LED lights found to kill coronavirus

by Tel Aviv University

Credit: CC0 Public Domain

Researchers from Tel Aviv University (TAU) have proven that the coronavirus can be killed efficiently, quickly, and cheaply using ultraviolet (UV) light-emitting diodes (UV-LEDs). They believe that the UV-LED technology will soon be available for private and commercial use.

17 december 2020--This is the first study conducted on the disinfection efficiency of UV-LED irradiation at different wavelengths or frequencies on a virus from the family of coronaviruses. The study was led by Professor Hadas Mamane, Head of the Environmental Engineering Program at TAU's School of Mechnical Engineering, Iby and Aladar Fleischman Faculty of Engineering. The article was published in November 2020 issue of the Journal of Photochemistry and Photobiology B: Biology.

"The entire world is currently looking for effective solutions to disinfect the coronavirus," said Professor Mamane. "The problem is that in order to disinfect a bus, train, sports hall, or plane by chemical spraying, you need physical manpower, and in order for the spraying to be effective, you have to give the chemical time to act on the surface. Disinfection systems based on LED bulbs, however, can be installed in the ventilation system and air conditioner, for example, and sterilize the air sucked in and then emitted into the room.

"We discovered that it is quite simple to kill the coronavirus using LED bulbs that radiate ultraviolet light," she explained. "We killed the viruses using cheaper and more readily available LED bulbs, which consume little energy and do not contain mercury like regular bulbs. Our research has commercial and societal implications, given the possibility of using such LED bulbs in all areas of our lives, safely and quickly."

The researchers tested the optimal wavelength for killing the coronavirus and found that a length of 285 nanometers (nm) was almost as efficient in disinfecting the virus as a wavelength of 265 nm, requiring less than half a minute to destroy more than 99.9% of the coronaviruses. This result is significant because the cost of 285 nm LED bulbs is much lower than that of 265 nm bulbs, and the former are also more readily available.

Eventually, as the science develops, the industry will be able to make the necessary adjustments and install the bulbs in robotic systems or air conditioning, vacuum, and water systems, and thereby be able to efficiently disinfect large surfaces and spaces. Professor Mamane believes that the technology will be available for use in the near future.

It is important to note that it is very dangerous to try to use this method to disinfect surfaces inside homes. To be fully effective, a system must be designed so that a person is not directly exposed to the light.

In the future, the researchers will test their unique combination of integrated damage mechanisms and more ideas they recently developed on combined efficient direct and indirect damage to bacteria and viruses on different surfaces, air, and water.

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More information: Yoram Gerchman et al, UV-LED disinfection of Coronavirus: Wavelength effect, Journal of Photochemistry and Photobiology B: Biology (2020). DOI: 10.1016/j.jphotobiol.2020.112044

Provided by Tel Aviv University 

Smartphone camera used to diagnose viral infections

by Bob Yirka , Medical Xpress

Three-dimensional schematic of the CNN–nanoparticle-enabled smartphone for virus detection. The detection process comprises three main steps. (A) Virus capture and labeling using Pt-nanoprobes. The samples are loaded into microchips modified with mAbs against the virus envelope protein and incubated to allow the capture of target virus for 20 min. The captured virus particles are then labeled with Pt-nanoprobes within 20 min. Each step of on-chip virus capture and labeling is followed by a washing step using 10 mM phosphate buffer (pH 7.4) (B) Catalyzer solution containing hydrogen peroxide (H2O2) is added to the chip and incubated for 10 min. In the presence of the captured virus, Pt-nanoprobe complex bubbles (oxygen) are formed because of the catalytic activity of PtNPs in contact with H2O2. Scale bar is set on the basis of the microchip dimensions. (C) The on-chip bubble signal is detected using the CNN–nanoparticle-enabled smartphone (NES). Photo credit: Mohamed S. Draz, Brigham and Women’s Hospital. (D) Screenshots of the results shown by the CNN-NES. Photo credit: Mohamed S. Draz, Brigham and Women’s Hospital. Credit: Science Advances (2020). DOI: 10.1126/sciadv.abd5354

A team of researchers at Brigham and Women's Hospital, Harvard Medical School, has developed a way to use a smartphone camera to test for viral infections. In their paper published in the journal Science Advances, the group describes their system, which also involves the use of an external catalytic microchip device and a smartphone system that uses a trained deep learning algorithm.

17 december 2020--As the pandemic has gripped the world for most of this year, scientists have been looking for ways to slow the spread of the next one. In this new effort, the team in Massachusetts has developed a smartphone-based system that can be used by non-medical people to test for a variety of viral infections.

The system is made up of a smartphone, an external catalytic microchip device and software. Body fluid samples are placed into a channel on the catalytic microchip device, which is then doused with a small amount of hydrogen peroxide. The resulting reaction leads to the formation of bubbles. The bubbles develop in unique patterns based in part on viruses in the fluid sample. The user points their smartphone camera at the bubbling sample and launches the deep-learning algorithm that has already been trained to identify the patterns and thereby recognize the presence of viruses. The whole process takes approximately 50 minutes. The researchers have thus far taught their system to recognize just three viruses, Zika and hepatitis B and C. But testing shows the system to be 99% accurate. They note that their system is more portable and cost effective than other solutions in the works.

The researchers suggest that their system could be rapidly trained to recognize new viruses if the need arises, and the catalytic microchip device could be sent to hot spots in the future. Such technology, the researchers suggest, could help to stop future pandemics if used widely. The researchers also note that the system could be immediately useful in infection prone areas lacking testing labs, such as third world countries.

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More information: Mohamed S. Draz et al. Virus detection using nanoparticles and deep neural network–enabled smartphone system, Science Advances (2020). DOI: 10.1126/sciadv.abd5354

Existing antihistamine drugs show effectiveness against COVID-19 virus in cell testing

by Sarah K. Carey, Doug Bennett, University of Florida

Leah Reznikov, Ph.D., and David Ostrov, Ph.D., are shown in Reznikov’s lab. Credit: UF Health/Jesse Jones

Three common antihistamine medications have been found in preliminary tests to inhibit infection of cells by the coronavirus that causes COVID-19, University of Florida Health researchers have found.

13 dec 2020--Their findings, based on laboratory tests of cells and a detailed analysis of nearly a quarter-million California patients' medical records, are published today in the journal Biochemical and Biophysical Research Communications. The data may support the launch of a randomized, controlled clinical trial to determine whether the specific antihistamines can treat or even prevent COVID-19 in humans, the researchers said.

Earlier this year, Leah Reznikov, Ph.D., an assistant professor of physiological sciences in the UF College of Veterinary Medicine and the study's principal investigator on the study, began collaborating with David A. Ostrov, Ph.D., an immunologist and associate professor in the UF College of Medicine's department of pathology, immunology and laboratory medicine. They and other colleagues set out to identify approved drugs that can interfere with the way the SARS-CoV-2 virus binds to cells. Blocking that connection essentially locks a cellular doorway that inhibits the virus's transmission to the respiratory system.

"We discovered epidemiological data showing that the usage of specific drugs was associated with a reduced likelihood of testing positive for SARS-CoV-2, the virus that causes COVID-19. We then found that these specific drugs exhibited direct antiviral activity against SARS-CoV-2 in the lab," Ostrov said.

While there is an association between the medications and infection rates, the researchers stressed there is much more to be learned and no cause and effect has been formally established.

"The fact that these drugs actually inhibit the virus in the lab does not necessarily mean that they will inhibit it actively in people—but they might," Ostrov said.

To establish their findings, the collaborators focused on angiotensin-converting enzyme-2, or ACE2, a "gateway" protein the virus uses to invade human cells. Working with a colleague at the University of California San Francisco, they analyzed medical records of nearly a quarter million California patients. People age 61 and older who had used certain antihistamines were less likely to test positive for the SARS-CoV-2 virus than those who did not take the medications, the researchers found.

Next, the researchers tested this group of antihistamines for their ability to inhibit the coronavirus in a combination of human and primate cells. Three of the drugs—hydroxyzine, diphenhydramine and azelastine—showed direct, statistically significant antiviral effects on the SARS-CoV-2 virus.

Hydroxyzine, sold as Atarax, and the nasal spray azelastine are prescription medications while diphenhydramine is sold over-the-counter as Benadryl, a treatment for cold and allergy symptoms.

The drugs were tested at different concentrations to measure how much is required to inhibit the virus.

While the findings are encouraging, Ostrov cautions against self-medicating with antihistamines as a COVID-19 prevention or treatment. So-called "off-label" use of medications should only take place after a detailed consultation with a physician, he said.

Among the three medications, azelastine was found to inhibit the SARS-CoV-2 virus at a dose that was smaller than the amount prescribed as a nasal spray. The other two antihistamines required higher drug concentrations than currently recommended dosing levels to achieve antiviral activity in cells. That doesn't make diphenhydramine any less of a potential COVID-19 therapy for now, especially considering its ubiquity and over-the-counter status, Ostrov said. Clinical trials will be necessary to establish the drugs' effectiveness in prevention, early treatment and as a secondary therapy for severe COVID-19.

Reznikov said the data suggest these three antihistamines may work by either disrupting the virus's interactions with ACE2 or by binding with another protein that may interfere with viral replication. The protein, known as a sigma receptor, is part of a cell's communications network.

Reznikov approached Ostrov in March with a hypothesis and an idea: Drugs that bind ACE2 could change disease outcomes, so she asked Ostrov to develop a list of small-molecule drug candidates.

She then pursued a strategy to screen the drugs against virus isolates of SARS-CoV-2 with Michael Norris, Ph.D., an assistant research professor of medical geography in the department of geography and the UF Emerging Pathogens Institute. In May, Reznikov was included in the UF Clinical and Translational Science Institute's Rapid-Response Translational Research Funding initiative to facilitate this project.

Although the findings are intriguing, Reznikov and Ostrov note there is still much to be learned about the mechanisms of how antihistamines interact with the SARS-CoV-2 virus.

Because of the urgency of the COVID-19 pandemic, Ostrov said there is a possibility that the antihistamine candidates could go directly to human clinical trials without first being tested in animal models. That is the case with famotidine, an antihistamine and antacid that is undergoing clinical trials elsewhere as a therapy for severely ill COVID-19 patients.

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More information: Leah R. Reznikov et al. Identification of antiviral antihistamines for COVID-19 repurposing, Biochemical and Biophysical Research Communications (2020). DOI: 10.1016/j.bbrc.2020.11.095

Provided by University of Florida 

Gut microbiota plays a role in brain function and mood regulation

by Pasteur Institute

Credit: Pascal Marseaud

Depression is a mental disorder that affects more than 264 million people of all ages worldwide. Understanding its mechanisms is vital for the development of effective therapeutic strategies. Scientists from the Institut Pasteur, Inserm and the CNRS recently conducted a study showing that an imbalance in the gut bacterial community can cause a reduction in some metabolites, resulting in depressive-like behaviors. These findings, which show that a healthy gut microbiota contributes to normal brain function, were published in Nature Communications on December 11, 2020.

11 december 2020--The bacterial population in the gut, known as the gut microbiota, is the largest reservoir of bacteria in the body. Research has increasingly shown that the host and the gut microbiota are an excellent example of systems with mutually beneficial interactions. Recent observations also revealed a link between mood disorders and damage to the gut microbiota. This was demonstrated by a consortium of scientists from the Institut Pasteur, the CNRS and Inserm, who identified a correlation between the gut microbiota and the efficacy of fluoxetine, a molecule frequently used as an antidepressant. But some of the mechanisms governing depression, the leading cause of disability worldwide, remained unknown.

Using animal models, scientists recently discovered that a change to the gut microbiota brought about by chronic stress can lead to depressive-like behaviors, in particular by causing a reduction in lipid metabolites (small molecules resulting from metabolism) in the blood and the brain.

These lipid metabolites, known as endogenous cannabinoids (or endocannabinoids), coordinate a communication system in the body which is significantly hindered by the reduction in metabolites. Gut microbiota plays a role in brain function and mood regulation

Endocannabinoids bind to receptors that are also the main target of THC, the most widely known active component of cannabis. The scientists discovered that an absence of endocannabinoids in the hippocampus, a key brain region involved in the formation of memories and emotions, resulted in depressive-like behaviors.

The scientists obtained these results by studying the microbiotas of healthy animals and animals with mood disorders. As Pierre-Marie Lledo, Head of the Perception and Memory Unit at the Institut Pasteur (CNRS/Institut Pasteur) and joint last author of the study, explains: "Surprisingly, simply transferring the microbiota from an animal with mood disorders to an animal in good health was enough to bring about biochemical changes and confer depressive-like behaviors in the latter."

The scientists identified some bacterial species that are significantly reduced in animals with mood disorders. They then demonstrated that an oral treatment with the same bacteria restored normal levels of lipid derivatives, thereby alleviating the depressive-like behaviors. These bacteria could therefore serve as an antidepressant. Such treatments are known as "psychobiotics".

"This discovery shows the role played by the gut microbiota in normal brain function," continues Gérard Eberl, Head of the Microenvironment and Immunity Unit (Institut Pasteur/Inserm) and joint last author of the study. If there is an imbalance in the gut bacterial community, some lipids that are vital for brain function disappear, encouraging the emergence of depressive-like behaviors. In this particular case, the use of specific bacteria could be a promising method for restoring a healthy microbiota and treating mood disorders more effectively.

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More information: Grégoire Chevalier et al, Effect of gut microbiota on depressive-like behaviors in mice is mediated by the endocannabinoid system, Nature Communications (2020). DOI: 10.1038/s41467-020-19931-2

Provided by Pasteur Institute 

 How are older adults coping with the mental health effects of COVID-19?

by McLean Hospital

McLean researchers indicate that older adults may be withstanding the mental health strains of the COVID-19 pandemic better than other age groups. Credit: McLean Hospital

Older adults are especially vulnerable to the effects of the COVID-19 pandemic—with higher risks of severe complications and death, and potentially greater difficulties accessing care and adapting to technologies such as telemedicine. A viewpoint article published in the Journal of the American Medical Association notes that there's also a concern that isolation during the pandemic could be more difficult for older individuals, which could exacerbate existing mental health conditions. Information gathered over the past several months suggests a much more nuanced picture, however.

05 december 2020--"Over the spring and summer of 2020, we were struck by a number of individual studies from all over the world that reported a consistent theme: Older adults, as a group, appeared to be withstanding the strains on mental health from the pandemic better than all other age groups," said lead author Ipsit Vahia, MD, medical director of the Geriatric Psychiatry Outpatient Services and the Institute for Technology in Psychiatryat McLean Hospital. "In this article, we highlight some of these studies and discuss resilience in older adults and what factors may be driving it."

Resilience may reflect an interaction among internal factors—such as an individual's stress response, cognitive capacity, personality traits, and physical health—and external resources like social connections and financial stability. For older adults experiencing isolation during the pandemic, having more meaningful relationships seems to be more important than having more interactions with others, and maintaining these relationships may require the use of technology to connect with loved ones.

Resilience can be supported through increased physical activity, enhanced compassion and emotional regulation, and greater social connectivity. Technology can play an important role in achieving these. "It can help maintain social connectivity, provide access to care via telemedicine, and also facilitate a range of other activities that may help cope with isolation," said Vahia. "It is increasingly becoming important for clinicians to assess patients' access and proficiency with technology as a part of care."

The authors stressed that although findings from the early months of the pandemic are encouraging and provide cause for cautious optimism, they may not reflect individual realities. "Older adults are a highly diverse group, and each person's response to the stresses of the pandemic depends on a unique set of circumstances," Vahia explained. "In addition, the current studies may not reflect specific high-risk populations with unique stressors, such as those living in underserved areas or those suffering with dementia or caregivers for people with dementia."

Importantly, the pandemic continues without a defined timeline or clear end in sight. The longer-term effects of COVID-19 on older adults' mental health, especially in countries with very high rates of disease, are unclear.

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More information: Ipsit V. Vahia et al, Older Adults and the Mental Health Effects of COVID-19, JAMA (2020). DOI: 10.1001/jama.2020.21753

Provided by McLean Hospital 

Older adults with dementia exhibit financial 'symptoms' up to six years before diagnosis

by Johns Hopkins University Bloomberg School of Public Health

Credit: CC0 Public Domain

A new study led by researchers at the Johns Hopkins Bloomberg School of Public Health and the Federal Reserve Board of Governors found that Medicare beneficiaries who go on to be diagnosed with dementia are more likely to miss payments on bills as early as six years before a clinical diagnosis.

01 december 2020--The study also found that beneficiaries diagnosed with dementia who had a lower educational status missed payments on bills beginning as early as seven years before a clinical diagnosis as compared to 2.5 years prior to a diagnosis for beneficiaries with higher educational status.

The study, which included researchers from the University of Michigan Medical School, also found that these missed payments and other adverse financial outcomes lead to increased risk of developing subprime credit scores starting 2.5 years before a dementia diagnosis. Subprime credit scores fall in the fair and lower range.

The findings, published online November 30 in JAMA Internal Medicine, suggest that financial symptoms such as missing payments on routine bills could be used as early predictors of dementia and highlight the benefits of earlier detection.

"Currently there are no effective treatments to delay or reverse symptoms of dementia," says lead author Lauren Hersch Nicholas, Ph.D., associate professor in the Department of Health Policy and Management at the Bloomberg School. "However, earlier screening and detection, combined with information about the risk of irreversible financial events, like foreclosure and repossession, are important to protect the financial well-being of the patient and their families."

The analysis found that the elevated risk of payment delinquency with dementia accounted for 5.2 percent of delinquencies among those six years prior to diagnosis, reaching a maximum of 17.9 percent nine months after diagnosis. Rates of elevated payment delinquency and subprime credit risk persisted for up to 3.5 years after beneficiaries received dementia diagnoses, suggesting an ongoing need for assistance managing money.

Dementia, identified as diagnostic codes for Alzheimer's Disease and related dementias in the study, is a progressive brain disorder that slowly diminishes memory and cognitive skills and limits the ability to carry out basic daily activities, including managing personal finances. About 14.7 percent of American adults over the age of 70 are diagnosed with the disease. The onset of dementia can lead to costly financial errors, irregular bill payments, and increased susceptibility to financial fraud.

For their study, the researchers linked de-identified Medicare claims and credit report data. They analyzed information on 81,364 Medicare beneficiaries living in single-person households, with 54,062 never receiving a dementia diagnosis between 1999 and 2014 and 27,302 with a dementia diagnosis during the same period. The researchers compared financial outcomes spanning 1999 to 2018 of those with and without a clinical diagnosis of dementia for up to seven years prior to a diagnosis and four years following a diagnosis. The researchers focused on missing payments for one or more credit accounts that were at least 30 days past due, and subprime credit scores, indicative of an individual's risk of defaulting on loans based on credit history.

To determine whether the financial symptoms observed were unique to dementia, the researchers also compared financial outcomes of missed payments and subprime credit scores to other health outcomes including arthritis, glaucoma, heart attacks, and hip fractures. They found no association of increased missed payments or subprime credit scores prior to a diagnosis for arthritis, glaucoma, or a hip fracture. No long-term associations were found with heart attacks.

"We don't see the same pattern with other health conditions," says Nicholas. "Dementia was the only medical condition where we saw consistent financial symptoms, especially the long period of deteriorating outcomes before clinical recognition. Our study is the first to provide large-scale quantitative evidence of the medical adage that the first place to look for dementia is in the checkbook."

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More information: Lauren Hersch Nicholas et al. Financial Presentation of Alzheimer Disease and Related Dementias, JAMA Internal Medicine (2020). DOI: 10.1001/jamainternmed.2020.6432

Journal information: JAMA Internal Medicine