Speech as a New Diagnostic Tool in ALS and FTD – Neuroscience News

Summary: With the help of AI, researchers are developing digital biomarkers that use speech data to identify ALS and frontotemporal dementia.

Source: DZNE

With the help of speech tests, an initial diagnosis of severe neurodegenerative diseases should be possible in the future.

Researchers at the DZNE are developing so-called digital biomarkers for this purpose these are criteria that artificial intelligence can use to detect whether a patients speech pattern has changed as a result of a disease. The technology manages to detect even the slightest speech changes that are inaudible to the human ear.

The DZNE project, PROSA (A High-Frequency PROgnostic Digital Speech Biomarker with Low Stress), is now funded with $200,000 from the Alzheimers Drug Discovery Foundation and the Target ALS Initiative, both based in the United States.

Frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) are the focus of interest for the involved DZNE researchers. In FTD, nerve cells die primarily in the frontal and temporal areas of the brain in the frontal and temporal lobes, which are responsible for controlling emotions and social behavior, among other things.

In ALS, nerve cells in the brain and spinal cord die off. Up to now, both diseases have been extremely difficult to diagnose.

Language has long been considered by researchers as a conceivable indicator of neurodegenerative diseases.

There have been earlier approaches in which scientists have evaluated textual factors: How complex grammar did the subjects use, how large is their vocabulary, how do they string words together? explains Prof. Dr. Anja Schneider, working group leader at the DZNE and director of the Department of Neurodegenerative Diseases and Gerontopsychiatry at Bonn University Hospital.

However, it was tedious and slow work based on detailed transcripts of what was said. Modern technology now offers new possibilities: Artificial intelligence can perform such analyses much faster and also take melodic aspects of speech into account. Anja Schneider is leading the study on linguistic changes in FTD patients as part of the now-funded project, while her DZNE colleague Prof. Dr. Andreas Hermann is focusing on ALS patients. Two private companies are also involved in the project.

The procedure of a language test is very simple for the patients: They are asked three open questions about their leisure activities, for example, or about their career. Free descriptions of a picture presented are also conceivable. The decisive factor is that the test subjects speak spontaneously.

The artificial intelligence then analyzes the complexity of the speech and it also takes into account pauses between words, the speed of speech and other melodic aspects of the language.

In ALS patients, whose breathing is typically restricted by the progression of the disease, the artificial intelligence can additionally detect abnormalities here as well at a very early stage.

Dialects and other individual characteristics of speech have no influence on the accuracy of the results, says Anja Schneider.

Her observation: Artificial intelligence detects such subtle nuances of speech changes that a normal listener would not recognize at all without technical aids.

The Bonn researchers are incorporating data from two DZNE studies in the development of the method: In Describe FTD and Describe ALS, patients are followed over a longer course of the disease with complex clinical examinations. For the PROSA project, some subjects also undergo various language tests. Their results are combined with cognitive examinations.

Thanks to these multi-layered insights, the researchers hope, the language indicators can be further developed: If brain recordings and genetic testing show how far the disease has progressed then scientists can use language recordings from the exact same stage of the diseases progression to determine how language is changing.

We also want to find answers to other questions, says Anja Schneider:

For example, is the precision of the speech test related to the patients daily form? Does language deteriorate linearly in the course of the disease, so that we could use a linguistic marker not only to make a diagnosis, but even to draw conclusions about how quickly the disease is progressing in the respective patient?

100 patients from the ALS cohort and 100 patients from the FTD cohort will be included in the study; additional subjects will be added for the control group.

Up to now, the diagnosis of FTD and ALS patients has been extremely complex. It can usually only be made in highly specialized expert centers. The necessary examinations take at least ten hours, and the waiting time for an appointment is up to half a year.

With the help of a language test, potential patients could be examined beforehand, ideally even by telephone, to provide doctors with support for their diagnosis.

Author: Sabine HoffmannSource: DZNEContact: Sabine Hoffmann DZNEImage: The image is in the public domain

See original here:
Speech as a New Diagnostic Tool in ALS and FTD - Neuroscience News

Can resilience be learned? Study finds that prior stressful events can help build resilience – EurekAlert

image:A new study published in the journal Nature found that mice who defended themselves against aggressors learned to be more resilient to aggression, and that the neurotransmitter dopamine plays a role in reinforcing resilience. view more

Credit: Danielle Capparella, Princeton University

Faced with climate change, a pandemic, and political unrest around the globe, it can feel all too easy to succumb to a sense of hopelessness. How do some people bounce back from adversity faster than others, and can those who struggle teach themselves to be more resilient over time?

A new study conducted in mice and published Oct. 19 in the journal Nature suggests resilience can be learned, and can even be reinforced. A team of researchers from the Princeton Neuroscience Institute placed small mice in close proximity with larger, aggressive mice and found that a display of defensive behaviors predicted the mices ability to be resilient after the stressful event. Further, the team found that by activating dopamine while the mice fought back, they could further reinforce resilience.

From the researchs inception, Lindsay Willmore, who earned her Ph.D. in 2022 and is lead author on the paper, was intrigued by the relatively rare subset of mice who would defend themselves tenaciously when faced with an aggressor.

Theyd turn back towards the aggressor, theyd throw their paws out, theyd jump on him, and they would just not give up, said Willmore. I thought, wow, theres something going on in these guys brains thats super interesting and could be the key to resilience.

In the study, the researchers gauged resilience by monitoring the mices behaviors in the 10 days during which they sustained attacks by the aggressor.

The mice that tended not to defend themselves ended up displaying depression-like behaviors such as social avoidance following the stressful event. Meanwhile, the mice that fought back displayed greater resilience.

By stimulating dopamine while the mice were fighting back, the researchers found they could make the mice even more likely to become resilient. On the flip side, stimulating dopamine during avoidant behavior did not make the mice more resilient.

Its a complicated environment where a mouse has to decide what to do around a bully mouse, said Ilana Witten, a professor of neuroscience and author on the study. What decision it makes has profound consequences in terms of how it ends up.

While the defensive stances associated with fighting back were key in predicting a mouses resilience in the face of attack, Willmore said, Even more strongly related to resilience was how much dopamine the animals had in their reward system during the time when they were starting to fight back. Thats what was really cool to me that an animal that is not just fighting back but is rewarded for fighting back is the one that becomes resilient.

For the study, the researchers put a smaller mouse in a cage with a larger, more aggressive mouse that typically would attack its smaller cage-mate. Afterward, the two mice would stay in the enclosure but this time separated by a wall so that they could not interact physically.

Im very interested in the question of whether we can teach resilience, said said Annegret Falkner, an assistant professor of neuroscience and author on the paper. The series of experiments the team conducted seemed to suggest the answer was indeed yes, that the mice could be nudged toward performing resilient behaviors.

While the researchers began the project before the start of the COVID-19 pandemic, Falkner said since the pandemic hit, shes been thinking more than ever about resilience. We need to think about ways to help the people who seem to be more susceptible to cope with the stresses of the world, said Falkner.

As the researchers continue their studies on resilience, they hope that in the future such work could be applied beyond animals to human health. For example, devices such as smart watches could give real-time feedback about good habits to promote healthy mechanisms like resilience. Information about our dynamic interactions with the environment will be useful for tracking our habits that might be helpful or harmful, said Willmore.

The study was funded by the New York Stem Cell Foundation, the Esther A. and Joseph Klingenstein Fund, the Simons Foundation, the Alfred P. Sloan Foundation, the National Science Foundation, and the National Institutes of Health.

The study, Behavioral and dopaminergic signatures of resilience, by Lindsay Willmore, Courtney Cameron, John Yang, Ilana Witten and Annegret Falkner, was published in the journal Nature on Oct. 19, 2022. DOI 10.1038/s41586-022-05328-2.

Experimental study

Animals

Behavioral and dopaminergic signatures of resilience

19-Oct-2022

The authors declare no competing interests.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

More:
Can resilience be learned? Study finds that prior stressful events can help build resilience - EurekAlert

Timely Interventions for Depression Might Lower the Future Risk of Dementia – Neuroscience News

Summary: Symptomatic depression increases the risk of developing dementia by 51%, but those being treated for depression had a significantly lower risk of being diagnosed with depression later in life.

Source: Elsevier

Depression has long been associated with an increased risk of dementia, and now anew studyprovides evidence that timely treatment of depression could lower the risk of dementia in specific groups of patients.

Over 55 million people worldwide live with dementia, a disabling neurocognitive condition that mainly affects older adults. No effective treatment for dementia exists but identifying ways to help minimize or prevent dementia would help to lessen the burden of the disease.

The study, led by Jin-Tai Yu, MD, PhD, Huashan Hospital, Shanghai Medical College, Fudan University, and Wei Cheng, PhD, Institute of Science and Technology for Brain-Inspired Intelligence, Fudan University, Shanghai, China, appears inBiological Psychiatry.

Professor Yu and Professor Cheng used data collected by the UK Biobank, a population-based cohort of over 500,000 participants. The current study included more than 350,000 participants, including 46,280 participants with depression. During the course of the study, 725 of the depressed patients developed dementia.

Previous studies examining whether depression therapies such as pharmacotherapy and psychotherapy could lower the risk for dementia produced mixed results, leaving the question unresolved.

Older individuals appear to experience different depression patterns over time, said Professor Yu.

Therefore, intra-individual variability in symptoms might confer different risk of dementia as well as heterogeneity in effectiveness of depression treatment in relation to dementia prevention.

To address that heterogeneity, the researchers then categorized participants into one of four courses of depression: increasing course, in which mild initial symptoms steadily increase; decreasing course, starting with moderate- or high-severity symptoms but subsequently decreasing; chronically high course of ongoing severe depressive symptoms; and chronically low course, where mild or moderate depressive symptoms are consistently maintained.

As expected, the study found that depression elevated the risk of dementia by a striking 51% compared to non-depressed participants. However, the degree of risk depended on the course of depression; those with increasing, chronically high, or chronically low course depression were more vulnerable to dementia, whereas those with decreasing course faced no greater risk than participants without depression.

The researchers most wanted to know whether the increased risk for dementia could be lowered by receiving depression treatment. Overall, depressed participants who received treatment had reduced risk of dementia compared to untreated participants by about 30%.

When the researchers separated the participants by depression course, they saw that those with increasing and chronically low courses of depression saw lower risk of dementia with treatment, but those with a chronically high course saw no benefit of treatment in terms of dementia risk.

Once again, the course of ineffectively treated depression carries significant medical risk, saidBiological Psychiatryeditor John Krystal, MD. He notes that, in this case, symptomatic depression increases dementia risk by 51%, whereas treatment was associated with a significant reduction in this risk.

This indicates that timely treatment of depression is needed among those with late-life depression, added Professor Cheng. Providing depression treatment for those with late-life depression might not only remit affective symptoms but also postpone the onset of dementia.

The new findings shed some light on previous work as well, said Professor Cheng. The differences of effectiveness across depression courses might explain the discrepancy between previous studies.

Author: Eileen LeahySource: ElsevierContact: Eileen Leahy ElsevierImage: The image is in the public domain

Original Research: Closed access.Depression, Depression Treatments, and Risk of Incident Dementia: A Prospective Cohort Study of 354,313 Participants by Wei Cheng et al. Biological Psychiatry

Abstract

Depression, Depression Treatments, and Risk of Incident Dementia: A Prospective Cohort Study of 354,313 Participants

To investigate the associations between courses of depression, the application of depression treatment, and the risk of incident dementia.

In this prospective cohort study, 354,313 participants aged 50 to 70 years were recruited from the UK Biobank between 2006 and 2010, and were followed-up until 2020, with a total of 4,212,929 person-years. We initially studied the effect of depression on dementia incidence across four subgroups characterized by courses of depressive symptoms. Then, 46,820 participants with depression diagnose were further categorized into the treated and untreated groups. We compared the risks of dementia among different depression treatments groups in all participants that depressed as well as four courses of depressive symptoms by performing survival analyses.

Depression was associated with a 51% higher risk of dementia, among which the increasing, chronically high and chronically low courses were associated with increased dementia risk while no association was found in the decreasing course. Compare to those who were depressed but untreated, receiving depression treatments corresponded to a hazard ratio of 0.7 (95% confidence interval= 0.62-0.77). Among the three detrimental courses, treatments for increasing and chronically low symptoms of depression were associated with a 42% and 29% lower risk of dementia while the reduction effect for chronically high symptoms was insignificant.

The negative association between depression treatment and incident dementia was significant in the increasing and chronically low course, highlighting the necessity of timely interventional strategies before depression progress to a chronically severe state.

Visit link:
Timely Interventions for Depression Might Lower the Future Risk of Dementia - Neuroscience News

The Appeal of Scientific Heroism – The New Yorker

In 2008, the journalist Jonah Lehrer paid a visit to a lab in Lausanne, Switzerland, to profile Henry Markram, a world-renowned neuroscientist. Markram, a South African, had trained at a series of lite institutions in Israel, the United States, and Germany; in the nineties, he published foundational papers on neural connections and synaptic activity. Markrams work in the laboratory, which involved piercing neural membranes with what Lehrer described as an invisibly sharp glass pipette, was known for its painstaking precision. Lehrers visit, however, had been occasioned not by Markrams incremental contributions to the fieldits not easy to sell a colorful profile on the basis of such publications as The neural code between neocortical pyramidal neurons depends on neurotransmitter release probabilitybut by Markrams pivot, in the early two-thousands, to brain simulation.

Neuroscience, Markram declaimed to Lehrer, had reached an impasse. Researchers had generated an enormous wealth of fine-grained data, but the marginal returns had begun to diminish. If there was to be real progress in understanding what exactly was going on in our heads, a more enterprising approach would be required. With the help of supercomputers descended from I.B.M.s Deep Blue, he planned to construct a full-scale model of the brain from the ground up: each individual neuron would have a digital analogue. A by-product of this computational strategy would be a solution to the mystery of consciousness. Of his effort, Lehrer wrote in the sadly long-defunct Seed magazine, Markram hopes that it represents a whole new kind of neuroscience. As Markram put it to Lehrer, You need to look at the history of physics. He continued, From Copernicus to Einstein, the big breakthroughs always came from conceptual models.

Such unapologetic self-mythologizing on the part of a subject is difficult for a journalist to resist, and Lehrer was patently captivated by Markram, who had an aquiline nose and a lustrous mop of dirty blond hair that he likes to run his hands through when contemplating a difficult problem. Though his eyes were bloodshot from lack of sleep, Lehrer comments, Markram could pass for a European playboy. Lehrer was primed to believe Markram, and, when treated to a theatrical visualization of one of the teams preliminary achievements, of a simulated portion of a mouse brains neocortex, he was not disappointed. One of Markrams scientists told Lehrer that their study of neurons in silicothat is, on a chipwas more propitious than the in-vivo and in-vitro processes used by actual experimenters: they enjoyed access to much cleaner data than their error-prone human colleagues did. Lehrer wrote, The model, in other words, has exceeded its own inputs. The virtual neurons are more real than reality.

At the time, Noah Hutton was studying neuroscience as an undergraduate at Wesleyan University. Hutton was an aspiring filmmakerhis first documentary, Crude Independence, which he shot in a North Dakota boomtown between his junior and senior years, premiered at SXSW before he graduated from college. Hutton had encountered Markrams seminal early work in a class on mammalian cortical circuits, but, as with Lehrer, it was the brain-simulation effortthe attempt to construct the legendary brain in a vat, with all of the philosophical issues it entailedthat took hold of his imagination. In 2009, when Hutton was in his final year of college, Markram delivered a viral TED talk in which he claimed that he could simulate a human brain within ten years.

I was fully awe-inspired, Hutton told me recently. Markram was a hero of mine, and I thought, I need to get in on the ground floor of this. Lehrers profile had ended with the usual backside-covering caveatsto be sure, Markram might not succeed, etc.but Hutton wanted the entire glorious arc. He e-mailed Markram a few times but received no response. Hutton had recently shot a music video for a band called the Amygdaloids, a side project of the N.Y.U. neuroscientist Joseph LeDoux, and LeDoux offered to vouch for Hutton. With LeDouxs endorsement, Hutton secured an invitation to Lausanne to make his pitch. There were other documentarians circling the program, which was called the Blue Brain Project, but, if Markram was committed to seeing the whole thing through in ten years, Hutton said, he was prepared to make the same investment. Hutton was twenty-two. There was no one else crazy enough to commit to that timeline, Hutton told me, and Markram was won over by an ambition that seemed commensurate with his own. Hutton was taken to a screening room to experience an updated version of the fly-through that the team had shown Lehrer, and he shared Lehrers fervor. I was just awestruck by the visuals. I was an acolyte, and we immediately had a kind of teacher-student relationship. I had not a shred of critical energy.

For the next decade, Hutton made an annual pilgrimage to Lausanne to check in on the project and interview Markram. The first eight visits were self-fundedHutton was supporting himself as a commercial editor in New Yorkand all of them were solo; Hutton had no one to help schlep his equipment around or set up his shots. His final product, the excellent In Silico, had its streaming dbut in September. Hutton is a talented filmmakerLapsis, a low-budget sci-fi movie that he wrote and directed himself, appeared last year, and portends a career in the conceptual mode of someone like Alex Garlandbut few documentary projects extend for more than a year or two, and in most instances their trajectories are rigged up to fit an arbitrary ending. Had Hutton encountered his subject over the standard documentary interval, he almost inevitably would have come away with a version of the story that Lehrer told: a familiar tale of a bold, charismatic visionary destined to triumph over the forces of cautious bureaucracy, opening up expansive new vistas of inquiry. As it turned out, however, Hutton found himself narrating a much more complicated storyone in which his own personal hopes for the project would be implicated.

An early montage sets us up for what seems like the first version of the story: a series of neuroscientists at prestigious institutions explain that we dont know nearly enough about the brains intricacies to permit wholesale simulation, and that it might be a century or more before we have such knowledge. In his TED talk, Markram explains that hell have nothing to do with such prognoses of impossibility, and in his year-one interview with Hutton he goes even further: as he sees it, the epistemic modesty of the neuroscience community is an alibi for timidity and self-preservation. A full-brain simulation, in his view, is the necessary basis we need to solve such problems as Alzheimers and severe autism; his son is autistic, which gives his work a particular personal urgency. As a scientist, you want to sit back and say, O.K., its enough for me to study my microcircuit, and Im happy, he tells Hutton, shuffling papers in front of himself with feigned dismissiveness, as he nods in imitation of scientific paper shufflers. I dont think thats enough. And thats what keeps me going.

If Markram succeeds, Hutton explains, in voice-over, brain researchers will neither need to experiment with animals anymore, nor run up against the limits of invasive procedures on human subjects. Markram goes on, Well have an intelligence. Youll be able to dial down a molecule and see that you dropped the I.Q., dial up a molecule, see that you raised the I.Q. I believe that we will understand the brain before we finish building it. With nave admiration, Hutton asks Markram what keeps him going, and Markram responds to the softball with a gentle head pat of a smile. Well, I want to see this built. In ten years, as I said, its going to be built. Hutton is ushered into a screening room and shown a fly-through of a portion of simulated mouse brain; the Blue Danube waltz plays, and stunning visuals unfurl before his eyes. Hutton says, Though it was just a tiny piece of the whole, this was the first rendering of the most detailed brain simulation ever attempted. He told me, I thought, Holy shit! No one else has ever seen thisIm seeing inside of a brain! I had a few years of that feeling.

When Hutton returns for another visit, in 2011, the team has made what they describe as a significant leap: they have seen, for the first time, glimmers of brain activity that they hadnt themselves programmed, a sign that the simulated brain has begun to exhibit emergent properties. Hutton lingers on a shot of their computer displays, where a wave of color washes over the digital neurons. Their promotional apparatus has also been upgraded, and Hutton notes the introduction of giant touch screens. One of Markrams lieutenants shows him a bottle of champagne theyve locked in a desk drawer for future celebrations of breakthroughs they feel certain are imminent.

That year, Hutton read a new book by the neuroscientist Sebastian Seung, then at M.I.T., that described his skepticism of Markrams brain-simulation project. In an interview, Seung, who is just as good-looking, charismatic, and camera-ready as Markram, seems unable to take Markrams venture seriously: If we dont have detailed knowledge about the connections in neural networks that we can really depend on, I think that the endeavor of simulating them is really bound to fail. Seung explains that the fundamental problem with Blue Brain is that there are no intermediate benchmarks. Absent some connection to the real, experimental world of rats in mazes or humans in MRI machines, Seung explains, theres no way to know whether Markrams team is simulating something like actual brain activity or merely producing cool graphics. Hutton cuts back and forth between his interviews with Seung, who calls brain simulation highly unrealistic and a waste of time, and Markram, who calmly explains that his efforts have been severely distorted by his critics, who are hopelessly limited by the old, plodding ways of doing things. Markram seems to pity them in their attachment to a superannuated model, as if they were still hard at work refining inquiries into the Ptolemaic spheres; as he puts it to Hutton, Were dealing with a cultural change.

Hutton, for the most part, gives Markram the final word; after all, he had hitched his own ten-year project to Markrams. Privately, however, Hutton was less sure. He told me, I thought, Do I need to jump over and follow Sebastian now? Have I picked the right vessel for the film? But I felt I had to stay with it. Hutton felt malleable, tossed in two directions. When he met with Markrams critics, he found their storythat Markram represented the conquest of traditional neuroscience by computational colonistspersuasive, but, when he relayed versions of these opinions to Markram, he was once again convinced that Markram was misunderstood, a maverick visionary. Hutton realized that his own role in the documentary had to change. He told me, Id made two documentaries before, and I wasnt in those films at allthey were vrit-style. Id thought this film would be the same. But then I thought: whos the narrator? It wasnt Henry, because at that point I couldnt place him at the center of the film. I had to step in, which meant I had to figure out my own point of view. Before Hutton returned to Lausanne for the third year, a short portion of his work in progress, including his interview with Seung, was published by the Scientific American. When he arrived for the next shoot, he was steered aside by one of Markrams subordinates; in the future, they told him, they wanted to know who else he was talking to. Hutton put the warning into the film.

On a superficial level, the rest of In Silico is about Markrams rise and fall: through the brute force of his salesmanship, he brings together hundreds of researchers from as many institutions to win a flagship billion-dollar grant from the European Commission, and his efforts at Blue Brain become the centerpiece of whats known as the Human Brain Project. Hutton is swept up in the renewed enthusiasm for a far-reaching effort now described as akin to the Human Genome Project, or to CERN, the European Organization for Nuclear Research; at one point, he appeared on MSNBC to announce that he had updated his own timeline to fifteen years, to track Markrams, and he was partway through what was now a fifteen-year documentary. Markrams imperial stewardship of the Human Brain Project was, however, short-lived: eight hundred neuroscientists signed an open letter of protest, arguing that the neuroscientific community had been sold a bill of goods, and that participants had been enlisted against their better judgment in what was no longer a cordinated effort to study the brain but a monumental boondoggle and an egregious squandering of scientific resources on expensive information technology. Markram was pushed out of the Human Brain Project, and resumed his old position at Blue Brain, which was supported by the Swiss government.

By year seven, Markram has begun to fully turn inward; he tells Hutton that hes tired of fighting for his position in the media, and that hes decided that this is his silent year, that hes going into hibernation. His science, he believes, will speak for itself. He removes his microphone, ending the interview early. In voice-over, Hutton explains the way hes been buffeted back and forth between the outside critics and Blue Brains spellbinding visuals. (Huttons own animated sequences, by the wonderful illustrator Andrew Khosravani, are, by deliberate contrast, decidedly anti-realistic; cartoonishly florid and surreal, they bring to mind the interstitial scenes from Monty Python.) Now, Huttons narration continues, something else was starting to creep in, a sense of multiplying touch screens, curved screens, headsets, but a lack of meaning to anything and anyone outside this glass-and-steel building in Geneva. Markram now suggests, against all evidence, that the ten-year timeline was never supposed to be taken literally, he insists that his team remains on track to complete the construction of a digital mouse brain; he produces as confirmation the fact that their simulations are growing larger and more theatrically vivid with the passage of time. Where Jonah Lehrer, the journalist, had to conclude with boilerplate about how Markram might very well fail, Hutton has put himself in the opposite position: Markram, he grants, might be vindicated in the end. But, even if that never proves to be the case, Hutton goes on, the story of scientific progress is as much a story of mistakes as it is one of successes. He allows that theres a certain grandeur in Markrams ability to make mistakes on such a tremendous scale, and with such tremendous initiative.

All of this is, of course, true enough, but Huttons more profound point is that there remains an important difference between being wrong and being not even wrong. The danger isnt that Markram has made mistakes, but that the mistakes hes making arent productiveor are only productive on a meta level, insofar as they suggest that science is only on rare occasion the proper realm for Nietzschean heroism, and that layers of bureaucratic oversight tend to exist for good reason. The portrait of Markram that ultimately emerges is of a lordly sovereign stalking the halls of an island mansion, an autumn of the scientific patriarch. Perhaps Lehrer was caught in the usual short-term trapthat, had he had Huttons longitudinal Sitzfleisch, he would have discovered that the whole thing was a castle in the air. (As the blogger Scott Alexander recently put it, just as economists have predicted ten of the last two recessions, so science journalists have predicted ten of the last two paradigm shifts.) But there were clues available to Lehrer even thenones that made their way, unexamined, into his own article. Markram had compared himself to Copernicus, suggesting that his own conceptual breakthrough would be of the same order. But Copernicus did not begin with a new conceptual framework. Copernicus began with the sense that there was something about our astronomical measurements that didn't quite add up. It may have been a conceptual breakthrough that solved the problem, but it was the painstaking incremental workwhat Thomas Kuhn called the practice of normal sciencethat demonstrated that there was in fact a problem to be solved.

Go here to see the original:
The Appeal of Scientific Heroism - The New Yorker

Kenworthy links quantity to theory – ASBMB Today

Anne Kenworthy began doing lab science as an undergraduate at Kenyon College in Gambier, Ohio, but it was only after she moved on to graduate school and postdoctoral opportunities that she realized the breadth of research at R1 institutions.

Kenworthy began doing biophysical studies as a grad student in the cell biology department at Duke University. Her advisor, Tom McIntosh, was a physicist by training and was known for his work investigating the forces between bilayers in the cell membrane.

Anne Kenworthy

I found that work appealing, Kenworthy said. It was very quantitative, and I enjoyed being able to take measurements that you could then relate back to a physical theory.

Now a professor of cell biology and molecular physiology and biological physics at the University of Virginia School of Medicine, Kenworthy is the recipient of the American Society for Biochemistry and Molecular Biologys 2023 Mildred Cohn Award in Biological Chemistry. The award is named for the first female president of the ASBMB and honors scientists who have used innovative physical approaches to understand biological chemistry.

Kenworthy was nominated by Avril Somlyo, a UVA School of Medicine colleague WHO was previously Cohns colleague at the University of Pennsylvania, for her contributions to the study of membrane structure and dynamics, including being one of the first researchers to apply fluorescence resonance energy transfer, or FRET, microscopy to the study of lipid rafts.

Knowing Anne and having known Mildred as a colleague at the University of Pennsylvania, I believe it is an ideal match, Somlyo wrote.

I honestly couldnt believe it, Kenworthy said of winning the award. Sometimes you dont realize the impact that some of your discoveries have actually made.

In addition to her research, Kenworthy serves as an associate editor in the Cell Biophysics section of the Biophysical Journal and as faculty in the FLIM (fluorescence lifetime imaging microscopy) and FRET workshop at the Keck Center for Cellular Imaging at UVA. She considers it a natural part of her evolution as a researcher to contribute to the community by serving on editorial boards and study sections.

You have an important role in helping to make sure that applicants get fair reviews, Kenworthy said. You know that the best science can go on for funding agencies to make those final decisions.

Anne Kenworthys lab in the Center for Membrane and Cell Physiology at the UVA School of Medicine studies cell membranes and the microdomains inside them, such as lipid rafts. Lipid raft microdomains contain certain concentrations of proteins in a small area that allow them to perform activities such as signaling and extracellular sensing. Caveolae, a special type of lipid raft, are dips in the plasma membrane that are built by caveolin proteins and that function in signaling and lipid homeostasis. Together with collaborators, the Kenworthy lab recently determined a high-resolution cryo-electron microscopy structure of the 3D form of a caveolin protein, a landmark achievement.

The lab also studies the structure and dynamics of lipid rafts themselves using techniques such as quantitative fluorescence microscopy, where the brightness level of fluorescence proteins is given a number compared to a control level of brightness and undergoes mathematical model analysis. Using florescence, the Kenworthy lab can measure on and off rates of transient protein binding events and measure the diffusion rate of lipids and proteins in the membrane.

Original post:
Kenworthy links quantity to theory - ASBMB Today

Newly identified process keeps some immune cells on their toes – News-Medical.Net

Cancer cells use an unusual mechanism to migrate into new tissue and form metastases there. The same process probably also keeps some immune cells on their toes. This is the result of a recent study led by the University of Bonn. According to the study, certain structures, the centrioles, increase in number. This makes it easier for them to maintain their direction and thus migrate more quickly to the lymph nodes, where they activate other immune cells. The results have now been published in the Journal of Cell Biology.

Like the police, the immune system relies on division of labor. First of all, there are the dendritic cells. They search the tissue around the clock for traces of suspicious intruders, called antigens. If they are successful, they rush to the lymphatic vessels and from there to the draining lymph nodes. There they present their findings to a powerful search team, the T cells. These endogenous troops now know which enemy to fight.

This attack must take place before the invaders cause major damage or multiply too much. It is therefore important that dendritic cells migrate as quickly as possible to the briefing in the lymph node.

We have discovered a mechanism that helps them doing this. To do so, they form more of certain structures called centrosomes. These help them maintain their direction for longer and thus reach the lymphatic vessels more quickly."

Prof. Dr. Eva Kiermaier, LIMES Institute (Life and Medical Sciences), University of Bonn

Centrosomes belong to the organelles - these are molecular complexes that are responsible for specific tasks in cells, much like the organs in the body. Normally, there is exactly one centrosome in each human cell. Shortly before cell division, it doubles. The two copies migrate to opposite poles of the cell and stretch a bundle of fibers between them, the microtubules. With them, they pull the chromosomes (which have also doubled) apart during division. Each of the resulting daughter cells thus receives a complete set of genetic material as well as one of the two centrosomes.

"However, centrosomes are also responsible for organizing the cytoskeleton during cell migration," emphasizes Kiermaier, who was brought to the Rhine from Lower Austria (IST Austria, Klosterneuburg) in 2017 through the returnee program of the state of North Rhine-Westphalia. "By this we mean fiber-like structural proteins that give the cell its shape and provide it with stability." The cytoskeleton also decides where "front" and "back" are in a cell. And that, in turn, affects its direction of movement. "We have now been able to show that dendritic cells form multiple centrosomes as soon as they come into contact with an antigen," says Ann-Kathrin Weier. The PhD student at the LIMES Institute shares first authorship of the publication with her colleague Mirka Homrich. Both performed important parts of the experiments.

Dendritic cells have a problem: they do not know where the next lymphatic vessel is via which they can reach the lymph node. In their search, they proceed according to the strategy of "trial and error": they run in one direction for a short while and then change it if they have not encountered a vessel in the process. "The more centrosomes they have, the longer they stay on course before continuing to search in a different direction," says Mirka Homrich. "We were able to show in computer simulations that this allows them to find the lymphatic vessels much faster than they normally would." In the process, the proliferation of centrosomes adjusts their staying power just right - so they don't stick too stubbornly to their direction. This would increase the risk of them going astray and getting completely lost.

The mechanism identified in the study was previously completely unknown in healthy cells. Cancer cells were assumed to use it to form metastases. However, the multiplied centrosomes must not be freely distributed inside the cells. Otherwise, they would severely disrupt functions such as cell division. In both tumor and dendritic cells, the organelles therefore congregate at a single site - they cluster. "There are now agents that disrupt this clustering of centrosomes," says Kiermaier, who is also a member of the ImmunoSensation2 Cluster of Excellence and the Transdisciplinary Research Area "Life and Health" at the University of Bonn. "As a result, the cancer cells can no longer divide correctly, but die."

However, it is also possible that these substances interfere with the immune system - after all, the centrosomes cluster there as well. "We've tested several of these agents in cell cultures," she says. "We've actually found evidence that they could significantly impair the effectiveness of the immune defense." If that will be confirmed in clinical trials, it would be bad news as there could be considerable side effects if the active substances were used in cancer therapy.

In addition to the University of Bonn, the Charles University in Vestec, Czech Republic, and the Institutes of Science and Technology in Austria and Spain were involved in the work.

Source:

Journal reference:

Weier, A-K., et al. (2022) Multiple centrosomes enhance migration and immune cell effector functions of mature dendritic cells. Journal of Cell Biology. doi.org/10.1083/jcb.202107134.

Read the rest here:
Newly identified process keeps some immune cells on their toes - News-Medical.Net

What does biochemistry have to do with climate change? – ASBMB Today

Ask Karla Neugebauer about her journey to climate activism, and she highlights two moments.

The first was in 2006. She was on vacation in Australias Northern Territory with her family, camping in the outback not far from Alice Springs. That part of Australia, known to some as the Red Centre, is beautiful, severe desert country the kind of place where its unwise to start a road trip without a five-gallon water tank and a spare tire. The rocks are russet. In the deep shade of narrow gullies in the MacDonnell mountain range, small pools of water cool the air around them, making small miracles of oasis.

Yale University

Karla Neugebauer's interest in climate change was inspired by a driving tripin the Australian outback and a dinner conversation with her son.

Neugebauer read aloud on the road trip, as she often did when her children were young. She came to an article by paleontologist turned climate writer and activist Tim Flannery outlining the fiery future Australia faced if it maintained its inaction on climate change.

Being immersed in the natural environment and then reading this thing was just kind of devastating, Neugebauer said. I remember sitting in the back seat and just bawling.

At the time, she was a group leader at the Max Planck Institute of Molecular Cell Biology and Genetics in Germany. There was no clear link between her professional expertise, which concerns RNA splicing and gene expression, and the looming crisis.

More than decade later, she sat down to dinner with her son and a friend he had grown up with. The world had continued to careen down the path of escalating emissions and rising global temperatures Flannery had described. Neugebauer had moved to the U.S. by this time and had taken a faculty position at Yale, but her son, a young adult, had returned to Dresden for an internship. He and his friend had become involved in the Fridays for Future climate protests; sometimes, their friends had been arrested. If they did choose to go to college, both young men said, the only fields worth studying would be environmental engineering or politics disciplines that could save the planet.

Their deep concern for the future galvanized her to act and made her wonder why other areas of expertise did not also seem like productive tools for climate activists. It disappointed me that other disciplines didnt come to their minds, Neugebauer said.

The more closely she looked at biochemistry, the less she could blame young people for overlooking its relevance. When she canvassed other universities for ideas about how to teach the biology of climate science, she came up emptyhanded. At interdepartmental meetings she began to attend virtually a few years later, during the pandemic, she was the only biochemist in attendance.

Neugebauer argues that the field has become myopically focused on human health because of funding organized around diseases of individual organs. Even basic researchers must think and write in terms of curing disease to secure grants.

I submit to you the work Im doing on stress in HeLa cells is relevant to climate change because Im studying how gene expression changes to parameters that are going to change for the algae and the fish, Neugebauer said. Yet when she talks to her neighbors about her work, she hears herself describing applications in cancer. Im not curing cancer! Im a basic scientist. Im asking fundamental questions that I believe are terribly important for allof these reasons.

She illustrated that belief by launching an unconventional seminar in the fall of 2021. The course, called Biochemistry and our Changing Climate, explores the basic biochemistry that governs living systems response to a changing world.

Neugebauer guides her students through discussions of articles that illuminate the core concepts of biochemistry in a climate context. She talks about the aromatic amino acid synthesis pathways that the pesticide Roundup inhibits and about how cell biological responses to heat stress contribute to coral bleaching. She talks about nitrogen fixation a biochemical process that her departments core courses do not cover. She talks about engineering enzymes that could recycle plastics or entomb atmospheric carbon in building materials.

Karla Neugebauer

In her course, Karla Neugebauer encourages students to propose research projects that would answer open questions about the links between biochemistry and climate change such as why red algae reduces cows methane emissions.

People have a hard time understanding what I mean by a class about biochemistry and climate change, she said. The course isnt focused on ecology or on bioengineering. Instead, she seeks to explore on a molecular level the mechanisms by which climate change is affecting and will alter further the living world. It frustrates her when students ask questions that biochemistry clearly could answer for example, What molecule from red algae reduces cows methane emissions? but has not.

She aims to show her students that biochemists have a role to play in understanding climate change and a role to play in adapting to and mitigating the crisis.

Neugebauer has spent time recently visiting other departments to tell them about her course. By the time you receive this magazine, she will be immersed in teaching it for a second time. Im on a mission to make people aware of this, she said.

Karla Neugebauer and Henry Jakubowski (author of the climate change article How to be a climate activist) will host an interest group on Biochemistry and Climate Change on March 25 at Discover BMB 2023, the ASBMB annual meeting in Seattle.

Originally posted here:
What does biochemistry have to do with climate change? - ASBMB Today

Biology Alumna Named Conn.’s Teacher of the Year – Susquehanna University

October 13, 2022

What keeps Carolyn Kuhr 98 Kielma coming back to teaching year after year is not the biology content she teaches, but the connections she shares with her students.

Kielma was named Connecticuts Teacher of the Year by Gov. Ned Lamont and the Connecticut State Department of Education. She teaches biology and biotechnology and forensics at Bristol Eastern High School.

I am elated and honored to represent my students and my city, Kielma said. The longer the dust settles, the more overwhelmed with gratitude I am. So many former students, colleagues and parents are reaching out to congratulate me and wish me luck. I had no idea how much I was able to impact my community.

Growing up, Kielma said she was a curious child with an early passion for learning. Upon graduating from Susquehanna University, she worked several concurrent jobs while saving up to continue her education at graduate school which she did, graduating in 2002 with a Master of Education from the University of New Haven.

After my first few years in the profession, I discovered that learning science is not truly the goal for my students, Kielma said. I now believe teaching is not only about the content but about helping youth become better humans. I strive to be the type of teacher that I needed in my adolescent years the trusted adult that students can come to when they need help, whether inside or outside the classroom.

Now 20 years into her career, Kielma said she still gets excited when chatting with her current students about the research opportunities they could have if they find mentors like the ones she had at Susquehanna, including Jack Holt, professor of biology; Peggy Peeler, Charles B. Degenstein professor of biology; Tom Peeler, associate professor emeritus of biology; and David Richard, presidential professor of biology.

I will never forget being able to keep frog hearts beating in culture on a petri dish during cell biology lab and trudging through the waters collecting samples from the Susquehanna River during limnology, she said. They supported me by believing in me, even when I didnt. Thats one of the most important gifts I can give my current students too.

Kielma also believes in students shes never met those at Susquehanna who are just on the precipice of beginning their own careers in teaching.

I think the greatest advice I can offer is to be patient with yourself honing a craft like education takes time. Lean into the educators in your building; within your school will be a group of highly educated, motivated and courageous professionals who understand the power of lifelong learning. Trust in them and trust in yourself, Kielma said. Remember to stay positive and do not get caught up in negativity because you are making a difference, even if it is with one student at a time.

Read the original post:
Biology Alumna Named Conn.'s Teacher of the Year - Susquehanna University

Cell Isolation Global Market Report 2022: Increasing Emphasis on Cell-Based Research Bolstering Growth – PR Newswire

DUBLIN, Oct. 18, 2022 /PRNewswire/ --The "Cell Isolation Market: Global Industry Trends, Share, Size, Growth, Opportunity and Forecast 2022-2027" report has been added to ResearchAndMarkets.com's offering.

The global cell isolation market size reached US$ 10.3 Billion in 2021. Looking forward, the publisher expects the market to reach US$ 24.6 Billion by 2027, exhibiting a CAGR of 15.62% during 2021-2027. 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.

Cell isolation, or separation, refers to the process of identifying and removing one or more specific cells from a heterogeneous mixture of cell population. The targeted cells are identified, isolated and separated according to their type. Some commonly used methods for cell isolation include magnet-activated cell separation, filtration, centrifugation and flow cytometry.

Cell isolation is also used to diagnose diseases, cellular research and therapies by analyzing the ribonucleic acid (RNA) expressions. It aids in minimizing experimental complexity while analyzing the cells and reducing the interference from other cell types within the sample. As a result, it finds extensive application in cancer research, stem cell biology, immunology and neurology.

Cell Isolation Market Trends:

Significant growth in the medical and pharmaceutical industries is one of the key factors creating a positive outlook for the market. Furthermore, increasing emphasis on cell-based research is providing a thrust to the market growth. Researchers actively utilize isolated cells to develop novel cell therapies and cell-based treatments for various chronic medical ailments. Pharmaceutical manufacturers are also widely using cell isolation technologies to improve drug discovery and develop drugs with enhanced efficacies. In line with this, the increasing requirement for personalized medicines is also contributing to the growth of the market.

Additionally, the development of advanced separation tools for proteins, nucleic acids, chromatin and other complex cells for subsequent analysis is also contributing to the growth of the market. Other factors, including extensive research and development (R&D) activities in the field of biotechnology, along with the implementation of favorable government policies, are anticipated to drive the market toward growth.

Key Market Segmentation

Breakup by Technique:

Breakup by Cell Type:

Breakup by Product:

Breakup by Application:

Breakup by End Use:

Breakup by Region:

Key Questions Answered in This Report:

Key Topics Covered:

1 Preface

2 Scope and Methodology

3 Executive Summary

4 Introduction

5 Global Cell Isolation Market

6 Market Breakup by Technique

7 Market Breakup by Cell Type

8 Market Breakup by Product

9 Market Breakup by Application

10 Market Breakup by End Use

11 Market Breakup by Region

12 SWOT Analysis

13 Value Chain Analysis

14 Porters Five Forces Analysis

15 Price Analysis

16 Competitive Landscape

Companies Mentioned

For more information about this report visit https://www.researchandmarkets.com/r/a39mjl

Media Contact:

Research and MarketsLaura Wood, Senior Manager[emailprotected]

For E.S.T Office Hours Call +1-917-300-0470For U.S./CAN Toll Free Call +1-800-526-8630For GMT Office Hours Call +353-1-416-8900

U.S. Fax: 646-607-1907Fax (outside U.S.): +353-1-481-1716

Logo: https://mma.prnewswire.com/media/539438/Research_and_Markets_Logo.jpg

SOURCE Research and Markets

Read the original:
Cell Isolation Global Market Report 2022: Increasing Emphasis on Cell-Based Research Bolstering Growth - PR Newswire

Replay establishes distinguished Scientific Advisory Board of genomic medicine and cell therapy … – The Bakersfield Californian

Replay establishes distinguished Scientific Advisory Board of genomic medicine and cell therapy experts

San Diego, California and London, UK, October 17, 2022 Replay, a genome writing company reprogramming biology by writing and delivering big DNA, today announced that it has established a scientific advisory board (SAB) comprising ten experts across a broad range of areas of scientific importance in genomic medicine and cell therapy.

The newly formed SAB will provide input into Replays strategy, portfolio of next-generation genomic and cell therapy medicines, and associated technology platforms. The SAB complements Replays industry seasoned management team and board.

Adrian Woolfson, Executive Chairman, President and Co-founder of Replay, commented: The multi-disciplinary nature of our scientific advisory board reflects Replays commitment to invoking innovation from a broad range of scientific specialties and leveraging this across our research and development programs. Our new advisors represent some of the best scientific minds of their generation and bring a unique and differentiated portfolio of expertise into the Company. Their contribution to Replay will be invaluable as we continue to address some of the most significant challenges in genomic medicine and cell therapy.

Lachlan MacKinnon, Chief Executive Officer and Co-founder of Replay, added: Following on from our recent launch, the formation of our uniquely distinguished scientific advisory board further demonstrates Replays commitment to developing a cutting-edge portfolio of medicines guided by world-class science. The combined inter-disciplinary expertise of our scientific advisory board brings tremendous knowledge and experience into the Company as we continue to expand our operations, with a view to developing transformative genomic medicines.

Replays SAB will be chaired by Professor Roger Kornberg, PhD, a biochemist whose laboratory work has focused on the molecular basis of eukaryotic transcription and in particular the structure of RNA polymerase and the nucleosome.

Professor Roger Kornberg, PhD, Chairman of Replays Scientific Advisory Board, said: Replays scientific advisory board incorporates expertise across several areas relevant to Replays genomic medicine and cell therapy technology platforms. I am excited to be working with this exceptional group of scientists and believe we can make a compelling contribution and help Replay realize its vision for genomic medicine.

Replays SAB members are as follows:

Professor Roger D. Kornberg PhD (Chairman), is the Winzer Professor of Medicine in the Department of Structural Biology at Stanford University School of Medicine. He was awarded the Nobel Prize in Chemistry (2006).

Professor Carl H. June, MD, is the Richard W. Vague Professor in Immunotherapy in the Department of Pathology and Laboratory Medicine at the Perelman School of Medicine at the University of Pennsylvania. He is Director of the Parker Institute for Cancer Immunotherapy at the University of Pennsylvania, Director of the Center for Cellular Immunotherapies at the Perelman School of Medicine, and Director of Translational Research at the Abramson Cancer Center. He was the co-founder of TMunity.

Professor Robert S. Langer, ScD, FREng,is one of 12 Institute Professors at the Massachusetts Institute of Technology (MIT), co-founder of Moderna, and was formerly Chair of the FDAs Science Board. He has been awarded 40 honorary doctorates, written over 1,500 articles, and received over 220 awards.

Professor Lynne E. Maquat, PhD, is the J. Lowell Orbinson Endowed Chair and Professor of Biochemistry and Biophysics, University of Rochester Medical Center, and founding Director of the Center for RNA Biology, University of Rochester, Rochester NY. She was awarded the Wolf Prize in Medicine from Israel (2021) and the Warren Alpert Foundation Prize from Harvard Medical School (2021).

Professor Dame Carol Robinson, DBE FRS FMedSci FRSC, is the Dr Lees Professor of Physical and Theoretical Chemistry, the Founding Director of the Kavli Institute for Nanoscience Discovery at Oxford, and a Founder of OMass Therapeutics. She is a Professorial Fellow at Exeter College, Oxford, and was formerly President of the Royal Society of Chemistry.

Professor David V. Schaffer, PhD, is the Hubbard Howe Professor of Chemical and Biomolecular Engineering, Bioengineering, and Neuroscience at the University of California, Berkeley, where he is Director of theBakar BioEnginuity Hub and Director of the California Institute for Quantitative Biosciences (QB3). He was the co-founder of 4D Molecular Therapeutics, Ignite Immunotherapies, Rewrite, and 5 additional companies.

Professor Stuart L. Schreiber, PhD, is the Morris Loeb Professor of Chemistry and Chemical Biology at Harvard University. He is a co-founder of the Broad Institute at Harvard University and MIT and co-founder of Harvards Institute of Chemistry and Cell Biology. He was awarded the Wolf Prize in Chemistry (2016).

Professor Pamela Silver, PhD, is the Elliot T. and Onie H. Adams Professor of Biochemistry and Systems Biology in the Department of Systems Biology at Harvard Medical School, and a founding member of the Wyss Institute for Biologically Inspired Engineering at Harvard Medical School.

Professor Sir John E. Walker, FRS FMedSci, is Emeritus Director and Professor at the MRC Mitochondrial Biology Unit at the University of Cambridge, England, and a fellow of Sidney Sussex College, Cambridge. He was awarded the Nobel Prize in Chemistry (1997).

Professor John Fraser Wright, PhD, is Professor of Pediatrics, Division of Hematology, Oncology, Stem Cell Transplantation and Regenerative Medicine, and Director of Technology Innovation at the Center for Definitive and Curative Medicine at Stanford University. He is co-founder and was Chief Technology Officer at Spark Therapeutics and is co-founder and Chief Scientific Advisor at Kriya Therapeutics.

Ends

About Replay

Replay is a genome writing company, which aims to define the future of genomic medicine through reprogramming biology by writing and delivering big DNA. The Company has assembled a toolkit of disruptive platform technologies including a high payload capacity HSV platform, a hypoimmunogenic cell therapy platform, and a genome writing platform to address the scientific challenges currently limiting clinical progress and preventing genomic medicine from realizing its full potential. The Companys hub-and-spoke business model separates technology development within Replay from therapeutic development in product companies that leverage its technology platforms. For example, Replays synHSV technology, a high payload capacity HSV vector capable of delivering up to 30 times the payload of AAV, is utilized by Replays four gene therapy product companies, bringing big DNA treatments to diseases affecting the skin, eye, brain, and muscle. The Company has, additionally, established an enzyme writing product company that leverages its evolutionary inference machine learning and genome writing technology to optimize enzyme functionality. Replay is led by a world-class team of academics, entrepreneurs, and industry experts.

The Company raised $55 million in seed financing in July 2022 and is supported by an international syndicate of investors including: KKR, OMX Ventures, ARTIS Ventures, and Lansdowne Partners.

Replay is headquartered in San Diego, California, and London, UK. For further information please visit http://www.replay.bio and follow us on LinkedIn and Twitter.

Contacts:

Replay

Dr Adrian Woolfson/Lachlan MacKinnon

info@replay.bio

Consilium Strategic Communications Media relations

Amber Fennell/Tracy Cheung/Andrew Stern

replay@consilium-comms.com

See original here:
Replay establishes distinguished Scientific Advisory Board of genomic medicine and cell therapy ... - The Bakersfield Californian