Category Archives: Biochemistry

Biochemistry

Global Automatic Veterinary Biochemistry Analyzer Market 2020 Analysis, Types, Applications, Forecast and COVID-19 Impact Analysis 2026 – Jewish Life…

Global Automatic Veterinary Biochemistry Analyzer Market 2020 by Manufacturers, Regions, Type and Application, Forecast to 2026 designed through detailed investigation procedure provides an all in all compilation of the historical, current, and future outlook of the market. The report gives a forecast of the various segments and sub-segments. It analyzes the revenue generated from the market analysis and provides opportunity analysis to estimate the market size. The brief profile of leading players in the global Automatic Veterinary Biochemistry Analyzer industry is presented along with their plans and current developments. The report describes the development of the industry by type segment & market application as well as upstream and downstream, industry overall and development, key companies.

Several major manufacturers mention in the global Automatic Veterinary Biochemistry Analyzer market research report is focusing on expanding operations in regions. The report offers a complete evaluation of sales enterprise, detailed market records, and penetrating insights. Several aspects including technology, supplies, capacity, production, profit, and price are considered while classifying the market dynamics and trends in the market. The research study determines the statistical analysis of the market covering factors such as capacity, production, production value, cost/profit, supply/demand, and import/export.

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Popular Players:

For the competitor segment, the report includes global key players of the market as well as some small players. Global Automatic Veterinary Biochemistry Analyzer market contains a set of manufacturers, vendors, and consumers that define that market and their every move and achievements becomes a subject of studying for market researchers and other stakeholders. The report introduces the market competition situation among the vendors and company profile, and market price analysis and value chain features are covered in this report. In addition, their market share, production, revenue, sales growth, gross margin, product portfolio, and other significant factors are also taken into consideration.

Top players covered in this global Automatic Veterinary Biochemistry Analyzer market share report: Biochemical Systems International, BPC BioSed, Carolina Liquid Chemistries, Abaxis Europe, AMS Alliance, Randox Laboratories, Rayto Life and Analytical Sciences, Scil Animal Care, Crony Instruments, DiaSys Diagnostic Systems, Eurolyser Diagnostica, Gesan Production, Heska, Idexx Laboratories, LITEON IT Corporation, Shenzhen Icubio Biomedical Technology, URIT Medical Electronic,

Geographically, this report is segmented into several key regions, with sales, revenue, market share and global market growth in these regions, covering: North America (United States, Canada and Mexico), Europe (Germany, France, UK, Russia and Italy), Asia-Pacific (China, Japan, Korea, India and Southeast Asia), South America (Brazil, Argentina, Colombia etc.), Middle East and Africa (Saudi Arabia, UAE, Egypt, Nigeria and South Africa)

Breakdown data by type: Bench-Top Veterinary Biochemistry Analyzer, Portable Veterinary Biochemistry Analyzer

Breakdown data by application: Pet Hospital, Veterinary Station, Other

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Global Automatic Veterinary Biochemistry Analyzer Market 2020 Analysis, Types, Applications, Forecast and COVID-19 Impact Analysis 2026 - Jewish Life...

Biochemistry

Researchers are developing a diagnostic test that predicts the advanced stages of COVID-19 patients – News-Medical.Net

A research team from the University of Valencia, led by Professor Juan Saus from the Department of Biochemistry and Molecular Biology, is developing a project to provide the healthcare system with a diagnostic test that anticipates the entry into advanced stages of patients with COVID-19 and a scalable oral treatment for the disease.

The proposal has the support of the Valencian Government, within the call "Capacities of the Valencian System of Innovation in the fight against COVID-19", which finances actions that provide innovative solutions to the new coronavirus.

Goodpasture syndrome has been the subject of study by the research group led by Juan Saus at the University of Valencia since 1988. It is a pulmonary haemorrhage with kidney failure that currently manifests itself very sporadically and that, thanks to new discoveries made by Saus' team, has given way to a therapeutic proposal for COVID-19.

GPBP (Goodpasture antigen binding protein), when overexpressed and accumulates outside the cell, causes a destructuring of the microenvironment and transforms thin membranous structures into thick fibrous walls that make it difficult for oxygenation and blood purification in the lung and kidney."

Juan Saus, Professor, Department of Biochemistry and Molecular Biology, University of Valencia

"This established the basis for the development of EMTEST, a prototype to measure GPBP in blood and T12, a compound specifically designed to inhibit it", explains Juan Saus.

The research team observed that GPBP accumulates in the lungs of patients with a condition of severe respiratory distress called adult respiratory distress syndrome (ARDS), caused by infections or sepsis.

"There are increasing amounts of evidence that a sepsis with a predominance of lung involvement is the cause of fatality in COVID-19", explains Saus.

"With sepsis, antibacterial or antiviral treatments are not effective enough in stopping the process. Once ARDS has been triggered in COVID-19 patients, a treatment that eliminates the coronavirus is not expected to significantly modify the fatal course of the disease", concludes the expert.

For this reason, the project wants to use EMTEST to measure GPBP in the blood of COVID-19 patients and anticipate the appearance of ARDS. Then, with controlled GPBP levels, administer T12 to COVID-19 patients at risk of respiratory distress to avoid the onset of this disease.

"With this proposal we want to develop a diagnosis of the imminence of ARDS and a specific treatment to improve the survival of people with COVID-19 and avoid collapses in the Health System", says Juan Saus.

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Researchers are developing a diagnostic test that predicts the advanced stages of COVID-19 patients - News-Medical.Net

Biochemistry

Why the ACE2 receptor could be key to treating Covid-19 – ThePrint

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In the search for treatments for COVID-19, many researchers are focusing their attention on a specific protein that allows the virus to infect human cells. Called the angiotensin-converting enzyme 2, or ACE2 receptor, the protein provides the entry point for the coronavirus to hook into and infect a wide range of human cells. Might this be central in how to treat this disease?

We are scientists with expertise in pharmacology, molecular biology and biochemistry, with a strong commitment to applying these skills to the discovery of novel therapies for human disease. In particular, all three authors have experience studying angiotensin signaling in various disease settings, a biochemical pathway that appears to be central in COVID-19. Here are some of the key issues to understand about why theres so much focus on this protein.

ACE2 is a protein on the surface of many cell types. It is an enzyme that generates small proteins by cutting up the larger protein angiotensinogen that then go on to regulate functions in the cell.

Using the spike-like protein on its surface, the SARS-CoV-2 virus binds to ACE2 like a key being inserted into a lock prior to entry and infection of cells. Hence, ACE2 acts as a cellular doorway a receptor for the virus that causes COVID-19.

ACE2 is present in many cell types and tissues including the lungs, heart, blood vessels, kidneys, liver and gastrointestinal tract. It is present in epithelial cells, which line certain tissues and create protective barriers.

The exchange of oxygen and carbon dioxide between the lungs and blood vessels occurs across this epithelial lining in the lung. ACE2 is present in epithelium in the nose, mouth and lungs. In the lungs, ACE2 is highly abundant on type 2 pneumocytes, an important cell type present in chambers within the lung called alveoli, where oxygen is absorbed and waste carbon dioxide is released.

ACE2 is a vital element in a biochemical pathway that is critical to regulating processes such as blood pressure, wound healing and inflammation, called the renin-angiotensin-aldosterone system (RAAS) pathway.

ACE2 helps modulate the many activities of a protein called angiotensin II (ANG II) that increases blood pressure and inflammation, increasing damage to blood vessel linings and various types of tissue injury. ACE2 converts ANG II to other molecules that counteract the effects of ANG II.

Of greatest relevance to COVID-19, ANG II can increase inflammation and the death of cells in the alveoli which are critical for bringing oxygen into the body; these harmful effects of ANG II are reduced by ACE2.

When the SARS-CoV-2 virus binds to ACE2, it prevents ACE2 from performing its normal function to regulate ANG II signaling. Thus, ACE2 action is inhibited, removing the brakes from ANG II signaling and making more ANG II available to injure tissues. This decreased braking likely contributes to injury, especially to the lungs and heart, in COVID-19 patients.

Also read: Study suggests HCQ does not significantly reduce risk of severe infection in Covid patients

No. ACE2 is present in all people but the quantity can vary among individuals and in different tissues and cells. Some evidence suggests that ACE2 may be higher in patients with hypertension, diabetes and coronary heart disease. Studies have found that a lack of ACE2 (in mice) is associated with severe tissue injury in the heart, lungs and other tissue types.

This is unclear. The SARS-CoV-2 virus requires ACE2 to infect cells but the precise relationship between ACE2 levels, viral infectivity and severity of infection are not well understood.

Even so, aside from its ability to bind the SARS-CoV-2 virus, ACE2 has protective effects against tissue injury, by mitigating the pathological effects of ANG II.

When the amount of ACE2 is reduced because the virus is occupying the receptor, individuals may be more susceptible to severe illness from COVID-19. That is because enough ACE2 is available to facilitate viral entry but the decrease in available ACE2 contributes to more ANG II-mediated injury. In particular, reducing ACE2 will increase susceptibility to inflammation, cell death and organ failure, especially in the heart and the lung.

The lungs are the primary site of injury by SARS-CoV-2 infection, which causes COVID-19. The virus reaches the lungs after entry in the nose or mouth.

ANG II drives lung injury. If there is a decrease in ACE2 activity (because the virus is binding to it), then ACE2 cant break down the ANG II protein, which means there is more of it to cause inflammation and damage in the body.

The virus also impacts other tissues that express ACE2, including the heart, where damage and inflammation (myocarditis) can occur. The kidneys, liver and digestive tract can also be injured. Blood vessels may also be a site for damage.

In a recent research paper, we argued that a key factor that determines severity of damage in patients with COVID-19 is abnormally high ANG II activity.

Angiotensin converting enzyme (ACE, aka ACE1) is another protein, also found in tissues such as the lung and heart, where ACE2 is present. Drugs that inhibit the actions of ACE1 are called ACE inhibitors. Examples of these drugs are ramipril, lisinopril, and enalapril. These drugs block the actions of ACE1 but not ACE2. ACE1 drives the production of ANG II. In effect, ACE1 and ACE2 have a yin-yang relationship; ACE1 increases the amount of ANG II, whereas ACE2 reduces ANG II.

By inhibiting ACE1, ACE inhibitors reduce the levels of ANG II and its ability to increase blood pressure and tissue injury. ACE inhibitors are commonly prescribed for patients with hypertension, heart failure and kidney disease.

Another commonly prescribed class of drugs, angiotensin receptor blockers (ARBs, e.g., losartan, valsartan, etc.) have similar effects to ACE inhibitors and may also be useful in treating COVID-19.

Evidence for a protective effect of ACE inhibitors and angiotensin receptor blockers in patients with COVID-19 was shown in recent work co-authored by one of us Dr. Loomba.

No evidence exists to suggest prophylactic use of these drugs; we do not advise readers to take these drugs in the hopes that they will prevent COVID-19. We wish to emphasize that patients should only take these drugs as instructed by their health care provider.

In collaboration with a multidisciplinary group of investigators, Dr. Loomba has initiated a multicenter (randomized, double-blinded, placebo-controlled) clinical trial to examine the efficacy of ramipril an ACE inhibitor compared to a placebo in reducing mortality, ICU admission or need for mechanical ventilation in patients with COVID-19.

[Get facts about coronavirus and the latest research. Sign up for The Conversations newsletter.]

Krishna Sriram, Postdoctoral Fellow, University of California San Diego; Paul Insel, Professor of Pharmacology and Medicine, University of California San Diego, and Rohit Loomba, Professor of Medicine, University of California San Diego

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Also read: Ashwagandha the new HCQ? Modi govt begins study to see if herb keeps coronavirus away

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Why the ACE2 receptor could be key to treating Covid-19 - ThePrint

Biochemistry

What is the ACE2 receptor, how is it connected to coronavirus and why might it be key to treating COVID-19? The experts explain – TheStreet

Courtesy of Krishna Sriram, University of California San Diego; Paul Insel, University of California San Diego, and Rohit Loomba, University of California San Diego

In the search for treatments for COVID-19, many researchers are focusing their attention on a specific protein that allows the virus to infect human cells. Called the angiotensin-converting enzyme 2, or ACE2 receptor, the protein provides the entry point for the coronavirus to hook into and infect a wide range of human cells. Might this be central in how to treat this disease?

We are scientists with expertise in pharmacology, molecular biology and biochemistry, with a strong commitment to applying these skills to the discovery of novel therapies for human disease. In particular, all three authors have experience studying angiotensin signaling in various disease settings, a biochemical pathway that appears to be central in COVID-19. Here are some of the key issues to understand about why theres so much focus on this protein.

ACE2 is a protein on the surface of many cell types. It is an enzyme that generates small proteins by cutting up the larger protein angiotensinogen that then go on to regulate functions in the cell.

Using the spike-like protein on its surface, the SARS-CoV-2 virus binds to ACE2 like a key being inserted into a lock prior to entry and infection of cells. Hence, ACE2 acts as a cellular doorway a receptor for the virus that causes COVID-19.

ACE2 is present in many cell types and tissues including the lungs, heart, blood vessels, kidneys, liver and gastrointestinal tract. It is present in epithelial cells, which line certain tissues and create protective barriers.

The exchange of oxygen and carbon dioxide between the lungs and blood vessels occurs across this epithelial lining in the lung. ACE2 is present in epithelium in the nose, mouth and lungs. In the lungs, ACE2 is highly abundant on type 2 pneumocytes, an important cell type present in chambers within the lung called alveoli, where oxygen is absorbed and waste carbon dioxide is released.

ACE2 is a vital element in a biochemical pathway that is critical to regulating processes such as blood pressure, wound healing and inflammation, called the renin-angiotensin-aldosterone system (RAAS) pathway.

ACE2 helps modulate the many activities of a protein called angiotensin II (ANG II) that increases blood pressure and inflammation, increasing damage to blood vessel linings and various types of tissue injury. ACE2 converts ANG II to other molecules that counteract the effects of ANG II.

Of greatest relevance to COVID-19, ANG II can increase inflammation and the death of cells in the alveoli which are critical for bringing oxygen into the body; these harmful effects of ANG II are reduced by ACE2.

When the SARS-CoV-2 virus binds to ACE2, it prevents ACE2 from performing its normal function to regulate ANG II signaling. Thus, ACE2 action is inhibited, removing the brakes from ANG II signaling and making more ANG II available to injure tissues. This decreased braking likely contributes to injury, especially to the lungs and heart, in COVID-19 patients.

No. ACE2 is present in all people but the quantity can vary among individuals and in different tissues and cells. Some evidence suggests that ACE2 may be higher in patients with hypertension, diabetes and coronary heart disease. Studies have found that a lack of ACE2 (in mice) is associated with severe tissue injury in the heart, lungs and other tissue types.

This is unclear. The SARS-CoV-2 virus requires ACE2 to infect cells but the precise relationship between ACE2 levels, viral infectivity and severity of infection are not well understood.

Even so, aside from its ability to bind the SARS-CoV-2 virus, ACE2 has protective effects against tissue injury, by mitigating the pathological effects of ANG II.

When the amount of ACE2 is reduced because the virus is occupying the receptor, individuals may be more susceptible to severe illness from COVID-19. That is because enough ACE2 is available to facilitate viral entry but the decrease in available ACE2 contributes to more ANG II-mediated injury. In particular, reducing ACE2 will increase susceptibility to inflammation, cell death and organ failure, especially in the heart and the lung.

The lungs are the primary site of injury by SARS-CoV-2 infection, which causes COVID-19. The virus reaches the lungs after entry in the nose or mouth.

ANG II drives lung injury. If there is a decrease in ACE2 activity (because the virus is binding to it), then ACE2 cant break down the ANG II protein, which means there is more of it to cause inflammation and damage in the body.

The virus also impacts other tissues that express ACE2, including the heart, where damage and inflammation (myocarditis) can occur. The kidneys, liver and digestive tract can also be injured. Blood vessels may also be a site for damage.

In a recent research paper, we argued that a key factor that determines severity of damage in patients with COVID-19 is abnormally high ANG II activity.

Angiotensin converting enzyme (ACE, aka ACE1) is another protein, also found in tissues such as the lung and heart, where ACE2 is present. Drugs that inhibit the actions of ACE1 are called ACE inhibitors. Examples of these drugs are ramipril, lisinopril, and enalapril. These drugs block the actions of ACE1 but not ACE2. ACE1 drives the production of ANG II. In effect, ACE1 and ACE2 have a yin-yang relationship; ACE1 increases the amount of ANG II, whereas ACE2 reduces ANG II.

By inhibiting ACE1, ACE inhibitors reduce the levels of ANG II and its ability to increase blood pressure and tissue injury. ACE inhibitors are commonly prescribed for patients with hypertension, heart failure and kidney disease.

Another commonly prescribed class of drugs, angiotensin receptor blockers (ARBs, e.g., losartan, valsartan, etc.) have similar effects to ACE inhibitors and may also be useful in treating COVID-19.

Evidence for a protective effect of ACE inhibitors and angiotensin receptor blockers in patients with COVID-19 was shown in recent work co-authored by one of us Dr. Loomba.

No evidence exists to suggest prophylactic use of these drugs; we do not advise readers to take these drugs in the hopes that they will prevent COVID-19. We wish to emphasize that patients should only take these drugs as instructed by their health care provider.

In collaboration with a multidisciplinary group of investigators, Dr. Loomba has initiated a multicenter (randomized, double-blinded, placebo-controlled) clinical trial to examine the efficacy of ramipril an ACE inhibitor compared to a placebo in reducing mortality, ICU admission or need for mechanical ventilation in patients with COVID-19.

[Get facts about coronavirus and the latest research. Sign up for The Conversations newsletter.]

Krishna Sriram, Postdoctoral Fellow, University of California San Diego; Paul Insel, Professor of Pharmacology and Medicine, University of California San Diego, and Rohit Loomba, Professor of Medicine, University of California San Diego

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Here is the original post:
What is the ACE2 receptor, how is it connected to coronavirus and why might it be key to treating COVID-19? The experts explain - TheStreet

Biochemistry

May: Prof Cullen Fellow announcement | News and features – University of Bristol

Peter Cullen, Professor of Biochemistry and Wellcome Trust Senior Investigator, has been elected to a Fellowship by the Academy of Medical Sciences.

The new Fellows have been chosen for their exceptional contributions to advancing biomedical science via world-leading research discoveries, running national science communication and engagement programmes and translating scientific advances into benefits for patients and the public.

Professor Cullen is internationally recognised for his identification and characterisation of the molecular mechanisms that orchestrate protein and lipid transport through the endosomal network, a complex intracellular maze found in all human cells.

His world-leading research has laid the foundations for understanding how altered function of the network contributes to an array of human diseases, ranging from cardiovascular disease and neurological disorders, most notably Alzheimer's disease and Parkinson's disease, through to metabolic disorders such a type 2 diabetes, hypercholesterolemia and non-alcoholic fatty liver disease, and subversion of the network by a wide range of viruses and bacteria.

Professor Cullen said: "This accolade really reflects the talent, endeavour and friendship of the current and past members of my laboratory and the amazingly stimulating and supportive research environment within the School of Biochemistry and the Faculty of Life Sciences. I must also express my extreme gratitude to the Medical Research Council, the Lister Institute of Preventive Medicine and, in particular, the Wellcome Trust for their continued and long-term funding of our research".

Indeed, the Cullen laboratory was recently awarded a prestigious 1.8-million Wellcome Trust Investigator Award to continue its groundbreaking research into 2026.

The value of medical science has never been more apparent than during the current COVID-19 global health crisis. From testing and vaccine development, public health and behavioural science to addressing the impacts of lockdown measures on mental health, biomedical and health scientists are helping to guide the UK through unprecedented challenges. Many of the Academys newly elected Fellows are at the forefront of the efforts to tackle coronavirus.

Professor Sir Robert Lechler PMedSci, President of the Academy of Medical Sciences said:This year our new Fellows announcement happens amidst a global health crisis. Some will face the challenge of how to continue to lead on some of the most pressing health challenges our society faces beyond coronavirus, such as heart disease, diabetes or cancer. Others have joined the global research effort to tackle the coronavirus pandemic, whether that be through working out how to treat those with the virus, joining efforts to develop a vaccine, or looking to limit the impact of the pandemic more broadly on our physical and mental health.

Never has there been a more important time to recognise and celebrate the people behind ground-breaking biomedical and health research, working harder than ever to further knowledge and protect patients and the public.

It brings me great pleasure to congratulate the new Fellows, and see our Fellowship grow to even greater heights of evidence-based advice, leadership and expertise.

The Academy of Medical Sciencesis the independent body in the UK representing the diversity of medical science. Their mission is to advance biomedical and health research and its translation into benefits for society.

The Academy is working to secure a future in which the UK and global health is improved by the best research; the UK leads the world in biomedical and health research and is renowned for the quality of its research outputs, talent and collaborations; independent, high-quality medical science advice informs the decisions that affect society and more have a say in the future of health and research.

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May: Prof Cullen Fellow announcement | News and features - University of Bristol

Biochemistry

The coronavirus might have weak spots. Machine learning could help find them. – News@Northeastern

Chemically speaking, proteins might be the most sophisticated molecules out there. Millions of different kinds of them live within our cells and work together as a fine-tuned orchestra catalyzing the biochemical reactions that keep us alive.

Few things in the world would function without proteinsnot the cells within your body, and certainly not SARS-CoV-2, the coronavirus responsible for COVID-19.

The proteins in the coronavirus facilitate its remarkable ability to infect human cells without resulting in visible symptoms of COVID-19 for long periods of time. Thats why researchers around the world have been investigating the roles of each of the 29 proteins packed inside SARS-CoV-2.

By learning more about each of those proteins at the molecular level, researchers want to pin down the exact parts of the SARS-CoV-2 proteins that enable it to bind itself to other proteins on the surface of human cells and enable the virus to replicate. The idea is to inhibit those chemical reactions right from the start, and render the coronavirus ineffective.

To analyze those protein interactions, Northeastern researchers are bringing another set of tools to study the coronavirus proteins down to their amino acids, the building blocks of all proteins.

Mary Jo Ondrechen, a professor of chemistry and chemical biology, wants to identify all of the amino acids responsible for the abilities of the coronavirus to infect and thrive at the expense of human cells. Together with Penny Beuning, a professor of chemistry and chemical biology, Ondrechen recently received a grant from the National Science Foundation to use machine learning algorithms and experimental lab work to do just that.

Proteins are long chains of molecules that function through cascading interactions with amino acids form other proteins. But those interactions dont always occur in the same place within the structure of a protein where the protein carries out its chemical reaction. Often, although the interactions happen outside of that site, they still control the reaction. A specific site within a protein can also control the action of different proteins, helping or hindering a specific chemical reaction.

Changes in protein behavior resulting from these networks of interactions, or from preventing interactions, are known as allosteric regulation. Ondrechens algorithm predicts many of these and other types of interactions based on the specific molecular structures of proteins.

Research led by her and Beuning could help researchers gain a better understanding of the biochemistry of SARS-CoV-2, and serve as the basis for developing new drugs to inhibit its infectious abilities.

Researchers around the world have been rushing to develop new chemicals that show promise as compounds that could hinder the coronavirus by interacting with its main active proteins.

Still, scientists are just beginning to understand many of the coronavirus proteins. And, Ondrechen says, there might be sites within those poorly understood proteins that researchers might be failing to notice.

The program, which Ondrechens lab invented in 2009, analyzes the chemical properties of each of the individual amino acids within a protein. It could predict the roles of important but subtle interactions in SARS-CoV-2 involving amino acids that arent directly linked to the main reaction sites, and which would be too difficult to analyze with conventional bioinformatic research.

In the main protease, everybody knows where the catalytic site is, in the RNA transferase, everybody knows where the catalytic site is, Ondrechen says. Our technology is special because we could predict exo-sites, allosteric sites, and other binding sites or interaction sites that can control.

The program will run those predictions against databases that include tens of thousands of compounds with anti-viral properties and compounds found in food, all in a major attempt to find proteins that might hit the predicted sites of protein interaction.

Once the program runs the computational analysis to find candidate proteins to inhibit SARS-CoV-2, it will guide Beunings experimental tests in her lab.

Well be looking at the protein level: Do the compounds actually bind those proteins, and do they modulate the activity of the protein? Beuning says. Ideally, they would inhibit the activity of the protein, and then impair the virus.

For the past 10 years, Ondrechen and Beuning have been combining their computational and experimental power to understand such questions as how proteins control the production of our DNA, and how proteins enable our bodies to carry out some of the most important metabolic functions.

Now, they are planning to move as fast as possible to identify important protein interactions in SARS-CoV-2, test them in the lab, and move on with further tests in live organisms.

Our plans are to finish in six months, Ondrechen says. If we come up with interesting compounds in vitro, hopefully we can find a collaborator that could do in vivo testing.

For media inquiries, please contact media@northeastern.edu.

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The coronavirus might have weak spots. Machine learning could help find them. - News@Northeastern

Biochemistry

New research discovered how the body reacts to coronavirus, how we can support defenses – WSAW

(WZAW) -- A breakthrough, preclinical study may provide some answers. It found that the coronavirus infection stresses cells and depletes cellular NAD+ levels, more than three-fold.

On Friday, Dr. Charles Brenner, Chair of Biochemistry at the University of Iowa, broke down the findings and how they could help inform how we deal with the coronavirus.

My laboratory is interested in NAD, which is the central co-enzyme, the central catalyst of metabolism. This is a molecule that is so intrinsic to life that its required for us to convert everything that we eat, not only into ATP, the biological energy to power our cells, but its required to convert everything that we eat, really into everything that we are, everything that we do, Dr. Brenner explained.

In his research, he team found that coronavirus attacks the NAD system. NAD is required for an innate immune defense against the virus.

This appears to be actionable, because not only are some of the genes that use up NAD turned on by our viral infection, but some of the genes that we use to make NAD are turned up by the viral infection, he added. We think that gives us a way to boost NAD and potentially boost our defense against viral infection.

He said there are many stressors that disturb the NAD system, such as age, obesity, type 2 diabetes, nerve damage, alcohol use, time zone disruption, DNA damage and reactive oxygen stress.

Dr. Brenner said there is good news, though, that you can increase your NAD levels.

Our laboratory discovered NR nicotinamide riboside as an NAD precursor vitamin. Its not been tested yet as a viral preventative strategy, but our research is moving in the direction for testing NR for preventability in animal models and in human systems.

Click here for more information

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New research discovered how the body reacts to coronavirus, how we can support defenses - WSAW

Biochemistry

Pivoting the Lab | News – WPI News

D-Term 2020 was supposed to look like past D-Terms in Destin Heilmans Experimental Biochemistry labstudents were going to learn how to isolate proteins in e.coli, and experience the flow and feel of a lab on campus.

Kathleen Donovan 21

Then the COVID-19 pandemic hit, and all of WPIs classes were moved online, including Heilmans.

So, in typical WPI fashion, the teaching professor of chemistry & biochemistry pivoted, and transformed his in-person lab into a digital oneone that charged students to examine the coronavirus from stem-to-stern.

I thought, Why not study the very thing that has us locked in our houses? says Heilman, whose background is in virology (he even has a 3-D printed model of a virus protein on his desk).

With the term now over, he and his students reflected on the challenges and opportunities they had in virtually dissecting the coronavirus, with a particular focus on the viruss proteins, and which ones make it wreak havoc in humans. During the class, he gave his seven students documents on those proteins to read, including the work done on coronavirus by Dmitry Korkin, and challenged them to pick which one they wanted to study.

Heilman maintained his usual hands-on approach to experiments, even via remote learning. After all, some of the most important lessons students learn in the lab isnt content, he says. Its the nuances of the lab itself, being able to feel things in your hands, making mistakes. As a result, instead of physically working with students in the lab, he talked them through scenarios of mistakesmaterial spills, equipment mishapsthat could happen during their experiments, and asked them to figure out how to make the appropriate fixes.

Joe Dainis 20

The students really sank their teeth into it, he says.

Students werent champing at the bit to do a digital lab at first, and werent sure about online lab work.

I was nervous, Ive never taken online classes before, says Kathleen Donovan 21, a biochemistry major.

But, as D-Term progressed and students got their sea legs in Heilmans digital lab, their excitement blossomed.

Some students say Heilmans digital lab gave them valuable real-world experience. Being able to look at a lab and experiment from an entirely different perspective has a lot of beneficial uses, particularly in the research field, where you are developing your own protocols, says Joe Dainis 20, who is double majoring in biology & biotechnology and biochemistry.

My favorite part of the class was learning some of the techniques researchers use to study enzymes that are therapeutic targets, such as the SARS-CoV2 replicase,says Olivia Hunker 20, a biochemistry major. Im planning to pursue a PhD after I graduate and it gave me a better understanding of how to approach problems like this.

Olivia Hunker 20

Students say learning about the pandemic in the lab enables them and Heilman to learn from each other, too. Every meeting, there was an instance where we discussed COVID-19 and a student brought up a detail that Professor Heilman did not know regarding this virus, and vice versa, Dainis says. It was a unique experience to be in a professor-student relationship where you are both improving your knowledge regarding a topic that no one is an expert in.

Its nice to understand on a molecular level how the virus is working, says Donovan. Its nice to look at the research thats already been done on coronavirus. It puts into perspective how important research is, and that there is still so much to learn.

One of the most important things that Heilman learned from flipping his lab is that the process was easier than he thought it would be, and its helping to ready students for the world post-WPI.

The transition from a lab-based class to online was easy because WPI does projects, he says. Students can easily adapt, and theyll be able to digest information about coronavirus and other viruses for the greater community.

-By Jessica Messier

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Pivoting the Lab | News - WPI News

Biochemistry

Graduates Urged to Use Lessons From the Climb to Look Beyond the Summit – UANews

How does college compare to climbing the world's tallest mountain? There are a few ways, according to someone who's done it twice.

Alison Levine, a mountaineer, adventurer and university alumna, called on her trips up Mount Everest to show the class of 2020 that the challenges they overcame this spring will only make them stronger.

Levine's speech during the university's 156th Commencement on Friday addressed head-on the unpredictable and trying times that graduates face as they enter the workforce amid the COVID-19 pandemic. The speech was delivered via video from Levine's home during the university's first-ever virtual ceremony.

"When it comes down to it, what will help you more than math or history or biology or computer science is, indeed, resilience," Levine said as she stood before a closet full of parkas, backpacks, helmets and other expedition gear. "I would argue that you, class of 2020, are coming away with more of that than any class before."

Before Levine's address, Commencement viewers heard from university President Robert C. Robbins, Dean of Students Kendal Washington White, Provost Liesl Folks, college deans, this year's senior award winners and other speakers. The clips were filmed at various locations in recent weeks, with participants following physical distancing guidelines.

Robbins, in his opening remarks, addressed graduates from Arizona Stadium, where Commencement is usually held.

"The new format of celebration this year is out of necessity, and we know that it's not traditional; however, commitment to celebrating your achievement is as robust as ever," he said.

"You have reached a milestone in your lives by earning your degrees, and now, we are all excited to see the impact you will make on our world," he said.

Levine, in her address, likened the circumstances surrounding this year's Commencement to the challenge she faced when she led the first American Women's Everest Expedition in 2002. A storm turned the team back just 300 feet from the summit.

"I can absolutely relate to what it feels like to lose an opportunity that you worked so hard for," she said.

"Everything I learned during that failed attempt on Everest prepared me for life's challenges going forward including a successful Everest climb that would come eight years later," she said.

She urged graduates to embrace and brave their fears but to not be complacent. She also assured them that changing direction like retreating back to base camp on Everest is never something to be ashamed of.

"Backing up is not the same as backing down," she said.

She reminded graduates that their summit graduation is not the end, but a time to reflect on lessons from college and how those lessons will guide them through their professional lives.

"Reaching the top of a mountain is not nearly as important as the lessons you learn along the way when you're fighting with everything you've got in you to get up there and what you're going to do with that information to be better going forward," Levine said. "It's that fight during the journey that benefits us the most, because that struggle makes us stronger."

Despite the shared challenge for the class 2020, nothing can take away from the shared accomplishment of graduation, Levine said, adding that the class has "raised the bar" with its perseverance in uncertain times.

"You are resilient, you are creative, you have learned to sacrifice, to pivot and to keep going when you thought you couldn't," Levine said.

"You are the fiercest Wildcat class ever."

Levine, a New York Times bestselling author, speaker and businesswoman, graduated from UArizona in 1987 with a bachelor's degree in communication. She has climbed the highest peak on every continent and has skied to both the North and South poles a feat known as the Adventure Grand Slam, which only 20 people in the world have achieved. In 2016, she completed first ascents or the first successful documented climbs to the top of Hall Peak in Antarctica and Khang Karpo in Nepal.

Levine is one of five honorees to receive an honorary Doctor of Humane Letters degree this year. The other recipients are Bruce and Patricia Bartlett, benefactors and champions of the university's Strategic Alternative Learning Techniques Center; Melody S. Robidoux, a businesswoman, philanthropist and UArizona alumna who co-founded the Women's Foundation of Southern Arizona; and Linda Ronstadt, a 10-time Grammy Award-winning singer, Rock and Roll Hall of Fame inductee and Tucson native.

Seven graduating seniors also were recognized for their outstanding achievements and contributions during the ceremony. The Provost Award went to Lauren Easter (law and philosophy); the Robie Gold Medal went to Tony Viola IV (literacy, learning and leadership); the Robert Logan Nugent Awards went to Lily Keane Chavez (creative writing and global studies) and Meucci Watchman Ilunga (biochemistry); and the Merrill P. Freeman Medals went to Marcos Gomez Ambriz (physiology and biochemistry) and Ahmad B. Shahin (physiology).

The virtual ceremony will be available to watch in full on the Commencement website on Monday. The class of 2020 will be celebrated with an in-person ceremony during Homecoming Weekend on Oct. 30.

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Graduates Urged to Use Lessons From the Climb to Look Beyond the Summit - UANews

Biochemistry

Researchers discover a combination punch to treat drug-resistant infections – News-Medical.Net

Reviewed by Emily Henderson, B.Sc.May 14 2020

McMaster University researchers have discovered a combination punch to treat drug-resistant infections that is showing promise based on testing in mice.

Researchers found that a natural product called dephostatin is an effective partner for the antibiotic colistin in treating infections caused by the bacteria Salmonella.

Colistin is considered a last-resort antibiotic for multidrug-resistant bacterial infections due its toxic effect on the body, which has limited its use in medicine. However, when paired together, dephostatin allowed for drastically lower concentrations of colistin in a treatment regimen for Salmonella infection in mice that maintained the antibiotic's effectiveness.

The study details are published in Cell Chemical Biology.

The rise of antibiotic resistance has ushered in the post-antibiotic age, and alternatives to antibiotics are urgently required. Solving the antibiotic resistance crisis will require us to shift away from the traditional view of antibiotic discovery."

Caressa Tsai, first author of the study and a Ph.D. student in biochemistry and biomedical sciences in the Coombes lab at McMaster

The World Health Organization has classified antibiotic-resistant Salmonella, which can cause infection from eating contaminated foods, as a high-priority pathogen.

In their study, researchers found that dephostatin does not kill Salmonella or stop it from growing. Instead, dephostatin prevents Salmonella from causing infection in two ways: It blocks its ability to resist being killed by immune cells and it enhances its sensitivity to colistin.

While the initial findings were done using a method of experimentation called high-throughput screening, the researchers were excited to find that co-administering dephostatin and colistin in mice with a lethal Salmonella infection significantly prolonged animal survival and used a lower concentration of colistin than is normally required for treatment, thereby reducing its toxic effect.

By the numbers, treatment with colistin alone extended survival of almost 88 per cent of mice to approximately five days post infection and 25 per cent of mice survived to the end of the experiment. However, more than 62 per cent of mice treated with both dephostatin and colistin survived the infection, indicating a significant improvement over therapy with one antibiotic.

"Traditional antibiotics all work in a similar way - they clear infections by killing bacteria," said Tsai. "Here, we were interested in a different approach - keeping bacteria alive, but chemically inactivating important pathways to prevent them from causing infection."

Researchers are continuing their research to understand how dephostatin works against Salmonella. Their ongoing work will explore the activity of dephostatin alone and in combination therapies during the treatment of infected animals.

"Dephostatin appears to knock out two important regulatory pathways that control Salmonella virulence and antibiotic resistance mechanisms," said Coombes, corresponding author and a professor in the Department of Biochemistry and Biomedical Sciences at McMaster University. He holds the Canada Research Chair in Infectious Disease Pathogenesis.

"This research highlights the opportunities in taking a different approach than traditional antibiotic discovery and is enabling new drug combinations to emerge."

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Researchers discover a combination punch to treat drug-resistant infections - News-Medical.Net