human beings are the same, a biologic singularity encoded in the unique arrangement of the molecules that make up our individual DNA.
Variation is a cardinal feature of biology, the driver of diversity, and the engine of evolution, but it has a dark side. Alterations in DNA sequences and the resulting proteins that build our cells can sometimes lead to profound disruptions in physiologic function and cause disease.
But which gene alterations are normal or at least inconsequential, and which ones portend disease?
The answer is clear for a handful of well-known genetic mutations, yet despite dramatic leaps in genome sequencing technology over the past 20 years, our ability to interpret the meaning of millions of genetic variations identified through such sequencing still lags behind.
To make sense of it all, researchers at Harvard Medical School and Oxford University have designed an AI tool called EVE (Evolutionary model of Variant Effect), which uses a sophisticated type of machine learning to detect patterns of genetic variation across hundreds of thousands of nonhuman species and then use them to make predictions about the meaning of variations in human genes.
In an analysis published Oct. 27 in Nature, the researchers used EVE to assess 36 million protein sequences and 3,219 disease-associated genes across multiple species.

Kawasaki disease (KD) is rare, with fewer than 6,000 diagnosed cases per year in the United States. It is most common in infants and young children and causes inflammation in the walls of some blood vessels in the body. KD is a common cause of acquired heart disease in children around the world, causing coronary artery aneurysms in a quarter of untreated children.
Multisystem inflammatory syndrome in children (MIS-C) is also rare, a life-threatening illness that follows exposure to severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2). MIS-C is characterized by the acute onset of fever and variable symptoms, including rash, cardiovascular complications, shock and gastrointestinal symptoms, including abdominal pain, diarrhea and vomiting.
KD and MIS-C share several clinical features and immune responses. Both conditions are treated with intravenous immunoglobulin (IVIG), a therapeutic containing antibodies purified from blood products. Antibodies in the blood protect us from a number of viral, bacterial and fungal pathogens, but when administered as IVIG, can also suppress excessive inflammation. How it does this is an ongoing area of research worldwide.
In a pair of new studies, published online October 26 and August 31, 2021, two collaborating teams of researchers at University of California San Diego School of Medicine examined the use of IVIG in two groups; one group used a second dose of IVIG in children with KD who do not respond to the first dose of the drug, and the other group used IVIG as an effective treatment for MIS-C.
“Our research teams looked further into KD to improve treatment, and then used what we know about that disease to advance science in another illness,” said senior author Jane C. Burns, MD, professor and director of the Kawasaki Disease Research Center at UC San Diego School of Medicine and Rady Children’s Hospital-San Diego.
In a paper published in the October 26, 2021 online edition of the Lancet: Child and Adolescent Health, researchers found treating IVIG-resistant KD patients with infliximab, a targeted anti-inflammatory drug, was more effective than a second dose of IVIG.

Alzheimer’s disease is the most common cause of dementia in Western societies and it is estimated that 24 million people worldwide have this condition. ICREA researcher Dr. Patrick Aloy, head of the Structural Bioinformatics and Network Biology lab at IRB Barcelona, has headed a study that has managed to reverse the symptoms of Alzheimer’s disease in mice by administering drugs currently used to treat hypertension and inflammation in humans.
In this study, the scientists led by Dr. Aloy have characterised three stages of Alzheimer’s disease, namely initial, intermediate and advanced. For each of these stages, they have analysed the behaviour of the animals, studied the effects on the brain (specifically the hippocampus at the tissue level) and performed a molecular analysis to measure gene expression and protein levels.
The approach adopted has allowed them to describe the development of the disease at a level of detail hitherto unknown and also compare it with healthy ageing. “What we have observed is that, although Alzheimer’s disease shares some features of accelerated ageing, it is also affected by totally different ageing processes,” says Dr. Aloy. “This disease is caused by the abnormal accumulation of certain proteins, and we have seen that, in some cases, this is not caused by overproduction but by an error in their removal,” he adds.
Chemical Checker: detection of the most promising molecules
Having characterised the disease, the scientists used the Chemical Checker, a computational tool developed by the same research group to find drugs already on the market with the capacity to reverse the effects at the cellular level. This tool has allowed them to identify a series of possible candidates, which were tested in various mouse models of Alzheimer’s disease. Four drugs — two non-steroidal anti-inflammatories and two anti-hypertensives, proved effective at reversing the disease and neutralising symptoms in these mice.
“Epidemiological studies already indicated that people who regularly take antiinflammatories show a lower incidence of Alzheimer’s disease, but this had not been correlated with a specific medication or mechanism. The results that we are publishing are most promising, and we hope that further research can be done on them because they could give rise to a paradigm shift in the treatment of this disease,” says Dr. Aloy.
Early diagnosis of the disease
In addition to paving new avenues of research for the treatment of Alzheimer’s disease, the characterisation of the distinct stages of this condition published in this study favours early diagnosis. Diagnosing Alzheimer’s disease at an early stage, when damage to the brain is still minimal, is one of the main research focuses to tackle this condition and to reduce symptoms.
This work has been done in collaboration with the RIKEN Center for Brain Science and the Institute of Brain Science, both in Japan, and the Biostatistics/Bioinformatics and also Proteomics core facility at IRB Barcelona. The study was funded by the European Research Council, the Spanish Ministry of Science and Innovation and the Government of Catalonia.
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Low back pain (LBP) is no stranger to office workers. In Japan, 1 out of 10 otherwise healthy office workers suffer from LBP. Stretching and exercise help alleviate the pain, but workers often do this when it is too late. But what if our chairs could alert us before the pain worsens?
Now, researchers at Tohoku University have developed a new prediction method that employs pressure sensors installed on a conventional office chair. The “smart chairs” sensors detect workers’ movements on the chair dynamically and quantitatively.
The smart chair was tested in a real-life setting outside of the lab. Amassing data from 22 study participants over a period of three months, the research group combed through the information to investigate the dynamics of sitting behavior and identify a predictable LBP progression.
Further aided by various machine learning methods, the researchers discovered a common motif present in the sitting behavior of most participants. They pinpointed small motions in the body trunk that prevent the fixation of vertebral joints, therefore avoiding LBP’s progression. The frequency of this motif could be used to predict the worsening of LBP throughout the day when compared to a morning reference state.
The research group hopes to apply the technology to other areas of the body. “Although the current method focused on LBP, we hope to collect data relating to head and neck regions to be able to predict and prevent stiff necks and headaches, said paper coauthor Ryoichi Nagatomi.
The study was published in the journal Frontiers in Physiology.
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Bone mineral density at the femoral neck bone in postmenopausal women decreased by an average of 10% during a 25-year follow-up, according to a new study from the University of Eastern Finland. Being the world’s hitherto longest follow-up of changes in bone mineral density in postmenopausal women, the study shows that bone loss after menopause is significantly lower than has previously been assumed on the basis of earlier studies. Women with the highest bone mineral density at baseline had the highest bone loss percentage when compared to baseline.
The Kuopio Osteoporosis Risk Factor and Prevention (OSTPRE) study began in 1989 with a health survey that was sent to all women aged 47-56 living in the Kuopio region, eastern Finland. A total of 14,200 women received the survey, and it has been repeated at five-year intervals. In addition, a randomised sample of 3,000 women have participated in bone mineral density measurements every five years. The study is still ongoing, with 30-year measurements currently under way.
Published in Journal of Bone and Mineral Research, the present findings are from the 25-year follow-up. The study included all OSTPRE study participants who had participated in all of the bone mineral density measurements during the 25-year follow-up.
“The average decrease in bone mineral density was lower than has been assumed on the basis of earlier, shorter follow-ups where the bone loss rate at the femoral neck has been estimated to be even more than 20%. There were also surprisingly few risk factors affecting bone mineral density. The most significant factor protecting against bone loss was hormone replacement therapy. Weight gain during the follow-up also protected against bone loss,” Associate Professor Joonas Sirola from the University of Eastern Finland says.
“This new, long-term follow-up of bone mineral density sheds significant new light on osteoporosis and bone research, and also changes our understanding of bone loss in older women,” Professor Heikki Kröger from the University of Eastern Finland says.
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Individuals with Alzheimer’s disease or related dementias (ADRD) often experience behavioral and psychological symptoms such as depression, aggression and anxiety. Frequently, these symptoms are treated with antipsychotics, antidepressants and benzodiazepines, which often have side effects.
While pet therapy is known to be a cost effective and therapeutic intervention for improving mood and behavior in older adults, little is known about pet therapy in adult day centers, despite logistical advantages such as socialization and group activities.
With the help of a cuddly and “furry” companion, researchers from Florida Atlantic University’s Christine E. Lynn College of Nursing tested the effectiveness of affordable, interactive robotic pet cats to improve mood, behavior and cognition in older adults with mild to moderate dementia. The non-pharmacological intervention took place over the course of 12 visits in an adult day center. Participants were informed that their pet was a robot and not a live animal. Each of them selected a name for their cat, which was fitted with a collar and a personalized nametag.
For the study, published in the journal Issues in Mental Health Nursing, researchers assessed mood and behavioral symptoms using the Alzheimer’s Disease and Related Dementias Mood Scale, the Observed Emotion Rating Scale and the Cornell Scale for Depression in Dementia. They also assessed cognition via the Mini Mental State Examination.
Results showed that intervention with a robotic pet cat improved all mood scores over time, with significant improvements in the Observed Emotion Rating Scale and the Cornell Scale of Depression in Dementia. More than half of the participants scored higher on the Mini Mental State Examination post-test than pretest, with slight to moderate improvement in attention/calculation, language and registration. Post-test scores on the Alzheimer’s Disease and Related Dementias Mood Scale were six points higher than pretest conditions.
Researchers frequently observed study participants smiling and talking to their robotic cats and expressing sentiments such as, “the cat is looking at me like someone who listens to me and loves me.” They believed that the robotic pet was responding to their statements through meowing, turning their head or blinking their eyes and that they were having a conversation with the pet. Several of the caregivers reported that their loved one had slept with the cat, held onto the cat when sitting or consistently played with the cat. One participant even slept with her robotic pet cat while she was hospitalized.
“Since there is no cure for dementia, our project offers a way to address symptoms naturally and without the use of pharmacological treatments, which may or may not be effective and have possible detrimental side effects,” said Bryanna Streit LaRose, D.N.P., A.P.R.N., lead author who conducted the study as a doctoral nursing student at FAU, together with co-authors Lisa Kirk Wiese, Ph.D., R.N., an associate professor and Streit LaRose’s faculty chair, and María de los Ángeles Ortega, D.N.P., A.P.R.N., a professor, director of FAU’s Louis and Anne Green Memory and Wellness Center and Streit LaRose’s community chair on the project, both within the Christine E. Lynn College of Nursing. “Our intervention was affordable, safe, and noninvasive.”
By using therapeutic pets instead of live pets, there was no concern about the safety of the pet, feeding them, taking them outside, or making sure they are up-to-date with their vaccines. In addition, there were no fears about participant safety due to possible pet aggression, allergies, tripping over them and the costs associated with caring for a live animal.
“In addition to improving mood, behaviors and cognition, these robotic pet cats provided our participants with an alternative way to express themselves,” said Wiese. “Importantly, improving overall mood and behavior in individuals with Alzheimer’s disease and related dementias may also improve quality of life for their caregivers and family members.”
The researchers also examined the relationship between the Mini Mental State Examination and subscale post-intervention scores of the Cornell Scale of Depression in Dementia, Observed Emotion Rating Scale and Alzheimer’s Disease and Related Dementias Mood Scale. They found multiple significant and strong correlations between the 11 subscales of the Alzheimer’s Disease and Related Dementias Mood Scale and Mini Mental State Examination following the intervention. Nine categories regarding pleasant mood/behavior correlated favorably with the Mini Mental State Examination score, indicating a relationship between positive mood/behavior and increased Mini Mental State Examination scores.
“In the United States, one in three older adults dies with Alzheimer’s disease or a related dementia and there is currently no cure for the rapidly growing burden,” said Safiya George, Ph.D., dean, Christine E. Lynn College of Nursing. “This therapeutic interactive pet intervention has proven to be a safe alternative method to improving mood and behavior in people with dementia who are attending an adult day center.”
FAU’s Christine E. Lynn College of Nursing received the 12 robotic pets for the project with assistance from an FAU Iota Xi Sigma grant and funding supplementation from Ageless Innovation.

A UBC-led research team has uncovered how the virus responsible for causing COVID-19 escapes destruction in infected cells, allowing SARS-CoV-2 to persist and continue spreading in the human body.
The finding explains the cellular coup d’état staged by the novel coronavirus, and how it disrupts normal cell defences to hijack human host cells.
“We discovered that the virus attaches to and deactivates an important sensor protein in the host cell called galectin-8, which protects the cell against infection. By deactivating galectin-8, SARS-CoV-2 disarms a cell’s antiviral defence system and allows the virus to take over the host,” says Dr. Chris Overall, the study’s senior author, a Canada Research Chair, and a principal investigator at the UBC Centre for Blood Research, Life Sciences Institute and Faculty of Dentistry.
Overall assembled a team of local, national and international collaborators to provide samples for this study, which was published in the Oct. 26 issue of Cell Reports. The study’s co-lead authors, Dr. Isabel Pablos and Dr. Yoan Machado, are both postdoctoral fellows in his lab.
In order to turn host cells into virus-producing machines, SARS-CoV-2 uses spike proteins, which surround the outside of the virus, to attach to, invade and seize control of the host.
The researchers made the important discovery that galectin-8 attaches to the spike protein. The virus then deactivates galectin-8 by using one of its own key enzymes, called the 3CL protease, to target, attach to and cut galectin-8 in half, like a pair of molecular scissors.