Culture

Nurses and other long-term care workers in nursing homes who hold multiple jobs, may be one of the factors contributing to the spread of COVID-19 in these facilities, according to a new study published in Medical Care Research and Review. The nature of their work in providing essential care to patients in rather close proximity, and the limited access to personal protective equipment for some workers, has made this profession even riskier during the pandemic. The findings examine the likelihood that nurses and direct care workers in long-term care facilities hold a second job, and how demographic differences between the two may affect this probability.

Due to low wages and limited hours, some nurses (registered nurses and licensed practical nurses) and direct care workers (certified nursing assistants, and personal and home care aides) seek secondary employment: 6.41 percent of personal care and nursing aides and 6.23 percent of licensed practical nurses and licensed nurses hold second jobs. This rate of holding a second job is 35 percent and 32 percent, respectively, higher than that of other workers.

Most nurses and direct care workers with second jobs stay within the same occupation at another location, which increases their interaction with patients and the potential for COVID-19 transmission as compared to their counterparts who have one job. Approximately 34 percent of nurses in nursing homes take second jobs in other nursing homes while nearly 30 percent of those who work in hospitals work at other hospitals. Fifty percent of direct care workers work in direct care as a second job while others work as cashiers, in retail or as a janitor or maid. Fifteen percent of second jobs for personal care and nursing aides are in other "essential occupations."

"With higher rates of second job holding among direct care workers and nurses in long-term care than other workers, and many of these workers moving across health settings from their first to second jobs, this creates a potential pathway for COVID-19 transmission," explains co-author Kristin E. Smith, a visiting associate professor of sociology at Dartmouth. "In New Hampshire, 81 percent of COVID-19 deaths are to long-term care residents, representing the highest percentage of deaths to long-term care residents in the country, so understanding employment dynamics and disparities in this sector could never be more timely than now."

The study was based on second job holding data from 2010 to 2019 from the Current Population Survey. While low wages and limited hours were associated with holding a second job for direct care workers, lower hours were more strongly correlated with second job holding among nurses. The results also showed that nurses with children and African American nurses were more likely to hold second jobs than white nurses. Female and married nurses were less likely to have a second job. Nurses had higher wages than direct care workers and worked 30 percent more hours.

White direct care workers were more likely to have second jobs than Asian, American Indian, Alaskan Native workers. Similarly, African American direct care workers were also less likely to take on second jobs when work hours were excluded from the analysis, and Hispanic workers were less likely to have a second job than their non-Hispanic counterparts. Direct care workers with more education were more likely to have a second job.

"The COVID-19 pandemic is shining the spotlight on inequalities throughout our society, particularly in healthcare systems, where we are now seeing real-life implications for loved ones in nursing homes, who are such a vulnerable population," added Smith. "Federal and state-level initiatives aimed at raising wages through bonuses that are higher than unemployment benefits could potentially help decrease the likelihood that these essential care workers must take on a second job and help reduce exposure for COVID-19 transmission."

In recent years, debate has been intensifying over whether the noncompete agreements some companies use to bind employees help or hurt workers. It's an issue management professor Evan Starr at the University of Maryland's Robert H. Smith School of Business has studied extensively -- co-authoring four research papers on the topic forthcoming in top journals. All the results point to the same conclusion: Noncompetes stifle workers.

The findings will be published as "Low Wage Workers and the Enforceability of Non-compete Agreements" in Management Science, "Locked In? The Enforceability of Covenants Not to Compete and the Careers of High-Tech Workers" in the Journal of Human Resources, "The Behavioral Effects of (Unenforceable) Contracts" in the Journal of Law, Economics, and Organization, and "Noncompete Agreements in the U.S. Labor Force" in the Journal of Law and Economics.

The latter, says Starr, represents the most sweeping work and is the first systematic investigation of noncompetes in the United States. In it, he studies a nationally representative sample, looking at all sorts of workers. One of the key findings: Noncompetes are found even among low-wage workers. "There have been anecdotes of that fact, but this is the first systematic evidence," says Starr. "This is shocking because when you think about noncompetes, you think about tech workers and executives - you're not thinking about doggie-daycare sitters or hairstylists or yoga instructors, but that's the modal worker that's bound by a noncompete. Our paper launches from that fact, and the key question for policymakers is this a good or a bad thing?"

"The argument for why they are bad is pretty clear," Starr says. Take the case of the low-wage worker, earning $12 an hour, who gets a better offer at a competitor to make $15 an hour. "A noncompete could prevent them from making those sorts of moves that are going to enhance their social and economic mobility."

So how do companies justify using these restrictions? Starr says past research argues that noncompetes give firms incentive to invest in workers to develop their skills and knowledge to make them more productive, and that boost will help the individual workers make more money than they could have otherwise.

"All states in the U.S. that enforce noncompete agreements require that workers have some sort of 'protectable,' legitimate interest, which is exactly this sort of investment: That you're giving workers trade secrets or very specialized training."

Policymakers have taken up the issue. In late 2019, Starr testified about the use of noncompetes before the U.S. House of Representatives and the U.S. Senate. Even earlier, in 2016, the U.S. Treasury and the Obama Administration used Starr's findings as the basis of related reports, spurring states to reexamine noncompete policies. In the past two years, some - including Maryland, Virginia, and Washington DC - have moved to ban noncompetes for low-wage earners. But Oregon was the trailblazer, doing so back in 2008, making it the perfect case study for Starr (in the forthcoming in Management Science paper), with co-author Michael Lipsitz, an economist for the Federal Trade Commission.

The Oregon law banned noncompete agreements for all hourly workers and for workers earning below the median income for a family of four in the United States. It also banned noncompetes for certain occupations.

"We looked broadly at hourly workers, because hourly workers comprise 67% of working population in Oregon, and it was very clear in the bill that all noncompetes are banned for hourly workers," Starr says.

The findings were clear: Low-wage workers benefited from the ban, earning higher wages and changing jobs more. On average, hourly workers' wages grew by 6% five years after the ban. The positive wage effects were across the board, in all age groups and education levels. The researchers also found that workers' job-to-job mobility rose by 17% overall, with 79% of this increase in mobility driven by an increase in moves within an industry - "exactly the kinds of moves that a noncompete would prohibit," Starr says.

The findings show that not only are workers moving to new jobs within their industries, they are also moving up to better jobs. And while men benefit from this ban on noncompetes, women benefit almost twice as much, suggesting that noncompetes were holding down the earnings of low-income women more than men, Starr says. "It could be that women are less likely to negotiate over these sorts of provisions, and so they are harmed more when these are being enforced."

The researchers analyzed how companies responded to the noncompete ban and found that there was no impact on hours worked, so firms are still employing workers, on average, for the same amount of time. "What that means is workers' take-home pay ultimately goes up - hourly wage increases translate into actual earnings increases," Starr says.

They also looked at whether firms changed compensation structures in response to the new law, because Oregon only banned noncompetes for hourly workers and those who make less than the median household income for a family of four. They find that workers earning just above that threshold were more likely to become salaried. "One perk of the structure of this bill is to get workers into more stable situations, even if they are still using noncompetes with them," Starr says.

"Despite good arguments for noncompetes potentially benefiting workers, the evidence just doesn't support that claim. The evidence suggests that these are bad for low-wage workers."

Paralleling the Oregon study, Starr's research for the Journal of Human Resources looks at a 2015 Hawaii law that banned noncompetes in the high-tech industry. His findings are the same. "After Hawaii banned noncompetes for tech workers, their wages rise, their job mobility rises. It's basically the same story but in a very different set of occupations, where arguments about the investment effects of noncompetes seem more plausible."

And, the work in the Journal of Law, Economics and Organization looks at the influence of per se unenforceable noncompete agreements. "We find that they still do matter, in fact to a similar degree as in states where they are totally enforceable. We look at why that is and find evidence that workers are proactively turning down jobs, not because of the law, but because they are scared of a lawsuit."

Collectively, Starr's papers show that workers do better without noncompete agreements. But what about firms?

Firms may be less profitable if they have to pay workers more, Starr says, but there's definitely a benefit for them too: Without noncompetes, firms have unfettered access to the labor market and can hire the workers they want to hire, including those from a competitor. "It's not really a firm versus worker issue. It could be a win for both workers and firms."

URBANA, Ill. - Walking rows of soybeans in the mid-summer heat is an exhausting but essential chore in breeding new cultivars. Researchers brave the heat daily during crucial parts of the growing season to look for plants showing desirable traits, such as early pod maturity. But without a way to automate detection of these traits, breeders can't test as many plots as they'd like in a given year, elongating the time it takes to bring new cultivars to market.

In a new study from the University of Illinois, researchers predict soybean maturity date within two days using drone images and artificial intelligence, greatly reducing the need for boots on the ground.

"Assessing pod maturity is very time consuming and prone to errors. It's a scoring system based on the color of the pod, so it is also subject to human bias," says Nicolas Martin, assistant professor in the Department of Crop Sciences at Illinois and co-author on the study. "Many research groups are trying to use drone pictures to assess maturity, but can't do it at scale. So we came up with a more precise way to do that. It was really cool, actually."

Rodrigo Trevisan, a doctoral student working with Martin, trained computers to detect changes in canopy color from drone images collected across five trials, three growing seasons, and two countries. Importantly, he was able to account for "bad" images to maintain accuracy.

"Let's say we want to collect images every three days, but one day, there are clouds or it's raining, so we cannot. In the end, when you get the data from different years or different locations, they will all look different in terms of the number of images and the intervals and so on," Trevisan says. "The main innovation we developed is how we can account for whatever we are able to collect. Our model performs well independent of how often the data was collected."

Trevisan used a type of artificial intelligence called deep convolutional neural networks. He says CNNs are similar to the way human brains learn to interpret components of images - color, shape, texture - from our eyes.

"CNNs detect slight variations in color in addition to shapes, borders, and texture. For what we were trying to do, color was the most important thing," Trevisan says. "But the advantage of the artificial intelligence models we used is that it would be quite straightforward to use the same model to predict another trait, such as yield or lodging. So now that we have these models set up, it should be much easier for people to use the same architecture and the same strategy to do many more things."

Martin says commercial breeding companies are clamoring for these capabilities.

"We had industry partners on the study who definitely want to use this in the years to come. And they made very good, important contributions. They wanted to make sure the answers were relevant for breeders in the field making decisions, selecting plants, and for farmers," Martin says. "Finding a good method to help breeders actually make decisions on large scales is quite exciting."

Just like other organisms, plants must respond dynamically to a variety of cues over their lifetime. Going through different developmental stages, or altering their form in response to a drought or drastic temperature change requires altering which of their genes are expressed into proteins and when those processes occur.

In a new paper in Developmental Cell, a research team led by Penn biologists Brian Gregory and Xiang Yu identified a mechanism by which plants can conduct this agile regulation of gene expression. They unpacked the details of a process whereby hormone signaling triggers the removal of a structure called nicotinamide adenine dinucleotide (NAD+) from one end, called the 5' end, of certain messenger RNA (mRNA) molecules, the transcripts that give rise to proteins. When present, these caps direct the cell to break down the associated mRNA transcript, ensuring that its corresponding protein is not made.

"We saw changes in the level of mRNA NAD+ capping occurring in different plant tissues and in different developmental stages," says Gregory, senior author on the paper and an associate professor in the School of Arts & Sciences' Department of Biology. "This appears to be a potentially quick on/off switch that plants can use to regulate their RNA levels."

"Researchers working on mammalian cells had identified an enzyme that appears to perform an analogous action, removing these NAD+ caps," says Yu, a postdoctoral researcher in Greogry's lab and the paper's first author. "Ours is the first study to show this process in a whole, living organism."

This work has its origins in preliminary findings that Gregory's lab generated close to a decade ago. While teaching a class on RNA, Gregory had shared with his students a paper about a yeast version of the plant protein DX01, an enzyme now known to be responsible for removing NAD+ from mRNA.

"I became really intrigued about what it was doing in eurkaryotes," he says. At that time, his lab grew plants with a DX01 mutation and found that their growth was stunted, their leaves were pale green, their development was delayed, and they had defects in fertility.

"I thought, 'This is cool, we need to work on this,'" Gregory recalls.

Pursuing it, they found that the mutants had an abundance of small RNAs, molecules often associated with silencing the expression of other RNA molecules. But ultimately they couldn't piece together a sensible story of how the mutation was causing small RNAs to accumulate, and the work stalled.

It stalled that is, until a few years ago, when other scientists who work on mammalian RNA regulation began publishing work showing that mammalian cells possess DX01 as well, and that it could recognize and remove NAD+ caps.

With this new understanding of DX01's role, Gregory, Yu, and colleagues decided to pick their own work back up. By studying plants, the group could take the findings in mammals a step further, looking in vivo, at how the enzyme was acting in a live, growing organism.

The researchers first confirmed that DX01 acted similarly in plants as in mammals, removing the NAD+ from mRNA transcripts. Plants lacking DX01 developed the problems Gregory had seen years earlier: stunted growth and development. They also used a technique to isolate and sequence only the NAD+-capped mRNAs and found that mRNA transcripts with NAD+ caps occurred frequently for those encoding proteins related to stress response, as well as those involved in processing NAD+ itself. Further analysis confirmed that the NAD+ cap made mRNAs more likely to be broken down.

To follow up on the clues pointing to an involvement in stress response, the team applied varying levels of a plant stress hormone, abscisic acid, to plants with or without a functioning DX01. Plants with a mutant DX01 did not appear to be affected by the changing hormone concentration, while those with a functional DX01 were, pointing to a role for NAD+ capping in responding to this hormone.

And indeed, they found that the level of NAD+ capping of RNA in response to abscisic acid dynamically changed.

"It does look like NAD+ capping is tissue-specific and responds to at least one specific physiological cue," says Gregory, "at least in plants. That's pretty neat becaue it looks like it's a strong regulator of RNA stability, so the plant can destabilize different sets of mRNA transcripts, depending on where this process is acting and what cue is being given."

The group's findings even tied back to the unusual discovery they had made much earlier, of a build-up of small RNA molecules. In their DX01 mutant plants, they observed that the NAD+ capped mRNA transcripts were processed into small RNAs, which are also unstable. Gregory, Yu, and colleagues believe this may be a secondary mechanism to remove NAD+ and rid themselves of these noncanonically capped transcripts, even in the absence of DX01.

"What's going on is they're using another pathway, making small RNAs, perhaps to get back the NAD+ so they can use it for other processes," Yu says.

Indeed, NAD+ is a critical component in metabolism, so it makes sense that plants would have multiple strategies for ensuring they have enough available to them, the researchers say.

In future work, the Gregory lab hopes to continue exploring the NAD+ mark, including working out how it is added and not just removed.

"Once we learn how to add, recognize, and remove it, it gives us the power to use this process as a tool for regulating various responses in plants," Gregory says, a power that could possibly be used in agriculture.

But human health could benefit from these insights as well. The Penn researchers say that the work deserves follow-up in mammalian systems. "I'd be curious to see what types of mRNA transcripts in mammals respond to different hormones," says Gregory.

Addition and removal of the NAD+ cap may even be involved in cancer biology, Gregory and Yu say. The abnormal cell metabolism seen in cancer cells often owes to mishaps in the type of regulation that mRNA transcripts undergo, and there's a "real probability," Gregory says, that NAD+ capping and decapping could play a role.

For his part, Gregory is pleased to have been able to move forward with an area of research that eluded him years ago, one that is opening up a new area of study for his lab.

"This is definitely one of those stories that reminds me that science is not a sprint; it's a marathon," Gregory says.

Michael Gross, professor of chemistry in Arts & Sciences at Washington University in St. Louis and of immunology and internal medicine at the School of Medicine, and his team are experts in footprinting proteins -- that is, using advanced methods for investigating the structure and interactions of proteins within larger molecules.

By sharing their method for fast photochemical oxidation of proteins (FPOP), a means of protein footprinting, they hope to support other labs in developing broader applications of FPOP to better address outstanding questions in structural biology.

"FPOP has drawn significant attention because it complements existing footprinting," said Roger Liu, a graduate student working with Gross and first author of a new publication about protein footprinting in the journal Nature Protocols. "Its major advantages include fast labeling time frame, irreversible nature, high sensitivity and relatively broad amino acid residue coverage."

Despite the compelling advantages of FPOP, the technical difficulty of establishing the platform has caused a lag in broader applications. Liu cites challenges including choosing the proper laser, setting up the laser optics, establishing the flow system, acquiring the footprint and analyzing the results by mass spectrometry.

"We always thought that the best way to disseminate FPOP is by applications," Gross said. "Following its discovery, we have implemented it for problems in biochemistry and biophysics."

Fast protein folding could be beneficial for mapping epitopes, which are the parts of an antigen that are recognized by the immune system. This application is potentially important for scientists and medical professionals racing to address the COVID-19 pandemic.

Other applications could include understanding aggregating proteins, with implications in Alzheimer's disease; uncovering hidden conformational changes invisible to other structural methods; and determining binding sites and binding affinities of small molecules that bind to proteins.

Gross added: "Currently, in a collaboration with Weikai Li in the Department of Biochemistry and Molecular Biophysics, we are moving into transmembrane and membrane-associated proteins where new structural methods are desperately needed for this important class of proteins."

A new 5-month longitudinal analysis of 254 COVID-19 patients who displayed a wide range of disease severity - from asymptomatic to deadly illness - suggests that IgA and IgM antibodies to the SARS-CoV-2 virus disappear quickly during convalescence. IgG antibodies likely persist for longer, but Katharina Röltgen and colleagues nonetheless documented a slow, inexorable decline in this antibody class as well, even in severely ill patients who mounted very strong initial antibody responses. Studying 983 plasma samples collected up to 5 months post-infection from 79 hospitalized COVID-19 patients and 175 outpatients and asymptomatic people infected with SARS-CoV-2, Röltgen et al. found a higher ratio of antibodies that react to the viral spike protein complex (versus those that target the nucleocapsid protein) in patients with mild illness compared with the severely ill patients, suggesting that this preponderance of spike-reactive antibodies may have helped to blunt the severity of symptoms. To facilitate their work, the researchers also developed an immunoassay that can detect successful blocking of the viral receptor binding domain's interaction with the human ACE2 receptor in human samples, providing an effective surrogate for detecting neutralizing antibodies. The authors say their findings may raise important questions about the reliability of seroprevalence studies, since the rapid waning of antibody titers may lead to an underestimation of how many people may have been previously infected in a given population. "The decrease in antibodies after infection also raises the question of how long antibodies elicited by vaccination will last, and whether frequent boosting will be needed to maintain protection," the authors further note.

An Asian hornet sets its sights on a busy honey bee hive. If all goes according to plan, the hornet's attack will result in a haul of bee larvae, precious nourishment to pilfer and feed to its own hornet young.

But over time, predator-prey evolution has equipped some honey bees with a potent defense mechanism against such an attack. A signal from colony guard bees lets hornets know that their attack plans have been exposed, and also sends an alarm across the bee colony communicating that urgent reinforcements are needed due to the impending danger. This "I see you" (ISY) visual signal involves guard bees shaking their abdomens laterally and increases as the threat intensifies.

Hornets are ferocious bee predators that have invaded multiple countries around the world. Yet even the giant "murder" hornets that have generated much concern of late have come to recognize the ISY signal as a warning to back off. They are well aware that ISY can lead to a counter attack in which a mass of bees surrounds the hornet, forming a "heat ball" with a deadly mix of heat, carbon dioxide and stinging for the hornet inside.

University of California San Diego biologists studying Asian honey bees (Apis cerana) and hornets (Vespa velutina) have produced new research that deconstructs this ISY signal and shows for the first time that it is visually driven and contagious across the bee colony. The findings are described Dec. 7, 2020 in the Journal of Animal Ecology. A key point of the new study is that the bees can only succeed if they have sufficient numbers to effectively execute a heat ball.

"The beauty of the ISY signal is that hornets are only deterred if enough defending bees quickly gather to synchronously produce the signal, thereby showing the hornet that further attack is futile," said study senior author James Nieh, a professor in the Section of Ecology, Behavior and Evolution in UC San Diego's Division of Biological Sciences.

But how to gather this defense? Nieh says the ISY signal is contagious and attracts other defenders who immediately copy the signal and rush towards the signaler, even if they cannot directly see or sense the predator.

"Hornets give off smell and sound but we found that the visual of a hornet alone can elicit the signal, which was not known," said Nieh. Previous speculation held that guard bees might produce a pheromone to alert others in the colony of the impending danger. "Using just a contagious visual signal is better because guards who are too far away to smell or hear the hornet can immediately head towards the threat. In some ways, it's like a fast chain reaction," said Nieh.

Nieh says the concept links to the issue of "fake news" since animal communication often contains errors, and a false ISY alarm could rapidly spread within the colony.

One solution to the problem of false information spread is that the bees are very selective about what they consider a true threat. Using an iPad to display videos, researchers Shihao Dong, Ken Tan and Nieh found that the visual appearance and motion of the hornet alone could trigger ISY signals. Visual displays of a harmless butterfly, on the other hand, elicited no response. The second and most important safeguard against false reporting is that bees are even more choosy about what they consider to be a real ISY signal.

"We played back videos of bees performing ISY signals at different speeds, but only the correct bee image at the right speed caused other bees to respond. This helps keep the signal spread honest," said Nieh.

It is still true that a bee could occasionally "cry wolf" but Nieh thinks that evolution has limited these errors because nestmates must work together to fight these powerful predators and colonies prone to errors would suffer. Nieh and his colleagues are now testing the details of the visual cues behind ISY. They are developing animations that display related visuals that can be tested, such as whether a harmless butterfly can be depicted as threatening, or whether offshoots such as a hornet displayed without wings could be enough to trigger ISY.

Nieh believes that the findings provide a cautionary tale about fake news for all of us.

"Individuals in a honey bee colony are completely interdependent. They can't go out and make it on their own. Cooperation is paramount, especially when faced with a large, heavily armored predator like hornets," said Nieh. "A couple of hornets can kill thousands of bees in a single day. Yet through teamwork that correctly produces synchronized, massed ISY signals, they can get the hornet to back off without harming a single bee. Maybe that's a lesson for us all."

A new study of more than 150 COVID-19 patients shows that IgA antibodies dominate the early response to the SARS-CoV-2 virus, coming on more quickly and strongly than IgG and IgM antibodies. This is a somewhat unexpected result, as IgM antibodies are usually the immune system's first responders. The finding may also inform the development of vaccines that encourage the IgA response, as well as IgA-based tests to detect infection at early stages, Delphine Sterlin and colleagues say. The researchers measured antibody responses in blood, saliva, and fluid from a broncho-alveolar wash in the patients, whose disease symptoms ranged in severity. They found that IgA concentrations were higher than IgG and IgM concentrations in these fluids for the first 3 to 4 weeks after the first appearance of symptoms and then waned, but IgA persisted in saliva for several more weeks. The surge in IgA was associated with an increase in IgA-secreting cells called plasmablasts, which can preferentially target the mucosal surfaces in the respiratory tract that the virus attacks. Sterlin et al. also found that IgA was more potent than IgG at neutralizing SARS-CoV-2.
     

In a separate, unrelated study, Zijun Wang and colleagues took a closer look at IgA responses to SARS-CoV-2 in 149 individuals recovering from COVID-19. After cloning antibodies taken from the patients, Wang et al. discovered that the dimeric form of IgA - consisting of two IgA molecules linked together - was roughly fifteen times better at neutralizing the SARS-CoV-2 virus than the monomeric form. Dimeric IgA is typically considered the most prevalent antibody isotype in mucosal tissues of the upper respiratory tract, a major point of entry for the virus. Given the potency of the dimeric IgA antibodies, Wang et al. suggest that a vaccine designed to induce dimeric IgA, perhaps delivered orally or nasally to target mucosal tissues, could offer protection against the virus.

HOUSTON - (Dec. 7, 2020) - Indian women past childbearing age are dying at a higher rate than those in other countries because of poverty and limited access to resources such as food and health care, according to a study from Rice University.

"Why Are Older Women Missing in India? The Age Profile of Bargaining Power and Poverty" was published in a recent edition of the Journal of Political Economy. The research examines the impact of India's substantial gender inequality on the health, poverty and mortality of Indian women 45 and older.

Rossella Calvi, an assistant professor of economics at Rice and the study's author, developed a theoretical model of household resource allocation and analyzed consumer spending in India. She used the model to examine how women's access to family resources, such as food and health care, varies over their lifetimes.

"In India, only 1 in 3 women work outside the home, and traditional norms dictate that their primary role is childbearing and child-rearing," Calvi said. "When women enter their post-childbearing years, one of their main productive activities disappears. Meanwhile, men of the same age remain productive by continuing to work. This fact has critical consequences for women's bargaining power within their families.

"The estimates from my model indicate that the decline in women's intrahousehold bargaining power during post-reproductive ages could help explain the excessively high mortality rates of older women in India," she continued. "The decrease in women's bargaining power is reflected in their diminished ability to access household resources. As a result, at older ages poverty rates are significantly higher among women than men, which negatively affects women's health and increases their mortality risk. The excessive poverty rates of women are even more pronounced in households where women beyond childbearing ages have no children to care for."

Calvi said India's inheritance laws may have exacerbated inequality between women and men. Until the 1970s, an Indian woman's ability to inherit family land was limited, and some restrictions remained in place until 2005, when a national amendment improved women's rights.

"Moving forward, we should expect women to have a slightly higher share of resources because of their improved ability to inherit property, which may boost their bargaining power," Calvi said.

Calvi said she hopes her research will lead to policies that support older women and improve their mortality rates in countries such as India.

A drug currently prescribed to treat a rare enzyme deficiency can help cells clear the herpes simplex 1 and herpes simplex 2 viruses, according to a new study published in the journal Science Advances.

The new data shows that the antiviral activity of the drug -- called phenylbutyrate, or PBA -- was even better when used along with acyclovir, a common HSV-1 treatment. When used in combination, less acyclovir is needed to effectively suppress the virus compared to acyclovir alone -- this is important because acyclovir is also known to have toxic side effects in the kidneys.

"There are very few drugs available to treat herpes simplex viruses, so when new drugs become available, especially drugs that enable fewer side effects, it is a welcome discovery," said Dr. Deepak Shukla, the Marion Schenk Professor of Ophthalmology and UIC professor of microbiology and immunology at the College of Medicine and corresponding author on the paper. "Acyclovir can have very toxic effects on the kidneys, especially when it is given in higher doses for HSV-induced encephalitis, which is rare but can be deadly. By combining acyclovir with PBA, we need less acyclovir to effectively treat HSV-1."

There are two types of herpes simplex virus: herpes simplex 1, which infects the eyes and mouth and is a leading cause of blindness, and herpes simplex 2, a genital infection that may cause painful sores and can seriously impair quality of life.

Treatment for both infections often includes acyclovir -- a systemic medication taken orally. However, long-term use often results in resistance to the drug as well as kidney damage.

Shukla and colleagues investigated the antiviral effects of PBA and found that in cells the drug disrupts the ability of the virus to hijack the cellular machinery used to produce proteins. Normally, viruses infect cells and force them to produce viral proteins so the virus can replicate itself. But the cell also continues to produce proteins for its own use, leading to a lot of stress in the structure -- called the endoplasmic reticulum, or ER for short -- that makes protein.

"We found that PBA reduces stress on the ER, which allows the cell to focus on clearing the virus on its own," said Tejabhiram Yadavalli, a UIC ophthalmology and visual sciences postdoctoral fellow and first author of the paper.

The researchers found that in cells, PBA alone was able to clear HSV-1 from cells of donated human corneas or from donated human skin tissue just as well as acyclovir. In a mouse model of ocular HSV-1 infection, PBA administered intraperitoneally was able to clear the virus from the eyes.

In an animal model of HSV-2 vaginal infection, mice that received PBA had no signs of the HSV-2 virus in tissues, similar to mice treated with acyclovir.

When they tested a combination of PBA with acyclovir cells infected with HSV-1, the drug combo was able to completely clear the virus from the cells faster and better than either drug alone. Additionally, in a mouse model of HSV-induced encephalitis, mice treated with PBA or acyclovir alone had significantly reduced death rates, but a combination of PBA and acyclovir was able to prevent death in all mice given this combination.

"PBA is an exciting new therapeutic for treating herpes infections that can help reduce side effects associated with long term or high dose use of acyclovir, a commonly prescribed medication to treat herpes viruses," Shukla said. "The added bonus of this drug already being approved by the FDA to treat a rare enzyme disorder means that we may be able to quickly develop a marketable new combination therapy in the near future."

UCLA researchers are the first to create a version of COVID-19 in mice that shows how the disease damages organs other than the lungs. Using their model, the scientists discovered that the SARS-CoV-2 virus can shut down energy production in cells of the heart, kidneys, spleen and other organs.

"This mouse model is a really powerful tool for studying SARS-CoV-2 in a living system," said Dr. Arjun Deb, a co-senior author of a paper about the study and a member of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA. "Understanding how this virus can hijack our cells might eventually lead to new ways to prevent or treat the organ failure that can accompany COVID-19 in humans."

Deb said the same model could also help researchers learn more about other similar viruses that might emerge in the future, and it could be useful for testing eventual treatments.

The paper, published in the journal JCI Insight, was co-led by Vaithilingaraja Arumugaswami, an associate professor of molecular and medical pharmacology at the David Geffen School of Medicine at UCLA and a member of the Broad Stem Cell Research Center.

Researchers often study mice to understand the fundamentals of human disease, but translating human health conditions to animal models can be tricky. SARS-CoV-2, for instance, relies on the ACE2 protein to infect humans. But the virus doesn't recognize the mouse version of ACE2, so healthy mice exposed to the SARS-CoV-2 virus don't get sick.

In previous experiments by other research teams around the world, mice have been genetically engineered to have the human version of ACE2 in their lungs and then been infected -- through their noses -- with the SARS-CoV-2 virus. Although that enables the virus to infect the mice and cause pneumonia, animals in those experiments don't get as broad a range of other symptoms as humans do.

"Among COVID-19 patients, those who have organs involved other than the lungs are most at risk of a bad outcome," said Deb, who is also a cardiologist and professor of molecular cell and developmental biology. "So we felt it was really important to understand how the virus affects those other organs."

Research in humans has suggested that SARS-CoV-2 can circulate through the bloodstream to reach multiple organs. So in the UCLA experiment, the researchers first engineered mice to have the human version of ACE2 in the heart and other vital organs. Then, they infected half of the animals by injecting SARS-CoV-2 into their bloodstreams. Over the following days, the researchers tracked the animals' overall health and analyzed how levels of certain genes and proteins in their bodies changed.

Within seven days, all of the mice with COVID-19 had stopped eating and were completely inactive, and had lost, on average, about 20% of their body weight. Animals that had been engineered to carry the human ACE2 protein but had not been infected with the virus, on the other hand, did not lose a significant amount of weight.

Moreover, the COVID-19 infected animals had altered levels of immune cells, swelling of the heart tissue and wasting away of the spleen -- all symptoms that have been observed in people who are critically ill with COVID-19.

Deb's team also looked at which genes were turned on and off in the mice infected with SARS-CoV-2, and they discovered other signs of disease. Common molecular processes that help cells generate energy -- through mechanisms known as the tricarboxylic acid cycle, or TCA cycle, and electron transport chain -- were shut off in the heart, kidney, spleen and lungs.

"If a virus snuffs out the energy-generating pathways in multiple organs of the body, that's going to really wreak havoc," Deb said.

Finally, the study also revealed that some changes were long-lasting throughout the organs in mice with COVID-19. In addition to temporarily altering which genes were turned on and off in some cells, the virus made epigenetic changes -- chemical alterations to the structure of DNA that cause more lasting effects. Deb said that could explain why, in some people with COVID-19, symptoms persist for weeks or months after their bodies are rid of the virus.

Although the findings don't have immediate implications for treating COVID-19, Deb said the mouse model will be useful for ongoing studies on how the virus infects vital organs other than the lungs, and for trials of new drugs to treat the disease.

(December 7, 2020) - A team of UTSA researchers has discovered that economic implications because of COVID-19 can have a devastating ripple effect on children. Monica Lawson, assistant professor of psychology, Megan Piel, assistant professor of social work and Michaela Simon, psychology graduate student in the UTSA College for Health, Community and Policy, have recently published a research article on the effects of parental job loss during the COVID-19 pandemic and risk of psychological and physical abuse toward children.

Using a community sample of 342 parents of 4- to 10-year-olds living in the United States, the researchers investigated factors associated with child maltreatment during the pandemic.

"We know that risk for child abuse increases during economic crises. We saw this during the Great Depression and the Great Recession and our study expanded this research to the COVID-19 pandemic," said Lawson. "We found that job loss due to the pandemic was associated with abuse towards children. Our study is unique by showing that positive coping strategies, however, can mitigate the risk for physical abuse against children, even among families where a parent lost their job."

The study included parental job loss and whether cognitive reframing moderated associations between job loss and child maltreatment. The researchers asked study participants to complete online questionnaires regarding their experiences with COVID-19, parental behaviors towards children, including psychologically and physically abusive behaviors, and coping strategies.

The research findings demonstrate that parental job loss due to the pandemic can have negative consequences on young children, including increased risk for psychological and physical abuse at the hands of their parents.

Another research finding demonstrates, however, that among parents who lost their jobs, physical abuse toward children decreased as parents engaged in more positive coping strategies. That is, parents who view hardships as something they can overcome without becoming too discouraged were less likely to physically abuse their children during the pandemic, even if they lost their jobs.

Importantly, these findings emerged when statistically controlling for whether families had a history of psychological and physical abuse before the pandemic, child and parent age and gender, parental depression, and family financial stability.

The researchers also found that the findings have consequences for economic policies and employment practices, but also indicate that focusing on parental mental health and, in particular, fostering healthy coping strategies among families is important during times of economic crises and may help to reduce family violence, including child abuse.

Lawson explains "We're just starting to understand the impact of the pandemic on family functioning and well-being." She adds, "Understanding factors that contribute to child abuse during the pandemic is critical for identifying at-risk families and providing services to protect children. This is especially important within the unique context of the pandemic when many children are at home and out of sight of mandated reporters."

A disease common during the First World War, trench fever, has been found in some urban populations experiencing homelessness in Canada, and physicians should be aware of this potentially fatal disease, highlights a practice article in CMAJ (Canadian Medical Association Journal).

The article describes a 48-year-old man who visited an emergency department in Manitoba with chest pain and shortness of breath. In the previous 18 months, the patient had sought care for episodes of chest pain and body lice infestation.

Bartonella quintana is a bacterium that is transmitted by body lice and causes a disease called trench fever, which killed millions of people during the First World War. It can lead to an infection of the heart, known as endocarditis, that can be fatal if untreated.

"Our public health message is that this disease is present in Canada and that people and physicians aren't always aware," says Dr. Carl Boodman, an infectious disease physician at the University of Manitoba, Winnipeg, Manitoba. "It's associated with homelessness and homeless shelters, and physicians should consider B. quintana infection in people who are unwell and have a history of body lice infestation."

The authors are aware of only 4 other cases in Canada over the last 20 years.

Symptoms of trench fever include fever, headache and malaise. It can be difficult to detect, requiring molecular testing and consultation with infectious disease experts.

"Clinicians should consider Bartonella serology, echocardiography and infectious disease consultation when caring for individuals who present unwell with a history of body lice infestation. B. quintana infection likely remains underdiagnosed," the authors conclude.

A novel form of an Alzheimer's protein found in the fluid that surrounds the brain and spinal cord indicates what stage of the disease a person is in, and tracks with tangles of tau protein in the brain, according to a study from researchers at Washington University School of Medicine in St. Louis. Tau tangles are thought to be toxic to neurons, and their spread through the brain foretells the death of brain tissue and cognitive decline. Tangles appear as the early, asymptomatic stage of Alzheimer's develops into the symptomatic stage.

The discovery of so-called microtubule binding region tau (MTBR tau) in the cerebrospinal fluid could lead to a way to diagnose people in the earliest stages of Alzheimer's disease, before they have symptoms or when their symptoms are still mild and easily misdiagnosed. It also could accelerate efforts to find treatments for the devastating disease, by providing a relatively simple way to gauge whether an experimental treatment slows or stops the spread of toxic tangles.

The study is published Dec. 7 in the journal Brain.

"This MTBR tau fluid biomarker measures tau that makes up tangles and can confirm the stage of Alzheimer's disease by indicating how much tau pathology is in the brains of Alzheimer's disease patients," said senior author Randall J. Bateman, MD, the Charles F. and Joanne Knight Distinguished Professor of Neurology. Bateman treats patients with Alzheimer's disease on the Washington University Medical Campus. "If we can translate this into the clinic, we'd have a way of knowing whether a person's symptoms are due to tau pathology in Alzheimer's disease and where they are in the disease course, without needing to do a brain scan. As a physician, this information is invaluable in informing patient care, and in the future, to guide treatment decisions."

Alzheimer's begins when a brain protein called amyloid starts forming plaques in the brain. During this amyloid stage, which can last two decades or more, people show no signs of cognitive decline. However, soon after tangles of tau begin to spread in the neurons, people start exhibiting confusion and memory loss, and brain scans show increasing atrophy of brain tissue.

Tau tangles can be detected by positron emission tomography (PET) brain scans, but brain scans are time-consuming, expensive and not available everywhere. Bateman and colleagues are developing diagnostic blood tests for Alzheimer's disease based on amyloid or a different form of tau, but neither test can pin down the amount of tau tangles across the stages of disease.

MTBR tau is an insoluble piece of the tau protein, and the primary component of tau tangles. Bateman and first author Kanta Horie, PhD, a visiting scientist in Bateman's lab, realized that specific MTBR tau species were enriched in the brains of people with Alzheimer's disease, and that measuring levels of the species in the cerebrospinal fluid that bathes the brain might be a way to gauge how broadly the toxic tangles have spread through the brain. Previous researchers using antibodies against tau had failed to detect MTBR tau in the cerebrospinal fluid. But Horie and colleagues developed a new method based on using chemicals to purify tau out of a solution, followed by mass spectrometry.

Using this technique, Horie, Bateman and colleagues analyzed cerebrospinal fluid from 100 people in their 70s. Thirty had no cognitive impairment and no signs of Alzheimer's; 58 had amyloid plaques with no cognitive symptoms, or with mild or moderate Alzheimer's dementia; and 12 had cognitive impairment caused by other conditions. The researchers found that levels of a specific form -- MTBR tau 243 -- in the cerebrospinal fluid were elevated in the people with Alzheimer's and that it increased the more advanced a person's cognitive impairment and dementia were.

The researchers verified their results by following 28 members of the original group over two to nine years. Half of the participants had some degree of Alzheimer's at the start of the study. Over time, levels of MTBR tau 243 significantly increased in the Alzheimer's disease group, in step with a worsening of scores on tests of cognitive function.

The gold standard for measuring tau in the living brain is a tau-PET brain scan. The amount of tau visible in a brain scan correlates with cognitive impairment. To see how their technique matched up to the gold standard, the researchers compared the amount of tau visible in brain scans of 35 people -- 20 with Alzheimer's and 15 without -- with levels of MTBR tau 243 in the cerebrospinal fluid. MTBR tau 243 levels were highly correlated with the amount of tau identified in the brain scan, suggesting that their technique accurately measured how much tau -- and therefore damage -- had accumulated in the brain.

"Right now there is no biomarker that directly reflects brain tau pathology in cerebrospinal fluid or the blood," Horie said. "What we've found here is that a novel form of tau, MTBR tau 243, increases continuously as tau pathology progresses. This could be a way for us to not only diagnose Alzheimer's disease but tell where people are in the disease. We also found some specific MTBR tau species in the space between neurons in the brain, which suggests that they may be involved in spreading tau tangles from one neuron to another. That finding opens up new windows for novel therapeutics for Alzheimer's disease based on targeting MTBR tau to stop the spread of tangles."

Cold Spring Harbor Laboratory (CSHL) scientists developed the world's first mobile genome sequence analyzer, a new iPhone app called iGenomics. By pairing an iPhone with a handheld DNA sequencer, users can create a mobile genetics laboratory, reminiscent of the "tricorder" featured in Star Trek. The iGenomics app runs entirely on the iOS device, reducing the need for laptops or large equipment in the field, which is useful for pandemic and ecology workers. Aspyn Palatnick programmed iGenomics in CSHL Adjunct Associate Professor Michael Schatz's laboratory, over a period of eight years, starting when he was a 14-year-old high school intern.

The iPhone app was developed to complement the tiny DNA sequencing devices being made by Oxford Nanopore. Palatnick, now a software engineer at Facebook, was already experienced at building iPhone apps when joining the Schatz laboratory. He and Schatz realized that:

"As the sequencers continued to get even smaller, there were no technologies available to let you study that DNA on a mobile device. Most of the studying of DNA: aligning, analyzing, is done on large server clusters or high-end laptops."

Schatz recognized that scientists studying pandemics were "flying in suitcases full of Nanopores and laptops and other servers to do that analysis in the remote fields." iGenomics helps by making genome studies more portable, accessible, and affordable.

Users can AirDrop sequencing data to each other, enabling DNA analysis in the most remote locations--even those without internet access. iGenomics may soon even find its way into the hands of astronauts, Schatz describes:

"There's a lot of interest to do DNA sequencing in space. I'm trying to see if there's a way we can get iGenomics up there. There's a lot of people that are interested to do that. It's a real testament about how it would be impossible to do, you know, any sort of analysis on regular computers. It's just impossible to bring them with you."

In the journal Gigascience, Palatnick and Schatz report the iGenomics algorithm can quickly map DNA sequences of viral pathogens, such as a flu virus or Zika virus, and identify mutations important for diagnosis and treatment. They also provide an online tutorial for analyzing other viral genomes, such as from a SARS-CoV-2 patient.

Schatz dreams that this device will help field workers and citizen scientists alike:

"Today, we all carry professional cameras in our pockets, so it's not that hard to imagine in the next couple years, all of us carrying our own DNA sequencers on our smartphones, as well. There's just so many opportunities to do measurements of our environment and look for pathogens, maybe even do scans of yourself."