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Neuroscience

Book review: The BrainCanDo Handbook – TES News

The BrainCanDo Handbook of Teaching and Learning

Edited by: Julia Harrington, Jonathan Beale, Amy Fancourt and Catherine LutzPublisher: RoutledgeDetails: 263pp; 19.99ISBN: 978-0367187057

Prince Harry has reported how he has learned a huge amount about unconscious bias since being married to Meghan Markle. In a moment of honesty, he recalled that he had been raised in a context of luxury and privilege, and it had taken him many years to recognise his own prejudices.

This prejudice, or unconscious bias, creeps in whether we like it or not. We are born with a predisposition to prefer the sorts of people we are familiar with, and this colours our behaviour and attitudes towards others.

What has this got to do with a review of a book about the translation of educational neuroscience into teaching and learning practice?

Just as Prince Harry has come to realise, in order to understand anything with any nuance, it is necessary to become more familiar with the background and context from which it came. Rigorous research always makes strenuous attempts to acknowledge any possible bias that may limit the findings of the study no study is ever perfect, and it is important that we understand that.

One limitation we should always consider is the demographic make-up of the participants. It goes without saying that we would be suspicious of using a new drug that had been tested only in a laboratory in a test tube, under perfect conditions. We would expect the drug to have been applied to a normal, varied group of people, going about their lives in the everyday world before we used it.

The BrainCanDo Research Centre is based at Queen Annes School, a small, selective independent girls school, in Berkshire. In collaboration with other independent schools, including Eton and Westminster, the research centre has embraced the opportunity to run research studies with respected researchers, developing approaches to implementing educational neuroscience. At the same time, it is also challenging the scientism and scepticism they perceive across the education sector.

Undoubtedly, the book is an impressive collection of pieces, written by teachers in partnership with researchers exploring the latest research in educational neuroscience and psychology, and offering practical strategies for its application in secondary schools.

The chapters vary. Some provide careful, scholarly, impressively referenced reviews of the literature, followed by suggestions of how these findings could be translated into practice and evaluated.

In other cases, the weighty and erudite literature review acts as background to the description of a serious, well-funded and systematic research study constructed to document new practices and evaluate impact.

Refreshingly, the book starts with a philosophical exploration of the elusive concept of scientism:the dogmatic excessive belief in the power or value of science. We have, it suggests, a dogmatic assumption that scientific methods or findings can be immediately or straightforwardly applied in education. This is where schools and practitioners are misled.

We are wrong to consider it easy or to be easily swayed by the use of scientific language or concepts. It is perfectly possible to be a good teacher without a deep knowledge of educational neuroscience.

The main finding of this chapter is that we should be cautious,and recognise the limitations of science and how far the findings can be translated into messy, educational contexts. We should be aware of using scientific or quasi-scientific language to try to make work look more impressive.

The bulk of the book explores the familiar canon of educational neuroscience, including subjects such as executive function, cognitive-load theory and working memory, misconceptions and counterintuitive concepts in maths and science, growth-mindset theory and the importance of sleep.

There is a chapter describing a longitudinal study of girls at Queen Annes as they engaged in their high-quality musical learning and instructionover a year, and the impact and importance this may have on cognitive and social and emotional learning.

We read how Eton College developed a curriculum designed to build character in their pupils, including opportunities for the boys to volunteer in the local community to enable them to develop empathy and be more concerned with those not within their social circles (remember Prince Harry?).

Undeniably, the work they have accomplished is deeply impressive. The opportunities they have created for their staff to work on research projects with researchers of international standing is admirable and there is much we can draw from their descriptions of gains in learning their students have made.

But the world they describe is a very distant reality to the one most teachers and leaders face during these dark and challenging times. Perhaps we might consider it a description of the test tube of perfect conditions, where the participants have every available luxury and privilege.

So, whileI recognise their deep commitment to the study of the translation of evidence into practice and their interest and dedication to the subject, I am acknowledging the limitations of their research. In essence, this is not a book for the everyday, workaday, comprehensive teachers and leaders among us.

The takeaway for those of us struggling to secure enough digital equipment to enable all our pupils to access remote learning might just be: look what you could doif you had the money and time to do so.

It is, perhaps, a glimpse into how the others believe they can do these things better with a dose of educational neuroscientism thrown in.

Megan Dixon is director of research and development at the Aspire Educational Trust

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Book review: The BrainCanDo Handbook - TES News

Neuroscience

This Jamaican is now the first Black woman to get PhD in neuroscience from University of Rochester – Face2Face Africa

Monique Mendes, a Jamaican-born scientist, followed her passion for the sciences to pursue a Ph.D. in neuroscience. Now, she is the first Black woman to receive a doctorate in that field from the University of Rochester.

The Neuroscience program at the University of Rochester Medical Centers Del Monte Institute was established in 1925 and Mendes, being the first Black woman Ph.D. graduate from the program, is worth celebrating. The only other Black was a man, Dr. Nathan Anthony Smith, in 2013.

I feel empowered, I feel excited, said Mendes. Im just happy that I was able to get a Ph.D. and to show other Black women that it is possible, and they can succeed.

The 27-year-old successfully defended her thesis in July and she started her post-doctoral fellowship at Stanford University in September, according toDemocrat & Chronicle. For a post-doctoral fellowship at Stanford, Mendes conducts research using novel imaging techniques to better understand how learning and memory are impacted by specific cells called glia.

The journey in the laboratory began in her native country, Jamaica. Her sixth-grade teacher at St. Andrew Preparatory School in Kingston was the only Black woman teaching science at the time. She taught science with passion and always made the lessons fun and interesting. Little Mendes knew then that she wanted to know more.

Interestingly, Mendes realized that none of her professors or teachers as a child were women aside from her sixth-grade teacher. One of the big things I wish I had had over the years was faculty that looked like me, said Mendes. She however acknowledges that Rochester University has put measures in place since she has been there to retain Black women in the sciences.

Mendes earned her undergraduate degree in biology at the University of Florida where she was named a McNair Scholar. The award was named after Black physicist Dr. Ronald E. McNair, who died in the Challenger Space shuttle accident in 1986. It is conferred on students from underrepresented backgrounds to increase the number of graduate degrees awarded to people from such backgrounds. It also provides funding for two years of graduate school and four years of postdoctoral training.

The thing that stands out most about Monique is her energy and enthusiasm, said Ania Majewska, Ph.D., a neuroscience professor at the University of Rochester in whose lab Mendes worked for five years conducting research on brain development.

Shes a dynamo. Shes very creative, independent and has incredible ideas. As a mentor, a lot of how youre measured is how well you train your students and Im super excited to see Monique go out in the world.

There is no stopping Mendes. While at the University of Rochester, she became the first URMC graduate student to receive the coveted F99/K00 NIH Blueprint Diversity Specialized Predoctoral to Postdoctoral Advancement in Neuroscience fellowship from the National Institute of Neurological Disorders in Stroke.

Mendes is a decorated scientist and admired for her contributions to the sciences, however, she wanted to be a musician at a point in time. Her love for science tramped her music ambitions but she never left them behind entirely.

According to Mendes, during her studies, she played the violin and was part of the Florida Philharmonic Youth Orchestra. Also, while at School of Medicine and Dentistry (SMD), she played in the Brighton Symphony Orchestra and even performed in two side-by-side concerts with the Rochester Philharmonic Orchestra.

Mendes hopes to become a mentor for young Black girls and people of color in and outside her field. While on campus at Rochester, she created a diverse and inclusive community to mentor new students from diverse backgrounds and occasionally held events to help them have much-needed discussions pertaining to them.

During her Ph.D. program, Mendes was awarded theEdward Curtis Peck Awardfor Excellence in Teaching by a Graduate Student and theOutstanding Student Mentor award.

Her advice to her mentees is that they should be fearless, be inquisitive and follow their dreams. Advocate for yourself; advocate for others, she advised.

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This Jamaican is now the first Black woman to get PhD in neuroscience from University of Rochester - Face2Face Africa

Neuroscience

So your brain injury case involves diffusion tensor imagingnow what? – JD Supra

Defense attorneys and claims professionals evaluating traumatic brain injury claims are likely to come across a form of advanced neuroimaging known as diffusion tensor imaging (DTI). Diffusion tensor imaging uses data from MRI sequences to measure and patterns of water diffusion throughout brain tissue. It uses that data to map the structure of white matter tracts in the brain and draw broader conclusions about the integrity ofor subtle injuries tothose white matter tracts. The resulting colorful three-dimensional images may make for striking demonstrative evidence, but these often bely the complexity of this neuroimaging modality and what it means for the ultimate questions in a personal injury caseas well as the admissibility of DTI studies and expert opinions derived from them under Daubert v. Merrell Dow Pharmaceuticals.

In a recent column in Nautilus, An Existential Crisis in Neuroscience, writer Grigori Guitchounts discusses how technological advances in neuroscience are outpacing our ability to make sense of the incredible volumes of data researchers are now able to uncover about the brains structure and function. As he notes, Technology has made it easy for us to gather behemoth datasets, but Im not sure understanding the brain has kept pace with the size of the datasets.

The column describes further conversations with researchers involved in the field of connectomics, or attempts to map out brain structures at the level of neurons to create a wiring diagram. Those researchers note the lack of clear understanding of how brain structure relates to psychiatric illnesses like schizophrenia, and their attempts to use machine intelligence to understand the relationship between structure and function. Despite decades of progress and access to more detailed data than ever about how the brain is composed, a holistic understanding and ability to apply that data remains elusive. As Guitchounts notes, The machines we have builtthe ones architected after cortical anatomyfall short of capturing the nature of the human brain. But they have no trouble finding patterns in large datasets.

Proponents of diffusion tensor imagings forensic use in litigating traumatic brain injury claims often tout its sensitivity, or ability to identify subtle changes in brain structures, at a degree that was previously unattainable by other structural imaging methods such as computed tomography (CT) or standard MRI sequences like T1, T2, SWI, and FLAIR. But, proponents miss the fact that once a lesionoften described as an area of reduced fractional anisotropy, in neuroradiology parlanceis identified on DTI, its significance in the particular case is not always entirely clear. There is not always a definitive correlation between an identified white matter lesion and neurocognitive complaints, whether identified by neuropsychological testing or not. This is especially true given that white matter lesions have a host of other causes unrelated to traumasuch as hypertension, pre-existing psychiatric conditions, or even the normal aging process. And, in our firms work in litigating traumatic brain injury claims nationally, we have occasionally seen DTI studies that describe a totally normal brain despite the fact that other imaging modalities like MRI have documented obvious structural brain damage in a particular individual. In such cases, the inability of DTIs high-resolution data to identify lesions where they clearly should exist raises questions about the clinical and forensic significance of single, isolated lesions in concussion cases.

In evaluating the strength and admissibility of expert opinions interpreting diffusion tensor imaging, one should be aware of the host of potential issues surrounding DTI and its interpretation in any particular case, including partial volume effects, the multiple comparisons problem, normative datasets, and mapping errors. And, in addressing whether DTI evidence satisfies Daubert and Fed. R. Civ. P. 702 in a case, attorneys should consider whether a DTI study merely finds a pattern in a large dataset without a clear understanding, based on actual science, of how that pattern correlates with an identified neuropsychological deficit or symptom that is at issue in the case. DTI abnormalities are not per se evidence of a TBI, and an expert who opines that they are likely expresses a degree of certainty that goes beyond the current scope of neuroscientists understanding about the relationship between brain structure and function.

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So your brain injury case involves diffusion tensor imagingnow what? - JD Supra

Cell Biology

Astrocytes Identified as Master ‘Conductors’ of the Brain – Duke Today

DURHAM, N.C. -- In the orchestra of the brain, the firing of each neuron is controlled by two notesexcitatory and inhibitory that come from two distinct forms of a cellular structure called synapses. Synapses are essentially the connections between neurons, transmitting information from one cell to the other. The synaptic harmonies come together to create the most exquisite musicat least most of the time.

When the music becomes discordant and a person is diagnosed with a brain disease, scientists typically look to the synapses between neurons to determine what went wrong. But a new study from Duke University neuroscientists suggests that it would be more useful to look at the white-gloved conductor of the orchestra the astrocyte.

Astrocytes are star-shaped cells that form the glue-like framework of the brain. They are one kind of cell called glia, which is Greek for glue. Previously found to be involved in controlling excitatory synapses, a team of Duke scientists also found that astrocytes are involved in regulating inhibitory synapses by binding to neurons through an adhesion molecule called NrCAM. The astrocytes reach out thin, fine tentacles to the inhibitory synapse, and when they touch, the adhesion is formed by NrCAM. Their findings were published in Nature on November 11.

We really discovered that the astrocytes are the conductors that orchestrate the notes that make up the music of the brain, said Scott Soderling, PhD, chair of the Department of Cell Biology in the School of Medicine and senior author on the paper.

Excitatory synapses the brains accelerator and inhibitory synapses the brains brakes were previously thought to be the most important instruments in the brain. Too much excitation can lead to epilepsy, too much inhibition can lead to schizophrenia, and an imbalance either way can lead to autism.

However, this study shows that astrocytes are running the show in overall brain function, and could be important targets for brain therapies, said co-senior author Cagla Eroglu, PhD, associate professor of cell biology and neurobiology in the School of Medicine. Eroglu is a world expert in astrocytes and her lab discovered how astrocytes send their tentacles and connect to synapses in 2017.

A lot of the time, studies that investigate molecular aspects of brain development and disease study gene function or molecular function in neurons, or they only consider neurons to be the primary cells that are affected, said Eroglu. However, here we were able to show that by simply changing the interaction between astrocytes and neurons specifically by manipulating the astrocytes we were able to dramatically alter the wiring of the neurons as well.

Soderling and Eroglu collaborate often scientifically, and they hashed out the plan for the project over coffee and pastries. The plan was to apply a proteomic method developed in Soderlings lab that was further developed by his postdoctoral associate Tetsuya Takano, who is the papers lead author.

Takano designed a new method that allowed scientists to use a virus to insert an enzyme into the brain of a mouse that labeled the proteins connecting astrocytes and neurons. Once tagged with this label, the scientists could pluck the tagged proteins from the brain tissue and use Dukes mass spectrometry facility to identify the adhesion molecule NrCAM.

Then, Takano teamed up with Katie Baldwin, a postdoctoral associate in Eroglus lab, to run assays to determine how the adhesion molecule NrCAM plays a role in the connection between astrocyte and inhibitory synapses. Together the labs discovered NrCAM was a missing link that controlled how astrocytes influence inhibitory synapses, demonstrating they influence all of the notes of the brain.

We were very lucky that we had really cooperative team members, said Eroglu. They worked very hard and they were open to crazy ideas. I would call this a crazy idea.

The project was funded by the NIH BRAIN Initiative, National Institute on Drug Abuse, Kahn Neurotechnology Award, Uehara Memorial Foundation, and Japan Society for the Promotion of Science.

CITATION: Chemico-Genetic Discovery of Astrocytic Control of Inhibition In Vivo, Tetsuya Takano, John T. Wallace, Katherine T. Baldwin, Alicia Purkey, Akiyoshi Uezu, Jamie L. Courtland, Erik J. Soderblom, Tomomi Shimogori, Patricia F. Maness, Cagla Eroglu, Scott H. Soderling. Nature, Nov. 11, 2020. DOI: 10.1038/s41586-020-2926-0.

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Astrocytes Identified as Master 'Conductors' of the Brain - Duke Today

Cell Biology

T cell factor 1: A master regulator of the T cell response in disease – Science

Recent advances have redefined a role for T cell factor 1 (TCF1) that goes beyond T cell development and T memory formation and encompasses new functions in the regulation of T cell biology. Here, we discuss the multifaceted and context-dependent role of TCF1 in peripheral T cells, particularly during disease-induced inflammatory states such as autoimmunity, cancer, and chronic infections. Understanding how TCF1 fine-tunes peripheral T cell biology holds the potential to tailor improved immune-targeted therapies.

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T cell factor 1: A master regulator of the T cell response in disease - Science

Cell Biology

UB researcher narrows time window for administering specific treatment to infants with Krabbe disease – UB Now: News and views for UB faculty and…

A team of UB researchers has published a paper in Nature Communications that is helping to define the best time to give a specific treatment to infants born with Krabbe disease (KD). This treatment has been found to prolong life for these infants for as long as a few years.

The paper was published online in Nature Communication Oct. 23.

Daesung Shin, assistant professor in the Department of Biotechnical and Clinical Laboratory Sciences and the Neuroscience Program, both in the Jacobs School of Medicine and Biomedical Sciences at UB, is the lead investigator. He also conducts research at UBs Hunter James Kelly Research Institute.

KD is an inherited disorder that destroys myelin, the protective coating of nerve cells in the brain and throughout the nervous system. In most cases, signs and symptoms of Krabbe disease develop in babies before 6 months of age, and the disease usually results in death by age 2. When it develops in older children and adults, the course of the disease can vary greatly.

The progressive neurologic disorder is caused by a deficiency of galactosylceramidase (GALC). GALC is an enzyme that breaks down galactosylceramide, an important component of myelin, which ensures the rapid transmission of nerve impulses.

Although there is no cure for KD, hematopoietic stem cell therapy (HSCT), a therapy that makes blood cells, reduces neurologic deterioration and improves developmental advances. These benefits are dependent on the severity of the disease at the time the stem cells are transplanted, and are only beneficial if delivered at a clinically defined pre-symptomatic time point before symptoms appear.

Even though it is widely accepted that early treatment is essential for the most positive outcome, the precise therapeutic window for treatment and what happens during this early time have never been elucidated, Shin says.

To address that issue, his team used mutations to create a novel mouse model of KD.

We engineered an inducible knockout mouse for the GALC gene deletion in specific cells at specific times, which provided us with the opportunity to directly ask when and where GALC enzyme is required for brain development, Shin explains.

We were particularly interested in the role of early developmental GALC function, he says. Our study not only revealed a key developmental process that requires GALC in the perinatal period, but also demonstrated that temporal GALC expression is likely a major contributor to brainstem development.

The researchers found that by increasing GALC levels at or before this newly defined perinatal period they could improve the effectiveness of therapeutic interventions for KD.

For the first time, our work showed the mechanistic evidence to explain why treatment must occur so early, with the defined critical postnatal period at days 4-6 in mice, and demonstrated that temporal GALC expression during this time is a major contributor to brainstem development, Shin says. Augmenting GALC levels at or prior to this newly defined period would likely improve the efficacy of therapeutic interventions for Krabbe patients.

While the time scale between mice and humans is considerably different, the sequence of key events in brain maturation between the two is consistent, he notes. It was estimated that the mouse nervous system at postnatal days 4-6 corresponds to a gestational age of 32 weeks in humans. Therefore, we anticipate that if our result is correct, then in utero treatments at, or prior to, 32 weeks should have better outcomes than conventional postnatal treatment for Krabbe babies.

Shin says his team will further identify which cell type needs to be targeted with therapy.

This work will directly impact the design of novel treatment options for KD patients, he says, noting that KD studies are at the basis of research on other, more common neurodegenerative diseases, such as multiple sclerosis and Parkinsons disease. Therefore, the teams work will have implications beyond KD.

Co-authors on the research were Nadav I. Weinstock, MD-PhD student, and Conlan Kreher, former masters student, both of the HJKRI and the Department of Biochemistry in the Jacobs School; Jacob Favret, research technician in the Department of Biotechnical and Clinical Laboratory Sciences; Lawrence Wrabetz and M. Laura Feltri, both co-directors of the HJKRI and members of the departments of Biochemistry and Neurology, as well as the Neuroscience Program.

Duc Nguyen and Ernesto R. Bongarzone of the Department of Anatomy and Cell Biology in the College of Medicine at the University of Illinois at Chicago also participated in the research.

The project was initiated with the support from Empire State development fund for HJKRI, and further developed and finalized by the R01, R56 and R03 grants from National Institutes for Health-National Institute for Neurological Disorders and Stroke awarded to Shin.

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UB researcher narrows time window for administering specific treatment to infants with Krabbe disease - UB Now: News and views for UB faculty and...

Cell Biology

Prenatal CRISPR therapy blocks Angelman syndrome traits in mice – Spectrum

Tour guide: A short strand of RNA shuttles the CRISPR enzyme to the best spot to activate UBE3A.

Courtesy of Mark Zylka / University of North Carolina

Editing DNA in embryonic and newborn mice by using CRISPR technology can override mutations underlying Angelman syndrome and prevent many of the conditions traits, according to a new study1. The effects last for at least 17 months and may be permanent, the researchers say.

Its very exciting, says Steven Kushner, professor of psychiatry at Columbia University, who was not involved in the study.

Angelman syndrome usually stems from a mutation in or deletion of the UBE3A gene. People have two copies of the gene one from each parent but typically only the one passed down from the mother is active in neurons. Mutations that stymie that copy can lead to a lack of UBE3A protein in the brain, causing the syndromes core traits: developmental delays, motor dysfunction, speech impairments, seizures and, often, autism.

These traits improve in response to treatments that activate the silent yet intact paternal copy of UBE3A and boost production of the protein in Angelman syndrome model mice2,3. But these treatments wear off over time, requiring repeated injections into the spinal fluid or brain.

The new therapy is effective after only two doses, says lead researcher Mark Zylka, professor of cell biology and physiology at the University of North Carolina at Chapel Hill.

The strategy uses the enzyme CRISPR-Cas9 to cut and edit DNA encoding an antisense RNA molecule that ordinarily serves to block production of UBE3A protein from the paternal copy of the gene. The technique also rouses the silent paternal copy of the gene in cultured human neurons, suggesting that it might work in people.

Treated mice did not show any negative side effects or unintended mutations. But other researchers warn the approach may still have rare off-target effects that could lead to birth defects or cancer.

Thats one of the big reasons why the use of CRISPR in humans is still something that is being taken very, very cautiously, Kushner says.

Zylka and his colleagues used a modified virus to carry the gene-editing enzyme into mouse cortical neurons. They tested 260 different guide RNAs to find one that could escort the enzyme to the intended region of the genome without damaging other genes.

The team injected the therapy into the brains of Angelman mice first when the mice were in the womb and again when they were a day old.

The double dose delivered the treatment to all layers of developing cortex, the researchers found. And it activated the paternal copy of UBE3A in every brain region they checked, aside from the cerebellum, until the mice were 17 months old. The effects likely last even longer, they say.

Mounting data show that a virus like the one they used can insert itself into the genome, resulting in permanent changes to an animals DNA, Zylka says. When that happens, the viral genome can affect nearby genes.

In this case, the viral genome contains instructions to tack extra nucleotides the building blocks of the genetic code on to messenger RNA. These additions render ineffective the antisense RNA that normally silences paternal UBE3A.

The injections prevented behaviors typically seen in Angelman mice, the researchers reported in Nature in October. Treated mice showed less hind-limb clasping, considered akin to repetitive behaviors seen in autistic people. They also spent more time in the center of an open field, suggesting they are less anxious than untreated mice, and performed better on a test of motor coordination.

Mice that model Angelman syndrome tend to have smaller brains than typical mice, but this trait, too, was at least partially averted in the treated animals.

The approach did not block all Angelman traits, however: The mice still engaged in marble-burying, another repetitive behavior; and only female mice showed improvements in obesity.

The treatment may not have worked in enough cells to correct all traits: The researchers found UBE3A protein expressed in 58 percent of the model animals cortical neurons, whereas typical mice have it in all neurons.

It is also possible that different traits have unique critical windows for treatment, says Stormy Chamberlain, associate professor of genetics and genome sciences at the University of Connecticut in Farmington, who was not involved in the study. Studies have shown that the earlier UBE3A is reinstated, the more Angelman traits are ameliorated.

Further research may improve the treatments effectiveness in mice, but its utility for people could be limited by its reliance on active CRISPR enzyme, which can introduce unpredictable cuts and mutations in DNA, Chamberlain says.

Even so, its important to keep an open mind and try some of these the skys the limit approaches, she says.

Other gene-based therapies for Angelman syndrome also pose safety concerns. An ongoing trial of a different treatment, which activates paternal UBE3A using strands of modified RNA, had to be halted because it causes temporary leg weakness in children with Angelman syndrome. Researchers hope to resume that trial with a different dosing plan.

Zylka and his colleagues plan to try their approach with an alternate version of CRISPR one that cannot cut DNA but can still activate paternal UBE3A which may be safer for use in people.

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Prenatal CRISPR therapy blocks Angelman syndrome traits in mice - Spectrum

Cell Biology

Hamilton Thorne to Announce Q3 2020 Financial Results and Hold Conference Call on November 19, 2020 – Stockhouse

BEVERLY, Mass. and TORONTO, Nov. 12, 2020 (GLOBE NEWSWIRE) -- Hamilton Thorne Ltd. (TSX-V: HTL), a leading provider of precision instruments, consumables, software and services to the Assisted Reproductive Technologies (ART), research, and cell biology markets, today announced that it will release its financial results for the three- and nine-month periods ended September 30, 2020 before market open on Thursday, November 19, 2020. The press release, with accompanying financial information, will be posted on the Company’s website at http://www.hamiltonthorne.ltd and on http://www.sedar.com .

The Company will follow with a conference call on the same day at 11:00 a.m. EST to review highlights of the results. All interested parties are welcome to join the conference call by dialing toll free 1-855-223-7309 in North America, or 647-788-4929 from other locations, and requesting Conference ID 6491864. A recording of the call will be available on Hamilton Thorne’s website shortly after the call.

About Hamilton Thorne Ltd. ( http://www.hamiltonthorne.ltd )

Hamilton Thorne is a leading global provider of precision instruments, consumables, software and services that reduce cost, increase productivity, improve results and enable breakthroughs in Assisted Reproductive Technologies (ART), research, and cell biology markets. Hamilton Thorne markets its products and services under the Hamilton Thorne, Gynemed, Planer, and Embryotech Laboratories brands, through its growing sales force and distributors worldwide. Hamilton Thorne’s customer base consists of fertility clinics, university research centers, animal breeding facilities, pharmaceutical companies, biotechnology companies, and other commercial and academic research establishments.

Neither the TSX Venture Exchange, nor its regulation services provider (as that term is defined in the policies of the exchange), accepts responsibility for the adequacy or accuracy of this release.

For more information, please contact:

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Hamilton Thorne to Announce Q3 2020 Financial Results and Hold Conference Call on November 19, 2020 - Stockhouse

Cell Biology

Global Live Cell Imaging Consumables Market 2020 Industry Analysis, Key Players Data, Growth Factors, Share, Opportunities And Forecast To 2025 – The…

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Global Live Cell Imaging Consumables Market 2020 Industry Analysis, Key Players Data, Growth Factors, Share, Opportunities And Forecast To 2025 - The...

Cell Biology

4D Path Announces Patented Precision Oncology Platform for Instant Biomarker Profiling and Stratification Just From H&E Biopsy or Resection Images -…

NEWTON, Mass., Nov. 12, 2020 (GLOBE NEWSWIRE) -- 4D Path, a company conceived by an experienced team of scientists, clinicians and management from leading research institutions including MIT, Harvard Medical School and the University of Cambridge, has unveiled a faster, more efficient approach to cancer diagnosis and biomarker profiling with better accuracy that accelerates and democratizes precision medicine for optimized patient care and clinical trials. The company, which has raised $6.4 million in funding to date, applies its cloud-based, quantitative approach to finding the data previously hidden in an H&E biopsy image without adding extra load to the current standard of care. As a result, the initial biopsy will no longer be the first step in a lengthy process towards biomarker profiling and stratification, but perhaps the only step necessary without the need for additional molecular tests (e.g. immunohistochemistry, FISH, RNA-Seq, NGS).

Just from whole slide H&E biopsy/resection images, in seconds 4D Path can identify cancer type (in the pan cancer level), its prognostically significant subtypes, variants, grades, and molecular profile with overexpression status as well as benign lesions. Its accelerated and more accurate diagnostic tool is commercially available now for use in clinical trials to allow pharmaceutical and biopharmaceutical companies to efficiently focus more precisely on effective treatments and targeted therapies.

Delayed and sometimes inaccurate cancer diagnosis is due largely to subjectivity, experience, variability in sampling and mood bias. Ancillary tests, designed to extract molecular profiles of the tumor and direct the right and effective treatment are lengthy, expensive and sometimes not accessible to the broad population (like in remote location), said Rodrigo Navarro, president and CEO, 4D Path. By eliminating the need for acquiring additional data, 4D Paths patented methods and integrated platform accelerate complete, actionable and proven clinical insights that are completely objective. For both companion diagnostics and translational medicine, 4D Path can reduce the cost, time and complexity of clinical trials and patient management.

Professor Andrew Hanby, specialist consultant breast histopathologist, NHS, UK, whose practice relies entirely on whole slide images (WSI) reporting, states: Pathologists are an essential part of the patient care pathway in offering a gold standard diagnosis to which patients treatment is tailored. Unlike current rival AI methodologies, 4D Paths technology significantly augments and revolutionizes the goal of achieving high levels of accuracy in diagnostics. It promises to enhance both the quality and efficacy of the process, giving patients the assurance that their treatment pathway has a solid and safe foundation.The value of this technology also extends beyond the complexity of clinical diagnostics in offering a robust analytical tool in environments where histopathologists are often lacking, such as clinical trials and grass roots cancer research."

4D Path applies statistical physics, cancer cell biology and mathematical principles to extract hidden dynamics encoded in a static tissue image to identify tumor-specific phenotypic and genotypic fingerprints. The patented algorithm relies on causation instead of merely statistical correlation to compute digital biomarkers and output the decisions. As a result, unlike emerging AI technologies, 4D Paths platform does not involve any kind of training of the histopathology images to learn to recognize diagnostic entities, nor does it require any pre-annotation or any other human intervention (like selecting handcrafted features) to direct the algorithm to regions of interest, said Tathagata Dasgupta, founder & CKO/CTO, 4D Path. By using previously unseen data unveiled by the proven diagnostic platform, 4D Path is the first biomedical endeavor of its kind to transition from R&D to validation in real-life clinical settings.

Founded in 2016 and previously in stealth mode, the company has achieved significant milestones including the approval of its first utility patent application earlier this year. The company operates a robust IT infrastructure and is expanding its platform compatibilities and ways to integrate it with existing PACS (Picture Archiving and Communication System). It has also extended its ability to analyze H&E stained biopsy and resection images to cytology images with standard stains (H&E or Papanicolaou) and is digital slide scanner agnostic.

4D Path BoilerplateJust because you cannot see something, does not mean it is not there. 4D Paths patented precision oncology platform unveils previously hidden data to instantly provide biomarker profiling and stratification directly from H&E Whole Slide biopsy/resection images only. 4D Paths cloud-based, quantitative approach eliminates the need for additional molecular tests (e.g., immunohistochemistry, FISH, RNA-Seq, NGS), accelerating complete, actionable and objective insight leading to expedited and democratized precision medicine for optimized patient care and clinical trials. Visitwww.4dpath.comto learn more.

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4D Path Announces Patented Precision Oncology Platform for Instant Biomarker Profiling and Stratification Just From H&E Biopsy or Resection Images -...