Cell Biology

Insights on the High Content Screening Global Market to 2026 – by Product, Application, End-user and Region – ResearchAndMarkets.com – Business Wire

DUBLIN--(BUSINESS WIRE)--The "High Content Screening Market: Global Industry Trends, Share, Size, Growth, Opportunity and Forecast 2021-2026" report has been added to ResearchAndMarkets.com's offering.

The global high content screening market exhibited strong growth during 2015-2020. Looking forward, the publisher expects the market to grow at a CAGR of 8.2% during 2021-2026.

Keeping in mind the uncertainties of COVID-19, we are continuously tracking and evaluating the direct as well as the indirect influence of the pandemic on different end use sectors. These insights are included in the report as a major market contributor.

High content screening (HCS), or high content analysis, refers to an analytical method of automated microscopy that uses visualization tools to obtain quantitative data from cell populations. It is an integration of modern cell biology, flow cytometry and robotic handling that involves fluorescence imaging for analyzing various biochemical and physical characteristics of the sample cells. This aids in drug discovery, complex multivariate drug profiling and toxicity studies, while utilizing robots, detectors and software to monitor the entire process.

The increasing prevalence of neurodegenerative diseases across the globe, such as Alzheimer's and Parkinson's, is one of the key factors driving the market growth. The rising need for cost-effective drug discovery systems in the pharmaceutical industry is also providing a boost to the market growth. In comparison to the traditionally used methods, HCS solutions prove to be inexpensive and resource- and time-efficient for analyzing the potential toxicity of chemicals and complex substances. Advancements in informatics solutions and imaging instruments are acting as another growth-inducing factor. HCS equipment manufacturers are producing innovative equipment that is integrated with software platforms and artificial intelligence (AI) systems to enhance the visualization capabilities of the devices. In line with this, the development of automated systems for analyzing cell separation and scalability has further enhanced the adoption of HCS technology. Other factors, including the rising geriatric population and increasing investments in the research and development (R&D) of advanced screening systems, are projected to drive the market further.

Companies Mentioned

Key Questions Answered in This Report:

Key Topics Covered:

1 Preface

2 Scope and Methodology

3 Executive Summary

4 Introduction

4.1 Overview

4.2 Key Industry Trends

5 Global High Content Screening Market

5.1 Market Overview

5.2 Market Performance

5.3 Impact of COVID-19

5.4 Market Forecast

6 Market Breakup by Product

7 Market Breakup by Application

8 Market Breakup by End-User

9 Market Breakup by Region

10 SWOT Analysis

11 Value Chain Analysis

12 Porters Five Forces Analysis

13 Price Indicators

14 Competitive Landscape

14.1 Market Structure

14.2 Key Players

14.3 Profiles of Key Players

For more information about this report visit https://www.researchandmarkets.com/r/73fef0

Continue reading here:
Insights on the High Content Screening Global Market to 2026 - by Product, Application, End-user and Region - ResearchAndMarkets.com - Business Wire

Cell Biology

Protein That Puts the Brakes on Fat Burning Could Be Obesity Drug Target – Weill Cornell Medicine Newsroom

A protein called Them1 prevents fat burning in cells by blocking access to the fuel source, according to preclinical research by Weill Cornell Medicine, NewYork-Presbyterian and Harvard Medical School/Beth Israel Deaconess Medical Center investigators. The findings may contribute to the development of a new type of obesity treatment that targets this response.

When cold temperatures force mice to ramp up fat burning to generate heat, they produce an enzyme that sits on standby, ready to shut down energy-intensive heat production when the need has passed, according a study published June 9 in Nature Communications. The study was a collaboration between Dr. David Cohen, chief of the Division of Gastroenterology and Hepatology at Weill Cornell Medicine and NewYork-Presbyterian/Weill Cornell Medical Center and the Vincent Astor Distinguished Professor of Medicine at Weill Cornell Medicine, and cell biology and microscopy expert Dr. Susan Hagen, associate professor of surgery at Harvard Medical School.

The study explains a new mechanism that regulates metabolism, said Dr. Cohen. Them1 hacks the energy pipeline and cuts off the fuel supply to the energy-burning mitochondria.

Dr. Cohen and his colleagues first became interested in Them1 about a decade ago when they discovered cold mice produce a lot of the enzyme in their brown fat tissue. They knew mice were using brown fat tissue to generate heat, so they assumed that Them1 was helping to produce heat. To prove this, they genetically engineered mice lacking Them1 to see what would happen.

To our complete surprise, when you delete the gene for Them1, the mouse produces more heat, not less, he said. In fact, the mice lacking the gene for Them1 burned so much energy trying to make heat that they ate twice as much as a typical mouse and still lost weight.

The new study helps explain how Them1 turns off heat production. In the experiments, the team used light and electron microscopy to observe Them1 in action in mouse brown fat cells grown in the laboratory. The experiments showed that when the cells are stimulated to burn fat using a drug, a phosphate group is added to Them1. The chemical modification causes Them1 molecules to spread out throughout the cell. This frees cellular powerhouses called mitochondria to efficiently turn the cells fat stores into energy. But when the stimulation stops, the Them1 molecules quickly reorganize like a protein flash mob into a membrane-less structure situated between the mitochondria and the fats they use as fuel, which stops energy production.

Humans also have brown fat and produce more Them1 in cold conditions, so the findings may have exciting implications for the treatment of obesity. Dr. Cohen and his colleagues are already working to develop an anti-obesity drug that inhibits Them1.

If we could give humans a drug that inactivates Them1s energy expenditure-suppressing activity, we might be able to increase fat burning, Dr. Cohen said.

Read more:
Protein That Puts the Brakes on Fat Burning Could Be Obesity Drug Target - Weill Cornell Medicine Newsroom

Cell Biology

Protein Aggregation Diseases | In the Pipeline – Science Magazine

If you have occasion to study neurodegeneration, you will be struck by how many terrible high-profile diseases in this area seem to share a common theme. Alzheimers, ALS, progressive supranuclear palsy, Parkinsons, Lewy body dementia, some types of frontotemporal dementia, Huntingtons, prion diseases such as BSE and more all feature abnormal protein aggregates that appear in neural tissues. There are plenty of variations, naturally. These aggregates happen in different types of cells, involve different key proteins that seem to have a variety of structural features that lead them into this process, and the resulting diseases affect different regions of the brain. But the overlap of such aggregation with disease is impossible to ignore, and believe me, no one has been ignoring it.

Ever since Alois Alzheimer noticed what we now call amyloid plaques in the brains of deceased dementia patients over a hundred years ago, every advance in neuroscience, cell biology, and instrumentation has been brought to bear on this problem. And its a measure of how complex such diseases are that we still dont truly understand whats going on and we still have no disease-modifying treatments for any of them. Were still not sure how many of these aggregates are direct causes of the associated diseases, and how many might be side effects of some other disease process thats more proximal. Even the ones where we have the most detailed knowledge have escaped us Huntingtons for example. In that case, the protein that aggregates (Huntingtin) does so because it has a long tail of glutamine residues. This genetic basis for the disease was made clear in 1993. We know that if there are fewer than 28 of these, a patient will be completely normal. 28 to 35 of them takes you into a range where some signs might be picked up by post-mortem histopathlogy, but the affected patient is still asymptomatic. 36 to 40 glutamine repeats, thats a danger zone. Patients in this range show disease, but its severity, age of onset, and progression are variable. And greater than 40 repeats means full-blown, progressive, and fatal Huntingtons.

Isnt that enough clues? If this were a movie, the screenwriters would have us running into the labs with a cure in the third act, for sure. But were not even sure if the biggest problem in the disease is the amino acid repeats in the protein or the trinucleotide repeats in the precursor RNA. Even if we were absolutely sure that all we needed to do was to keep the Huntingtin protein from sticking to itself, we still cant manage that. Drug discovery organizations have been screening for aggregation inhibitors for decades now, and I have seen more papers than I can possibly remember on compounds that (theoretically) keep amyloid, tau, Huntingtin, alpha-synuclein, and other such proteins from aggregating. To the best of my knowledge, most of these have not even made it into clinical trials, and the ones that do have a flat zero per cent success rate. On the other end of the process, Alzheimers especially has seen a whole list of attempts to clear out such aggregates, especially before they become pathological, but as my recent hand-wringing about aducanumab should make clear, I dont see any successes so far in that approach, either.

This short review paper (open access) urges everyone to realize that these aggregates are even more complicated than they look. From one perspective thats not such cheerful news, but were always better off facing reality in these situations. Its easier to think of protein aggregation as happening with single proteins that have something wrong with them that form relatively pure clumps that are then cytotoxic. In vitro screening efforts often assume a picture something like this there are a lot of systems where aggregation of protein constructs (usually through formation of fibril structures) is used as the basis for such a screen, and one recommendation I take from this new paper is to just stop doing that sort of thing entirely.

Thats because, as numerous references show, these aggregates in vivo are far from homogeneous lumps of toxic protein. Amyloid plaques, neurofibrillary tangles, and Lewy bodies have hundreds of different proteins in them. They have varying amounts of lipids, RNA species, and carbohydrates as well, and were not very far along in characterizing these. Lewy bodies have entire membranous organelles tangled up in them! The lack of detailed knowledge is partly because of the sheer complexity of the problem, and partly (as with the carbohydrates) because of deficiencies in our techniques for analyzing such things in general.

We also have deficiencies with some of the tools used in cell biology studies. Watching protein fibrils form from purified starting materials can tell you a lot from a structural biology perspective, but its not the same as whats happening inside a neuron. Indeed, the structures of the fibrils themselves are different. One of the things I took from this paper is that my picture of the formation of the in vivo protein aggregates is way off its easy, especially for a chemist, to imagine something like a messy precipitation, with random clumps of stuff coming out of solution. But in reality, these things are probably forming under rather specific and controlled conditions, and it may be really hard to recapitulate these outside of the cell. The details of the various post-translational modification of the aggregated proteins also argue for specific conditions rather than random fallout.

Even studying them inside the cell is tricky. Close study by advanced microscopy in wild-type cells and tissues shows that the structure and composition of even a single type of aggregate can vary according to what compartment of the cell it appears in, although these may appear superficially similar. As the paper points out, using protein overexpression systems leads to unnatural artifacts, as can tagging the relevant proteins with fluorescent groups. Youre always worried about such effects, of course, but when the very process youre highlighting seem to depend on self-association of a key protein, then such assays are at their most vulnerable. At any rate, we have to rework our approaches here, because continuing to use (over)simplified assays mainly because theyre doable does not seem to be getting us very far.

Nobody likes to hear the Gosh, its more complicated than we thought news, but we get to hear it a lot in this business, and its generally an accurate view of the situation. Once in a great while its less complicated than we though, and those are memorable occasions, but mostly its like this when you study the causes of disease. Especially in neurology! The important thing is not to use this as an excuse to throw up your hands, but rather as a call to find something that can be improved.

Originally posted here:
Protein Aggregation Diseases | In the Pipeline - Science Magazine

Cell Biology

The hunt to find causes and treatments for deadly childhood cancer – Newswise

Newswise Australian researchers and oncologists have been awarded $2.4 million to investigate the causes and treatments for neuroblastoma, the deadliest and most common solid tumour in children under the age of five.

Associate Professor Yeesim Khew-Goodall and Associate Professor Quenten Schwarz from the University of South Australia and SA Pathologys Centre for Cancer Biology will lead two separate projects to identify the molecular drivers of neuroblastoma and find more effective drugs to fight it, using patient data in the first instance, and genetically engineered stem cells in the second.

The projects, involving the Womens and Childrens Hospital and Royal Adelaide Hospital, are two of 106 groundbreaking medical research projects announced by the Federal Government under the Medical Research Future Fund, including $5.7 million for UniSA.

Neuroblastoma is a devastating disease which accounts for 15 per cent of all childhood cancer deaths, with fewer than 50 per cent of high-risk patients living five years after diagnosis.

It typically affects very young children, mostly under the age of five years, with the average age of diagnosis around one to two years, says Assoc Prof Yeesim Khew-Goodall, a world expert in cancer and microRNA biology.

For high-risk neuroblastoma, relapse is not uncommon, and these children often need to undergo multiple rounds of therapy. Due to the young age of the children and the high toxicity of current treatments, which include chemotherapy and radiation therapy, those who survive can end up with debilitating side effects that stay with them for life.

Tumours form (typically in the abdominal region) when immature nerve cells called neuroblasts continue to divide and grow, developing into cancer cells instead of becoming functioning, mature nerve cells. Defective genes are thought to be partly responsible, but scientists are yet to find the definitive causes.

Despite the highly toxic nature of current therapies, they are only effective in some children, so being able to predict which patients will or will not respond to current treatments will be our priority. Currently, there is a lack of reliable diagnostic criteria to predict disease course or treatment outcomes, and our aim is to fill that void.

Assoc Prof Khew-Goodalls $1.4 million project aims to improve risk classification using clinical information linked to molecular profiles of patient samples, and to identify therapeutic drugs that can be personalised for each child.

We have found the first evidence that key microRNAs (molecules that regulate gene expression) are deleted in one type of neuroblastoma, for example. Increasing the expression of these microRNAs could be significant in stopping the progression of the cancer.

At the moment, we have a sledgehammer approach towards treating neuroblastoma that can lead to developmental effects, including deafness, and problems with speech, mobility and cognition.

Assoc Prof Schwarz, a world expert in neuron development, will use genetically engineered stem cells to model the fetal origins of the disease and screen FDA-approved drugs.

Stem cell modelling will help us mimic the disease process so that we can understand how different genetic alterations drive different forms of this cancer. We hope that this new information will allow us to identify the best therapies for each tumour type, as well as more accurately predict the patient outcomes, Assoc Prof Schwarz says.

A major flaw of current treatment strategies is that they fail to treat the underlying cause of tumour growth. By modelling the disease, we will have better resources to identify new drugs for this disorder that are already approved for clinical use in other disease settings he says.

The researchers will work with the families of current patients over the next three years, combining laboratory studies with patient profiling.

See the article here:
The hunt to find causes and treatments for deadly childhood cancer - Newswise

Cell Biology

People in the News: New Appointments at Genetron Health, BioSkryb, Geisinger, More – GenomeWeb

GenetronHealth: Chao Tang and Shan Fu

GenetronHealth has appointedChao Tang and Shan Fu to its board of directors. Tang replaces Weiwu He, who hadserved as chairman of the board beginning inMay 2015. Fu replaces Weidong Liu, who served as board director starting November 2019. According to Genetron, bothHe and Liu have resigned from its board due to personal reasons.He has since been appointed chairman emeritus in recognition of his prior contributions.

Tang is a chair professor of physics and systems biology at Peking University.His current research interest is at the interface between physics and biology. He is a fellow of the American Physical Society, an academician of the Chinese Academy of Sciences, the founding director of the Center for Quantitative Biology at Peking University, and the founding co-editor-in-chiefof the journal Quantitative Biology. He had his undergraduate training at the University of Science and Technology of China and received a Ph.D. in physics from the University of Chicago.

Fu has previously served as joint CEOof Vivo Capital, beginning inOctober 2013. Prior to Vivo, heworked as the chief representative of China at Blackstone Group, and in leadership positions at several other firms.Fu received both his B.A. andmaster's degree in history from Peking University.

Genetronalsosaid that it has named Sizhen Wang, the firm's co-founder, chairman, and CEO, as its new board chairman.In addition, effective June 30,Kevin Ying Hong will become the firm'ssenior adviser.

BioSkryb: Gary Harton

BioSkryb, a Durham, North Carolina-based developer of genomic amplification technologies, has appointed Gary Harton as CSO. Harton has more than 30 years of experience in single-cell diagnostic product development, and will apply BioSkrybs platform technology to develop new diagnostic technologies for cancer, neurological disorders, and assisted reproductive technologies, the company said. Prior to BioSkryb, he was the portfolio director for preimplantation genetic testing at PerkinElmer. He has also previously held a variety of product and portfolio-development positions at PerkinElmer, Igenomix US, Progyny, Illumina, BlueGnome, and Reprogenetics.

Geisinger: Christa Lese Martin

Geisinger Health System has named Christa Lese Martin as CSO. Martin, the founding director of the Autism & Developmental Medicine Institute at Geisinger, has served as interim CSO since December and previously was associate CSO at the health system. Shewill lead clinical research programs across the entire organization, directing a team of more than 500 researchers in precision health, genomics, data science, population health, implementation science, health services, bioethics, and clinical trials. Martin, cochair of theAmerican College of Medical Genetics and Genomics' Secondary Findings Working Group, was operations director of Emory Genetics Clinical Laboratory at Emory University before joining Geisinger in 2013.

For additional recent items on executive appointments and promotions in omics and molecular diagnostics, please see the People in the News page on our website.

Read more:
People in the News: New Appointments at Genetron Health, BioSkryb, Geisinger, More - GenomeWeb

Cell Biology

Uncovering Genetic Traces to Discover How Humans Adapted to Historical Coronavirus Outbreaks – SciTechDaily

Coronavirus graphic. Credit: Gerd Altmann

An international team of researchers co-led by the University of Adelaide and the University of Arizona has analyzed the genomes of more than 2,500 modern humans from 26 worldwide populations, to better understand how humans have adapted to historical coronavirus outbreaks.

In a paper published in Current Biology, the researchers used cutting-edge computational methods to uncover genetic traces of adaptation to coronaviruses, the family of viruses responsible for three major outbreaks in the last 20 years, including the ongoing pandemic.

Modern human genomes contain evolutionary information tracing back hundreds of thousands of years, however, its only in the past few decades geneticists have learned how to decode the extensive information captured within our genomes, said lead author Dr. Yassine Souilmi, with the University of Adelaides School of Biological Sciences.

This includes physiological and immunological adaptions that have enabled humans to survive new threats, including viruses.

Viruses are very simple creatures with the sole objective to make more copies of themselves. Their simple biological structure renders them incapable of reproducing by themselves so they must invade the cells of other organisms and hijack their molecular machinery to exist.

Lead author Dr. Yassine Souilmi Australian Centre for Ancient DNA, School of Biological Sciences, The University of Adelaide. Credit: The University of Adelaide

Viral invasions involve attaching and interacting with specific proteins produced by the host cell known as viral interacting proteins (VIPs).

In the study, researchers found signs of adaptation in 42 different human genes encoding VIPs.

We found VIP signals in five populations from East Asia and suggest the ancestors of modern East Asians were first exposed to coronaviruses over 20,000 years ago, said Dr. Souilmi.

We found the 42 VIPs are primarily active in the lungs the tissue most affected by coronaviruses and confirmed that they interact directly with the virus underlying the current pandemic.

Dr. Ray Tobler, Australian Centre for Ancient DNA, within the University of Adelaides School of Biological Sciences. Credit: The University of Adelaide

Other independent studies have shown that mutations in VIP genes may mediate coronavirus susceptibility and also the severity of COVID-19 symptoms. And several VIPs are either currently being used in drugs for COVID-19 treatments or are part of clinical trials for further drug development.

Our past interactions with viruses have left telltale genetic signals that we can leverage to identify genes influencing infection and disease in modern populations, and can inform drug repurposing efforts and the development of new treatments, said co-author Dr. Ray Tobler, from the University of Adelaides School of Biological Sciences.

By uncovering the genes previously impacted by historical viral outbreaks, our study points to the promise of evolutionary genetic analyses as a new tool in fighting the outbreaks of the future, said Dr. Souilmi.

The researchers also note that their results in no way supersede pre-existing public health policies and protections, such as mask-wearing, social distancing, and vaccinations.

Reference: An ancient viral epidemic involving host coronavirus interacting genes more than 20,000 years ago in East Asia by Yassine Souilmi, M. Elise Lauterbur, Ray Tobler, Christian D. Huber, Angad S. Johar, Shayli Varasteh Moradi, Wayne A. Johnston, Nevan J. Krogan, Kirill Alexandrov and David Enard, 24 June 2021, Current Biology.DOI: 10.1016/j.cub.2021.05.067

The team involved in this study also included researchers from Australian National University and Queensland University of Technology.

Read the rest here:
Uncovering Genetic Traces to Discover How Humans Adapted to Historical Coronavirus Outbreaks - SciTechDaily

Cell Biology

How does a regulatory protein know where to bind to modulate insulin production? | Penn State University – Penn State News

UNIVERSITY PARK, Pa. Some proteins in the body ensure that genes are turned on and off at the correct times. For example, the transcription factor protein Pdx1 (pancreatic and duodenal homeobox 1) turns on the gene that codes for insulin, and the protein SPOP (speckle-type POZ protein) in turn binds to Pdx1 so that the body doesnt make too much insulin. But its unclear how SPOP binds to Pdx1. Understanding where SPOP binds may help researchers predict what predisposes individuals to developing diabetes and clarify how SPOP regulates other important proteins. In a recent study, a team of researchers from Penn State and St. Jude Childrens Research Hospital imaged the proteins and determined just how this important interaction occurs.

A paper describing the interaction was recently published in the Journal of Biological Chemistry. We talked to two of the authors of the paper, Scott Showalter, professor of chemistry and of biochemistry and molecular biology, and Emery Usher, graduate student in Biochemistry, Microbiology and Molecular Biology (BMMB) program, about this work.

Q: Why is Pdx1 important for the human body, and how does SPOP support its function?

Showalter: Pdx1 is a transcription factor, which is a protein that binds to the DNA in your genome and controls whether nearby genes will be turned on or off. In humans, Pdx1 is primarily found in the pancreas, where it turns on the gene that codes for the protein insulin when more of it is needed. When enough insulin is stored up for the future, SPOP binds to Pdx1 and causes it to be destroyed by the cellular protein recycling machinery, thus turning off insulin production.

Usher: Ultimately, Pdx1 and SPOP work together to maintain glucose homeostasis; that is, the careful balance of glucose levels in the cells and in your bloodstream. Notably, SPOP performs a similar regulatory role for dozens of other proteins in lots of different types of cells, all of which are critical to appropriate cell function.

Q:What was your motivation for this study?

Showalter: Although we knew that Pdx1 and SPOP work together to regulate the insulin-coding gene, prior to this study the details of this interaction was unclear. It was known from other work that SPOP turns proteins off by attaching a molecular signal to them that targets these proteins for destruction, but Pdx1 does not look like any other proteins that SPOP regulates. Almost all proteins known to be regulated by SPOP possess multiple recognition sequences, or sequences of amino acids that act like a password. However, Pdx1 does not contain any of the sequences that SPOP was known to bind to. My laboratory has invested a great deal of effort over the past decade to develop techniques that can be used to characterize interactions like the ones that we knew must exist between Pdx1 and SPOP. In this study, we set out to determine where SPOP binds to Pdx1 and how it knows that it has found the correct site(s).

Usher: SPOP can actually recognize more than one of these amino acid password sequences and can thus target many partners, so it is difficult to produce a comprehensive list of the amino acid sequences that SPOP looks for. Investigating the interaction between Pdx1 and SPOP could also provide insight into other proteins SPOP might bind to.

Penn State researchers used a variety of techniques regarding cell biology, structural biology, and protein biophysics to determine how the proteins SPOP and Pdx1 work together to ensure the gene that codes for insulin is turned on and off at the correct time.

IMAGE: Showalter Lab, Penn State

Q:What were the main results of this study?

Showalter: We were very happy to find that there is not just one SPOP binding site on Pdx1, but two. It is known that SPOP generally binds multiple sites in the proteins it controls, so this result was very satisfying because it brings Pdx1 regulation into alignment with the communitys more general understanding of how SPOP functions. After we found the second binding site, we used X-ray crystallography to image the complex that forms when SPOP is bound to Pdx1 at these newly discovered binding sites. This structure revealed that even though an unusual sequence of amino acids in Pdx1 was involved in SPOP binding, the geometric and chemical details actually were very similar to previously determined structures. Our results suggest that the previous definition of a SPOP binding site was too narrow.

Usher: We now have a better understanding of the chemical rules that define whether a sequence is a good candidate to bind or not. Our structure also suggests a plausible mechanism to disrupt Pdx1 binding by SPOP when this interaction is unwanted for example, when Pdx1 is needed to produce more insulin.

Q:Why are these findings important?

Showalter: It is important to understand the molecular details of biological processes like glucose-dependent insulin production and how they are regulated because these are the deciding factors between normal health and disease. Understanding the sequences SPOP binds to helps us to predict why certain genetic variations may predispose individuals and families that carry them to developing diabetes. Similarly, by clarifying the rules that SPOP uses to identify the proteins it should bind to and regulate, we can better predict other proteins it regulates. We may also be able to predict how naturally occurring variations in their amino acid sequences may disrupt normal SPOP binding, leading to poor health outcomes.

Usher: SPOP is also known for its role in certain cancers, including prostate and endometrial cancer. While beyond the scope of our current work, better defining how SPOP selects binding partners will likely impact future research in this area as well.

Go here to read the rest:
How does a regulatory protein know where to bind to modulate insulin production? | Penn State University - Penn State News

Cell Biology

Frequent testing improves the detection of SARS-CoV-2 – News-Medical.Net

Detecting SARS-CoV-2, the virus that causes COVID-19, improves with regularity of testing, whether using rapid antigen tests or PCR molecular tests. The PCR test is considered the gold standard for diagnosing COVID-19 infection, but cost and infrastructure issues, as well as wait times for PCR results, have limited its use more broadly as a screening tool for asymptomatic people because rapid results are needed to interrupt the chain of transmission.

In a highly anticipated study that compares rapid antigen and laboratory PCR approaches for COVID-19 serial screening, researchers affiliated with the National Institutes of Health's Rapid Acceleration of Diagnostics (RADx) initiative reported results from 43 people infected with the virus. They found that both testing methods were equally effective in detecting SARS-CoV-2 infection when tests were given on a regular cadence every three days.

While individual PCR tests are more sensitive than antigen tests, particularly early in infection, the results showed that both testing approaches can give 98% sensitivity when taken regularly as part of a screening program. Because antigen tests at the point of care or at home can deliver immediate results and are less costly than laboratory tests, these results suggest that they could be a highly effective screening tool to prevent disease outbreaks.

Rapid antigen testing at home, two to three times per week, is a powerful and convenient way for individuals to screen for COVID-19 infection. With schools and businesses reopening, an individual's risk of infection can change from day to day. Serial antigen testing can help people manage this risk and quickly take action to prevent spread of the virus."

Bruce Tromberg, PhD, Director of the National Institute of Biomedical Imaging and Bioengineering, National Institues of Health

Dr. Tromberg leads the RADx Tech program, which supported the study. For the past year, the RADx initiative has been a catalyst for dozens of diagnostic device technologies-;including both antigen and PCR tests-;accelerating the development and commercialization of COVID-19 diagnostic tests.

Authors of the study in the June 30, 2021, Journal of Infectious Diseases, are researchers at the University of Illinois at Urbana-Champaign (UIUC); University of Massachusetts Medical School, Worcester; Johns Hopkins School of Medicine, Baltimore; and NIBIB.

Employees and students at UIUC participate in SHIELD Illinois, a COVID-19 screening program implemented this past year on campus. SHIELD Illinois participants who tested positive or lived in close contact with a person who received a positive result were invited to participate in this research study. The goal was to investigate the sensitivity of specific types of diagnostic tests during infection by having participants take PCR and antigen tests daily during the course of their infection. Daily samples were also tested for the presence of infectious virus as a measure of how easily individuals may transmit virus to others at different stages of infection.

The team began their participant recruitment in early December 2020, which continued into spring 2021. To capture daily test results across the entire course of infection, participants were enrolled within days after their exposure to the virus, having received negative test results in the seven days prior to enrollment. None of the participants in the study experienced symptoms that required hospitalization.

Participants supplied a saliva sample and two forms of nasal swabs for 14 consecutive days. A courier retrieved the samples daily. To obtain a rough measure of the period during which subjects could spread infection to others, the research team sent one of the nasal samples to a laboratory at Johns Hopkins University to observe the growth of live virus in culture. Viral culture is labor- and cost-intensive and is not practical for testing large numbers of people but provides a high degree of certainty that live virus can be derived from the sample. By culturing samples in this study, the researchers could estimate the onset and duration of COVID-19 infectiousness.

"Antigen tests and PCR tests detect the presence of different molecules found in virus particles," explained Christopher B. Brooke, senior author and assistant professor of molecular and cell biology at UIUC. "Most tests detect genetic material associated with the virus, but that doesn't mean there is live virus there. The only way to tell with certainty if live, infectious virus is present is to perform an infectivity assay, or culture," such as was performed at the Johns Hopkins laboratory.

The researchers then compared three COVID-19 viral testing modalities-;PCR testing of saliva, PCR testing of nasal samples and rapid antigen testing of nasal samples. The saliva sample results were performed with an authorized saliva-based PCR test developed at UIUC, called covidSHIELD, that can generate a result after about 12 hours.

A separate PCR test performed with an Abbott Alinity device was used to obtain results from a nasal swab. Rapid antigen testing was performed using a Quidel Sofia SARS Antigen Fluorescent Immunoassay device that is authorized for use at the point of care and can generate a result after 15 minutes.

The researchers calculated the sensitivity of each test modality to detect SARS-CoV-2 and measured the presence of live virus over a two-week period following initial infection. They found that PCR molecular tests-;both from saliva and nasal samples-;are more sensitive than rapid antigen tests at detecting the SARS-CoV-2 virus prior to the infectious period. If the result from PCR tests could be quickly returned, the person receiving the result could undertake measures much sooner to prevent transmitting the virus to others. Unfortunately, results from PCR are rarely returned the day of testing.

The authors calculated test sensitivity based on test frequency, finding that a cadence of tests every three days achieved better than 98% sensitivity to detect infection, whether using rapid antigen tests or PCR tests. When they assessed frequency of testing once per week, nasal and saliva PCR testing sensitivity remained high, at around 98%, but antigen test sensitivity declined to 80%. These results show, for the first time, that testing at least twice per week with rapid antigen tests has comparable performance with PCR testing and maximizes the likelihood of detecting people infected with SARS-CoV-2.

The sensitivity of PCR molecular tests and rapid antigen tests is highest when viral cultures are positive for SARS-CoV-2, as might be expected. Even beyond this infectivity period, though, PCR tests continue to detect particles of virus, when the virus is most likely no longer transmissible.

"Silent transmission of the SARS-CoV-2 virus from individuals with no symptoms contributes significantly to the spread of the virus," said co-author William Heetderks, M.D., Ph.D., a RADx Tech program advisor at NIBIB. "Faster, cheaper and broader testing with antigen tests can be a big help in the kind of large-scale screening scenarios that can find these silent transmitters."

Source:

Journal reference:

Smith, R. L., et al. (2021) Longitudinal assessment of diagnostic test performance over the course of acute SARS-CoV-2 infection. The Journal of Infectious Diseases. doi.org/10.1093/infdis/jiab337.

Follow this link:
Frequent testing improves the detection of SARS-CoV-2 - News-Medical.Net

Genetics

New CRISPR/Cas9 Plant Genetics Technology to Improve Agricultural Yield and Resist the Effects of Climate Change – SciTechDaily

Arabidopsis plants were used to develop the first CRISPR-Cas9-based gene drive in plants. Credit: Zhao Lab, UC San Diego

New technology designed to breed more robust crops to improve agricultural yield and resist the effects of climate change.

With a goal of breeding resilient crops that are better able to withstand drought and disease, University of California San Diego scientists have developed the first CRISPR-Cas9-based gene drive in plants.

While gene drive technology has been developed in insects to help stop the spread of vector-borne diseases such as malaria, researchers in Professor Yunde Zhaos lab, along with colleagues at the Salk Institute for Biological Studies, demonstrated the successful design of a CRISPR-Cas9-based gene drive that cuts and copies genetic elements inArabidopsisplants.

Breaking from the traditional inheritance rules that dictate that offspring acquire genetic materials equally from each parent (Mendelian genetics), the new research uses CRISPR-Cas9 editing to transmit specific, targeted traits from a single parent in subsequent generations. Such genetic engineering could be used in agriculture to help plants defend against diseases to grow more productive crops. The technology also could help fortify plants against the impacts of climate change such as increased drought conditions in a warming world.

A schematic representation of a new plant gene drive using CRISPR/Cas9 technology. Credit: Zhao Lab, UC San Diego

The research, led by postdoctoral scholar Tao Zhang and graduate student Michael Mudgett in Zhaos lab, ispublished in the journalNature Communications.

This work defies the genetic constraints of sexual reproduction that an offspring inherits 50% of their genetic materials from each parent, said Zhao, a member of the Division of Biological Sciences Section of Cell and Developmental Biology. This work enables inheritance of both copies of the desired genes from only a single parent.The findings can greatly reduce the generations needed for plant breeding.

The study is the latest development by researchers in theTata Institute for Genetics and Society(TIGS) at UC San Diego, which was built upon the foundation of anew technology called active genetics with potential to influence population inheritance in a variety of applications.

Developing superior crops through traditional genetic inheritance can be expensive and time-consuming as genes are passed through multiple generations. Using the new active genetics technology based on CRISPR-Cas9, such genetic bias can be achieved much more quickly, the researchers say.

I am delighted that this gene drive success, now achieved by scientists affiliated with TIGS in plants, extends the generality of this work previously demonstrated at UC San Diego, to be applicable in insects and mammals, said TIGS Global Director Suresh Subramani. This advance will revolutionize plant and crop breeding and help address the global food security problem.

Reference: Selective inheritance of target genes from only one parent of sexually reproduced F1 progeny in Arabidopsis by Tao Zhang, Michael Mudgett, Ratnala Rambabu, Bradley Abramson, Xinhua Dai, Todd P. Michael and Yunde Zhao, 22 June 2021, Nature Communications.DOI: 10.1038/s41467-021-24195-5

Coauthors of the paper include: Tao Zhang, Michael Mudgett, Ratnala Rambabu, Bradley Abramson, Xinhua Dai, Todd Michael and Yunde Zhao.

The research was funded by TIGS-UC San Diego and a training grant from the National Institutes of Health.

The rest is here:
New CRISPR/Cas9 Plant Genetics Technology to Improve Agricultural Yield and Resist the Effects of Climate Change - SciTechDaily

Genetics

In Brief This Week: Foundation Medicine, Myriad Genetics, Genetron Health, and More – GenomeWeb

NEW YORK Foundation Medicine and Flatiron Health announced this week that Foundations comprehensive genomic profiling tests will be available to order through Flatiron's OncoEMR platform. The integration will allow clinicians to electronically order, track, and receive Foundations test through OncoEMR, the companies said. Both Flatiron and Foundation are planning further integrations with the others comprehensive genomic profiling tests and electronic medical record systems, respectively.

Myriad Genetics this week said it has completed the sale of its Myriad RBM unit which specializes in providing laboratory research services to pharmaceutical companies to IQVIA subsidiary Q2 Solutions. When Myriad announced its intent to sell this business unit in May, it did not disclose the deal's financial details.

GenetronHealth said this week that it has entered a new partnership with the World Economic Forum under its Health and Healthcare Platform, where it is contributing its research insights, technologies, and industry experience. The platform's overall goal is to ensure worldwide equal access to the highest standards of health and healthcare.Genetroniscurrentlyparticipating in a sub-project,dubbedMoving Genomics to the Clinic, which seeks to promote the use of genetic testing in routine clinical practices by proving its utility and efficacy.

AccessHope, a City of Hope subsidiary, said this week that it has partnered with the Dana-Farber Cancer Institute to bring the latest cancer care expertise to patients and oncologists in the community. By partnering withAccessHope, Dana-Farber's experts will support oncologistswiththe latest advances in oncology,includingpersonalized treatments, clinical trials, promising investigational medications, and molecular testing. Patients in Massachusetts, Maine, New Hampshire, Vermont, Connecticut, Rhode Island, New York,and New Jersey, as well asthosein other parts of the country,can access these services through their employee benefits programs. City of Hope and Northwestern University's Robert H. Lurie Comprehensive Cancer Center are also foundational members ofAccessHope.

Molecular breath analysis startup Deep Breath Intelligencesaid this week that it has entered a collaboration with Lwenstein Medical, a sleep and respiratory medicine firm based inRheinland-Pfalz, Germany.Rotkreuz, Switzerland-based DBI said that it is applying artificial intelligence to identify breath biomarkers related to obstructive sleep apnea syndrome. DBIsaid ithas initiated a study on OSASin collaboration with Lwenstein Medical,using participantsbreath samples and applying DBIs patterned analytical algorithms to provide results.

Enable Biosciences said this week it is partnering with the California Department of Public Health to survey state residents for the presence of antibodies against SARS-CoV-2. As part of the program, more than 200,000 households in California will be invited to submit dried blood samples collected at home using kits developed by Enable Bio andtheCDPH. The samples will then be tested by Enable Bio for the presence of antibodies against SARS-CoV-2 to distinguish antibody response fromviralinfection versusresponse fromvaccination. Test results will provide information about the spread of COVID-19 in California and the uptake of vaccines for the disease, South San Francisco, California-based Enable Bio said. The project is a collaboration betweenthe company,theCDPH, Stanford University, and Gauss Surgical. The first survey period concluded June 15 with the second and third enrollment periods slated tobeginat the start of 2022.

NeoGensaid this week that it has extended itsglobalanimal genomicspartnership withGencove. Thepartnership allowsNeoGento offerGencove'sSkimSeeklow-pass sequencing technology to customers in the agricultural sector, including those in the bovine, canine,poultry, and swine industries. UsingGencove'ssequencingimputationplatform,NeoGensaid it can deliver increased genomics data with improved accuracy and flexibility.

Bioceptsaid this week ithas been added to the Russell Microcap Index. Michael Nall, Biocept's president and CEO,called the nodexceptionally exciting, as a driver ofawarenessfor the cancer liquid biopsy firm within thelargerglobal investment community.

Immunoviasaid this week that its American subsidiary hasreceived a CLIA Certificate of Registration,which isan important step in the accreditation of its laboratory in Marlborough, Massachusetts, and a prerequisite to receiving clinical laboratory licensure fromtheMassachusetts Department of Public Health. Clinical laboratory licensure is required beforeImmunoviacan begin testing patients with itsImmrayPanCan-d test, the firm said.According to the Centers for Medicare and Medicaid Services, a Certificate of Registration allows a laboratory toconduct moderate and/or high complexity testing until it is inspected to determine its compliance with the CLIA regulations.

In Brief This Week is a selection of news items that may be of interest to our readers but had not previously appeared onGenomeWeb.

Follow this link:
In Brief This Week: Foundation Medicine, Myriad Genetics, Genetron Health, and More - GenomeWeb