Publisher Health

Researchers at the Texas A&M University School of Public Health have developed a new COVID-19 test distribution method that uses drones to quickly deliver at-home diagnostic tests to individuals who suspect they have COVID-19.
The coronavirus pandemic showed that a key part of controlling the spread of a contagious disease is to quickly and accurately identify who has been infected. This allows for distancing and quarantining of infectious people to reduce transmission. At the same time, it is important to limit contact between people who need to be tested, others seeking diagnosis and health care workers administering tests. Home test kits have made it possible for people to get an accurate diagnosis without coming into contact with others but getting tests to people who need them can be a challenge, something drone deliveries could overcome.
COVID-19 diagnostic tests that use a polymerase chain reaction (PCR) technique are highly accurate but take hours to process, and it can sometimes take days for patients to get results back. In contrast, faster antigen-based tests can give results in as little as 15 to 30 minutes. Home antigen test kits allow people who suspect they may have COVID-19 to test themselves at home, which can limit exposure to other patients at testing sites as well as health care workers administering tests. Getting faster results while minimizing exposure to other people is a one way to further limit the spread of the disease.
In a new article published in the Journal of Intelligent & Robotic Systems, Murray Côté, associate professor at the Texas A&M School of Public Health, and colleagues from the University of Houston developed a new technique for scheduling the delivery of COVID-19 diagnostic tests using a truck to dispatch the drones and drones to deliver the tests. The researchers tested various scenarios to better understand the capability of their approach.
Côté and colleagues’ approach examine their problem as separate truck and drone components. First, they optimize the truck schedule to minimize travel distance and then focus on minimizing drone delivery time. The first stage of their proposed method works to find a feasible set of truck and drone routes. The second stage uses a heuristic algorithm that tries different combinations of routes to find improvements to their initial solution.
Using a real-world scenario, they were able to find a good routing schedule within approximately one hour of computing time. The researchers then developed a way of showing their method’s effectiveness based on the total time needed to complete the deliveries, the number of people involved in the process and the virus transmission rate compared to face-to-face testing. They found that the proposed truck and drone delivery method could reduce transmission during testing by a factor of 7.5. For example, if the rate of transmission was 100 per day, the proposed research has the potential to reduce this rate to 13.3 per day.
Their study demonstrated the effectiveness of the proposed delivery scheduling method, which could also be used in other applications such as testing of other infectious diseases like influenza. The researchers also note that their model could be used for both rural areas, where patients are spread over long distances, and urban areas, where many patients live in a single region. Another future direction the researchers note is investigating how driving restrictions like speed limits, traffic lights and traffic congestion influence truck and drone scheduling methods.
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Materials provided by Texas A&M University. Original written by Rae Lynn Mitchell. Note: Content may be edited for style and length.

Black adolescents who lived in poverty and were less optimistic about the future showed accelerated aging in their immune cells and were more likely to have elevated insulin resistance at ages 25-29, researchers found.
Allen W. Barton, a professor of human development and family studies at the University of Illinois Urbana-Champaign is the first author of the study, which tracked the health of 342 African Americans for 20 years, from adolescence to their mid- to late twenties. The researchers’ goal was to explore links between the individuals’ childhood social environment and insulin resistance, a precursor to diabetes where cells don’t respond well to insulin or use blood glucose for energy.
The participants lived in rural Georgia, a region with one of the highest poverty rates and shortest life expectancies in the U.S.
“Once we found some compelling evidence that family poverty during childhood was associated with participants’ insulin resistance in their late 20s, we looked at immune cell aging as a possible mediator, something that transmits the effect,” Barton said. “And we found support for that. Immune cell aging was a pathway, a mechanism through which poverty was associated with insulin resistance.”
Published in the journal Child Development, the findings support the hypothesis that chronic diseases such as diabetes and metabolic syndrome that occur at significantly higher rates among Black adults and low-income populations may partially originate with experiences much earlier in life – even during childhood – and that such disadvantages can influence individuals’ cognition and physiology.
“Understanding these health disparities associated with race and socioeconomic status really requires a developmental perspective, but prospective research with these populations is sparse,” Barton said.

Black patients have a dramatically higher risk of advanced vision loss after a new diagnosis of primary open angle glaucoma (POAG) when compared to white patients, according to a new study from New York Eye and Ear Infirmary of Mount Sinai (NYEE).
The work, published July 25 in Translational Vision Science and Technology, shows that being of African heritage is an independent risk factor for this drastic decline in vision, and should prompt more eye screening in this population for early glaucoma detection. This is the first study to use an artificial intelligence algorithm to break down visual field loss in new-onset glaucoma cases among United States-based population groups.
The work is important because glaucoma is the leading cause of blindness in the United States and primary open angle glaucoma is the most common type. POAG is the leading cause of optic nerve degeneration that is related to the pressure level inside the eye, but other factors also contribute to this condition. Patients typically experience few or no symptoms until the disease progresses and they have irreversible vision loss — underscoring the need for early glaucoma screening and detection in high-risk patient groups.
“This study has tremendous implications for glaucoma screening of Blacks, who we already knew were a population at increased risk of glaucoma,” says senior author Louis R. Pasquale, MD, FARVO, Deputy Chair for Ophthalmology Research at the Icahn School of Medicine at Mount Sinai and Director of the NYEE Eye and Vision Research Institute. “Screening earlier in life could significantly increase the chance of detecting glaucoma and slowing down progression before it reaches one of the advanced patterns shown in our research.”
A team of researchers analyzed nearly 210,000 participants from three population-based databases of nurses and health professionals from the Nurses’ Health Study (enrolled between 1980 and 2018, and 1989-2019), and the Health Professionals Follow-up Study (enrolled between 1986 and 2018). Participants were over the age of 40 and their data was collected during comprehensive eye exams — none had glaucoma at baseline. They were followed biennially and provided updated information on their lifestyle, diet, and medical status, including glaucoma diagnosis.
Within the study group, 1,946 patients developed glaucoma. Researchers analyzed their earliest record of visual field loss using archetype analysis, a form of artificial intelligence. The algorithm identified 14 archetypes: four representing advanced loss patterns, nine of early loss, and one of no visual field loss.
Black patients made up 1.3 percent of the study, but had a nearly twofold increased risk of early visual field loss archetypes, and a sixfold higher risk for advanced field loss archetypes, when compared to white patients. Asian participants, who constituted 1.2 percent of the participants, had a nearly two-fold higher risk of early visual field loss compared to white patients, but did not have a dramatically higher rate of advanced patterns of visual field loss. Hispanic patients made up 1.1 percent of the study population, and did not have an increased risk of any archetypes compared to white patients; however, the study showed they were at risk of an archetype showing initial loss near the center of their visual field. The results were controlled for a number of variables including socioeconomics, frequency of eye exams, heart disease, diabetes, and exercise.
“This study started decades ago in three health professional cohorts that were not as diverse as current numbers — and if we collected more representation of people of color, the results would likely be even more profound,” Dr. Pasquale adds. “African descent is a risk factor for glaucoma blindness, and this work provides insight into why that might be the case. We suspect that the reason why Blacks presented with more advanced patterns of loss compared to whites is because the disease starts one to two decades earlier in the former group compared to the latter group. This emphasizes the importance of early screening strategies in Blacks to identify early-onset glaucoma so that visual disability in this population is averted.”
Dr. Pasquale says the next step for this work is to figure out the specific risk factors for the different patterns of visual loss seen in glaucoma patients — including genetic and environmental factors — so as to fully disentangle the pathogenesis of primary open angle glaucoma.
This study was done with collaborators at Brigham and Women’s Hospital and Massachusetts Eye and Ear. This work was supported by the National Eye Institute, part of the National Institutes of Health.

Exposure to extreme heat increases both chronic and acute malnutrition among infants and young children in low-income countries — threatening to reverse decades of progress, Cornell University research finds.
Linking survey and geocoded weather data over more than 20 years, a study of more than 32,000 West African children ages 3-36 months found that average heat exposure had increased the prevalence of stunted growth from chronic malnutrition by 12%, and of low weight from acute malnutrition by 29%.
The researchers estimate that if the average global temperature rises 2 degrees Celsius — which scientists warn is likely without significant reductions in carbon emissions — the average effect of heat exposure on stunting would nearly double, erasing gains recorded during the study period (1993 to 2014).
The findings are worrying, the researchers said, because temperatures in West Africa are rising and expected to continue to do so for several decades. And the effects of acute and chronic malnutrition in early childhood, which are linked to higher mortality rates and to lower education and incomes in adulthood, are irreversible.
“We’re talking about children at a very young age that will have changes for the rest of their lives, so this is permanently scarring their potential,” said Ariel Ortiz-Bobea, an associate professor and applied agricultural economist at Cornell. “What we are doing to reduce global poverty is being eroded by our lack of action on climate.”
Ortiz-Bobea is a co-author of “Heat exposure and child nutrition: Evidence from West Africa,” published in the Journal of Environmental Economics and Management, with John Hoddinott, a professor of food and nutrition economics and policy at Cornell.
The paper’s lead author is Sylvia Blom, a Cornell Ph.D. graduate, now a postdoctoral research associate at the University of Notre Dame.
Strategies to reduce child malnutrition, the researchers conclude, will need to consider increased needs for programs during periods of prolonged heat exposure.
Meanwhile, improved incomes, infrastructure and child care practices during the study period helped reduce stunting across the five West African countries by 5.8 percentage points on average.
“While this progress has been welcomed in West Africa and in other low- and middle-income countries, it’s occurring against the backdrop of rising temperatures and an increased likelihood of extreme weather events,” Hoddinott said. “Our work suggests these rising temperatures risk wiping out that progress.”
The researchers acknowledged funding support from the African Development Bank through the Structural Transformation of African Agriculture and Rural Spaces (STAARS) project.
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Materials provided by Cornell University. Original written by James Dean, courtesy of the Cornell Chronicle. Note: Content may be edited for style and length.

Researchers at the University of Colorado Anschutz Medical Campus have investigated how antiviral proteins called interferons interact with SARS-CoV-2, the cause of COVID-19. The study, published in Proceedings of the National Academy of Sciences USA, focuses on how the innate arm of the immune system defends against this coronavirus. The work resulted from a collaborative effort by multiple scientists, including the laboratories of Mario Santiago, PhD, associate professor of medicine and Eric Poeschla, MD, professor of medicine, both at the University of Colorado School of Medicine.
While the adaptive arm of the immune system responds definitively to infection by generating antibodies and T cells, the innate arm forms an earlier, first line of defense by recognizing conserved molecular patterns in pathogens. “SARS-CoV-2 just recently crossed the species barrier into humans and continues to adapt to its new host,” says Poeschla. “Much attention has deservedly focused on the virus’s serial evasions of neutralizing antibodies. The virus seems to be adapting to evade innate responses as well.”
Interferons are central molecules in the innate immune system that trigger a cascade of antiviral responses in cells within minutes of infection. As such, the interferon pathway could significantly reduce the levels of virus initially produced by an infected individual.
“They are clinically viable therapeutic agents that have been studied for viruses like HIV-1 for years,” says Santiago. “Here we looked at up to 17 different human interferons and found that some interferons, such as IFNalpha8, more strongly inhibited SARS-CoV-2. Importantly, later variants of the virus have developed significant resistance to their antiviral effects. For example, substantially more interferon would be needed to inhibit the omicron variant than the strains isolated during the earliest days of the pandemic.”
The data suggests that COVID-19 clinical trials on interferons — dozens of which are listed in clinicaltrials.gov — may need to be interpreted based on which variants were circulating when the study was conducted. Researchers say that future work to decipher which of SARS-CoV-2’s multitude of proteins might be evolving to confer interferon resistance may contribute in that direction.
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Materials provided by University of Colorado Anschutz Medical Campus. Original written by Kelsea Pieters. Note: Content may be edited for style and length.

Most drugs developed to treat Alzheimer’s disease have for years been ineffective in clinical trials. Researchers from Indiana University School of Medicine recently evaluated the efficacy of a failed clinical trial drug using their rigorous pipeline.
Researchers from Model Organism Development and Evaluation for Late-Onset Alzheimer’s Disease (MODEL-AD), a consortium of experts at IU School of Medicine, The Jackson Laboratory, Sage Bionetworks, The University of Pittsburgh School of Medicine and University of California, Irvine, recently published their study in Alzheimer’s & Dementia: Translational Research & Clinical Intervention, a journal of the Alzheimer’s Association.
Adrian Oblak, PhD, assistant professor of radiology and imaging sciences at IU School of Medicine and first author on the publication, said the study investigated the efficacy of the drug verubecestat — a beta-secretase (BACE) inhibitor — administered in the early stages of Alzheimer’s disease, using the MODEL-AD Preclinical Testing Core Drug Screening Pipeline.
“Although BACE inhibitors lowered amyloid beta plaque in patients with late-stage Alzheimer’s disease during clinical trials, many of those studies stopped due to adverse events or lack of clinical efficacy,” Oblak said. “The drug was also under-investigated in its effectiveness prior to the onset of Alzheimer’s disease, making it an ideal compound for MODEL-AD to study.”
The researchers conducted in vivo PET/MRI imaging to measure amyloid deposition and glucose uptake in the brain of the animal models, measured plasma and brain amyloid beta and assessed the clinical and behavioral characteristics.
Stacey Rizzo, PhD, associate professor of neurobiology and geriatric medicine at the University of Pittsburgh Aging Institute and senior author on the paper, said this study validates the importance of the consortium in advancing Alzheimer’s disease research.
“The MODEL-AD consortium brings together experts from the fields of Alzheimer’s disease biology, mouse models, genetics, behavioral research, neuropharmacology and medical imaging to develop the research infrastructure that will benefit the entire Alzheimer’s research community,” Rizzo said. “There is currently no cure for Alzheimer’s disease and so there is an absolute need to find a treatment and develop prevention strategies.”
The National Institute on Aging, part of the National Institutes of Health, funded the MODEL-AD consortium to establish robust infrastructure for the greater research community to improve preclinical to clinical translational studies and accelerate the pace of bringing effective and safe treatments to patients at risk for Alzheimer’s disease, Rizzo said.
“Under our rigorous unbiased screening strategy, we were able to prevent significant amyloid beta deposition, which was expected; however, the same dose range that was efficacious in preventing amyloid beta plaque formation resulted in similar side effects reported in the clinic and in the absence of cognitive improvement,” Oblak said about the study. “Therefore, we would not have prioritized this compound for advancement into clinical trials had we vetted the compound using this rigorous unbiased approach.”
The results from this investigation, Oblak said, like all animal models, protocols and validation data studied by MODEL-AD, are rapidly made available to all researchers for preclinical drug development, thanks to support of the NIA.

Researchers at Mayo Clinic’s Center for Individualized Medicine have discovered key human genomic signatures that could help explain why COVID-19 is severe in some people and mild in others. After analyzing volumes of diverse worldwide DNA sequence data, the scientists identified mutations in two human proteins that might sway the course of SARS-CoV-2 — the virus responsible for COVID-19.
Their study reveals that variants in the genes for ACE2 and TMPRESS2 can lead to an increase or decrease in protein expression. An increase in protein expression might result in elevated COVID-19 susceptibility and severity, while a decrease might have a protective effect against the virus. Proteins play many critical roles in the body. In this case, ACE2 and TMPRESS2 provide critical entry points for SARS-CoV-2 to invade and infect human cells.
The study findings, published in Human Molecular Genetics, suggest a potential new diagnostic approach that is based on variation in the host cells rather than the constantly evolving virus itself.
“COVID-19 is a master of frequency in changing the sequences of its genes, but that only tells half of the story. Our findings suggest that the virus’s interaction with proteins encoded by the human genome may also be a contributor to a person’s disease outcome,” says Lingxin Zhang, Ph.D., the lead author of the study and a researcher in the Pharmacogenomics Program of the Center for Individualized Medicine.
“These results can now be applied to DNA sequence data for patients infected with SARS-CoV-2 to potentially determine the degree of susceptibility to the disease,” Dr. Zhang adds. “I hope this methodology can be expanded for other genes involved in COVID-19, and that scientists and clinicians across the world can use this information to help their patients.”
For the study, Dr. Zhang and her team delved deep into the DNA sequencing data of nearly 71,000 people worldwide, including nearly 30,000 racial and ethnic minorities, to identify sequence variants in the ACE2 and TMPRESS2 genes. The team then analyzed hundreds of protein variants encoded by those genes and identified variant genes that generated high and low expression levels. To do that, Dr. Zhang engineered cells capable of expressing the protein variants, and then, using color-coding, she and her team analyzed the variants to see which were more or less stable.
The study used nearly a million generated cells and produced billions of data points, which the team analyzed using a series of technologies, including cell sorting, modern genomics, high throughput DNA sequencing and a computer algorithm.
“To our knowledge, it’s the first time anyone has applied this approach to COVID-19,” says Richard Weinshilboum, M.D., co-author of the study and a pharmacologist in the Center for Individualized Medicine, and Department of Molecular Pharmacology and Experimental Therapeutics. “This work would not have been possible without the dramatic advances that have occurred in DNA sequencing, joined together with parallel advances in our ability to test the functional and medical implications of individual variations in DNA sequence — and, as a result — of individual variation in the proteins encoded by our genes.”
Dr. Weinshilboum says the study also was made possible by the large quantity of human DNA sequence information that is now publically available — with the proviso that those data must be carefully protected and must have their use reviewed and approved to avoid any possible violation of privacy.
As of July 11, 2022, more than 6.3 million people worldwide have died from COVID-19 since the start of the pandemic.
Acknowledgements
This study was funded by NIH grants U19 GM61388 (The Pharmacogenomics Research Network), R01 GM028157, R01 GM125633, R01 AA027486, K01 AA28050 and by the Mayo Clinic Center for Individualized Medicine.
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Materials provided by Mayo Clinic. Original written by Colette Gallagher. Note: Content may be edited for style and length.

Long Covid sufferers have experienced a wider set of symptoms than previously thought including hair loss and sexual dysfunction, new research has found.
A study published in Nature Medicine today (25 July 2022) found that patients with a primary care record of infection with the virus that causes Covid-19 (SARS-CoV-2 coronavirus) reported 62 symptoms much more frequently 12 weeks after initial infection than those who hadn’t contracted the virus.
Anonymised electronic health records of 2.4 million people in the UK were analysed by researchers from the University of Birmingham alongside a team of clinicians and researchers across England, and was funded by the National Institute for Health and Care Research and UK Research and Innovation. The data taken between January 2020 and April 2021 comprised of 486,149 people with prior infection, and 1.9 million people with no indication of coronavirus infection after matching for other clinical diagnoses.
Using only non-hospitalised patients, the team of researchers were able to identify three categories of distinct symptoms reported by people with persistent health problems after infection.
Patterns of symptoms tended to be grouped into respiratory symptoms, mental health and cognitive problems, and then a broader range of symptoms. While the most common symptoms include anosmia (loss of sense of smell), shortness of breath, chest pain and fever; others include: amnesia, apraxia (inability to perform familiar movements or commands), bowel incontinence, erectile dysfunction, hallucinations, limb swellingDr Shamil Haroon, Associate Clinical Professor in Public Health at the University of Birmingham is the senior author on the study. Dr Haroon said:
“This research validates what patients have been telling clinicians and policy makers throughout the pandemic, that the symptoms of Long Covid are extremely broad and cannot be fully accounted for by other factors such as lifestyle risk factors or chronic health conditions.”

Scientists from the RIKEN Center for Integrative Medical Sciences in Japan in collaboration with other researchers from around the world have discovered that recombinations of specific genomic sequences that are repeated millions of times in the genome of each of our cells are pervasively found in both normal and in disease states. Identifying the mechanisms that lead to this myriad of recombinations involving DNA sequences that were once considered as “junk”, may be crucial to understanding how our cells develop and what can make them unhealthy.  
Following the discovery of DNA, it was long believed that all the cells in our body share the same genetic code, safely guarded within the nucleus. However, modern advances in DNA sequencing have challenged this view: we now know that mutations accumulate in the genome of single cells starting from the very early stages of development. However, the magnitude of this phenomenon and how it contributes to disease is not well understood.  
In this work, published in Cell, the authors looked at certain repeated genomic sequences, called Alu and L1, and developed a method to study these specific sequences of DNA that are repeated millions of times in the genome of each cell. It was already known that they recombine with each other, generating mutations often found in cancer and other genetic disorders. By analyzing the DNA of donors unaffected by disease, the researchers identified millions of DNA mutations caused by the recombination of these repeated sequences, and further discovered that different tissues in the body are characterized by different recombination signatures. 
The researchers also found that the differentiation of human stem cells into neuronal cells is accompanied by distinct changes of recombination of repeat sequences. This indicates that this particular type of DNA mutation may be a physiological phenomenon involved in human development.  
Finally, the researchers looked at the recombination of repeated sequences in samples from people affected by Alzheimer’s and Parkinson’s disorders, the two most prominent neurodegenerative disorders in the developed world. They found signatures of recombination that are specific to each disease, suggesting that genomic recombinations caused by these repeated sequences are involved in brain diseases. 
According to Giovanni Pascarella, first author of the study, “We have shown in this study that the recombination of repeat elements in the human genome is a widespread phenomenon that contributes to the complex constellation of genomic variants making up our genomes.” 
According to, Piero Carninci, Principal Investigator and co-corresponding author of the study, “We hypothesize that it might be that random recombinations of Alu and LI in somatic cells may occasionally prime the genome of individual cells at vulnerable sites and drive the transition from healthy to pathological states.” 
“However,” he continues, “what is difficult to know at this point is to determine whether the recombinations in disease are truly causative or if they are effects of the disease state. Further studies need to be done to understand this important question.” 
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Materials provided by RIKEN. Note: Content may be edited for style and length.

Researchers at the University of Toronto, Johns Hopkins University and Vanderbilt University have discovered that certain cells move surprisingly faster in thicker fluid — think honey as opposed to water, or mucus as opposed to blood — because their ruffled edges sense the viscosity of their environment and adapt to increase their speed.
Their combined results in cancer and fibroblast cells — the type that often creates scars in tissues — suggest that the viscosity of a cell’s surrounding environment is an important contributor to disease, and may help explain tumour progression, scarring in mucus-filled lungs affected by cystic fibrosis, and the wound-healing process.
The study, “Membrane ruffling is a mechanosensor of extracellular fluid viscosity,” published today in Nature Physics, sheds new light on cell environments, an under-explored area of research.
“This link between cell viscosity and attachment has never been demonstrated before,” says Sergey Plotnikov, assistant professor in the Department of Cell and Systems Biology in the Faculty of Arts & Science at the University of Toronto and a co-corresponding author of the study. “We found that the thicker the surrounding environment, the stronger the cells adhere to the substrate and the faster they move — much like walking on an icy surface with shoes that have spikes, versus shoes with no grip at all.”
Understanding why cells behave in this surprising way is important because cancer tumours create a viscous environment, which means spreading cells can move into tumours faster than non-cancerous tissues. Since the researchers observed that cancer cells speed up in a thickened environment, they concluded that the development of ruffled edges in cancer cells may contribute to cancer spreading to other areas of the body.
Targeting the spreading response in fibroblasts, on the other hand, may reduce tissue damage in the mucus-filled lungs affected by cystic fibrosis. Because ruffled fibroblasts move quickly, they are the first type of cells to move through the mucus to the wound, contributing to scarring rather than healing. These results also may imply that by changing the viscosity of the lung’s mucus, one can control the cell movement.