Publisher Health

A point-of-care COVID-19 test developed by researchers at the University of Illinois Urbana-Champaign can now detect and differentiate the alpha variant of the SARS-CoV-2 virus from earlier strains in saliva samples.
The new test builds on the group’s previous developments, which allowed samples to bypass the laboratory — first using nasopharyngeal swabs, then with saliva samples. The point-of-care amplification and testing process, called LAMP, is more efficient than PCR because it does not require expensive thermal cycling machines. The researchers said the assay does not need RNA extraction and purification steps, similar to the Illinois saliva test.
The results of the study, co-led by Rashid Bashir, a professor of bioengineering and the dean of the Grainger College of Engineering at Illinois, mechanical science and engineering professor Bill King and bioengineering professor Enrique Valera, are published in the journal Lab on a Chip.
“Our study shows that it is possible to test for variants of the same coronavirus strain in a single point-of-care test that takes 30 minutes using a portable handheld device,” Bashir said. “The new test is scalable to suit future pandemics, COVID-19 or otherwise, and could be used at home or other settings.”
The updated process takes advantage of a genetic phenomenon called S-gene target failure — which is present in the alpha variant but not in the SARS-CoV-2 virus early strains — to differentiate between the two alpha variants, the researchers said.
“The new omicron variant also exhibits S-gene target failure and could be tested for by adapting the approach developed in this study,” Valera said.

When babies are born with alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV), their skin starts to turn blue from the under-oxygenated blood in their systems. But unlike most other breathing problems a newborn might experience, there’s little to nothing that can be done to save these children unless they get a lung transplant.
That’s because their lungs lack the ability to grow enough alveolar capillaries to support healthy gas exchange, which in most cases leads to death within a month after birth. Now, after conducting a cell-by-cell analysis of genetic activity occurring among many different cell types within the lung, scientists at Cincinnati Children’s are shedding new light on how ACDMPV develops — and a possible way to treat it.
Detailed findings were published online April 19, 2022, in Nature Communications. The study was led by first author Guolun Wang, PhD, corresponding author Vladimir Kalinichenko, MD, PhD, and seven other experts collaborating with the Center for Lung Regenerative Medicine at Cincinnati Children’s Perinatal Institute.
“Treatment with BMP9 effectively restored capillary density, improved alveolarization, increased arterial oxygenation, increased expression of BMP9 receptor on the surface of capillary endothelial cells called Acvrl1, and improved survival in the ACDMPV mouse model,” Kalinichenko says. “The improvements are striking. However, several more research steps are needed before BMP9 therapy could be ready for human clinical trials.”
Intricate Detective Work Isolates Key Molecular Signaling Pathway
The study in Nature Communications describes how the research team sifted through a mountain of single-cell RNA sequencing data collected from more than 7,000 lung cells from mice carrying a gene mutation linked to ACDMPV (a loss-of-function for the gene FOXF1 in humans) and another nearly 6,000 normal lung cells to find the one cell type where the disease creates its devastating results.

The Journal of the National Cancer Institute (JNCI) published a commentary today on the significant cancer disparities facing Asian Americans. The article is authored by seven researchers from across the country who participated in the U.S. Food and Drug Administration (FDA) Oncology Center of Excellence “Conversations on Cancer” held on July 29, 2021. The virtual “conversation,” the first by the FDA, focused on the unfair cancer burden impacting Asian Americans. The lead author of the commentary is Moon Chen, associate director for community outreach and engagement with the UC Davis Comprehensive Cancer Center.
In percentage terms, Asian Americans are the fastest-growing U.S. racial group for the past three censuses, yet data aggregation obscure distinctions within subgroups of the more than 24 million Asians living in the United States. The JNCI commentary illustrates the harmful impacts this is having on Asian American communities.
Chen said the neglect of Asian American cancer inequities stems from multiple factors. They include historical prejudices against Asian Americans and the myth of Asian Americans as the model healthy minority, compounded by language and cultural barriers as well as racism.
“Asian Americans are unique as the first U.S. population to experience cancer as the leading cause of death,” said Chen. “Bigotry against Asian Americans, pervasive since the 19th century, but especially during the COVID-19 pandemic, is only exacerbating the cancer disparities that are costing Asian Americans their lives.”
High rates of certain cancer in Asian Americans
The authors cite a disproportionate rate of certain cancers affecting Asian Americans including: Cancers due to infectious origin such as the human papillomavirus. For example, Vietnamese American women experience the highest U.S rates of cervical cancer. High rates of liver cancer caused by chronic hepatitis B virus (HBV) infection rates in Asian and Southeast Asian Americans, including Hmong Americans. Nasopharyngeal cancers, occurring in the upper part of the throat behind the nose, affecting Chinese Americans at high rates. Stomach cancers, which have the highest rates among Korean Americans. Lung cancer among never-smokers that disproportionately affects Asian American women at a rate of more than twice that of non-Hispanic white women.The authors note an “infinitesimal proportion” of the National Institutes of Health (NIH) budget funded Asian American research even though the population is experiencing the highest percentage increases of any U.S. racial population for the past three decades. Between 1992 and 2018, only 0.17% of the total budget of the NIH funded research on Asian Americans. A portfolio analysis of grants funded by the National Cancer Institute’s Division of Cancer Control and Population Sciences showed a very limited number of studies focused on Asian Americans, with none at the time addressing the causes of cancer.

A new study from the from the University of Missouri School of Medicine and MU Health Care shows patients hospitalized with COVID-19 pneumonia have a higher risk of developing dementia than those with other types of pneumonia.
A team of MU researchers pulled Cerner Real World Data from 1.4 billion medical encounters prior to July 31, 2021. They selected patients hospitalized with pneumonia for more than 24 hours. Among 10,403 patients with COVID-19 pneumonia, 312 (3%) developed new onset dementia after recovering, compared to 263 (2.5%) of the 10,403 patients with other types of pneumonia diagnosed with dementia.
“The risk of new onset dementia was more common in COVID-19 pneumonia patients over the age of 70 in our study,” said lead researcher Adnan I. Qureshi, MD, a professor of clinical neurology at the MU School of Medicine. “The type of dementia seen in survivors of COVID-19 infection mainly affects memory, ability to perform everyday tasks and self-regulation. Language and awareness of time and location remained relatively preserved.”
The median time interval between infection and dementia diagnosis was 182 days for COVID-19 patients. The study only included new onset dementia associated with hospital admission during a short follow-up period. Qureshi said further study over longer periods of time would provide a more complete picture and may help to determine the underlying reasons why COVID-19 pneumonia might increase dementia risk.
“The findings suggest a role for screening for cognitive deficits among COVID-19 survivors,” Qureshi said. “If there is evidence of impairment during screening and if the patient continues to report cognitive symptoms, a referral for comprehensive assessment may be necessary.”
In addition to Qureshi, the study authors include fellow MU School of Medicine collaborators S. Hasan Naqvi, MD, associate professor of clinical medicine; William Baskett, graduate student; Wei Huang, graduate student; and Chi-Ren Shyu, PhD, director, MO Informatics Institute.
Their study, “New Onset Dementia Among Survivors of Pneumonia Associated with Sevre Acute Respiratory Syndrome Coronavirus 2 Infection,” was recently published in the journal Open Forum Infectious Diseases. Part of the support for this study was provided by the National Institutes of Health. The content does not necessarily represent the official views of the funding agency. Qureshi has received consultation fees from AstraZeneca. The authors declare no other potential conflicts of interest.
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Scientists have identified a mechanism that explains how fine air pollution particles might cause lung cancer, according to a study published today in eLife.
The findings could lead to new approaches for preventing or treating the initial lung changes that lead to the disease.
Tiny, inhalable fine particulate matter (FPM) found in air pollutants has been recognised as a Group 1 carcinogen and a substantial threat to global health. However, the cancer-causing mechanism of FPM remains unclear.
“Despite its potential to cause mutations, recent research suggests that FPM does not directly promote — and may even inhibit — the growth of lung cancer cells,” explains first author Zhenzhen Wang, an associate researcher at Nanjing University (NJU), Nanjing, China, who carried out the study between labs at NJU and the University of Macau where she was sponsored by a University of Macau Fellowship. “This suggests that FPM might lead to cancer through indirect means that support tumour growth. For example, some studies suggest FPM can prevent immune cells from moving to where they are needed.”
To explore this possibility, Wang and the team collected FPM from seven locations in China and studied its effects on the main immune cells that defend against tumour growth — called cytotoxic T-cells (CTLs). In mice administered with lung cancer cells that were not exposed to FPM, CTLs were recruited to the lung to destroy the tumour cells. By contrast, in the mice whose lungs were exposed to FPM, the infiltration of CTLs was delayed — potentially allowing the tumour cells to establish in lung tissue.
To investigate why the CTLs did not enter the lung as quickly in the FPM-exposed lungs, the team studied both the CTLs themselves and the lung tissue structure. They found that CTLs exposed to FPM still retained their migratory ability, but that FPM exposure dramatically compressed the lung tissue structure and the spaces that immune cells move between. There were also much higher levels of collagen — a protein that provides biomechanical support for cells and tissues. When the team studied the movement of CTLs in the mice, in lung tissue exposed to FPM, CTLs struggled to move, whereas those in the untreated tissue were able to move freely.
Further analysis of the tissue showed that the structural changes were caused by increases in a collagen subtype called collagen IV, but the team still did not know how FPM triggered this. They found the answer when they looked more closely at the structural changes to collagen IV and the enzyme responsible for making them — called peroxidasin. This enzyme drives a specific type of cross-linking that exposure to FPM was found to cause and aggravate in the lung tissue.
“The most surprising find was the mechanism by which this process occurred,” Wang says. “The peroxidasin enzyme stuck to the FPM in the lung, which increased its activity. Taken together, this means that wherever FPM lands in the lung, increased peroxidasin activity leads to structural changes in the lung tissue that can keep immune cells out and away from growing tumour cells.”
“Our study reveals a completely new mechanism by which inhaled fine particles promote lung tumour development,” concludes senior author Lei Dong, Professor at the School of Life Sciences, Nanjing University. “We provide direct evidence that proteins that stick to fine particulate matter can cause a significant and adverse effect, giving rise to pathogenic activity. Our discovery that peroxidasin is the mediator of this effect in lung tissue identifies it as a specific and unexpected target for preventing lung disease caused by air pollution.”
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By analysing samples from patients who have been treated for malaria in Sweden, researchers at Karolinska Institutet can now describe how the immune system acts to protect the body after a malaria infection. The results, published in the journal Cell Reports, provide knowledge that can aid in the development of more effective vaccines against the disease.
“Our results contribute to a better understanding of how humans fight this serious disease and may help in the development of better vaccines,” says Christopher Sundling, principal researcher at the Department of Medicine, Solna, at Karolinska Institutet, and last author of the study. “This sheds new light on the question of how the body’s immunse system deals with malaria.”
Malaria is caused by parasites that are spread to humans by mosquitoes. The disease caused more than 600,000 deaths in 2020, mainly among young children in sub-Saharan Africa.
People who contract malaria repeatedly may gradually become immune to the disease. But even before that, the body can build up a so-called tolerance, which provides protection against severe disease.
To find out more about how disease tolerance develops, KI researchers have investigated immune cells and proteins in blood samples from patients who have been treated for acute malaria infection at Karolinska University Hospital in Solna, Sweden and have recovered.
This patient group was monitored by being tested on six occasions during one year following the onset of the disease. A total of 53 patients were included, 17 of whom had contracted malaria for the first time, while 36 had grown up in malaria endemic areas, had had malaria many times before and now contracted the disease again after travel.

Dengue is the most widespread mosquito-borne disease in the world, and to date, there are no medical treatments for people suffering from this disease. The virus causes symptoms ranging from high fevers to severe bleeding and shock, can be life-threatening, and presents an enormous burden on health systems.
In Chaos, by AIP Publishing, researchers from Spain, Portugal, and Colombia developed a model the virus. In 2009, researchers discovered mosquitoes carrying Wolbachia bacteria lessen the chances for the dengue virus to impact humans.
Mosquitoes do not acquire Wolbachia bacteria in their natural environment, however. This bacterium must be introduced in vitro in mosquitoes’ eggs, which are later released in areas affected by dengue transmission. Mosquitoes infected with Wolbachia naturally take over the local mosquito population.
The researchers use real data on human and vector activity in a framework that can be analyzed from a mathematical point of view, allowing them to re-create and understand the epidemiological situation. In this way, they can identify those geographical areas with the greatest vulnerability, creating a ranking of areas that prioritizes those where Wolbachia-carrying mosquitoes can have the strongest and most beneficial impact on the spread of the dengue virus.
“One might think that the most populated areas are those in which Wolbachia release would be most beneficial. However, this is not always true,” said co-author Jesus Gomez-Gardenes, from Universidad del Valle in Colombia.
The authors found once they immunize the most vulnerable geographical area, the ranking of the remaining areas is affected, giving rise to a new scenario that tells them where they should concentrate resources in the second instance and beyond.
The findings from this research will be beneficial to many groups, such as the World Mosquito Program, which is currently releasing Wolbachia-infected mosquitoes to protect the global community from diseases such as dengue, chikungunya, yellow fever, and Zika.
In these kinds of initiatives, the information about the most vulnerable areas within cities or regions proved the researchers’ model could complement field studies to find targets that maximize the benefit for the whole community.
“Data-driven models have also proven useful to tackle the evolution and mitigation of other diseases such as COVID-19,” said Gomez-Gardenes. “Hopefully, the framework developed for dengue can be further generalized for tackling the control of other vector-borne diseases.”
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Materials provided by American Institute of Physics. Note: Content may be edited for style and length.

Not only the villas of the rich and famous have a direct line to the police. The cells in our body also have a sophisticated alarm system, the inflammasome. Its central component is the so-called ASC protein. In the event of danger, such as an attack by a pathogen, many of these molecules join together to form a large complex, the ASC speck. This ensures two things: First, its activity causes the cell to accumulate large quantities of messenger substances, which can be used to summon the help of the immune system. And secondly, numerous pores are formed in the cell membrane through which these alarm molecules can reach the outside and fulfill their task.
Last cry for help from the dying cell
These holes ultimately lead to the demise of the cell: “At some point, the cell basically explodes and empties its entire contents into the tissue,” explains Prof. Dr. Bernardo Franklin of the Institute of Innate Immunity at the University Hospital Bonn. “The messenger substances that are now abruptly released then act like a last great cry for help. This triggers the immune system to mount a strong inflammatory response that contains the infection.” That is why this mechanism of innate immune defense is hugely important.
However, in this process, ASC specks also accumulate in the tissue and may persist there for a long time. “We have now been able to show in mice that their activity activates the immune system even after the threat has been averted,” Franklin says. “This can result in chronic inflammation, which severely damages the tissue.” Together with researchers from the University of Sao Paulo, Franklin’s team has succeeded in preventing this undesirable effect. They used so-called nanobodies for this purpose.
These agents are antibody fragments with a very simple structure. “In collaboration with Prof. Dr. Florian Schmidt from the Institute of Innate Immunity, we generated nanobodies that specifically target ASC and can dissolve the specks,” explains Franklin’s collaborator Dr. Damien Bertheloot. The researchers got help from an alpaca: They injected the animal with the ASC protein so that it developed matching antibodies. Some of the alpaca antibodies have a very simple structure. This makes it possible to produce and test fragments of these antibodies as so-called nanobodies.
Rheumatism and gout symptoms alleviated in mice
The researchers were able to obtain the genetic information for the ASC nanobodies from blood samples of the animal using a complex technique. “We then incorporated this genetic makeup into bacteria so that we could have them produce the nanobody in large quantities,” Bertheloot explains. The team demonstrated that the compound can dissolve ASC specks using human cell cultures as well as mice. “The mice in our experiments have rheumatoid and gout-like symptoms,” Bertheloot explains. “After administration of the nanobody, the inflammation and also the general health of the rodents improved significantly.”
Nanobodies are very small compared to normal antibodies. They are therefore excellent for breaking up such molecular complexes. This is because they can still reach sites that would be too cramped for large agents. Moreover, normal antibodies provide additional stimulation to the immune system and can therefore exacerbate inflammation — a property that nanobodies lack.
The results are also interesting for another reason: Studies indicate that ASC specks can also cause significant damage to the brain. There, they seem to serve as a kind of “crystallization nucleus” for the Aß protein. In the brains of Alzheimer’s patients, Aß clumps together to form large protein complexes called plaques. Presumably, ASC specks can trigger this clumping. “So perhaps it’s possible to slow down this process with the help of our nanobodies,” Franklin hopes. “We now plan to investigate this possibility in a follow-up study.” Bernardo Franklin is a member of the ImmunoSensation2 Cluster of Excellence at the University of Bonn.
At the same time, however, he warns against overly high expectations: Even in the ideal case, it will be years before the results might translate into new drugs.
The Institute of Innate Immunity and the Nanobody Core Facility at the University Hospital Bonn were involved in the study. Partners on the part of the University of Sao Paulo were the Center for the Study of Inflammatory Diseases and the Department of Pharmacology.
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In what is believed to be the largest study to date on race and dementia, researchers from UCSF and the San Francisco Veterans Affairs Health Care System tracked health and demographic data from close to two million veterans. It compared rates of dementia across five racial groups and showed significant race-based variations in the incidence of the condition.
This study is also believed to be the first to report the rate of dementia in Native Americans using a nationwide sample, the researchers stated in their paper, publishing in JAMA on April 19, 2022.
Of the 1.87 million veterans, whose average age was 69, 88.6% were white, 9.5% were Black, 1% Hispanic, 0.5% Asian and 0.4% Native American. Just 2.3% were female, consistent with the gender distribution of the older veteran population. All received their health care at medical centers of the Veterans Health Administration (VHA) located throughout the continental United States.
Among the 13% of participants who were diagnosed with dementia over the course of the 10-year study, the researchers found that rates were markedly higher for Hispanic and Black veterans than they were for whites: 99% and 55% respectively. These results reinforce previous research that showed elevated rates for both groups.
Rates for Asian veterans have not been as widely documented and in this study were 24% higher than for whites. Among Native Americans, the rate was 8% higher than for whites, a finding that enhances prior research that has focused on smaller, geographically limited populations and has shown conflicting results, according to the researchers.
When adjusting for sex, education, and underlying medical and psychiatric conditions, differences in dementia rates for all four groups were narrowed slightly in relation to whites: 92% higher for Hispanics, 54% for Blacks, 20% for Asians and 5% for Native Americans. This finding for Native Americans shows no significant difference with whites, the researchers noted.

If you become ill with COVID-19, your smartwatch can track the progression of your symptoms, and could even show how sick you become.
That’s according to a University of Michigan study that examined the effects of COVID-19 with six factors derived from heart rate data. The same method could be used to detect other diseases such as influenza, and the researchers say the approach could be used to track disease at home or when medical resources are scarce, such as during a pandemic or in developing countries. Their results are published in the journal Cell Reports Medicine.
Following U-M students and medical interns throughout the country, the researchers discovered new signals embedded in heart rate indicating when individuals were infected with COVID and how sick they became. The researchers found that individuals with COVID experienced an increase in heart rate per step after symptom onset, and those with a cough had a much higher heart rate per step than those without a cough.
“We found that COVID dampened biological timekeeping signals, changed how your heart rate responds to activity, altered basal heart rate and caused stress signals,” said Daniel Forger, professor of mathematics and research professor of computational medicine and bioinformatics. “What we realized was knowledge of physiology, how the body works and mathematics can help us get more information from these wearables.”
The researchers found that these measures were significantly altered and could show symptomatic vs. healthy periods in the wearers’ lives.
“There’s been some previous work on understanding disease through wearable heart rate data, but I think we really take a different approach by focusing on decomposing the heart rate signal into multiple different components to take a multidimensional view of heart rate,” said Caleb Mayer, a doctoral student in mathematics.