Publisher Health

In the summer of 2021, as the third wave of the COVID-19 pandemic wore on in the United States, infectious disease forecasters began to call attention to a disturbing trend.
The previous January, as models warned that U.S. infections would continue to rise, cases plummeted instead. In July, as forecasts predicted infections would flatten, the Delta variant soared, leaving public health agencies scrambling to reinstate mask mandates and social distancing measures.
“Existing forecast models generally did not predict the big surges and peaks,” said geospatial data scientist Morteza Karimzadeh, an assistant professor of geography at CU Boulder. “They failed when we needed them most.”
New research from Karimzadeh and his colleagues suggests a new approach, using artificial intelligence and vast, anonymized datasets from Facebook could not only yield more accurate COVID-19 forecasts, but also revolutionize the way we track other infectious diseases, including the flu.
Their findings, published in the International Journal of Data Science and Analytics, conclude this short-term forecasting method significantly outperforms conventional models for projecting COVID trends at the county level.
Karimzadeh’s team is now one of about a dozen, including those from Columbia University and the Massachusetts Institute of Technology (MIT), submitting weekly projections to the COVID-19 Forecast Hub, a repository that aggregates the best data possible to create an “ensemble forecast” for the Centers for Disease Control. Their forecasts generally rank in the top two for accuracy each week.

An international team of scientists from Nanyang Technological University, Singapore (NTU Singapore) and Waseda University in Japan have found that fermented soybean waste, or okara, could improve fat metabolism and mitigate effects of diet-induced obesity.
Through laboratory experiments reported in the peer-reviewed scientific journal Metabolites in February, the scientists from NTU Singapore and Waseda showed that mice on a high fat diet supplemented with fermented okara gained less body mass and had lower levels of fat and cholesterol after three weeks as compared to mice on the same diet but not fed any fermented okara.
With 14 million tonnes of okara generated every year, and nearly a third of the world’s population overweight or obese, the scientists hope their findings can pave the way for fermented okara to be integrated into health foods one day, addressing the problems of food waste and obesity at the same time.
Dr Ken Lee, senior lecturer at the NTU School of Physical and Mathematical Sciences and co-lead author of the paper, said: “Using a process akin to what is used to produce miso and soy sauce, we fermented okara and fed it to mice on a high-fat diet. Three weeks later, we found that these mice gained less weight as compared to mice on a high-fat diet but without fermented okara. The mice that were fed fermented okara also had less fat and lower cholesterol levels.
“Our findings suggest that fermented okara could help to mitigate the harmful effects of a high-fat diet, and could potentially be integrated in the diets of obese patients who find it difficult to make immediate lifestyle changes.”
Dr Shigenobu Shibata, Professor at the Waseda University Graduate School of Advanced Science and Engineering and co-lead author of the paper, said: “Aspergillus oryzae and Aspergillus sojae, whichare typical aspergillus fungi used to produce soy sauce and miso, were successfully combined to ferment okara. Compared to unfermented okara, fermented okara was found to be able to reduce obesity and improve abnormal lipid metabolism in mice. Tofu and soymilk are now widely accepted as health foods not only in Japan but in the world, and the effective use of okara, which is an industrial waste, is in line with the United Nations Sustainable Development Goals. I hope NTU and Waseda University, each with their unique strength, will continue to promote such joint research centred on graduate students and young researchers.”
The okara study supports the goals of the NTU 2025 five-year strategic plan, which prioritises the University’s commitment to sustainability, as well as its focus on health and society as one of the research clusters with potential for significant intellectual and societal impact.

Just one dose of a new nanoparticle-based COVID-19 vaccine was enough to produce an immune response in animals on track with vaccines currently in clinical use. And with minor changes, Northwestern University researchers hope the same vaccine platform could target other infectious diseases.
In a new study, 100% of mice who received the protein-based immunization survived when challenged with lethal doses of the SARS-CoV-2 virus, which causes COVID-19. None of the mice experienced lung damage due to SARS-CoV-2 exposure. All mice who did not receive this nanoparticle vaccine died in a 14-day trial.
The results, published this week in the Proceedings of the National Academy of Sciences, outline the structure-function relationships between the first spherical nucleic acid (SNA) vaccine developed to protect against viral infections.
“What makes this vaccine different than other vaccines is the approach we take to design them,” said Dr. Michelle Teplensky, co-first author of the paper. “Even as recently as a few years ago people focused on selecting the right target to train the immune system and the right stimulant to activate it, not on how those components were arranged structurally and presented to the body.”
Called SNAs, the nanoparticles that house the immune target are a form of globular DNA that can enter and stimulate immune cells with extreme efficiency. SNAs have been tested in more than 60 cell types. Researchers experimentally determined the ideal ratio between the SNA’s shell and core density that produces the most potent response.
SNA vaccines have been used to treat mice with triple negative breast cancer — and more vaccines for other cancers are in development.

People often think of salmon when they think of omega-3 fatty acids, but a new research review found that the major plant-based version of the nutrient, alpha-linolenic acid (ALA), can benefit heart health and reduce the risk of heart disease for those who don’t eat seafood.
In a comprehensive literature review, the researchers found that consuming ALA that is found in plant-based foods like walnuts and flaxseeds was associated with a 10% lower risk of cardiovascular disease and a 20% reduced risk of fatal coronary heart disease.
Penny Kris-Etherton, Evan Pugh University Professor of Nutritional Sciences at Penn State, said the review suggests there are multiple ways of meeting the recommendations for omega-3 fatty acids.
“People may not want to eat seafood for a variety of reasons, but it’s still important for them to consume omega-3s to reduce the risk of heart disease and to promote overall health,” Kris-Etherton said. “Plant-based ALA in the form of walnuts or flaxseeds can also provide these benefits, especially when incorporated into a healthy diet rich in fruits, vegetables, and whole grains.”
Jennifer Fleming, assistant teaching professor of nutrition at Penn State, said they also found evidence that for people who do eat seafood, they could get extra benefits from eating plant-based omega-3s.
“When people with low levels of omega-3s in their diet ate ALA, they saw a benefit in terms of cardiovascular health,” Fleming said. “But when people with high levels of omega-3s from other sources ate more ALA, they also saw a benefit. It could be that ALA works synergistically with other omega-3s.”
The review was recently published in Advances in Nutrition.

Children and adolescents (aged 0-18 years) with disabilities experience physical, sexual, and emotional violence, and neglect at considerably higher rates than those without disability, despite advances in awareness and policy in recent years. This is according to a systematic review of research involving more than 16 million young people from 25 countries conducted between 1990 and 2020. The study provides the most comprehensive picture of the violence experienced by children with disabilities around the world. The findings are published in The Lancet Child & Adolescent Health.
Young people with mental illness and cognitive or learning disabilities (e.g., attention deficit hyperactivity disorder and autism) are especially likely to experience violence, and overall, children with disabilities are more than twice as likely to experience violence compared to those without disabilities, which can have a serious and long-lasting impact on their health and wellbeing.
The findings highlight the urgent need for collaborative efforts by governments, health and social care workers, and researchers to raise awareness of all forms of violence against children with disabilities and to strengthen prevention efforts, according to the authors.
“Children with disabilities face unacceptably high levels of violence worldwide,” says Dr. Ilan Cerna-Turoff in the Department of Environmental Health Sciences at Columbia University Mailman School of Public Health, who co-led the study. “Governments face a challenging time in which resources are spread thin in responding to the COVID-19 pandemic and economic and social change. We know that violence prevention leads to better development indicators for our societies. Now, more than ever, violence prevention is a worthy and important investment to secure a better future. Moreover, all people deserve the right to live in a world in which they are safe from violence. Protecting children with disabilities from violence is a fundamental aspect of social justice and equity.”
An estimated 291 million children and adolescents have epilepsy, intellectual disability, vision impairment, or hearing loss — representing about 11 percent of the total child and adolescent population globally. Many more have other physical and mental disabilities. The vast majority of children with disabilities — more than 94 percent — live in LMICs where multiple risks converge. Inadequate systems of social protection and access to support, stigma, discrimination, and a lack of information about disability contribute to the higher levels of violence experienced by children with disabilities. This can be further exacerbated by poverty and social isolation. The unique challenges faced by children with disabilities, such as the inability to verbalise or defend themselves, can also make them a target of violence.
In 2012, a systematic review published in The Lancet estimated that more than a quarter of children with disabilities in high-income countries experienced violence and that their odds of experiencing violence were more than three times higher than their non-disabled peers.

A novel system to control protein aggregation in a model of Parkinson’s disease may answer longstanding questions about how the disease begins and spreads, according to a new study published March 9 in the open-access journal PLOS Biology by Abid Oueslati of Laval University, Quebec, Canada, and colleagues. Initial results suggest that aggregation of the protein alpha-synuclein plays a critical role in disrupting neuronal homeostasis and triggering neurodegeneration.
Parkinson’s disease is a neurodegenerative disorder, marked clinically by tremor, stiffness, and slowed movements, as well as a host of nonmotor symptoms. Within affected neurons, molecules of a protein called alpha-synuclein can be seen to clump together, forming characteristic aggregates called Lewy bodies. But it has been hard to answer whether alpha-synuclein aggregation contributes to disease development or progression, and when it may act in the toxic disease cascade, or whether instead the aggregates are innocent bystanders to some other malevolent process, or are even protective. These elements have been difficult to determine, in part because aggregation in cellular and animal models has not been controllable in either time or space.
To address that problem, the authors turned to optobiology, a technique in which a protein of interest is fused to another protein that changes its conformation in response to light, allowing the behavior of the target protein to be manipulated selectively and reversibly. Here, the authors fused alpha-synuclein to a protein known as cryptochrome protein 2, from a mustard plant. They found that when light of the correct wavelength fell on the mustard protein, its conformational change triggered aggregation of its alpha-synuclein partner.
The aggregates that formed were reminiscent of Lewy bodies in multiple important ways, including that they included several other key proteins besides alpha-synuclein found in Lewy bodies in people with Parkinson’s disease, and that the alpha-synuclein in the aggregates adopted the characteristic beta-sheet conformation seen in many diseases of misfolded proteins. The aggregates induced dislocation of multiple cellular organelles, as Lewy bodies have been recently reported to do as well. They also induced misfolding in alpha-synuclein molecules not attached to the cryptochrome protein, mimicking the prion-like spread of aggregation seen with alpha-synuclein in the diseased brain and animal models.
Finally, the authors delivered the genes for the alpha-synuclein-cryptochrome fusion protein to mice, directly into the substantia nigra, the structure in the brain that is most prominently affected by Parkinson’s disease, and surgically placed an optic fiber to deliver light to the targeted cells. Light treatment led to formation of alpha-synuclein aggregates, neurodegeneration, disruption of calcium activity in downstream neuronal targets, and Parkinson-like motor deficits.
“Our results demonstrate the potential of this optobiological system to reliably and controllably induce formation of Lewy body-like aggregations in model systems, in order to better understand the dynamics and timing of Lewy body formation and spread, and their contribution to the pathogenesis of Parkinson’s disease,” Oueslati said.
Oueslati adds, “How do alpha-synuclein aggregates contribute to neuronal damage in Parkinson’s disease? To help address this question, we developed a new optogenetic-based experimental model allowing for the induction and real-time monitoring of alpha-synuclein clustering in vivo.”
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When a heavy alcohol drinker tries to take a night off, their body protests, with shaky hands, heart palpitations, anxiety and headaches. These acute symptoms of alcohol withdrawal — but even more so the enduring emotional distress that lingers into protracted abstinence — are one reason people with alcohol use disorders have a hard time quitting. Now, scientists at Scripps Research have made new headway in understanding the basis of alcohol withdrawal in the brain.
Previously, a signaling molecule called corticotropin-releasing factor (CRF) was linked to alcohol withdrawal; when researchers block CRF in rats or mice addicted to alcohol, the animals drink less. Scientists believed that the suspect CRF is produced by neurons in a brain area called the central nucleus of the amygdala. But in the new study, published in the journal Molecular Psychiatry in March 2022, the team found that — at least in mice — these cells aren’t required for alcohol withdrawal or alcohol dependence.
“Understanding the basis of withdrawal is incredibly important for treating alcohol addiction in humans, because this is one of the motivational drivers of excessive alcohol drinking,” says Candice Contet, PhD, associate professor in the Department of Molecular Medicine at Scripps Research. “These findings weren’t what we expected, but help us get closer to understanding alcohol addiction and the role of CRF.”
Many studies have established that CRF levels increase in the central nucleus of the amygdala of rats and mice during alcohol withdrawal as well as in response to other psychological stressors. Pharmaceutical companies are actively investigating how to target CRF signaling to treat a variety of psychological diseases including alcohol addiction. But results in humans have been inconclusive, and scientists have not been able to pin down which cells in the brain release CRF during alcohol withdrawal.
Contet’s group wanted to test the hypothesis that cells in the central amygdala produce the CRF necessary for alcohol withdrawal. In the new study, the researchers activated and blocked these amygdala-residing neurons in mice dependent on alcohol. First, they activated the neurons in various patterns designed to replicate cycles of repetitive drinking and withdrawal. However, activating these CRF-producing neurons had no effect on the drinking behavior of the mice, even though other experiments confirmed that CRF was getting released in the central amygdala. Next, the team showed that blocking these neurons also had no effect on the behavior of mice with alcohol dependence, which was surprising because it meant that the CRF known to signal in the amygdala to promote alcohol drinking wasn’t being produced in that area.
“We basically saw that activating these neurons within the central amygdala is not sufficient nor necessary for the escalation of drinking in mice,” says Contet. “So it means that the CRF is coming to the central amygdala from somewhere else in the brain.” Other neurons in the brain are known to produce CRF, but the team doesn’t yet know which might be involved in alcohol dependence.
“These findings were surprising but highlight the complexity of the CRF system and the changes in brain circuitry that occur following chronic alcohol exposure,” says Melissa Herman, a former Scripps Research postdoctoral research associate and co-first author of the new paper.
When the team looked at the spatial patterns of organization of the amygdala neurons they were studying, they made another unexpected observation — the CRF neurons weren’t organized the same way in mice brains as they are in rat brains. The observation, Contet says, suggests that there might be some variation in CRF between species. This also could explain why the amygdala neurons in question have been found to be necessary for alcohol withdrawal in rats but, according to the new data, not in mice.
“Our data has to be taken with a grain of salt when it comes to implications for humans,” she says. “Since there’s this important difference between rats and mice, more work is definitely needed to figure out the relevance to humans.”
The group is planning experiments to further understand the differences in CRF between rats and mice, as well as pin down which other neurons in the brain might be involved in its production during alcohol withdrawal.
This work was supported by funding from the National Institutes of Health (AA024198, AA026685, AA027636, AA027372, AA006420, AA021491, AA015566, AA02300, and AA024952).

Infants and toddlers who experienced community infection with SARS-CoV-2, the coronavirus that causes COVID-19, had significantly higher levels of antibodies against the virus compared to adults, according to a study led by researchers at the Johns Hopkins Bloomberg School of Public Health in collaboration with the Centers for Disease Control and Prevention.
The new study suggests that children tend to have strong antibody responses after SARS-CoV-2 infection. Understanding antibody responses to SARS-CoV-2 at different ages can inform COVID-19 vaccine strategies and policies.
The findings will be published online March 22 in the journal JCI Insight.
This analysis is based on samples taken at enrollment from 682 children and adults in 175 Maryland households who participated in a household surveillance study of SARS-CoV-2 infection and had not yet received a COVID-19 vaccine. Participants ranged in age from 0 to 62 years, and enrollment samples were collected between November 2020 and March 2021.
The researchers found evidence of SARS-CoV-2 antibodies, indicating prior infection with the virus, in 56 people at the time of enrollment. Of these 56 people with antibody evidence of previous SARS-CoV-2 infection, 15 were children ages 0 to 4 years, with the youngest three months old; 13 were children ages 5-17 years; and 28 were adults ages 18 years or older. Antibodies to a key site on the virus’s outer spike protein — the “receptor-binding domain” (RBD) — were present at much higher levels in children compared to adults: more than 13 times higher in children age 0-4, and nearly 9 times higher in children age 5-17. And levels of SARS-CoV-2 neutralizing antibodies, which may help to predict protection against severe COVID infection, were nearly twice as high in children ages 0-4 compared to adults.
In most households where both children and adults had antibody evidence of SARS-CoV-2 infection, children ages 0-4 years had the highest levels of SARS-CoV-2 RBD and neutralizing antibodies of all infected household members.

Fewer than 1 in 1,000 people who have been vaccinated or previously infected with COVID-19 were hospitalized with a new breakthrough infection, Mayo Clinic research finds. The study, which is published in Clinical Infectious Diseases, supports previous studies that show vaccination is the best way to prevent severe COVID-19 infection, hospitalization and death.
“In the general primary care patient population, those who have been vaccinated have very low risk of subsequent hospitalization for breakthrough COVID-19,” says lead author Benjamin Pollock, Ph.D., a researcher in the Mayo Clinic Robert D. and Patricia E. Kern Center for the Science of Health Care Delivery. “Our study shows that while it can and does happen, that these occurrences are extremely uncommon.”
The researchers created a longitudinal study of 106,349 primary care patients at Mayo Clinic in Rochester who were 18 or older and tested positive for COVID-19, and/or were vaccinated for COVID-19. Of those patients, only 69 were hospitalized because of a breakthrough COVID-19 infection.
The researchers found the hospitalization rate was: 0.06%, or 6 in 10,000 for vaccinated patients. 0.03%, or 3 in 10,000, in previously infected but unvaccinated people. 0.01%, or 1 in 10,000, among those who were both vaccinated and infected previously.While there were slight differences between the three groups, the researchers note the difference is not statistically significant.
“We found these results to be in line with previous studies, although the interpretation shouldn’t necessarily be that natural immunity provides the same protection as vaccination,” says Dr. Pollock. “Rather, this study found that among our primary care population, both natural immunity and vaccine immunity appeared to lead to very low rates of breakthrough hospitalizations.”
The researchers looked at breakthrough cases that resulted in hospitalization, but they did not compare immunity after infection and vaccination rates among mild or asymptomatic breakthrough cases.

To accurately diagnose and treat diseases, doctors and researchers need to see inside bodies. Medical imaging tools have come a long way since the humble x-ray, but most existing tools remain too coarse to quantify numbers or specific types of cells inside deep tissues of the body.
Quantum dots can do that, according to new research in mice from the University of Illinois.
“Quantum dots can measure things in the body that are very, very dynamic and complicated and that we can’t see currently. They give us the ability to count cells, detect their exact locations, and observe changes over time. I think it is really a huge advance,” says Andrew Smith, professor in the Department of Bioengineering at U of I and co-author on the ACS Nano study.
Quantum dots are lab-grown nanoparticles — just a few hundred atoms in size — with special optical properties detectable by standard microscopy, tomography (e.g., PET/CT scanners), and fluorescence imaging. Depending on their size and composition, bioengineers like Smith can make them glow in specific colors and emit light in the infrared spectrum.
“Emitting light in the infrared is rare. Very little light is emitted by tissues in the infrared, so if you put them in the body, they appear very bright. We can see deeply into the body and can more accurately measure things than we could using technology in the visible range,” Smith says.
In the ACS Nano study, Smith and colleagues let quantum dots loose on macrophages.