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PAWTUCKET The first acceptance letter came from Brown University. The next one from Harvard. When a thick envelope arrived from Yale University, Victoria Wijerathnayapa was totally blown away.

Wijerathnayapa is not only the first student from Blackstone Valley Prep to get into Harvard and Yale, she is the first one to be admitted to three Ivy League institutions.

Her first reaction?

"I was super happy," Wijerathnayapa said Thursday. "It was a really emotional experience, but a happy one."

The good news doesnt stop there. She was accepted at eight other colleges, including Brandeis, Swarthmore, Wellesley, Williams and Worcester Polytechnic Institute.

A first-generation college student whose mother is from Sri Lanka, Wijerathnayapa is not one to brag. She acknowledges that she doesnt fit the typical Ivy League mold. She didnt study abroad or attend a prestigious public or private school. In fact, shes never left New England.

She attributes her success to Blackstone Valley Prep, a cluster of charter schools in northern Rhode Island where college banners adorn classroom doors, where race and equity are part of the fabric of conversation.

In her Pawtucket elementary school, Wijerathnayapa says, she felt singled out for being bright.

In fifth grade, Wijerathnayapa won the lottery, literally. She was admitted to BVP, where her fortunes brightened.

"At BVP, my hard work and determination were not credited to my race but rather to my character," she said. "People here accepted me for who I was, not what I looked like."

Blackstone Valley Prep did more than encourage her academic brilliance. It allowed her to choose from a palette of enriching experiences, from attending a summer program at Brown University to taking a years worth of college classes at the Community College of Rhode Island, where she is currently taking cellular biology, English composition and public speaking.

At BVP, Wijerathnayapa said, she feels known. She ticked off the teachers who have been friends and mentors: Mr. Leger, her chemistry teacher and track coach; and Mr. Jose, one of her college and career counselors.

"Just this morning, I was stressed out about having to apply for scholarships, and online learning. So many things were coming at me," she said. "Being a first-generation student, not knowing how to navigate the system, I reached out to Ashley Gemma, my college counselor. We discussed how to arrange my time better. She helped me figure out what the next steps were."

Although she and her younger brother were born here, Wijerathnayapa still sees the world through an immigrants eyes, her mothers eyes.

"She sacrificed herself. She tells me theyve all been worth it."

Sri Lanka, a tropical island off the coast of India, was wracked by civil war for 26 years, from 1983 to 2009. In 2004, a typhoon killed some 30,000 residents.

"My mom is the rock in my life," she said. "Ever since I was born, she was pushing me to take advantage of all of the opportunities life gives you. I am eternally grateful to her."

A trip to the Museum of Science in Boston triggered Wijerathnayapas interest in neuroscience, her likely major in college. But an internship with the Rhode Island Board of Elections in eighth grade sent her in a separate direction: political science.

"I realized that youth voter apathy is a big problem," she said.

David Jose, the dean of BVPs college and careers, recalled how Wijerathnayapa walked around the cafeteria, imploring students to register to vote. Then she managed to get actual voting machines to the school for a student council election.

"She has so many interests," Jose said. "You could talk to her for hours about neuroscience and psychology. And you could talk to her for many hours about philosophy and political science."

Jose felt Wijerathnayapa was destined to have her choice of the most selective colleges. But he said getting admitted to an Ivy League school wasn't what motivated her.

"Her first goal was to learn as much as possible," Jose said. "That ethos drove her regardless. Nobody gets into three Ivies."

Her mother, he said, is her core influence.

"Her mom is a big cheerleader," he said. "But Victoria is also very connected to the Sri Lankan community. Its important for her to represent as much as possible the immigrant community. In a conversation we had the other day, she was asking, "What can I do to give back?"

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Brown, Harvard, Yale. Pawtucket teen has been accepted to all 3, and more - The Providence Journal

Neuroscience

Large-scale analysis links glucose metabolism proteins in the brain to Alzheimer’s disease biology – National Institute on Aging

April 13, 2020 medical

In the largest study to date of proteins related to Alzheimers disease, a team of researchers has identified disease-specific proteins and biological processes that could be developed into both new treatment targets and fluid biomarkers. The findings suggest that sets of proteins that regulate glucose metabolism, together with proteins related to a protective role of astrocytes and microglia the brains support cells are strongly associated with Alzheimers pathology and cognitive impairment.

The study, part of the Accelerating Medicines Partnership for Alzheimers Disease (AMP-AD), involved measuring the levels and analyzing the expression patterns of more than 3,000 proteins in a large number of brain and cerebrospinal fluid samples collected at multiple research centers across the United States. This research was funded by the National Institutes of Healths National Institute on Aging (NIA) and published April 13 in Nature Medicine.

This is an example of how the collaborative, open science platform of AMP-AD is creating a pipeline of discovery for new approaches to diagnosis, treatment and prevention of Alzheimers disease, said NIA Director Richard J. Hodes, M.D. This study exemplifies how research can be accelerated when multiple research groups share their biological samples and data resources.

The research team, led by Erik C.B. Johnson, M.D., Ph.D, Nicholas T. Seyfried, Ph.D., and Allan Levey, M.D., Ph.D., all at the Emory School of Medicine, Atlanta, analyzed patterns of protein expression in more than 2,000 human brain and nearly 400 cerebrospinal fluid samples from both healthy people and those with Alzheimers disease. The papers authors, which included Madhav Thambisetty, M.D., Ph.D., investigator and chief of the Clinical and Translational Neuroscience Section in the NIAs Laboratory of Behavioral Neuroscience, identified groups (or modules) of proteins that reflect biological processes in the brain.

The researchers then analyzed how the protein modules relate to various pathologic and clinical features of Alzheimers and other neurodegenerative disorders. They saw changes in proteins related to glucose metabolism and an anti-inflammatory response in glial cells in brain samples from both people with Alzheimers as well as in samples from individuals with documented brain pathology who were cognitively normal. This suggests, the researchers noted, that the anti-inflammatory processes designed to protect nerve cells may have been activated in response to the disease.

The researchers also set out to reproduce the findings in cerebrospinal fluid. The team found that, just like with brain tissue, the proteins involved in the way cells extract energy from glucose are increased in the spinal fluid from people with Alzheimers. Many of these proteins were also elevated in people with preclinical Alzheimers, i.e., individuals with brain pathology but without symptoms of cognitive decline. Importantly, the glucose metabolism/glial protein module was populated with proteins known to be genetic risk factors for Alzheimers, suggesting that the biological processes reflected by these protein families are involved in the actual disease process.

Weve been studying the possible links between abnormalities in the way the brain metabolizes glucose and Alzheimers-related changes for a while now, Thambisetty said. The latest analysis suggests that these proteins may also have potential as fluid biomarkers to detect the presence of early disease.

In a previous study, Thambisetty and colleagues, in collaboration with the Emory researchers, found a connection between abnormalities in how the brain breaks down glucose and the amount of the signature amyloid plaques and tangles in the brain, as well as the onset of symptoms such as problems with memory.

This large, comparative proteomic study points to massive changes across many biological processes in Alzheimers and offers new insights into the role of brain energy metabolism and neuroinflammation in the disease process, said Suzana Petanceska, Ph.D., program director at NIA overseeing the AMP-AD Target Discovery Program. The data and analyses from this study has already been made available to the research community and can be used as a rich source of new targets for the treatment and prevention of Alzheimers or serve as the foundation for developing fluid biomarkers.

Brain tissue samples came from autopsy of participants in Alzheimers disease research centers and several epidemiologic studies across the country, including the Baltimore Longitudinal Study of Aging (BLSA), Religious Orders Study (ROS) and Memory and Aging Project (MAP), and Adult Changes in Thought (ACT) initiatives. The brain collections also contained samples from individuals with six other neurodegenerative disorders as well as samples representing normal aging, which enabled the discovery of molecular signatures specific for Alzheimers. Cerebrospinal fluid samples were collected from study participants at the Emory Goizueta Alzheimers Disease Research Center. These and other datasets are available to the research community through the AD Knowledge Portal, the data repository for the AMP-AD Target Discovery Program, and other NIA supported team-science projects operating under open science principles.

This press release describes a basic research finding. Basic research increases our understanding of human behavior and biology, which is foundational to advancing new and better ways to prevent, diagnose, and treat disease. Science is an unpredictable and incremental process each research advance builds on past discoveries, often in unexpected ways. Most clinical advances would not be possible without the knowledge of fundamental basic research.

The research in this study is funded by NIH grants R01AG053960, R01AG057911, R01AG061800, RF1AG057471, RF1AG057470, R01AG061800, R01AG057911, R01AG057339, U01AG061357, P50AG025688, RF1AG057470, RF1AG051633, P30AG10161, R01AG15819, R01AG17917, U01AG61356, R01AG056533, K08NS099474, U01AG046170, RF1AG054014, RF1AG057440, R01AG057907, U01AG052411, P30AG10124, U01AG046161, R01AG050631, R01AG053960, R01AG057339, U01AG061357, P50AG005146, U24NS072026, and P30AG19610.

Reference: Johnson ECB et al. Large-scale proteomic analysis of Alzheimers disease brain and cerebrospinal fluid reveals early changes in energy metabolism associated with microglia and astrocyte activation. Nature Medicine. 2020 Apr 13. doi:10.1038/s41591-020-0815-6

About the National Institute on Aging (NIA): NIA leads the U.S. federal government effort to conduct and support research on aging and the health and well-being of older people. Learn more about age-related cognitive change and neurodegenerative diseases via NIAs Alzheimer's and related Dementias Education and Referral (ADEAR) Center website. For information about a broad range of aging topics, visit the main NIA website and stay connected.

About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit the NIH website.

NIH...Turning Discovery Into Health

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Large-scale analysis links glucose metabolism proteins in the brain to Alzheimer's disease biology - National Institute on Aging

Neuroscience

Brain Discovery Could Have Important Implications for Neurodegenerative Diseases – University of Virginia

April 13, 2020 medical

Improper removal of faulty brain cells during neurodevelopment may cause lifelong behavioral issues, new research from the University of Virginia School of Medicine suggests. The finding also could have important implications for a wide range of neurodegenerative diseases, such as Alzheimers and Parkinsons diseases.

UVA neuroscientists have discovered that an unexpected form of cellular cleanup takes place in developing brains. If this process goes wrong happening too little or too much it can cause permanent changes in the brains wiring. In lab mice, this results in anxiety-like behavior, and it may play a role in neurological conditions such as autism in humans.

You dont want [brain] cells to have genomic compromises. You dont want damaged DNA. So, this would be a normal mechanism to expel those cells from being incorporated into the central nervous system, researcher Catherine R. Lammert explained. When the damage isnt recognized, the cells that have DNA damage live on in the [central nervous system] and can be seen by accumulation of DNA damage in the brain.

The cellular cleaner the researchers spotted, the AIM2 inflammasome, has been associated primarily with the bodys immune response to infections, but has not been extensively studied in the brain. But there it plays a critical role in ensuring the developing brain is assembled properly and functions correctly, Lammert discovered in collaboration with principal investigator John Lukens.

Neurodevelopment is a very complicated process, said Lammert, a graduate student whose specialized skills were instrumental in the discovery. This form of cell death actually plays a role in removing unwanted cells from the brain to establish a healthy [central nervous system] with the correct connections and the right number of cells.

More than half the neurons created during brain development end up dying, so proper cleanup is essential, noted Lukens, of UVAs Department of Neuroscience. Too much or too little is thought to underlie everything from autism to intellectual disability any type of neurodevelopmental disorder, he said.

For example, ataxia is a condition that causes people to lose control of their movements. Theres a potential that this pathway could be contributing to the neuronal loss that is seen in ataxia, said Lukens, a researcher with UVAs Center for Brain Immunology and Glia, or BIG. On the one hand, you need it [the cleanup], but if you have too much of it, it can have negative consequences, like, potentially, ataxia. A lot of the early-onset neurodegenerative diseases are associated with mutations in DNA damage repair proteins, and this pathway could also be involved.

The discovery came about somewhat serendipitously, the result of an observation of the behavior of lab mice while the researchers were investigating traumatic brain injury. But following that unexpected lead has given scientists a better understanding of brain development, and that understanding may one day yield new treatments for neurological diseases.

Lukens, a member of UVAs Carter Immunology Center, cautioned that such treatments are likely a long way off, but he said a therapy based on the discovery might have widespread applications.

Hitting this pathway in the mature brain would likely provide a treatment strategy for any neurodegenerative disease associated with DNA damage, he said. And thats all the major heavy hitters: Alzheimers disease, Parkinsons, ALS.

The researchers havepublished their findings in the prestigious journal Nature. The studys authors were Lammert, Elizabeth L. Frost, Calli E. Bellinger, Ashley C. Bolte, Celia A. McKee, Mariah E. Hurt, Matt J. Paysour, Hannah E. Ennerfelt and Lukens.

The research was supported by the Hartwell Foundation; Rettsyndrome.org grant 22349; the Owens Family Foundation; and Brain & Behavior Research Foundation grant 27515. Lammert was supported by a predoctoral training grant from the National Institutes of Healths National Institute of General Medical Sciences and a Wagner Fellowship.

To keep up with the latest medical research news from UVA, subscribe to theMaking of Medicineblog.

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Brain Discovery Could Have Important Implications for Neurodegenerative Diseases - University of Virginia

Neuroscience

Event Cells in the Brain Help Organize Memory into Meaningful Segments – Scientific American

April 13, 2020 medical

Our recollection of events is usually not like a replay of digital video from a security cameraa passive observation that faithfully reconstructs the spatial and sensory details of everything that happened. More often memory segments what we experience into a string of discrete, connected events. For instance, you might remember that you went for a walk before lunch at a given time last week without recalling the soda bottle strewn on the sidewalk, the crow cawing in the oak tree in your yard or the chicken salad sandwich you ate upon your return. Your mind designates a mental basket for walk and a subsequent bin for lunch that, once accessed, make many of these finer details available. This arrangement raises the question of how the brain performs such categorization.

A new study by neuroscientist Susumu Tonegawa of the Massachusetts Institute of Technology and his colleagues claims to have discovered the neural processing that makes this organization of memory into discrete units possible. The work has implications for understanding how humans generalize knowledge, and it could aid efforts to develop AI systems that learn faster.

A brain region called the hippocampus is critical for memory formation and also seems to be involved in navigation. Neurons in the hippocampus called place cells selectively respond to being in specific locations, forming a cognitive map of the environment. Such spatial information is clearly important for episodic (autobiographical rather than factual) memory. But so, too, are other aspects of experience, such as changing sensory input. There is evidence that neurons in the hippocampus encode sensory changes by altering the frequency at which they fire, a phenomenon termed rate remapping. According to research by neuroscientist Loren Frank of the University of California, San Francisco, and his colleagues, such changes may also encode information about where an animal has been and where it is going, enabling rate remapping to represent trajectories of travel.

Besides coding continuously changing variables, whether sensory inputs or route trajectories, some imaging studies previously suggested that the brain also processes experience as segmented events. But exactly how it achieves this process at a neural level was not known. In the new study, published last week in Nature Neuroscience, the teamled by Chen Sun, a graduate student in Tonegawas labdevised a task that attempted to disentangle the discrete, segmented nature of events from the continuously changing spatial and sensory details of moment-to-moment experience. The researchers trained mice to run around a square track. After doing four laps, the animals were rewarded with a sweet treat. They visited the reward box after every lap, segmenting each trial into four events (with the reward defining the end of a trial). Each lap traversed the same route, so sensory and location information was constant from one event to the next, allowing the researchers to attribute brain activity differences to what did change: the laps, or events.

The researchers recorded activity in hundreds of hippocampal cells while the mice performed this task and found that around 30 percent of cells showed a lap-specific pattern. Some of them were highly active when a rodent ran through the location it responded to on the first lap and relatively quiet during the remaining three laps. Others responded on the second lap far more than the rest, and so on. These neurons, which the researchers termed event-specific rate remapping, or ESR, cells, seemed to signal which lap a mouse was on.

To confirm the ESR cells were really encoding events, the researchers conducted experiments using tracks that were elongated along one dimension, increasing their length. Even when lap length was randomly altered between trials, the cells were still much more active on their preferred lap, showing the activity could not be related to the time elapsed or distance travelled. The results support the idea that the hippocampus can express representations of relevant variables, including, in this case, the number of laps since a reward was delivered, says Frank, who was not involved in the study.

In another experiment, the team trained mice on a square track on the first day, then substituted a circular track on the next one. Shifting to a new environment resulted in the ESR cells spatial responses being completely remapped onto the circular track. Strikingly, though, the lap that those neurons preferentially responded to remained the same. These findings suggest that ESR activity represents segmented units of experienceand that this event code can be transferred between different experiences that share a common structure.

Tonegawa compares this process to a familiar scenario. If you go to a restaurant to have dinner with your friend, that episode is made up of different segments: you arrive at the restaurant, then order an appetizer, then you choose a main dish, and then, usually, you have dessert, he says. As all this is going on, the stimuli coming to you are changing. But at the same time, its made up with distinct events, where you switch from the appetizer, to eating a main dish, dessert, and so on. The coding revealed in the study may explain how the brain abstracts events such as main course across different visits to different restaurants with different friends. And this idea may offer insight into how the brain generalizes knowledge to learn efficiently. Youre transferring knowledge you already have, based on past experience, to learn new things, Tonegawa says. Thats why we can learn things much faster. These insights, he thinks, could help engineers develop AI systems with the ability to transfer competencies from one environment to another, such as for medical robots moved between hospitals.

The circular track experiment showed that brain responses that specify your precise location can be altered without affecting event-specific activity. In a final experiment, the team asked whether the reverse is also true. A region called the medial entorhinal cortex (MEC) works closely with the hippocampus in spatial cognition and navigation. There is also evidence that it is involved in segmenting experience into sequential events. The researchers used optogenetics (a technique involving genetically altering cells so they can be activated or inhibited using light) to switch off signals from the MEC to the hippocampus while mice performed the running task. Doing so had no effect on location-specific responses but completely disrupted lap-specific ones, suggesting place and event encoding can be separately manipulatedeven though the same cells process both aspects of experience.

One limitation of the study is that running repeatedly around a track is unlike most natural experiences. Theres no demonstration that these event-related patterns exist the first time an animal experiences a set of eventsonly that they appear after many repeats of a now familiar sequence, Frank says. This is not really the same as our episodic memories, where each new experience gets encoded separately and stored as an event the first (and often only) time it happens. He thinks the cells represent well-learned and relevant elements of an experience with repeating elements. That arrangement, he says, is reminiscent of reports from studies of hippocampal neurons that fire similarly, but not identically, in geometrically repeated elements of the same environment.

This is an insightful experiment, performed with the care and numerous controls characteristic of Tonegawas lab, says neuroscientist Gyrgy Buzski of the NYU Grossman School of Medicine, who was not involved with the study, though he provided comments to the researchers. But Buzski has a more radical take on what is happening. He thinks all of the properties researchers have assigned to hippocampal neurons are different aspects of the same fundamental mechanism. To explain this idea, he compares it to the relationship between the motion of a vehicles engine and its distance travelled and journey time different variables reflecting a single underlying process.

In the case of episodic memory, the hypothesized elements are what, where and when. The definition of episodic memory is: What happened to me, where and when? Buzski says. When you combine these elements, it re-creates the event. This is called memory, he adds. Researchers relate the activity they observe to what, where or when, but all the hippocampus is doing is efficiently encoding experience into a neuronal sequence. The hippocampus is like a librarian that tells you to go to shelf five, row two. Then the next book is this, then this, and so on, he says. But the librarian is blind to the content of these sequences, which is constructed in the cortex. Thus, Buzskis interpretation of the new findings is that cells do not encode abstract event-specific propertiessuch as which lap number or dinner course one is experiencingso much as they generate the ordinal sequences that give memory the order necessary for us to make sense of it.

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Event Cells in the Brain Help Organize Memory into Meaningful Segments - Scientific American

Neuroscience

AI researchers hope to ID healthcare workers with COVID-19 before they show symptoms – AI in Healthcare

April 13, 2020 medical

The goal is to ultimately detect when providers are infected with the virus as quickly as possible, limiting their ability to potentially spread COVID-19 to their colleagues, patients and loved ones back home.

We are continuously monitoring the mind-body connectivity through our integrated neuroscience platform measuring the autonomic nervous system, fatigue, anxiety, circadian rhythms, and other human resilience and recovery functions, Ali Rezai, MD, executive chair of the WVU Rockefeller Neuroscience Institute, said in a prepared statement. Our AI-driven models are currently predicting symptoms 24 hours prior to onset, and we are working toward a three-plus day forecast. This forecasting capability will help us get ahead of this pandemic; limit the spread to protect healthcare workers, their families, and our communities; and improve our understanding of health recovery.

At Oura, weve heard firsthand from our users how the physiological signals tracked by the ring have predicted the onset of the virus before other symptoms manifest, Harpreet Rai, CEO of Oura Health, said in the same statement. Were grateful we can apply this knowledge to help vulnerable caregivers swiftly identify the earliest signs of the disease, and take the appropriate protective measures to limit its spread.

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AI researchers hope to ID healthcare workers with COVID-19 before they show symptoms - AI in Healthcare

Cell Biology

Biology Basics: What is a Virus? Bacteria? Fungus? And How Can We Kill Them? – Clare County Review

April 13, 2020 medical

April 13, 2020

Dear Editor:With the coronavirus is on everyones mind, lets go back to some basics. Like what is a virus and how do we get rid of it? Modern medicine seems to cure most anything, so why is it so hard to destroy the coronavirus?There are three major pathogens (biological structures that can make humans ill). They are bacteria (bacterium), fungi (fungus), and viruses (virus). Each one is unique in its structure and complexity. Therefore, the way to destroy each of them is also unique.

We are exposed to thousands, if not millions, of unique pathogens. Our immune system must learn how to destroy each and every one. When we are born, we have almost no immune system; we are incredibly vulnerable to infection and sickness. We must build up our immune system with antibodies. Antibodies are how the immune system can identify, tag, and destroy the pathogens making a person sick. The only way an immune system can build up antibodies is to be exposed to a pathogen and learn how to identify, tag, and destroy the pathogen. The only short cut to this is when a mother can pass some antibodies to a nursing infant through her breast milk. (This is only one of the many reasons why a newborn should be breast fed.)

However, once our immune systems have the antibodies needed to identify, tag, and destroy a specific pathogen, it will remember that pathogen. So, the next time you are exposed to it, your immune system will produce the antibodies to destroy the pathogen much quicker, ideally even before you feel sick.

Sometimes our immune systems cannot do it on its own, that is where medicine is required. Remember, there are bacteria, fungal and viral pathogens.

First, fungi tend to be external organisms that live on surfaces. Mold, mushrooms, and mildew are some classic examples and good to use as a reference. They grow in dark, moist places on decaying matter. The hypha or roots borrow into the organic matter to extract the nutrients it needs for life. Athletes foot, jock itch, and yeast infections are all common pathogens many of us have suffered. Although, internally fungi are lethal, they are rare. Most external fungi can be destroyed with an anti-fungal cream or pill. Fungi tend to be on the low side of complexity and relatively easy to kill.Bacterial pathogens are individual living organisms. They are the germs that we think of swimming around under a microscope. There are millions of varieties of them. They live on their own, on surfaces within the air, in foods and water. Many ear, throat, and sinus infections are bacterial.

Fortunately, our immune system is pretty good at identifying these foreign organisms living within our bodies and can destroy them on its own. And if it cannot, a doctor can prescribe an antibiotic (penicillin) to finish the job.On the other hand, viruses are non-living, they are DNA pirates. They cannot live or reproduce on their own. Think of a virus as a blob of grease or oil with a single strand of DNA within it. No nucleus, no organelles, just a microscopic ball of fat with a code to cause some biological mutiny.

Viruses require a host cell for reproduction. The virus does this by taking over a host cell and forcing the cell to reproduce the virus and it fatty shell, much like a pirate hijacking a ship for its own purposes. Unfortunately, the cell will no longer able to perform the life sustaining job it was intended to be doing; hence you fell sick. The host cell will continue to perform the pirates task, reproduce the virus, until it destroys itself. Then, liberating more DNA pirates to repeat the process.

The fact that the virus lives inside the cell makes it hard for the immune system to identify the pathogen, let alone destroy it. The only way to destroy the virus is to destroy the cell itself. The pirate will never leave the ship, the ship must be destroyed to kill the pirate.

This is what our immune systems does, anti-bodies identify, tag, and destroy the living cells that have the virus within them. This explains our symptoms which can range from minor aches and pains to lethal tissue and organ damage. Your immune system is literally destroying your own cells.

Fortunately, we have billions of cells and our immune system can be very targeted once the anti-bodies have figure out which cells have been pirated by the virus. White blood cells can then effectively destroy only the pirated cells and recovering will begin.

A major problem with the Coronavirus in humans is our immune systems have hard time identifying which cells have been pirated by the virus and which cells are still healthy. Human immune systems seem to be over-reacting and destroying ALL the surrounding cells. Since the virus is often found in the lungs, heart, and kidneys these are the organs that seem to be suffering the most.

So how do we destroy the Coronavirus? They only thing that can destroy a virus is our own immune system. The medical field has had little success in developing anti-viral medications. We can only support our immune system to learn quicker, to produce the antibodies needed and then the immune system can become much more targeted.

Vaccines do this by providing a weaken version for the immune system to learn from. Anti-body therapy takes the anti-bodies from one immune system that has already learned how to identify the virus and directly gives it to an un-learned immune system.

Unfortunately, we do not have any solutions yet! So, the best way to be healthy is to not get sick in the first place. Stay away from the pirates! You all know what to do, washing your hand, social distance, etc. Be safe.

Andrew J. FrischFarwell High School.

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Biology Basics: What is a Virus? Bacteria? Fungus? And How Can We Kill Them? - Clare County Review

Cell Biology

Fast-tracked research projects aim to respond quickly to mitigate effects of COVID-19 – University of Miami

April 13, 2020 medical

Twenty-four University of Miami research teams have received rapid response grants to undertake innovative projects that will provide critical information about the novel coronavirus.

Imagine this: developing an oral rinse test to detect COVID-19 earlier, creating a behavior therapy program for parents so that they do not pass on the stress they are feeling to their children during the pandemic, and gauging the effects of COVID-19 on pregnant women and trying to determine the impacts on their new babies.

These are just a few of the 24 projects recently awarded rapid response grants from the University of Miamis Office of the Vice Provost for Research. The grants, which range from $5,000 to $40,000, require faculty members and students to develop and execute research that will somehow broaden our understanding of COVID-19 and begin to mitigate its impacts within the next four months.

Our idea was to take advantage of researchers creativity and commitment in tackling some of the most pressing problems around the COVID-19 epidemic, said John Bixby, vice provost for research and professor of molecular and cellular pharmacology and neurological surgery. We challenged them to examine the effects of the pandemic on multiple aspects of peoples livesnot just the physical ones, but the social aspects, the economic ones, and the environmental.

With just 10 days to submit proposals, faculty members across the university flooded the office with applications and more than 70 ideas were submitted. Each award was reviewed by three individuals, and the awardees were selected based on novelty, potential impact on the effort to combat COVID-19, and whether the study could be completed in short turnaround time.

The faculty response was inspiring, said Erin Kobetz, co-vice provost for research. There was a level of innovation across multiple disciplines that demonstrates an institutional commitment to addressing the COVID-19 pandemic. We look forward to the outcomes of those applications that were funded and imagine that they will lead to positive, measurable impact now and in the future.

After the four months are over, teams will be asked to report their progress, Bixby said. Below is a list of all the projects awarded grants:

This team will evaluate the potential benefits of nitric oxide in treating COVID-19 utilizing the iNOpulse technology, which may potentially allow future patients to be treated outside of the hospital.

Principal investigator: Roger Alvarez, assistant professor of clinical medicine,

This team will develop a novel vaccine to protect against the current coronavirus pandemic caused by SARS-CoV-2. Its strategy involves replacing the envelope glycoprotein (G) of vesicular stomatitis virus (VSV) with the spike of COVID-19. The resulting virus will form the basis of a vaccine to generate neutralizing antibody to the SARS-CoV-2 spike that could prevent disease if exposed to the real virus.

Principal investigator: Glen Barber, professor and chair of cell biology

This study will exploit the enzyme TMPRSS2 as a potential link between androgen receptors and COVID-19 by providing preliminary data on whether certain drugscalled androgen receptor antagoniststhat are effective and safe for treating prostate cancer, might also be effective in treating COVID-19.

Principal investigator: Kerry Burnstein, professor of molecular and cellular pharmacology

Artist Xavier Cortada will develop a socially engaged art platform online to mitigate stress related to COVID-19 infection and/or social distancing. He is also working to develop participatory art projects and an online message mural to capture stories from individuals across South Florida as they are affected by the pandemic. https://cortadaprojects.org/projects/corona/

Principal investigator: Xavier Cortada, professor of practice, art and art history

Public health emergencies pose huge challenges to the behavioral health system, and consequences on the psychosocial well-being of people in at-risk communities largely go overlooked. This project will first identify community psychosocial needs and then create and disseminate a multilingual COVID-19 online toolkit and resource hub to mitigate negative mental health outcomes throughout the pandemic.

Principal investigator: Bridget Davidson, assistant professor of clinical pediatrics

This team will develop a prototype for a socially engaging online experience targeting vulnerable and older adults where future University live cultural offerings could benefit from a secondary virtual platform.

Principal investigator: Joy Doan, head of Marta and Austin Weeks Music Library

Since parental stress during disasters or quarantine may be associated with child traumatic stress and/or subsequent incidents of abuse or neglect, this study will examine how parent-directed telehealth interventions using motivational, opposite action, and mindfulness strategies can be deployed during crisis situations to mitigate risk for parents exhibiting mental health concerns during our current COVID-19 pandemic.

Principal investigator: Jill Ehrenreich-May, professor of psychology

This project will enable the development of an oral rinse test that detects COVID-19 earlier and saves lives by directing resources and quarantine efforts to patients who need them most. Researchers will perform testing with the current prototype on a confirmed COVID-19 patient to determine the best antigen and concentration.

Principal investigator: Elizabeth Franzmann, associate professor of otolaryngology

This team will take blood samples from asymptomatic health care personnel working in any patient care capacity in three high-risk medical specialtiesotolaryngology, anesthesiology, and ophthalmologyand examine them for the presence of immunity. The results could help South Florida hospitals consider strategies for resource and personnel deployment.

Principal investigator: Michael Hoffer, professor of otolaryngology and neurological surgery

This team will gather data and insight on loneliness and other behaviors in the wake of CDC recommendations for social distancing during the COVID-19 pandemic. Results will demonstrate the effects of this public health crisis on loneliness, as well as other psychosocial symptoms. The team will also assist public health professionals in preparation for post-pandemic interventions and future global health emergencies.

Principal investigator: Viviana Horigian, associate professor of public health sciences

More than 20 models of the viral protease (which if targeted, might stop the virus) have been openly shared on Twitter, prompting labs around the world to begin a collective search for protease inhibitors. This project will provide a cheap, accessible screening test for characterizing potential protease inhibitors and use the available crystal structures to develop effective protease inhibitors through computational techniques.

Principal investigator: Daniel Isom, assistant professor, molecular and cellular pharmacology

Researchers will investigate the ability to detect the COVID-19 virus in donor allograft tissue and frozen tissue. They will also attempt to determine whether the COVID-19 virus in the donor tissue is associated with transmission to the recipient and influences short- or long-term survival, as well as the health of the recipient.

Principal investigators: Hugo Kaneku Nagahama, assistant professor, surgery and Phillip Ruiz, professor of surgery and pathology and director of Transplantation Laboratories and immunopathology

Partnering with Breakthrough Miami, a community-based academic enrichment organization for low-income students, this study will contact families involved with this organization to understand the educational and health-related challenges as a result of COVID-19. Researchers will also investigate the role of community-based organizations in the mitigation of stress related to the concerns of infection and social distancing.

Principal Investigator: Laura Kohn Wood, dean and professor in the School of Education and Human Development.

Ear, nose, and throat (ENT) doctors play a key role in the treatment of COVID-19, but they are at high risk of exposure. This team will identify ENT issues in COVID-19 patients at the University of Miami and Jackson Memorial Hospital and evaluate new approaches to case identification and health care worker protection.

Principal investigator: Xue Liu, professor and Marian and Walter Hotchkiss Endowed Chair in otolaryngology

Mindfulness training has emerged as an effective program to enhance cognitive functioning, improve psychological and physical health, and to reduce loneliness in young to mid-aged adults. But little is known about its effects in elderly adults. This proposal aims to offer mindfulness training via online delivery to elderly adults and to assess the trainings potential to protect against cognitive decline and degradation in psychological and physical health during the COVID-19 pandemic.

Principal investigator: Ekaterina Ninova (Denkova), research assistant professor, psychology

Individuals who have hypertension, diabetes, or underlying cardiovascular disease have higher rates of mortality from COVID-19 than the average person. Patients with these diseases have a high likelihood of being prescribed ACE inhibitors or angiotensin receptor blockers (ARBs) in order to treat their underlying ailments. This project will examine whether there is a link between drugs that are given to patients with hypertension, coronary artery disease, diabetes, or cardiovascular disease and the outcomes of COVID-19 patients.

Principal investigator: Savita Pahwa, professor, microbiology and immunology

This project aims to determine the rate of COVID-19 positivity among pregnant women and their newborns delivering at a tertiary care center in Miami with the highest rates of coronavirus in Florida. They also want to identify cases of maternal transmission of COVID-19, which is critical to establish treatment guidelines, while also answering questions about disease progression, perinatal transmission, and effects on the newborn.

Principal investigator: JoNell Potter, professor of clinical, obstetrics, gynecology, and reproductive services

This team will test, evaluate, and create new reusable mask designs for use in the health care setting to limit exposure and protect medical personnel and first responders who treat coronavirus patients. The aim is to provide masks to workers within the University of Miami and Jackson Memorial Hospital first. Finalized mask designs can be shared with other medical facilities.

Principal investigator: Carl Schulman, executive dean for research and professor

This project hopes to develop a deep learning program that could classify X-ray or CT scan imaging characteristics in COVID-19 patients that could help radiologists categorize them into those patients who require hospitalization, those who will need Intensive Care Unit admission, and those at risk for death. In addition, such a deep learning network could be used to predict the patients response to current experimental drugs.

Principal investigator: Radka Stoyanova, research professor in radiation oncology

This project aims to understand the relationship between cardiac injury and COVID-19 severity. The team will conduct an extensive evaluation of 50 patients with a new COVID-19 infection who require hospital admission and will test myocardial injury and inflammatory biomarkers, use cardiac magnetic resonance imaging (CMR), and offer a social determinants of health survey. Blood will be saved for future biomarker discovery and genomic evaluation.

Principal investigator: Leonardo Tamariz, professor of medicine

While respiratory distress dominates acute symptoms of COVID-19, ruptures in the brains capillary cells accompanied by bleeding within the brain have fatal consequences in patients with COVID-19.Moreover, impacts of COVID-19 on the brain depend largely on the ability of the SARS-CoV-2 virus to leak in through brain capillaries, the cells of which express the SARS-CoV-2 receptor (ACE2). This study is based on the hypothesis that interaction of the virus with ACE2 disrupts the normal barrier function of brain capillary cells, and induces inflammatory responses derived from these cells.

Principal Investigator: Michal Toborek, vice-chair for research and professor, biochemistry and molecular biology

Given the surfeit of social media data accompanying the recent outbreak of COVID-19, this group will take a computational and big data-driven approach to uncovering information about viral transmission, social sentiment and response, decision-making, and public health policy recommendations. The group proposes to develop algorithm(s), as well as an online early alert system, to provide early warnings for disease surveillance tied to geographical data.

Principal investigator: Nicholas Tsinoremas, director of the Institute for Data Science and Computing

This team will investigate Florida citizens opinions on COVID-19, including their thoughts about the causes and consequences of the pandemic, their preferred sources of information, and subsequent behavior changes. They will also assess public perceptions of government responses to COVID-19 to determine how Floridians change their perceptions and behaviors over time in response to changing policies, messaging, and conditionsparticularly if they or someone they know becomes ill. This will be one of very few studies to track a statewide populations opinions, lifestyle factors, and health behaviors during an ongoing pandemicwith clear implications for policymakers, health communicators, and disaster specialists.

Principal investigator: Joseph Uscinski, associate professor of political science

Because young adults appear to experience fewer cases of the COVID-19 virus, this population may engage in behaviors that contribute to the spread of COVID-19. Yet, little is known about the impact of COVID-19 on adolescent mental and physical health and their substance-use behaviors. This project hopes to collect epidemiologic data on the patterns of mental and physical health, substance use (frequency and dose), and potential disease transmission behaviors among young adults during the COVID-19 pandemic.

Principal investigator: Denise Vidot, assistant professor in the School of Nursing and Health Studies

Cell Biology

Supervisor Dean Preston and UC Berkley researchers team up to deliver hand sanitizer to MUNI operators – KRON4

April 13, 2020 medical

SAN FRANCISCO, Calif., (KRON) San Francisco District 5 Supervisor Dean Preston and UC Berkeley researchers partner to deliver 500 bottles of hand sanitizer to MUNI operators early Monday morning.A group of volunteers helped deliver hand sanitizers in an effort to assist in the citys response to COVID-19.

During this public health crisis, we must protect our essential workers, and that includes MUNI operators said Preston. For all of the MUNI operators who are bravely providing essential services, the least we can do is ensure they have basic protective supplies on the job.

Since the start of the outbreak Presidentof Transit Workers Union 250A Roger Marenco has urged the Metropolitan Transportation Authority to protect operators and its passengers.

If the city is requiring essential workers to come to work and provide essential services, then we need to be issued essential protective equipment, Marenco said.

Supervisor Prestons office and UC Berkeley researchers have been working together to help deliver hand sanitizer to people who need it the most since the start of sheltering-in-place orders.

Abrar Abidi and Yvonne Hao, researchers from UC Berkeleys Department of Molecular and Cell Biology reached out Supervisor Prestons office with a goal to help Bay Area residents.

Our goal is to make and distribute hand sanitizer to every homeless person, every MUNI operator, every jail inmate, every senior home, and every frontline healthcare worker in the Bay, said Yvonne Hao.

The group has been able to deliver approximately 200 gallons of hand sanitizer to homeless shelters, county jails and MUNI operators in San Francisco.

We are extremely grateful for the district 5 team stepping up to support our Muni Operators, said Marenco.

Do you know someone who deserves to be recognized?Click here to submit themto be a KRON4 Hero.

Why coronavirus is so lethal & fast-spreading: Its biology, disease, cure & call for united action – MyNation

April 13, 2020 medical

1. What is a virus?

We have to first understand the simple structure of a typical cell very briefly. Then, even as laymen, we will be able to understand how the structure of the coronavirus is different from that of a typical cell. A common mans understanding and knowledge of the coronavirus holds the key to implementation of preventive measures and solutions to contain the pandemic.

That "protoplasm is the physical basis of life" is a fundamental concept of cell biology and life science defined by William Huxley, an English biologist and anthropologist. The cell content within the cell membrane is called protoplasm. The matrix residing within the cell membrane and outside the centrally located nucleus is called cytoplasm. So, cytoplasm with organelles and nucleus containing the genetic material (DNA) are the constituents of protoplasm.

2. Virus as a bridge between the living and non-living: A virus is an unusual, very primitive parasitic entity that has both living and non-living characteristics. It is a mysterious invisible, non-living, micro-crystal or dust particle when outside a living host. But it assumes life soon after it enters a living host (ranging from amoeba to man and also plants). Therefore, it is an obligatory parasite. It has neither cytoplasm nor cell organelles. It has only genetic material, either DNA or RNA, surrounded by a protein coat. Therefore, the virus is considered as a bridge between the living and the non-living by those who have studied biology and theories of the origin of life.

3. Understanding the nature of the coronavirus: The coronavirus is a virus belonging to the family Coronaviridae. It is opined that the original reservoir of this virus is a non-human host, the horse-shoe bat (in which it causes no harm), from which it jumped to humans. The immune system of the bat is distinct from the human immune system and allows the virus to rapidly multiply within the bat while also protecting it from the harmful effects. Accordingly, bats have been the source of other recent viral disease outbreaks such as SARS, MERS and Ebola This coronavirus emerged in the Chinese city of Wuhan in November 2019 and spread all over the world in a short period. The epidemic is now known as COVID-19 and the virus is known as SARS-CoV-2. The virus is a mutant variety of the SARS (Severe Acute Respiratory Syndrome) coronavirus. This non-living micro dust-like form of the virus is transmitted between people through respiratory droplets when an infected person sneezes or coughs.

4. Structure of the coronavirus: This coronavirus is a spherical, single-stranded RNA (genetic material) virus with a protein coat. It has corona-like extensions called spike proteins on its surface. Hence the name coronavirus. The spike proteins bind to the receptors on the host cell. It is called novel coronavirus (nCoV) because of these spike proteins, which are different from those of other coronaviruses.

5. Fast replication process once it enters the host: In general, the coronavirus multiplies swiftly once it enters the living host. Its RNA replicates after entering the host and produces multiple copies of itself. The RNA particles get themselves covered by protein coats and then come out of the host cells, only to infect new cells. During infection, they enter through the mouth or nostrils through respiratory droplets, make their way into the bronchial tract and lungs gradually, and then they multiply in the alveoli of the lungs. This reduces the expanding and contracting mechanism of the alveoli, leading to fibrosis of the lung. As a result, the function of our oxygen-supplying organ, the lung, gets badly mutilated and respiration gets hindered, making us unable to breathe. This results in a shortage of oxygen supply to the brain and the entire body and the patient dies within a few days.

6. Why is the coronavirus so lethal and fast- spreading? How to break the protein coat of the virus and paralyze its RNA when it is in the non-living form outside the host and in a living form inside the host is a matter of research. Of course, its duration of life outside the host is very limited, to the extent of 3 or 4 days, especially in a tropical hot climate like in India, where the relative humidity is also relatively high. It is believed that a type of WBCs called the natural killer cells (NK cells), which are a component of our innate immunity and which resist any pathogen as the first line of defence, are not very effective against these viruses. People may be carriers of infection of the virus for 1 to 14 days before developing symptoms. The most common symptoms are fever, dry cough, tiredness, and excessive drowsiness. In severe cases, breathing will be difficult. If not contained, it can be fatal, particularly in individuals with co-morbid health conditions like diabetes, high blood pressure, and chronic diseases of heart, lungs, kidneys and liver, and infants aged 12 months and under. Since the coronavirus is spread through respiratory droplets, it is advised not to touch the nose and mouth as these viruses stay on the surface of the hand in a viable state for quite a long time. Also, it is advised to wash the hands thoroughly for at least 20-25 seconds frequently with soap. Sanitizers can also be used to keep the hands clean.

7. Prevention of COVID-19 -- the scientific and social approach: Our body's immune system is yet to develop a new strategy to counter this novel mutant coronavirus. Presently, our WBCs can kill many other invading pathogenic forms like bacteria and others. But we have not yet developed an immune system that can kill the SARS-CoV-2. So, we are neither able to effectively deal with the coronavirus outside the body nor inside. The greater challenge is to find a way for our defence mechanism to deactivate the RNA of coronavirus when it enters the human body or by antibiotics or in developing a vaccine. Since it is fast-spreading through human agency, the epidemic has now become a pandemic, killing human beings fast without yielding to any known medical system. That is the reason thousands have died in such a short time, in China, Italy, Spain and South Korea. As a result of the deeply inter-connected world we now live in involving convenient air travel and cruises, it has spread to nearly 200 countries now. As of 31st March 2020, there were 750,890 confirmed cases and 36,405 deaths. Realizing the magnitude of the epidemic, the Government of India has decided that the only way to contain the epidemic is by making humans not accessible to it by social distancing. People affected by coronavirus have to be isolated in quarantine. Thus, the virus chain has to be broken by not allowing it to enter the human host, so that it perishes after being deprived of a host for a considerable period.

8. Social distancing and Stay at Home are the only Mantra: That is why we have messages of preventing the coronavirus infection on the telephone ringtone. We should broadcast it in all media and all possible manners. It is with this intention that the Government of India and all the States have announced a strict lockdown. That is why the COVID-19 preventing "mantras" are "stay at home" and maintain social distance everywhere. Even while shopping for essentials, one must maintain a distance of one or two meters from the next person. 'Prevention is better than cure' is the golden proverb we all have heard, but in the context of the coronavirus, prevention is the only cure thus far.

9. The absolute need for a strict, nation-wide lockdown: If we see the extent of devastation caused by the coronavirus in developed countries like Italy, China, Spain, UK, and America, India with its less developed medical infrastructure and habitual group-living in cities and slums, especially in villages, needs to be extra vigilant and cautious in preventing the entry and spread of coronavirus. Our national lockdown may have to be inevitably continued for some more reasonable time and all of us have to educate fellow citizens about the preventive measures more aggressively and convincingly.

10. Therapeutic approaches being tested for potential treatment of COVID-19 in the future: Scientists and physicians all around the world are working together to explore potential treatments for coronavirus. Clinical trials are underway to test a number of candidate treatments that are already approved and safely administered to patients for other diseases. These include the anti-malarial agents chloroquine and hydroxychloroquine; HIV treatments lopinavir and ritonavir. An experimental antiviral agent called Remdesivir that was previously developed for treating Ebola is also being explored. Another treatment called convalescent plasma is also under investigation that involves transfusion of critically ill patients with plasma obtained from the blood of patients who have recovered from COVID-19 and built up high levels of antibodies to SARS-CoV-2 to help stimulate a stronger immune response. Several unconventional approaches for rapid vaccine development are being explored that are expected to deliver results in 12-18 months. The first patient was recently dosed in a clinical trial in the USA for a candidate mRNA based vaccine which encodes for a stabilized form of the coronavirus spike protein.

11. Need for a positive attitude at the time of fear and uncertainty: It is very hard to retain positive energy when we are being constantly bombarded with the news of death and economic crisis. However, this time of lockdown is a golden opportunity for reflection, spending quality time with family and exploring hobbies we never had a chance to pursue due to the unending grind of routine life. While social media is a blessing in times of a lockdown to keep in touch with family and friends, it is also a source of rumours and misinformation. We should only rely on government agencies for the most accurate information and guidelines.

12.Need for basic existential solidarity transcending the barriers of caste, creed and religion: It is time that we Indians demonstrate that we are all solidly united, transcending barriers of caste, creed, religious customs and traditions to protect not only our country but the world. Let us pray intensely for the wellbeing of all. Let us invoke the noble and powerful survival instinct and motherly caring instinct hidden in all of us. Let us work together constructively, lovingly, as Indians. This feeling of unity, amity, and love for each other is needed now to keep the COVID-19 pandemic away. This should be our religion, throb of life, the wave of mind, and line of action. So, let us together pray for the protection from this lethal coronavirus and wellbeing of all and take a pledge to stay at home. The famous French surgeon and Nobel laureate, Dr. Alexis Carrel, who was awarded the Nobel Prize in Physiology or Medicine in 1912, has said, "Prayer is the most powerful form of energy one can generate. As a physician, I have seen the patients coming out of melancholy and disease by the serene efforts of prayer."

Our united and the sincere cry of the soul shall be heard by the Almighty, the Omniscient, Spiritual Consciousness, which has created and is sustaining the universe. Let our patriotism, universal brotherhood, and unity find its true expression in this hour of unprecedented crisis. Let the scientific capability of the West and the spiritual capability of the East come together and work reciprocally to fight this terrible pandemic and stave off nemesis. If political and religious leaders, government employees, police, the medical, pharmaceutical and nursing brigades and the business community work with sincerity and honesty as per the scientifically defined line of action, we shall not only conquer the coronavirus pandemic, but also create a new eco-friendly, clean, and spiritually vibrant world of understanding, friendship and love.

Microbes in your blood could be the tell-tale of cancer | Forge – ForgeToday

April 13, 2020 medical

Scientists have developed a novel method of cancer detection and diagnosis from a single blood draw, even at early stages.

In 2017, Dr Ravid Straussman of the Weizmann Institute of Sciences Molecular Cell Biology Department and his team found live bacteria within pancreatic tumours. These bacteria metabolised a common chemotherapy drug and rendered it ineffective. This shone light onto the possibility that bacteria and viruses may influence prognosis to a larger extent than previously thought.

Recent investigation into these microbes revealed that they are detectable in the blood, even before symptoms arise. Researchers at the University of California San Diego School of Medicine have exploited this to develop a new method to determine who has cancer, and which type, by a simple analysis of microbial DNA in the patients blood.

The researchers were granted access to The Cancer Genome Atlas, which stores microbial data as well as genetic information from thousands of patients tumours. From this, distinct patterns of microbial DNA were found to be associated with specific types of cancer.

Of course, some of these associations are well-known. For example, human papillomavirus (HPV), has a clear link to cervical cancer. However, the team also found new microbial patterns, or signatures, which were previously unknown and were able to distinguish between specific cancer types. If these were found present in the blood of a patient, this would allow accurate and complete diagnosis.

The team tested thousands of cancer samples on computer-based models which were trained to associate the presence of certain microbial DNA with specific cancer types. They found that the computer was able to recognise a patients cancer type, even at early stages, using only a small blood sample.

Gregory Poore, MD/PhD, his supervisor Professor Rob Knight and their team have undertaken the largest-ever attempt (to their knowledge) to identify specific microbial DNA in human blood. They have successfully produced a technique to exploit non-human molecules in the diagnosis of a major human disease. The ability of this technique to detect traces of microbes at the earliest stage of disease progression gives it great therapeutic potential it is no secret that earlier diagnosis produces a better prognosis.

The team is now looking to introduce their method into the clinical setting and are encouraging other cancer researchers to invest their efforts into the study of microbes in the disease.

Original post:
Microbes in your blood could be the tell-tale of cancer | Forge - ForgeToday

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Why coronavirus is so lethal & fast-spreading: Its biology, disease, cure & call for united action – MyNation

Microbes in your blood could be the tell-tale of cancer | Forge – ForgeToday