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People with pre-diabetes or diabetes who live in ozone-polluted areas may have an increased risk for an irreversible disease with a high mortality rate. A new study published in the Environmental Health Perspectives connects insulin resistance and repetitive ozone exposure to the development of interstitial lung disease.

"Our findings are especially important today as we're in the midst of the COVID-19 pandemic, where we have great concern regarding the convergence of health effects from air pollution and SARS-CoV-2 in susceptible populations like people with diabetes," said James Wagner, lead author and associate professor for the MSU College of Veterinary Medicine's Department of Pathobiology and Diagnostic Investigation.

Ozone - a gas often referred to as "smog" - is known to exacerbate certain lung diseases, such as asthma and rhinitis, which are primarily upper airway diseases. But recent epidemiology (Johannson et al. and Sesé et al.) suggests an association between high ozone concentrations and adverse health effects in the deep lung, which cause difficulty breathing due to lung restriction and stiffness.

"More than 170,000 people in the U.S. suffer from interstitial lung disease. Furthermore, type 2 diabetes and insulin resistance are recently suggested risk factors for developing pulmonary fibrosis," said Jack Harkema, University Distinguished Professor, Albert C. and Lois E. Dehn Endowed Chair in Veterinary Medicine, and director of the Laboratory for Environmental and Toxicologic Pathology and the Mobile Air Research Laboratories at MSU.

In the study, Wagner, Harkema and their collaborators, Robert Tighe and Christina Barkauskas from Duke University's Department of Medicine, studied healthy mice, mice with mild insulin resistance and mice with marked insulin resistance. The study found a direct relationship between insulin resistance levels and the severity of lung inflammation and scarring (fibrosis); diabetes-prone mice were particularly susceptible to inflammation and tissue remodeling caused by repeated ozone exposure.

"Evidence suggests that ozone exposure could exacerbate pulmonary fibrosis, particularly in individuals that are diabetic," said Tighe, a pulmonologist who specializes in interstitial disease at Duke. "Poorly controlled diabetes, in particular, may be an important co-morbidity for worsened lung damage."

According to Wagner, these findings are of critical importance for public health.

"Our results propose a causal link for ozone exposure to preferentially promote early pulmonary fibrosis and interstitial lung disease in pre-diabetic mice. We only exposed these mice for three weeks, but there are millions of people living in cities like Los Angeles and New York who are exposed to high levels of ozone day after day," he said. "Then, you must consider the prevalence of pre-diabetes people--approximately 33% in this country. Our study results suggest that people who are borderline insulin resistant--or diabetic--and living in areas with high levels of ozone pollution might be at an increased risk for developing interstitial lung disease."

This study is just the latest in Wagner and Harkema's research efforts, which describe pre-diabetes as a risk factor for multiple possible adverse responses to air pollution. Wagner has previously shown deleterious effects on heart rate, blood pressure, and adipose tissue inflammation in pre-diabetic rodents that were exposed to ozone (Wagner et al. and Zhong et al.).

The authors believe this study is the first of its kind, as it describes exacerbated pulmonary inflammation and remodeling due to repetitive, short-term ozone exposures in insulin-resistant rodents that also exhibit other manifestations of type 2 diabetes. The work was supported in large part by the researchers' grant from the Environmental Protection Agency's Great Lakes Air Center for Integrative Environmental Research (GLACIER) at MSU. For more information about this research, contact Dr. James Wagner.

Could number two be number one when it comes to combating recurrent Clostridium difficile (CDI) infections?

Using genetic material analysis and machine learning, UBC researchers have pinpointed several key factors to ensure successful fecal microbiota transplants (FMT), which have proven successful in treating bacterial infections in the gut including illnesses like C. difficile, Crohn's Disease, Colitis and even obesity, explains lead author Negin Kazemian.

"This therapy is still in its infancy, but studies like ours are helping identify key contributors to its overall success," says Kazemian, a graduate student at UBC Okanagan's School of Engineering.

Kazemian and her supervisor, Assistant Professor Sepideh Pakpour, are investigating the internal dynamics of both donors and recipients to set out a formula for the effectiveness of the therapy.

C. difficile is one of the most frequently identified health care-associated infection in North America, she adds. Once a patient gets it, the illness often recurs, making a significant negative impact on a patient's gut microorganisms.

Kazemian explains that severely damaged gut ecosystems, like someone who has had C. difficile, are not self-renewing. Therefore, FMT can help by restoring damaged systems through the recreation of the original ecosystem, or the construction of an entirely new and alternative ecosystem.

"In our study, we showed that the success of gut ecological recovery through FMT is dependent on several factors, including the donor gut microbiome--the presence of specific bacteria--as well as the recipient's pre-FMT gut community structures and the absence of specific bacteria and fungi."

Some previous studies have pointed to the possibility of "super" donors, but these new findings indicate the relationship between donors and recipients is much more complex. Pakpour says the notion of the super-donor is oversimplified due to the observed short-term fluctuations. A recipient's microbiota may be just as important to consider when predicting treatment outcomes, especially in unbalanced conditions such as ulcerative colitis.

"Take, for example, blood transplants where we have a strong understanding of the four main blood groups or types, and how they interact with one another," says Pakpour. "With fecal transplants the research up to this point has not been as clear in what constitutes a good match or compatibility."

Working with data from the University of Alberta Hospital, Kazemian and Pakpour analyzed the gut composition and DNA from samples extracted before and after FMT.

According to Kazemian, their findings indicate that there isn't a "one stool fits all" approach to ensure transplant success.

"The data illustrates that the unique microorganisms in everyone's bodies respond differently over time, and this has profound implications on whether these transplants work well or not."

The researchers suggest that preparing donors and patients' gut ecosystems prior to transplant, maybe by using metabolites, would potentially sync their microbiota leading the way to a higher probability of transplant success.

New Rochelle, NY, December 9, 2020--Minority women and women in general aged 50-64 in Pennsylvania showed an increased proportion of early-stage breast cancer diagnosis since the implementation of the Affordable Care Act (ACA). Under the ACA, more women are able to get early breast health screening. The study is published in the peer-reviewed Journal of Women's Health. Click here to read the article now.

For women aged 50-64, both non-Hispanic white women (86.54% pre-ACA, 88.09% post-ACA) and minority women (83.12% pre-ACA, 85.83% post-ACA) had a significantly increased proportion of early stage breast cancer diagnosis post-ACA.

"The ACA expanded access to affordable insurance coverage, making it possible for more women to undergo regular breast cancer screening. This study demonstrates the benefits that this can have for early breast cancer diagnosis and the ability to begin to mitigate some of the racial disparities in early detection," says Journal of Women's Health Editor-in-Chief Susan G. Kornstein, MD, Executive Director of the Virginia Commonwealth University Institute for Women's Health, Richmond, VA.

"Future research should identify those disadvantaged populations for whom disparities in healthcare remain pronounced despite the ACA. It should also explore the variables that contribute to healthcare disparities, but are not addressed by the ACAs insurance expansion, such as social determinants of health that impact healthcare access and outcomes," state Neal Spade, MD and coauthors from the University of Pittsburgh.

For people in wealthy countries, diarrhea is usually nothing more than an uncomfortable inconvenience for a few days. But for a poor child in a developing country, repeated bouts of diarrhea can lead to serious health consequences such as malnutrition, stunted growth and cognitive deficits.

Researchers at Washington University School of Medicine in St. Louis have discovered that a toxin produced by the bacterium Escherichia coli (E. coli), long known to cause diarrhea, also has other effects on the human digestive tract. The toxin, they found, changes gene expression in the cells that line the inside of the gut, inducing them to manufacture a protein that the bacterium then uses to attach to the intestinal wall.

The findings, published Nov. 17 in Proceedings of the National Academy of Sciences, offer a clue to why recurrent but short-lived episodes of diarrhea could lead to long-term nutritional problems.

"There's more than meets the eye with this toxin," said senior author James M. Fleckenstein, MD, a professor of medicine and of molecular microbiology. "It is basically changing the surface of the intestine to benefit itself, probably ultimately to the detriment of the host. Decades ago, people worked out how the toxin causes diarrhea, but until recently, nobody really had the tools to delve into what else this toxin might be doing. We're trying to put together the pieces of the puzzle to find out how toxin-producing E. coli might be driving malnutrition and other ripple effects of diarrhea."

Fleckenstein and first author Alaullah Sheikh, PhD, a postdoctoral researcher, study enterotoxigenic E. coli (ETEC), a toxin-producing strain of E. coli that is a common cause of severe, watery diarrhea. The bacterium's so-called heat-labile toxin causes ion channels on intestinal cells to open, triggering an outpouring of water and electrolytes into the digestive tract -- in other words, diarrhea.

Since oral rehydration therapy was invented in the 1970s, deaths from diarrhea have dropped by more than 80% worldwide. While invaluable at helping people survive a bout of diarrhea, the therapy does nothing to reduce the number of cases. Worldwide, young children still develop diarrhea an average of three times a year, with the youngest and poorest children bearing the brunt of the caseload -- and of the long-term health consequences.

Fleckenstein and Sheikh speculated that ETEC's heat-labile toxin might be doing more than just causing acute diarrhea and dehydration. If so, it might explain the link between ETEC and malnutrition, stunting and other problems.

To find other ways the toxin affects the gut, the researchers grew human intestinal cells in a dish and treated the cells with the toxin. They found that the toxin activates a set of genes known as CEACAMs. One in particular -- CEACAM6 -- codes for a protein that is normally in cells of the small intestine at low levels. Further experiments revealed that the toxin causes cells to produce more CEACAM6 protein, which the bacteria then uses to attach to intestinal cells and deliver even more toxin. Moreover, using intestinal biopsy specimens from people in Bangladesh infected with ETEC, the researchers showed that CEACAM6 expression increases in the small intestine during natural infection.

"CEACAM6 is expressed in what is called the brush border of the small intestine, which is where all your vitamins and nutrients get absorbed," Sheikh said. "This is one of the first pieces of evidence that ETEC can change the intestinal surface. We don't yet know how long that lasts and what that means for people who are infected, but it stands to reason that damage to this part of the body could affect the ability to absorb nutrients."

Fleckenstein, Sheikh and colleagues are continuing to study the link between ETEC and malnutrition, stunting and other health consequences.

"We are trying in the lab to understand the role of ETEC and its toxins as they relate to nondiarrheal effects of ETEC infection, particularly in young children in developing countries," Fleckenstein said. "There's a lot of work to be done to explore how the toxins might be related to these long-term consequences of diarrhea."

Each day, at least half a million Danes take a small pill to keep their blood pressure down or to protect against heart disease, and they should continue to take the medicine during the pandemic - even if the pill they take is an ACE inhibitor or Angiotensin II receptor blocker such as Losartan, Enalapril or Ramipril.

This is underscored by a new reassuring study, which, unlike all previous studies, also includes all Danes who have been tested for corona over a five month period - and not 'just' the most ill patients who have been hospitalised.

The researcher behind the research result is Christian Fynbo Christiansen, who is consultant, clinical associate professor and PhD at the Department of Clinical Epidemiology, which is part of the Department of Clinical Medicine at Aarhus University and Aarhus University Hospital, Denmark.

"The study finally removes any lingering suspicion that this particular type of blood pressure medicine increases the risk of getting corona or of suffering a worse illness, which was something that many health professionals feared while we were learning about corona. But there is no evidence to conclude such fears are correct," says Christian Fynbo Christiansen.

In the study, which includes all Danes who were tested in the period from 27 February to 26 July this year, the researchers have examined whether users of the popular blood pressure medications had an increased probability of a positive corona test, and whether the outcome of any illness was different than that of users of other types of blood pressure medication. The comparison group also includes people who do not take blood pressure medication.

"The study shows that people who take ACE inhibitors and Angiotensin II receptor blockers had the same probability of a positive test - and no increased risk of being hospitalised or dying," says Christian Fynbo Christiansen, who can thus confirm in a large-scale study what other smaller studies have already hinted at.

The new study is published in the journal Thorax and is part of a discussion about treatment that peaked in the early summer, when the coronavirus was still a new acquaintance. At the time, medical doctors and researchers feared that ACE inhibitors could actually increase the risk of dying from COVID-19, because the SARS-CoV-2 virus which causes COVID-19 enters the lungs through the same ACE receptors as the ACE inhibitors.

The hypothesis was that when the ACE inhibitor does what its name states and reduces the level of ACE, the body compensates for this by activating a far greater number of ACE receptors on the surface of the cells, which the SARS-CoV-2 virus then utilises as a kind of access key. The more keys available on the surface of the cells, the easier it is for the virus to access the cells.

"The theory about increased mortality was nourished by the fact that many of the severely ill COVID-19 patients had elevated blood pressure, which is widely treated with these ACE inhibitors. This is also why it was important to include all the Danes who had been tested - and not just those who were hospitalised - in the study," says Christian Fynbo Christiansen.

"We have a qualified basis to reiterate the current recommendation that users of medicines of the type ACE inhibitors and Angiotensin II blockers should continue to take their medicine while the pandemic is raging," he says.

What The Study Did: Considering when health care resources need to be prioritized during special times, such as the COVID-19 pandemic, researchers in this observational study looked at whether delaying radical prostatectomy surgery for up to six months for high-risk prostate cancer was associated with worse outcomes.

Authors: Leilei Xia, M.D., of the University of Pennsylvania Perelman School of Medicine in Philadelphia, is the corresponding author.

To access the embargoed study: Visit our For The Media website at this link https://media.jamanetwork.com/

(doi:10.1001/jamanetworkopen.2020.28320)

Editor's Note: Please see the article for additional information, including other authors, author contributions and affiliations, conflict of interest and financial disclosures, and funding and support.

A mechanical engineering research team at the University of Hong Kong (HKU) has invented a novel light-controlled, contamination-free fluidic processor, which can serve as a useful tool to greatly reduce the risk of infection of front-line medical workers in testing virus or bacteria in big pandemics like the current COVID-19 pandemic, and to minimise the risk of contamination during the process.

The new technology has been published in Science Advances in an article titled "Photopyroelectric Microfluidics", co-authored by graduate student Mr Wei Li, postdoctoral researcher Dr Xin Tang and Chair Professor Liqiu Wang at the Department of Mechanical Engineering, Faculty of Engineering, HKU.

Precision manipulation of various liquids is essential in many fields. The team innovatively uses light as a stimulating force, allowing contactless manipulations in moving, merging, dispensing and splitting liquids, on a specifically designed photo-responsive platform. The platform is non-toxic and non-sticky to all fluids, making it an ideal contamination-free fluidic processor.

Professor Wang said the first applications of the new technology can be in biomedical testing and diagnosis, with the aim of lowering the risk of contamination and infection in the process.

"Testing infectious viruses and bacteria is highly risky, sometimes even fatal. A blood droplet from an Ebola patient can infect medical workers through the skin. For diagnosis, medial workers have to crash, filter and purify a patient's blood sample to obtain the virus's genetic materials. This series of operations, very often in a fluidic medium, is highly infectious. Moreover, fluids stick to surfaces, which will contaminate containers and handling tools, causing potential dangers if the medical wastes are not properly managed." He said.

According to WHO reports, healthcare workers are 21 to 32 times more likely to be infected with Ebola and nearly 14% of COVID-19 reported cases are among healthcare workers. Moreover, it is estimated that disposable plastics worth US$20 billion are consumed in testing annually. The used plastics are left with potentially infectious or toxic residues and hazardous wastes that cost another US$10 billion to handle.

"We hope the newly-invented technique can reduce and even replace the usage of disposable plastics in the biomedical and pharmaceutical industries. The light-control device outperforms its electrical counterpart in the market in terms of operational precision and convenience, whereas the cost is only one-hundredth of it." Professor Wang said.

The key technology of the light-controlled fluidic processor is a two-layer photo-responsive platform. With a thickness of only 2mm, it is portable and easy to handle. Its superomniphobic surface interfaces fluids in a frictionless manner, like dew drops rolling on a lotus leaf; and a photothermal pyroelectric layer, which senses the light stimuli and converts it into a force that move, split and dispense fluids.

It has great potential in advanced research and applications in DNA analysis, proteomics, cell assay and clinical diagnosis, chemical synthesis and drug discovery. It can handle a wide spectrum of liquids such as water, alcohol, alkanes, and particularly silicone oil, which is particularly challenging because of its ultra-low surface tension. Its maneuverable fluid volume can be from 1000 μl to tiny droplets at 0.001 μl, i.e. about 0.02% of the volume of blood in a mosquito bite, which is 100 times smaller than that manipulated by its electrical counterpart.

"The device functions as a "magic" wetting-proof hand to navigate, fuse, pinch, and cleave fluids on demand, enabling cargo carriers with droplet wheels and upgrading the limit of maximum concentration of deliverable protein by 4000-fold." Professor Wang said.

The team will seek to integrate the platform with artificial intelligence (AI) system to work out a fully automatic system for liquid processing. In future, gene editing can be done with the click of a button, instead of repeated pipetting.

Sore eyes are the most significant vision-based indicator of COVID-19, according to new research published in the journal BMJ Open Ophthalmology.

Researchers at Anglia Ruskin University (ARU) asked people who had a confirmed COVID-19 diagnosis to complete a questionnaire about their symptoms, and how those compared to before they tested positive.

The study found that sore eyes was significantly more common when the participants had COVID-19, with 16% reporting the issue as one of their symptoms. Just 5% reported having had the condition beforehand.

While 18% of people reported suffering from photophobia (light sensitivity) as one of their symptoms, this was only a 5% increase from their pre-COVID-19 state.

Of the 83 respondents, 81% reported ocular issues within two weeks of other COVID-19 symptoms. Of those, 80% reported their eye problems lasted less than two weeks.

The most common reported symptoms overall were fatigue (suffered by 90% of respondents), a fever (76%) and a dry cough (66%).

Lead author Professor Shahina Pardhan, Director of the Vision and Eye Research Institute at ARU, said: "This is the first study to investigate the various eye symptoms indicative of conjunctivitis in relation to COVID-19, their time frame in relation to other well-known COVID-19 symptoms and their duration.

"While it is important that ocular symptoms are included in the list of possible COVID-19 symptoms, we argue that sore eyes should replace 'conjunctivitis' as it is important to differentiate from symptoms of other types of infections, such as bacterial infections, which manifest as mucous discharge or gritty eyes.

"This study is important because it helps us understand more about how COVID-19 can infect the conjunctiva and how this then allows the virus to spread through the body."

A research group at the University of Turku, Finland, has led the development of a new method to evaluate vaccine safety. The new method may significantly reduce the use of animal testing in the vaccine industry.

Vaccines are safe and potent pharmaceutical products that prevent infectious diseases caused by viruses and bacteria, and reduce the spread of pathogens among the population. A vaccine prevents an infectious disease because the body develops an ability to recognise and destroy the pathogen. Vaccines are generally designed from a weakened pathogen, or parts of it. The vaccine industry uses effective methods to ensure vaccine safety, and constantly develops new methods as well.

The pertussis vaccine, which also belongs to the Finnish national vaccination programme, contains the surface structures of the pertussis bacteria and inactivated forms of the pertussis toxin produced by the bacteria. The pertussis toxin attaches to the surface of the cell, penetrates it, and destroys the vital control system of the cell.

The research group at the University of Turku has led the development of the new method that can be used to ensure the safety of the pertussis toxin in the pertussis vaccine. The new iGIST method (Interference in Gαi-mediated Signal Transduction) detects how the pertussis toxin destroys the vital control system of the cell.

- Compared to the current methods in the vaccine industry, iGIST is more effective and enables the detection of up to 100 times lower levels of pertussis toxin. iGIST is entirely based on using laboratory grown, human-based cells. Therefore, it may significantly reduce the use of animal testing in the vaccine industry, says Dr. Arto Pulliainen from the University of Turku who was the principal investigator of the research group that was in charge of developing the method.

A Brazilian study published in the Journal of Pineal Research describes a group of genes potentially regulated by the hormone melatonin in some types of cancer, especially breast cancer. According to the authors, the results can be used to guide future personalized therapies for the disease.

“Certain types of tumor appear to correlate directly with the amount of melatonin produced by cells. It’s essential to understand how the hormone influences molecular signaling at the genetic level as a guideline for personalized therapies based on melatonin,” Luiz Gustavo Chuffa, a professor at São Paulo State University’s Botucatu Institute of Biosciences (IBB-UNESP), told Agência FAPESP.

The study was supported by FAPESP and conducted in collaboration with researchers at the University of North Paraná (UENP) and São José do Rio Preto Medical School (FAMERP) in Brazil and the University of Texas Health Science Center at San Antonio in the United States.

Known as the “sleep hormone” because its functions include regulating the sleep-wake cycle, melatonin has been shown to have anti-tumor properties in laboratory trials. Evidence presented in the scientific literature suggests that low levels of melatonin are associated with a heightened risk of cancer. A possible explanation is that the hormone contributes to the modulation of gene expression and may intensify the activity of tumor suppressor genes, for example.

“Most tumor cells have low levels of melatonin, but laboratory trials have shown that treatment with the hormone increases tumor cell death and reduces tumor cell proliferation, both of which are important to avoid progression of the cancer and metastasis,” Chuffa said. “Ongoing clinical trials are evaluating the use of melatonin to treat cancer. Specific therapies for the different subtypes of breast cancer already exist, and some patients will probably respond well to alternative treatments based on melatonin, while others may not.”

In search of target genes

To identify molecular markers that serve as guides for cancer treatment, the researchers first conducted a study based on meta-analysis to find out how melatonin regulates microRNA expression in breast, head and neck, liver, stomach, prostate, central nervous system, and colorectal cancer.

Meta-analysis entails a systematic review of the literature using statistical methods to integrate the results of published research on the same subject. MicroRNAs are small RNA molecules that do not encode proteins but perform a regulatory function in the genome, controlling gene expression and hence several cellular processes.

“In this first stage, we found 14 quite recent studies that associated melatonin with altered microRNA expression. For the seven cancers on which we focused, we found 46 microRNAs with altered expression,” Chuffa said.

Next, the researchers used bioinformatics to identify pathways associated with the hormone’s action on tumor cells, basing their analysis on the association between these microRNAs and their regulatory targets. Regulatory and molecular networks were generated and analyzed in collaboration with researchers Robson Francisco Carvalho, Luis Antonio Justulin, and Sarah Santiloni.

“When we cross-referenced the information with The Cancer Genome Atlas [TCGA], a public database, we identified the target genes for these 46 microRNAs with altered expression,” Chuffa said.

As a result, they were able to understand how melatonin works in several cellular signaling pathways. “These genes targeted by melatonin relate to important biological processes in cancer, such as cell cycle regulation, cell death, and cell migration and senescence,” he explained. “Melatonin appears to act more strongly on breast, oral, and stomach cancer. Prostate and colorectal tumors, as well as glioblastoma, showed few changes induced by the microRNAs concerned.”

Breast cancer was associated with the most genes and microRNAs in this first stage of the study, so the researchers compared the target genes for the microRNAs concerned with the data obtained by RNA-seq analysis of breast tumors in mice treated with melatonin.

RNA-seq uses next-generation sequencing technology to study the expression of several genes at the same time and hence to obtain the entire transcriptome, i.e. the complete set of RNA molecules expressed in a tissue.

These analyses were performed in partnership with FAMERP researchers Débora Aparecida Pires de Campos Zuccari and Bruna Victorasso Jardim-Perassi.

“In the animals treated with 40 milligrams of melatonin, there was an enrichment of signaling pathways related to the immune system and apoptosis, and a reduction of pathways associated with tumor aggressiveness and metastasis,” Chuffa said.

The group also investigated certain proteins (transcription factors and kinases) that are active in such processes as transcription and the cellular cycle. “The goal of this part of the study was to find common targets in cellular processes and the breast cancer public database,” he said.

According to Chuffa, genes regulated by melatonin in breast cancer are potential targets for the treatment of the disease. “Melatonin is a multitasking molecule and acts on various cellular substrates, so we’re now taking the study deeper to find out how the hormone influences microRNA expression and hence the regulation of the cellular mechanisms identified,” he said.

New research could shed light on the mystery cause of a lung disease that is a major killer, and potentially unlock new treatments.

Idiopathic pulmonary fibrosis (IPF) affects at least 32,000 people in the UK, and accounts for one per cent of all UK deaths, with patients having a life expectancy of three to five years once diagnosed. The disease involves scar tissue developing abnormally in the lungs, which progressively reduces the ability to breathe.

Up to now, the cause has been unknown - however, a new largescale research study led by the University of Exeter and published in The Lancet Respiratory Medicine has found that short telomeres - a protective component found on the ends of DNA - are linked to higher risk of having IPF.

Moreover, using a complex genetic analysis approach called Mendelian randomisation, researchers found evidence that it's likely that the short telomeres cause IPF, as opposed to the disease itself causing telomere shortening.

The Exeter-based research team collaborated with the Royal Devon & Exeter NHS Foundation Trust, and the universities of Bath and Leicester, as well as patients affected by IPF. They examined data from 1,300 participants with IPF in UK Biobank, and compared it with similar cohorts to ensure their results were replicated.

Senior researcher Dr Chris Scotton, of the University of Exeter Medical School, said: "The cause of idiopathic pulmonary fibrosis has always been difficult to pin down, and it's proven hugely challenging to develop effective treatments. Our research provides the strongest evidence to date that having short telomeres may contribute to the cause of this terrible disease. This means we can look for new ways to prevent or treat IPF, and it's another reason to adopt a healthier lifestyle - because reducing stress and increasing exercise may help keep telomeres longer."

In healthy people, telomeres naturally get shorter as we age. But if this shortening is accelerated, it is thought to be one of the contributing factors to the health issues that we may encounter as we get older. Having less protection at the ends of our DNA can impair our bodies' ability to heal or fight off infection.

LOWELL, Mass. - Tens of thousands of Massachusetts residents depend on home care to support their health as they age or cope with physical challenges. That care often requires close personal contact, increasing the risk of contracting COVID-19 among both home-care clients and the aides who provide their care.

Findings from a survey issued today by the Safe Home Care Project at UMass Lowell and the Betsy Lehman Center for Patient Safety underscore the need to act now to sustain the safety of home-care services and protect both workers and clients.

"Home care is an important alternative to hospitals and nursing homes, especially for infection prevention during the COVID-19 pandemic. But keeping clients and workers safe at home carries different challenges than in hospitals. The findings of this report underscore the needs to incorporate home care into all health-care pandemic planning and to tailor educational materials, practice guidance and other resources for the delivery of care in homes," said Safe Home Care Project lead and report co-author Margaret Quinn, ScD, professor emeritus of UMass Lowell Department of Public Health.

According to managers at home-care agencies who participated in the June survey, potential exposure to COVID-19 is a significant concern among home-care aides and clients. A majority of agencies surveyed reported having both workers and clients test positive for COVID-19 or exhibit symptoms of the virus.

The survey findings also include:

Provisioning staff with personal protective equipment (PPE) is both a top priority and a challenge for agencies;

Guidance and policies to protect against COVID-19 are difficult to interpret and apply to the home-care environment;

Inconsistent communication about COVID-19 exposure compromises prevention and safety efforts.

The results of the survey, along with the expectation that COVID-19 will continue to circulate until a vaccine is readily available, suggests that efforts to stem the spread of COVID-19 in the state need to account for the role of home care in the health care, disability and elder care systems by providing a framework for practice guidance and securing resources to prevent the spread of infection among workers and clients.

The authors of the report indicate that home care will be enhanced by affording the same consideration to agencies and workers that are given to other frontline health organizations and workers. That includes providing:

Actionable information about COVID-19 infection status of clients;

Access to and funding for PPE and disinfection supplies;

Robust training on proper use of PPE including effective fit testing of N95s;

Access to timely, free COVID-19 testing upon occupational exposure or development of symptoms;

Informational resources on COVID-19 policies relevant to the home-care setting.

Irvine, Calif., Dec. 8, 2020 -- A new class of epidemiological models based on alternative thinking about how contagions propagate, particularly in the early phases of a pandemic, provide a blueprint for more accurate epidemic modeling and improved disease spread predictions and responses, according to a study published recently in Scientific Reports by researchers at the University of California, Irvine and other institutions.

In the paper, the scientists said that standard epidemic models incorrectly assume that the rate in which an infectious disease spreads depends on a simple product of the number of infected and susceptible people. The authors instead suggest that transmission happens not through complete mingling of entire populations but at the boundary of sub-groups of infected individuals.

"Standard epidemiological models rely on the presumption of strong mixing between infected and non-infected individuals, with widespread contact between members of those groups," said co-author Tryphon Georgiou, UCI Distinguished Professor of mechanical & aerospace engineering. "We stress, rather, that transmission occurs in geographically concentrated cells. Therefore, in our view, the use of fractional exponents helps us more accurately predict rates of infection and disease spread."

The researchers proposed a "fractional power alternative" to customary models that takes into account susceptible, infected and recovered populations. The value of the exponents in these fractional (fSIR) models depends on factors such as the nature and extent of contact between infected and healthy sub-populations.

The authors explained that during the initial phase of an epidemic, infection proceeds outwards from contagion carriers to the general population. Since the number of susceptible people is much larger than that of the infected, the boundary of infected cells scales at a fractional power of less than one of the area of the cells.

The researchers tested their theory through a series of numerical simulations. They also fitted their fractional models to actual data from Johns Hopkins University Center for Systems Science and Engineering. Those data covered the first few months of the COVID-19 pandemic in Italy, Germany, France and Spain. Through both processes they found the exponent to be in the range of .6 and .8.

"The fractional exponent impacts in substantially different ways how the epidemic progresses during early and later phases, and as a result, identifying the correct exponent extends the duration over which reliable predictions can be made as compared to previous models," Georgiou said.

In the context of the current COVID-19 pandemic, better knowledge about propagation of infections could aid in decisions related to the institution of masking and social distancing mandates in communities.

"Accurate epidemiological models can help policy makers choose the right course of action to help prevent further spread of infectious diseases," Georgiou said.

COVID-19 has changed the way we live and work, as various health and safety restrictions keep more of us at home more often. The resulting changes to our behavior are already impacting the environment around us in myriad ways, according to comparisons of remote sensing data before and during the pandemic collected by NASA, U.S. Geological Survey (USGS), and ESA (European Space Agency) Earth-observing satellites and others.

Researchers from several institutions presented their early results in a virtual press conference on Dec. 7 at the American Geophysical Union's 2020 fall meeting. They found that the environment is quickly changing, and the timing of those changes seems to indicate that the pandemic may be a reason. Deforestation rates are changing in some places, air pollution is diminishing, water quality is improving, and snow is becoming more reflective in some areas since the pandemic began earlier this year.

"But we will need more research to clearly attribute environmental change to COVID," said Timothy Newman, National Land Imaging Program Coordinator for the United States Geological Survey (USGS).

Scientists and engineers like Newman use remote sensing data to observe how the world is changing during the COVID-19 pandemic, comparing current remote sensing data to pre-pandemic trends. Newman's program monitors weekly changes with satellite images from the joint NASA/USGS Landsat satellites and the ESA's Sentinel-2 satellites.

Newman's program observed that large swaths of the Brazilian Amazon rainforest were cleared from June to September of this year, since the start of the COVID-19 pandemic. Rapid deforestation also is occurring in the tropics near Indonesia and the Congo. Yet, in other parts of the Amazon rainforest such as Colombia and Peru, deforestation appears to have slowed somewhat since the onset of the pandemic.

Satellite images and data from Landsat also show a reduction in environmental pollution in this time period. Industrial activities in India, including extracting and crushing stone for construction projects, slowed or ground to a halt because of COVID-19 lockdowns. Soon after, surface air measurements and Landsat thermal infrared data showed that air pollution levels had dropped significantly. One study found that the concentration of an air pollutant called particulate matter (PM) 10 decreased around a third to a fourth of the pre-pandemic level in India.

For years, Ned Bair has been studying snow in the Indus River Basin - a network of mountain ranges and rivers near India, China, and Pakistan that supplies water for more than 300 million people.

"Once the COVID-19 lockdown started in India, I immediately thought that it would have an impact on the snowpack," said Bair, a snow hydrologist with the University of California Santa Barbara's Earth Research Institute.

Bair saw posts on social media about how clear the air was in Delhi and preliminary data that air quality was improving during the pandemic. With less pollution in the air, he thought, there would be less dust and soot accumulating on nearby snow. Dust and other air pollutants affect snow albedo - how white and, therefore, reflective the snow is - as they accumulate on the surface of snow. Cleaner snow has a higher albedo, which means it reflects more light energy and, thus, melts at a slower rate.

Bair and his team found that snow albedo was higher during pandemic-related lockdowns than in the 20 years prior - likely a result of the significant reduction in travel and industrial activity as fewer people were leaving home and workplaces were shut down or reduced operations.

They used data from the Moderate Resolution Imaging Spectroradiometer (MODIS) instrument aboard NASA's Terra satellite, and two computer models to filter out clouds, rocks, trees, and anything that wasn't snow. Both models showed that snow in the Indus was significantly cleaner during the COVID-19 lockdowns. Using dust to approximate all pollutants, the models showed that pollutants accumulating on the snow decreased by 36 parts per million below the pre-pandemic average - a change that could delay the melting of enough snow to fill up Lake Tahoe Dam in California, or about 0.17-0.22 cubic miles (0.73- 0.93 cubic kilometers).

Snowmelt is an important source of drinking water for more than 300 million people living in the Indus River Basin. While changes in albedo won't change the overall amount of snowmelt, it will change the timing of when that snow melts - potentially affecting the available water supply in the region.

Nima Pahlevan, a research scientist at NASA's Goddard Space Flight Center, dove into examining the pandemic's impact on water quality around the world. He looked at Landsat-8 and Sentinel-2 data on water quality by analyzing proxies like chlorophyll-a, solid material suspended in the water, and turbidity - essentially a measure of how clear water is based on things like suspended particles of inorganic sediment or phytoplankton in the water - during the pandemic and compared those measurements to years prior.

The findings were murky in some areas. For example, in San Francisco, California changes in rainfall made it difficult to tell whether the pandemic impacted water quality. But a clearer picture surfaced in the western Manhattan area of New York City.

"The water has become clearer in the western Manhattan area because there were fewer people commuting to Manhattan during the lockdown," he explained.

Sewage water from homes and businesses, as well as runoff from streets, are treated in wastewater treatment plants before being released into nearby rivers. When the city imposed a stay-at-home order in mid-March, many of Manhattan's 2.1 million commuters began working from home or left the city. Fewer people producing those pollutants means that fewer particles end up in the water in the Hudson River. Satellite data showed a more than 40% drop in turbidity during the pandemic in a section of the Hudson River.

The better water quality probably won't last, though, Pahlevan says. Once we return to pre-pandemic behaviors, water quality will revert as well. Many of the environmental improvements that researchers are seeing won't last if the world goes back to its pre-pandemic ways.

Researchers from Tokyo Medical and Dental University (TMDU) identify a novel mechanism by which periodontal disease may cause diabetes

Tokyo, Japan - Periodontal or gum disease is known to be a significant risk factor of metabolic syndrome, a group of conditions increasing the risk for heart disease and diabetes. In a new study, researchers from Tokyo Medical and Dental University (TMDU) discovered that infection with Porphyromonas gingivalis, the bacterium causing periodontal disease, causes skeletal muscle metabolic dysfunction, the precursor to metabolic syndrome, by altering the composition of the gut microbiome.

Periodontal bacteria have long been known to cause inflammation within the oral cavity, but also systemically increase inflammatory mediators. As a result, sustained infection with periodontal bacteria can lead to increases in body weight and lead to increased insulin resistance, a hallmark of type 2 diabetes. The function of insulin is to help shuttle glucose from the blood into tissues, most importantly to skeletal muscle, where one quarter of all glucose in stored. Unsurprisingly, insulin resistance plays a key role in the development of metabolic syndrome, a group of conditions including obesity, altered lipid metabolism, high blood pressure, high blood glucose levels, and systemic inflammation. Although skeletal muscle plays a key role in decreasing blood glucose levels, a direct connection between periodontal bacterial infection and the metabolic function of skeletal muscle has not been established yet.

"Metabolic syndrome has become a widespread health problem in the developed world," says first author of the study Kazuki Watanabe. "The goal of our study was to investigate how periodontal bacterial infection might lead to metabolic alterations in skeletal muscle and thus to the development of metabolic syndrome."

To achieve their goal, the researchers first investigated antibody titers to Porphyromonas gingivalis in the blood of patients with metabolic syndrome and found a positive correlation between antibody titers and increased insulin resistance. These results showed that patients with metabolic syndrome were likely to have undergone infection with Porphyromonas gingivalis and thus have mounted an immune response yielding antibodies against the germ. To understand the mechanism behind the clinical observation, the researchers then turned to an animal model. When they gave mice that were fed a high-fat diet (a pre-requisite to developing metabolic syndrome) Porphyromonas gingivalis by mouth, the mice developed increased insulin resistance, and fat infiltration and lower glucose uptake in the skeletal muscle compared with mice that did not receive the bacteria.

But how was this bacterium capable of causing systemic inflammation and metabolic syndrome? To answer this question, the researchers focused on the gut microbiome, the network of bacteria present in the gut and with which the organism co-exists symbiotically. Intriguingly, the researchers found that in mice administered with Porphyromonas gingivalis the gut microbiome was significantly altered, which might decrease insulin sensitivity.

"These are striking results that provide a mechanism underlying the relationship between infection with the periodontal bacterium Porphyromonas gingivalis and the development of metabolic syndrome and metabolic dysfunction in skeletal muscle," says corresponding author of the study Professor Sayaka Katagiri.