Category Archives: Molecular Genetics

WALTHAM, Mass.--(BUSINESS WIRE)--BostonGene Corporation, a biomedical software company focused on defining optimal precision medicine-based therapies for cancer patients, today announced that three abstracts were selected for poster presentations at the 2020 American Association for Cancer Research (AACR) Virtual Annual Meeting II, which will be conducted from June 22 - 24, 2020.

The presentations describe findings obtained by using BostonGenes technologies and analytical tools designed to improve diagnosis and treatment decisions for cancer patients. Results include validation of bulk RNAseq utility for accurate reconstruction of tumor microenvironment and identification of four prominent microenvironment types conserved among solid tumors. Application of BostonGene computational tools lead to better understanding of the role of microenvironment compartments in tumor pathogenesis and supporting clinical decision making for the treatment of cancer.

We are excited to present at the 2020 AACR Virtual Annual Meeting to share the clinical utility of the BostonGene solution and demonstrate how it improves diagnosis and treatment decisions for cancer patients, said Andrew Feinberg, President and CEO of BostonGene.

Details of the poster presentations are as follows:

Abstract Number: 6168 Title: Integrated whole exome and transcriptome analyses of the tumor and microenvironment provide new opportunities for rational design of cancer therapy Session: Tumor Heterogeneity and Microenvironment: Next-Generation Sequencing, Single Cell, and ImagingPoster: 4418Presenter: Alexander Bagaev, BostonGene

BostonGene developed and validated a new analytic platform for multi-parametric analyses of malignant and nonmalignant tumor compartments using genomic and transcriptomic sequencing data. Application of BostonGene platform to more than 8,500 patient data sets revealed four types of tumor microenvironment (TME) that are conserved across cancer types and demonstrate high prognostic significance and differential response to immunotherapy. This novel Molecular-Functional (MF) portrait platform, involving analytic and visualization methods, provides a robust tool for prediction of response to immunotherapy and for future tailoring of personalized therapeutic combinations.

Abstract Number: 6997 Title: Novel machine learning based deconvolution algorithm results in accurate description of tumor microenvironment from bulk RNAseq Session: Machine Learning and Artificial Intelligence for Omics, Imaging, and Diagnostics Poster: 853Presenter: Alexander Bagaev, BostonGene

BostonGene developed a novel machine learning-based algorithm for cellular deconvolution of tumor microenvironment (TME) from bulk RNAseq data. This tool accurately reconstructs proportions of major immune and stromal cell populations, as well as T cell subtypes and M1 and M2 macrophages. Validation of BostonGene algorithm performance by comparison of flow cytometry, single cell RNAseq and bulk RNAseq analysis performed on samples from different tissues will be presented. The result demonstrates utility of bulk RNAseq for accurate and robust reconstruction of TME composition and paves the road for application of the BostonGene computational tool for support of clinical decision making for the treatment of cancer.

Research conducted with Massachusetts General Hospital

Abstract Number: 7544 Title: HER2 expression and M2-like tumor infiltrating macrophages associated with Cabazitaxel activity in gastric cancer Session: Predictive Biomarkers for Treatment Efficacy 1Poster: 2011Presenter: Sandipto Sarkar, Weill Cornell Medicine

In the clinical study of cabazitaxel efficacy in gastric cancer, comprehensive whole exome sequencing (WES) and RNAseq data analysis identified genetic aberrations and tumor microenvironment signatures associated with favorable response. In particular, this analysis resulted in identification of two novel biomarkers, HER2 overexpression and M2-high tumor macrophage signature, both of which associated with improved outcomes. RNAseq-based deconvolution demonstrating M2 macrophages enrichment in patients with improved PFS, was further validated by immunohistochemistry using M1 and M2 macrophage-specific markers.

Research conducted with Weill Cornell Medicine

The e-poster website will be launched June 22, 2020, the first day of the AACR Virtual Annual Meeting II. All e-posters will be made available for browsing on this date.

Additionally the abstracts will be published in an online-only Proceedings supplement to the AACR journal Cancer Research after the completion of the AACR Virtual Annual Meeting II.

About BostonGene Corporation

BostonGene Corporation is pioneering the use of biomedical software for advanced patient analysis and personalized therapy decision making in the fight against cancer. BostonGenes unique solution performs sophisticated analytics to aid clinicians in their evaluation of viable treatment options for each patient's individual genetics, tumor and tumor microenvironment, clinical characteristics and disease profile. BostonGenes mission is to enable physicians to provide every patient with the highest probability of survival through optimal cancer treatments using advanced, personalized therapies. For more information, visit BostonGene at http://www.BostonGene.com.

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BostonGene to Present Three Abstracts at the 2020 American Association for Cancer Research (AACR) Annual Meeting - Business Wire

Amid the COVID-19 pandemic, Val Sheffield is pivoting his research focus to find a way to test patients without using high demand cotton swabs.

University of Iowa Molecular Genetics Chair in the Carver College of Medicine Val Sheffield has made research breakthroughs in linking gene research and was recently named to a prestigious American research institutes class of 2020.

But amid the COVID-19 pandemic, Sheffield is pivoting his work to research an alternate way to test patients for novel coronavirus to alleviate a nationwide shortage of the parts in a COVID-19 test.

Sheffield and his team submitted a document April 1 to the FDA requesting emergency-use authorization to utilize a patient-sample collection method for COVID-19 testing.

My laboratory decided early on that we have the capability to help with [COVID-19] testing, Sheffield said. Testing is really important, but its behind where it should be because there arent enough official, FDA-approved swabs to collect samples from patients For the last month weve been trying to get FDA approval for our testing method where patients snort through the nose and spit into a tube, and the saliva sample is tested for the virus.

When the method is approved by the FDA, Sheffield said researchers can use it to test anyone. The most common coronavirus tests involve inserting a long cotton swab into a patients nostril. Sheffield anticipates beginning testing soon, with a limited number of patients in a study that will be the final step in getting FDA approval.

Iowa Gov. Kim Reynolds launched Test Iowa, a partnership between the state and private technology companies Domo, Qualtrics, and NomiHealth. But, the Test Iowa equipment was pending certification by the State Hygienic Lab to run tests as of Friday.

In Iowa, tests are being prioritized for those over the age of 60, with chronic health conditions, are in the hospital, or live in congregate living facilities such as a nursing home.

Iowa has tested more than 63,000 people and reported more than 10,000 cases as of Wednesday. Reynolds is using widespread testing as a signal that the state can begin the steps of reopening, seemingly going against the advice of University of Iowa researchers, who concluded that a second wave of COVID-19 cases could emerge without precautions in place.

In late April, amid his shifting work, Sheffield was elected to the 2020 class of the American Academy of Arts and Sciences.

Sheffield began as a faculty member at the UI 30 years ago and contributes to campus clinical work and research. He started as an assistant professor and has since branched out to administrative work, instruction, and research. He served as the UI Division Director of Medical Genetics for 22 years and stepped down in January to spend more time on research.

RELATED: National registrar association awards Sarah Harris with honorary membership after 30 years at UI

Sheffield has co-authored 330 peer-reviewed scientific papers, and said he has found supportive and outstanding collaborators who have been pivotal to his researchs success in his time at the UI.

My research focuses on hereditary blindness, he said. Ive worked on identifying genes that play a role in hereditary blindness. More recently, my team and I have been focusing on figuring out mechanisms by which mutations cause disease and developing treatments.

Sheffield said that his election has reinforced his obligation to serve and help others with his science. This will continue to fuel his desire to work hard and continue to further his research, Sheffield said.

David Ginsburg, James V. Neel Distinguished university professor at the University of Michigan Medical School, is also a member of the American Academy of Arts and Sciences. He first met Sheffield at the Howard Hughes Medical Institution.

Ginsburg said Sheffields research has been crucial to developing human genetic maps. Only a few academic scientists are elected to the U.S. organization a year, and Ginsburg said Sheffields election was well deserved.

Val is a fantastic physician scientist, Ginsburg said. Hes done landmark work figuring out what gene is defective for a whole variety of different, rare genetic diseases. He was one of the real pioneers tracking down these genes. He identified where the corresponding disease gene is located in our chromosomes for about 35 diseases When I was in medical school, we only knew the responsible gene for one human disease Today, we know the gene for about 6,000 human diseases, and Val was one of the early leaders in this work.

Ginsburg said he has seen how much members of the organization can grow once theyre inducted. Sheffield will be able to continue expanding his horizons in academia when he is inducted next spring, he added.

A big part of what drives what we do in academic medicine is interaction with colleagues and the new ideas that you get when meeting, talking, and interacting with colleagues in diverse fields, he said. Thats one of the greatest things the American Academy has to offer. I know it will give Val an opportunity to expand his research and intellectual contributions to the academic enterprise.

According to the American Academy of Arts and Sciences website, the 240-year-old American Academy of Arts and Sciences was founded by John Adams and John Hancock and aims to recognize scholars and leaders in various disciplines. Sheffield joins 11 other Hawkeyes already in the organization, including UI Cardiovascular Research Chair and Professor Francois Abboud.

Abboud said Sheffield, who he has known since 1990, is an internationally recognized leader in the field of human molecular genetics and genomics as well as someone he admires.

[Sheffield] is more than a great scientist, Abboud said. Ive always been impressed by his true commitment to his patients. What drives his scientific research is his extraordinary commitment to the patients. Science is his true passion. He is a brilliant scientist and an even more remarkable person.

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University of Iowa molecular genetics researcher studying COVID-19 testing methods to alleviate test shortages - UI The Daily Iowan

Transmission electron micrograph of SARS-CoV-2 virus particles, isolated from a patient. Image: National Institute of Allergy and Infectious Diseases, Flickr

For the sake of both science and action in the COVID-19 pandemic, we need collaboration among specialists, not sects.

The Brazilian-British biologist Peter Medawar won the Nobel Prize in 1960 for his study of acquired immune tolerance. Beyond his scientific work, he was also a gifted writer and expositor of scientific culture. One of the many treasures of his Advice to a Young Scientist (1979) is a passage in his chapter on Aspects of Scientific Life and Manners where he discusses techniques used in the hope of enlarging ones reputation as a scientist or diminishing the reputation of others by nonscientific means.

One such trick, Medawar writes, is to affect the possession of a mind so finely critical that no evidence is ever quite good enough (I am not very happy about. . . .; I must say I am not at all convinced by. . . .). After all, as he writes in a different passage, no hypothesis in science and no scientific theory ever achieves . . . a degree of certainty beyond the reach of criticism or the possibility of modification.

Scientists must resist the temptation to excessive skepticism: the kind that says no evidence is ever quite good enough. Instead they should keep their eyes open for any kind of information that can help them solve problems.

I share Medawars pragmatic vision of scientific reasoning. Scientists must resist the temptation to excessive skepticism: the kind that says no evidence is ever quite good enough. Instead they should keep their eyes open for any kind of information that can help them solve problems. Deciding, on principle, to reject some kinds of information outright, or to consider only particular kinds of studies, is counterproductive. Instead of succumbing to what Medawar calls habitual disbelief, the scientist should pursue all possible inputs that can sharpen ones understanding, test ones preconceptions, suggest novel hypotheses, and identify previously unrecognized inconsistencies and limitations in ones view of a problem.

This conception of science leads me to disagree with some elements of the philosopher of medicine Jonathan Fullers recent essay about two sects within epidemiology, defined by what kinds of evidence they consider meaningful and how they think decisions should be made when evidence is uncertain. Fuller sees in the contrast two competing philosophies of scientific practice. One, he says, is characteristic of public health epidemiologists like me, who are methodologically liberal and pragmatic and use models and diverse sources of data. The other, he explains, is characteristic of clinical epidemiologists like Stanfords John Ioannidis, who draw on a tradition of skepticism about medical interventions in the literature of what has been known since the 1980s as evidence-based medicine, privilege gold standard evidence from randomized controlled trials (as opposed to mere data), and counsel inaction until a certain ideal form of evidenceEvidence with a capital Ejustifies intervening.

Fuller rightly points out that this distinction is only a rough approximation; indeed, there are many clinical epidemiologists who do not share the hardline skepticism associated with the most extreme wing of the evidence-based medicine community. But the distinction is also misleading in a subtle way. If the COVID-19 crisis has revealed two competing ways of thinking in distinct scientific traditions, it is not between two philosophies of science or two philosophies of evidence so much as between two philosophies of action.

If the COVID-19 crisis has revealed two competing ways of thinking, it is not between two philosophies of science or two philosophies of evidence so much as between two philosophies of action.

In March, as health systems in Wuhan, Iran, and Northern Italy teetered under the weight of COVID-19 cases, Ioannidis cautioned that we really didnt know enough to say whether a response was appropriate, warning of a once-in a-century evidence fiasco and suggesting that the epidemic might dissipate on its own. (I replied to that argument, explaining why we do know enough to act decisively against this pandemic.) To my knowledge, Ioannidis has never stated that early interventions should have been avoided, but by repeatedly criticizing the evidence on which they were based, he gives that impression.

On the question of how we interpret evidence, Fuller concludes that to understand the scientific disagreements being aired about COVID-19, we need to blend the insights of each camp. Cooperation in society should be matched by cooperation across disciplinary divides, he writes. I dont understand what this kind of bothsidesism means when one side is characterized as accepting many types of evidence and the other as insisting on only certain kinds. On the question of how we should make decisions under uncertainty, of course more data are better. But decisions are urgent and must be made with the evidence weve got.

This is not to deny that there are different and valuable perspectives on epidemiology. Like any other field, there are many specialties and subspecialties. They have different methods for how they study the world, how they analyze data, and how they filter new information. No one person can keep up with the flood of scientific information in even one field, and specialization is necessary for progress: different scientists need to use different approaches given their skills, interests, and resources. But specialization should not lead to sectsin this case, a group of scientists who accept only certain kinds of evidence and too rigidly adhere to a philosophy of non-interventionism.

Infectious disease epidemiologists must embrace diverse forms of evidence by the very nature of their subject. We study a wide range of questions: how and under what conditions infectious diseases are transmitted, how pathogens change genetically as they spread among populations and across regions, how those changes affect our health, and how our immune systems protect us and, sometimes, make us vulnerable to severe illness when immune responses get out of control. We also seek to understand what kinds of control measures are most effective in limiting transmission. To understand these issues for even one type of diseasesay, coronavirus diseasesrequires drawing on a wide range of methodologies and disciplines.

On the question of how we should make decisions under uncertainty, of course more data are better. But decisions are urgent and must be made with the evidence weve got.

We consider evidence from classical epidemiological studies of transmission in households and other settings. We consider immunological studies that show us how markers of immunity develop, whether they protect us against future disease, and how particular markers (say a certain type of antibody directed at a certain part of the virus) change infection and mortality rates. We consider molecular genetics experiments, including those conducted in animal models, that tell us how changes in a viruss genome affect the course of disease. We consider evolutionary patterns in the viruss genetic code, seasonal patterns in its transmission and that of other related viruses, and observational studies of the risk factors and circumstances favoring transmission. And, of course, we also consider randomized trials of treatments and prevention measures, when they exist, as we seek to understand which interventions work and which ones may do more harm than good.

The upshot is that, done well, epidemiology synthesizes many branches of science using many methods, approaches, and forms of evidence. No one can be expert in all of these specialties, and few can even be conversant in all of them. But a scientist should be open to learning about all of these kinds of evidence and more.

Thinking about evidence from diverse specialties is critical not only for weighing evidence and deciding how to act but also for developing hypotheses that, when tested, can shed light across specialties. Appropriate humility dictates that molecular virologists should not assume they are experts in social epidemiology, and vice versa. To say Im a virologist, so Im not going to account for any findings from social epidemiology in my work gives up the chance to understand the world better.

Heres an example. In the case of a new virus like SARS-CoV-2, the fact that socioeconomically disadvantaged people get sick more often than the wealthy gives clues, which we dont yet know how to interpret, about the way the virus interacts with hosts. It would be informative to a virologist to distinguish the following two hypotheses (among others): (a) exposure to high doses of virus tends to cause severe disease, and disadvantaged people are often exposed to higher doses due to confined living and working conditions, or (b) comorbidities such as heart disease and obesity are higher among disadvantaged people, and lead to more severe outcomes. Of course, either, both, or neither of these hypotheses may turn out to be important explanations, but the canny virologist should wonder and think about how to distinguish them experimentally and test results against data from human populations. Reciprocally, a canny social epidemiologist should look to virological studies for clues about why COVID-19, like so many other illnesses, disproportionately harms the least advantaged in our society.

Done well, epidemiology synthesizes many branches of science. No one can be expert in all of these specialties, and few can even be conversant in all of them, but a scientist should be open to learning about all of these kinds of evidenceand more.

In practice, virologists, immunologists, and epidemiologists are different specialists who often work far apart and almost never attend each others seminars. I do not think we should spend all our time learning each others disciplines. But I do think that a scientist who genuinely wants to solve an important problem should be open to evidence from many sources, should welcome the opportunity to expand their list of hypotheses, and should seek to increase their chances both of making a novel contribution to their field and of being right. Central to this effort is considering information from diverse kinds of studies performed by people with diverse job titles in diverse departments of the universityas well as their diverse forms of data and argumentation.

When we move from the realm of understanding to the realm of intervention, the need for openness to different sources of evidence grows further. In some cases, like whether to use a drug to treat infection or whether to use a mask to prevent transmission, we can draw on evidence from experiments, sometimes even randomized, controlled, double-blind experiments. But in deciding whether to impose social distancing during an outbreak of a novel pathogenand in thinking about how the course of the epidemic might play outit would be crazy not to consider whatever data we can, including from mathematical models and from other epidemics throughout history. With infectious diseases, especially new and fast-spreading pandemics, action cant wait for the degree of evidentiary purity we get from fully randomized and controlled experiments, or from the ideal observational study. At the same time, we must continue to improve our understanding while we act and change our actions as our knowledge changesleaving both our beliefs and our actions open, as Medawar says, to the reach of criticism and the possibility of modification.

Where does the skepticism so characteristic of the evidence-based tradition come from? One reason may be the habits and heuristics we absorb from textbooks, colleagues, and mentors.

In supervising students and postdocs, inculcating these habits is one of the most challenging, gratifying, and time-consuming parts of scientific trainingfar more than teaching technical skills. Some of these rules of thumb are well suited to science in general and serve us well throughout our careers, no matter the field. Among these are workaday but important heuristics like: consider alternative hypotheses; look at raw data whenever possible before looking at processed data; and repeat experiments, especially those whose results surprise you. Indeed, these heuristics can be summarized as a form of intense skepticism directed at ones own work and that of ones team: find all the flaws you can before someone else does; fix those you can and highlight as limitations those which are unfixable. Recently an advanced PhD student said to me: I read your new idea that you shared on Slack this morning and Ive been doing my best all afternoon to break it. It made my day, and made me think I probably had very little left to teach her.

Scientists of all stripes should work together to improve public health, and none should mistake a professional tendency or a specialists rule of thumb for an unshakable epistemological principle.

Other heuristics, however, are more specific to a narrow field and may be ill suited to other contexts. Insisting on gold standard, randomized trial evidence before prescribing drugs to prevent heart attacks or before performing a certain surgical operation may be a good rule of thumb in medicine (though not all physicians or even philosophers agree). But randomized controlled trials are not available for huge swaths of scientific inquiry, and the narrow populations often studied in such trials can limit their applicability to real-world decision making. Nor are they always available when we need them: they require a lot of time and administrative resources to execute (and money, for that matter). Stumping for Evidence is thus useful in many parts of clinical medicine but impractical in many other aspects of science-informed decision making. Applying this doctrine indiscriminately across all areas of science turns the tools of a specialist into the weapons of a sectarian.

This point was appreciated by some of the pioneers of evidence-based medicine: David Sackett, William Rosenberg, J. A. Muir Gray, R. Brian Haynes, and W. Scott Richardson. Evidence-based medicine is not restricted to randomized trials and meta-analyses, they wrote in 1996. It involves tracking down the best external evidence with which to answer our clinical questions. And last week the Oxford professor of primary care Trisha Greenhalgh, another major contributor to this field and author of a popular textbook on evidence-based medicine, suggested that in the realm of social interventions to control the spread of COVID-19, the evidence-based clinical paradigmwaiting for the definitive [randomized controlled trial] before taking actionshould not be seen as inviolable, or as always defining good science.

Indeed, on the question of how we ought to act during an outbreak, two leading epidemiologists in the clinical tradition, Hans-Olov Adami and the late Dimitrios Trichopoulos, argued that the non-interventionist rule of thumb is suitable for chronic, noncommunicable diseases but foolish for fast-moving infectious diseases. In an editorial accompanying an article that showed that the impact of cell phones in causing brain cancer was not large but might be larger than zero, they counseled cautious inaction in regulating cell phones. But they noted this is not how you would reason in the case of a transmissible disease:

There is another lesson to be learned about the alarms that have been sounded about public health during the past few years. When the real or presumed risk involves communicable agents, such as the prions that cause bovine spongiform encephalopathy (mad cow disease), no precaution, however extreme, can be considered excessive. By contrast, for noncommunicable agents, such as radio-frequency energy, the lack of a theoretical foundation and the absence of empirical evidence of a substantial increase in risk legitimize cautious inaction, unless and until a small excess risk is firmly documented.

In my ideal public health world wed have a lot more good sense like that proposed by Adami and Trichopoulos, acting not only on the strength of the evidence we have but on the relative harms of being wrong in each direction. And whether waiting or acting, wed work hard to get the evidence to meet the challenges of skeptics and improve our decision-making, all with an eye to the possibility of criticism and modification Medawar describes.

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Good Science Is Good Science - Boston Review

Wayne W. Grody, Joshua L. Deignan, in Emery and Rimoin's Principles and Practice of Medical Genetics, 2013

This article is a revision of the previous edition article by Wayne W Grody, volume 1, pp 601626, 2007, Elsevier Ltd.

Molecular genetic testing has a unique range of indications, most of which are quite different from the uses of traditional clinical laboratory testing and even molecular biologic testing in other disease classes (e.g. infectious disease, cancer). The technical approaches as well as the psychosocial and ethical implications of molecular genetic tests may vary substantially depending on the reason for testing (e.g. diagnostic, carrier screening). Just as many of the applications are unique, so too the types of patient samples collected for molecular genetic testing may be different from those obtained for other types of clinical laboratory testing. In addition, the choice of technique will depend on the nature of the disease gene being studied (especially its size and mutational heterogeneity), the purpose of the test, and to some extent the condition of the specimen, and examples of specific conditions are discussed. Finally, high complexity laboratories performing molecular genetic testing need to be aware of the specific regulatory considerations involved.

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Molecular Genetics - an overview | ScienceDirect Topics

History is written by the victors. Its a quote often attributed to Winston Churchill, and its certainly true of many discoveries in science, where being the first to publish a major finding is enough to secure your name in the history books (or at least in the science textbooks)

The book, The Double Helix, is a dramatic tale of how American geneticist James Watson and British molecular biologist Francis Crick discovered the structure of DNA back in the early 1950s. Of course, being written by Watson himself, its no surprise that hes the dashing hero of the story.

Big names like Watson and Crick take much of the glory for the discovery of the structure of DNA, while others like Maurice Wilkins, Rosalind Franklin and Ray Gosling are increasingly recognized for their contributions. But there are still many others whose work contributed to our understanding of the structure and function of DNA, such as Johannes Friedrich Miescher, Fred Griffith, Oswald Avery, Rudolf Signer and Elwyn Beighton.

In this episode of Genetics Unzipped, geneticist Kat Arney talks with Gareth Williams, professor emeritus at the University of Bristol and author of Unravelling the Double Helix: The Lost Heroes of DNA, to explore some of the lesser-known stories and names behind the discovery of the structure and function of DNA.

Full transcript, links and references available online atGeneticsUnzipped.com

Genetics Unzippedis the podcast from the UKGenetics Society,presented by award-winning science communicator and biologistKat Arneyand produced byFirst Create the Media.Follow Kat on Twitter@Kat_Arney,Genetics Unzipped@geneticsunzip,and the Genetics Society at@GenSocUK

Listen to Genetics Unzipped onApple Podcasts(iTunes)Google Play,Spotify,orwherever you get your podcasts

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Podcast: Twisted historyThe true story of how the DNA double helix was discovered - Genetic Literacy Project

In Avatar, James Camerons 2009 science-fiction epic, the resource-rich world of Pandora is covered in tropical rainforests, all glowing with luscious phosphorescence like some kind of underwater paradise. According to a Wired article published at the time of the movies release, Cameron hired a plant sciences specialist from the University of California, Riverside. The specialist spent weeks writing detailed scientific explanations for the dozens of flora on Pandora, explaining exactly how their alien bioluminescence works. After all, no such thing exists on our planet. Right?

Hold that thought. Because a team of international researchers this month announced that they have created plants that produce a visible, glowing green luminescence. The results could potentially be used for everything from better studying the inner workings of plants to producing aesthetically interesting flower displays for rave-inspired weddings. Its probably too early to write to your city council to suggest swapping out street lighting for glowing trees, but its not entirely out of the question either!

There are many possible applications of this technology, Keith Wood, CEO of Light Bio, the company that could one day bring this work to market, told Digital Trends. Most notably [it could] allow scientists to observe the living processes occurring within plants, and to allow the general public to experience the internal living energy within [these same] plants. Specifically, we are referring to the possibility of house plants and flowers that glow in the dark.

The light-emitting plants were developed by inserting bioluminescent DNA from a mushroom into a tobacco plant. Tobacco plants were used because of their simple genetics and rapid growth, although other plants could be utilized in the future. Feasibility has already been shown with plants including periwinkle, petunia, and rose. Plants that contain the mushroom DNA glow continuously throughout their lifespan (not just at night), all the way from seedling through to mature plant.

The project was carried out by researchers at Moscow biotech company Planta, working with the Institute of Bioorganic Chemistry of the Russian Academy of Sciences, MRC London Institute of Medical Sciences, and the Institute of Science and Technology Austria, and others. Light Bio is the company spun out to bring these luminescent plants to market in ornamental house plants, in partnership with Planta.

Bioluminescence is one of the most fascinating and diverse phenomena found in nature, Wood explained. Many scientists worldwide are working to better understand the underlying foundations for these living lights. They also recognize that these have many practical and aesthetic applications.

The work was led by Dr. Ilia Yampolsky, who discovered the biochemical basis for bioluminescence in mushrooms. The unique insight was not just discovering the natural bioluminescence found in some mushrooms, but also that it was unexpectedly compatible with the basic metabolism common to all plants. Through collaboration, the researchers formulated their hypothesis that glowing plants may be a real feasible possibility.

This is not the first time that researchers have explored bioluminescence in plants. In 1985, Light Bios founder Wood was harnessing the underlying chemistry and molecular biology responsible for the fireflys glow to create glowing plants (again, of the tobacco variety) by inserting the relevant DNA. Since then, researchers have continued to explore the concept every few years. In 2017, for instance, Massachusetts Institute of Technology researchers were able to get an otherwise ordinary watercress plant to emit a dim light for a period of 3.5 hours by embedding specialized nanoparticles into its leaves.

The problem with all of these attempts? That the resulting plants simply were not that bright. This is what the new work, published in a recent paper in the journal Nature Biotechnology corrects. As its authors write:

Autoluminescent plants engineered to express a bacterial bioluminescence gene cluster in plastids have not been widely adopted because of low light output. We engineered tobacco plants with a fungal bioluminescence system that converts caffeic acid (present in all plants) into luciferin and report self-sustained luminescence that is visible to the naked eye. Our findings could underpin development of a suite of imaging tools for plants.

According to the researchers, the plants can reportedly produce more than a billion photons per minute. Thats enough that the results should be clearly visible. And it should be entirely possible to use the same technique to make future plants glow even brighter. It might even be feasible to integrate features like changing levels of brightness as a direct response to a plants surroundings. Or for the colors to cycle accordingly.

Smart home lights that change their brightness or hue depending on what youre doing are commonplace now. But a plant that does the same thing? Thats sure to start a conversation or two at your next house party. (When such things are once again possible.) Where do we place our pre-orders?

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Avatar IRL? Scientists have cracked the code to bioengineering plants that glow - Digital Trends

Lou Siminovitch, circa 1963, studying viruses.

John Dirks is the emeritus president and scientific director of the Gairdner Foundation.

At a time when medical science is playing the key role in treating the global COVID-19 pandemic, it is only appropriate that we celebrate the 100th birthday of molecular biologist, scientific leader and genetics pioneer Dr. Louis Siminovitch today. After all, Lou as he is affectionately known is considered by many to have had the most substantial impact on Canadian medical science in our time.

The works of English architect Christopher Wren are so prominent in London that his bequest can be found, as the famous quote goes, if you just look around you, and the same can be said of Lou in Toronto, where a constellation of notable research institutes, hospitals and networks of top scientists will speak to his legacy. And when Lou has felt Canadian science was running behind in quality or slow to engage new advances like genomics, he has energetically stepped up to the plate to forcefully challenge the political and academic powers of the day through his powerful pen lots and lots of letters to turn things around.

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One can only stand in awe," said Henry Friesen, the founder of the Canadian Institutes of Health Research, of the profound influence Lou Siminovitch has had in inspiring so many young students, building and developing major scientific institutions, and offering decision makers wise counsel in cultivating a more robust science culture in Canada.

So how did Lou become such a respected icon? He was born in Montreal of Eastern European parents who lived near the poverty line and had little interest in learning and culture. In high school, Lou was a so-so student, surrounded by many who spent their time in leftist politics. He entered McGill with an interest in chemistry and, stimulated by a top professor, made science his career choice.

Lou embarked on a PhD in physical chemistry, graduating in 1944. He married Elinore, who typed his thesis, and they moved to Ottawa and Chalk River. There, he worked on nuclear research, meeting every day with bright scientists such as Italian physicist Bruno Pontecorvo (who later defected to the Soviet Union), kindling Lous excitement in science.

Lou has a habit of riding the ways of fortune between opportunity, despair and joy. When his interest turned to biology he likes to say that he has a high mutation rate, seeking new challenges and new fields every 10 years he met French and Canadian scientist Louis Rapkine, who invited Lou to join his lab in Paris where he became a successful experimenter. But Rapkine died suddenly, leaving Lou with no mentor and no lab.

Instead, Lou managed to join the high-level lab of Andr Lwoff, Jacques Monod and Franois Jacob at the Pasteur Institute. Those three men shared the Nobel Prize in Medicine in 1965, and in that period, Lou produced some of his most original scientific work. Collaborating with those giants, who rigorously explored big questions, branded Lou with the principle that defines him: Nothing less than excellence is good enough. What distinguishes Lou was that he has had no tolerance for compromise on excellence in science," said Calvin Stiller, a colleague of Lous for 50 years. "He literally snorts when he observes mediocrity; he senses bogus in a blink.

In 1953, ready to return to Canada, Lou joined the famed Connaught Laboratories in Toronto the city he has made his home, and where he began distinguishing himself through a parade of remarkable opportunities. In 1956, prominent Canadian histologist Arthur Ham appointed Lou to the Ontario Cancer Institute, where he established his independent research career with critical studies in the stem cell discovery and cancer research, and rapidly became the head of biological research. In 1968, he was invited to chair a new department in the University of Torontos medical school that incorporated genetics and immunology, two themes that had been missing in the faculty; this grew into a major research unit.

In 1978, Lou became head of genetics at SickKids hospital, again bringing in new talent and technologies, and setting the stage for world-class accomplishment in cloning genes like cystic fibrosis. And in 1984, while concurrently shaping a new research institute at the Baycrest geriatric centre for Joe Rotman, he was asked to develop a brand new research institute at Mount Sinai Hospital, with up-to-date molecular biology related to major diseases. He recruited stars like Tony Pawson, Janet Rossant and many more in the creation of the Lunenfeld-Tanenbaum Research Institute arguably the pinnacle of his achievements.

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Lou deeply influenced research development at the University of Toronto and many Canadian institutions, as well as the national and provincial research funding agencies. But in building all these institutions, he was the one sought out to lead he never applied for any position.

His advice is constantly and widely sought and usually heeded. Its impossible for me to convey how much I learned from Lou through all those years and how much I owe him," said David Naylor, the former president of the University of Toronto. The advice came at lunches where the real menu was on Lous cue cards with its list of topics to be discussed or at other times in long, meticulously argued emails. Many Canadian leaders had the same experience.

Highly esteemed, Lou has received many awards and honorary degrees, including the Companion of the Order of Canada, the Canada Gairdner Wightman Award and induction to the Canadian Medical Hall of Fame. Internationally, he is one of few Canadians elected to both the Royal Society of the U.K. and the U.S. National Academy. He was truly one of the great medical builders of his day, a list that includes John Evans, Fraser Mustard and Jacques Genest, to name just a few.

Lou placed major emphasis on cultivating talent, creating intellectual descendants and finding outstanding leaders who have truly innovated and not many make his A-list. Lous science will never die, in that he has generated not only ideas, but offspring who will continue to carry out his work," said Montreal physician Phil Gold.

Lou can be described in many ways. Hes a driver of excellence and deeply committed to the idea that science can solve societal problems. Hes an institution, remembering how things happened and still worrying about where Canada stands as a nation in the world of science today. Hes a disturber of the status quo and a skilled science politician. Hes a passionate family man and, prompted by his playwright wife, he became an avid pursuer of culture in the arts and humanities, and the Elinore & Lou Siminovitch Prize in Theatre was developed by friends. Clearly, Lou could bridge the sciences and the arts.

And he is still the same old Lou. He goes to the office most days, surrounding himself with pictures of great art, mentors and family. He reads voraciously, absorbing daily newspapers, journals such as Science and Nature, as well as the books of the day. As he always says: I am still here.

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As a centenarian who still stimulates and provokes, and who still yearns to build a better place, Lou deserves a public toast. We might not be able to do that right now, as we wrestle with the novel coronavirus and all its devastation. But as scientists fight the deadly infection, its a perfect time to remember the scientific foundations that this giant of Canadian medicine laid down. So on behalf of scientists from coast to coast to coast Canada has been good to me, he likes to say, and the same is true in reverse we raise a glass to you, Lou.

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Im still here: Celebrating the 100th birthday of Lou Siminovitch, a giant of Canadian science - The Globe and Mail

Six weeks ago, with little fanfare, a network of geneticists launched an obscure but potentially game-changing initiative. Their aim: to learn why people with particular DNA profiles end up dying from the coronavirusor completely avoiding its effects. Ultimately, they want to devise ways for scientists to cook up new therapies that might alter how our nanosize genes operate as a way of reversing or accelerating the pathogens progress. Called the COVID-19 Host Genetics Initiative, the project now involves close to 700 scientists and researchers, worldwide, who are busily comparing DNA data from pandemic victims to literally millions of existing DNA profiles of millions of people.

To appreciate how our genes might be impacted by the onslaught of COVID-19, imagine this: that a tiny, invisible bug is hovering over the surface of a cell inside your bodysay a lung cell. You dont know it yet, but youve just been infected with SARS-Cov-2. Maybe it came from that jogger who whizzed past you on the sidewalk, or that tabletop you touched before rubbing your eyes. Whatever its source, there it is, circulating inside you: a fuzzy, sphere-shaped pathogen thats less than 1/1000 the width of a human hair. Prickly, with spikes on its outside, its searching for a place to plug into and enter your cell. Its a little like a key and a lock, where the key (the virus) wants to slip into the keyhole (a receptor on the cell) and then release a payload that will be up to no good.

Except that, in some people, the virus-key doesnt fit the lock and is blocked from entering the cell. In others, it slips right in, leading to illness and sometimes to rapid deterioration and even death. One potential differencesay geneticists who are working day and night to better understand how SARS-Cov-2 invades and attacks our cellsmight be because your DNA code differs from mine. Yours might inherently spurn the virus at the cellular level; mine might make me more susceptible.

So what determines who gets dangerously sick? We know that people who are older and have underlying diseases like diabetes and heart disease are at higher risk for having a bad response to COVID-19, explained Mark Daly, a 52-year-old geneticist and the director of the Institute for Molecular Medicine in Helsinki, Finland. Other factors include higher risk biases that involve ethnicity, class, vocation, geographic location, and the medical resources available at the time of treatment. And yet, according to Daly, this doesnt explain why relatively healthy people, including young people, are sometimes having severe and life-threatening reactions such as very high fevers, pneumonia, and difficulty with breathing that requires oxygen and sometimes a ventilator. Most likely this has something to do with differences in their genes.

Daly should know. With his Paul Reverelike ponytail, circular hippie glasses, and lean, determined face, hes a pioneer of modern genetics who was a key player during and after the Human Genome Project, the huge international effort in the 1990s and early 2000s that sequenced the first-ever human genome. And as the pandemic has been raging, Daly, a physicist, decided to help spearhead a remarkable hive-mind effort: the COVID-19 Host Genetics Initiative.

The project was announced on March 16 in a tweet posted by Dalys cohort Andrea Ganna: Goal: aggregate genetic and clinical information on individuals affected by COVID-19. The response was immediate. Within days, scientists from over 150 organizations in more than 30 countries on six continents agreed to join. Thats the ideal use of the hive mind: a conglomeration of big brains and, in this case, their disparate data sources, to solve one huge problem. Participants have come not only from Harvard and MIT (institutions with which Daly has ongoing affiliations) and the usual institutional suspects in North America, Europe, and the wealthier Asian countries, but also from the Qatar Genome Program, Vietnams SARS-Cov-2 Susceptibility Program, and CLHORAZbased in Burkina Faso.

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What Do Your Genetics Have to Do With Your Chances of Dying From Coronavirus? - Vanity Fair

Hunters and wild meat lovers are being warned that the practice of eating wild meat could result in the spread of more viruses.

Dr Christine Carrington, Professor of Molecular Genetics and Virology and Head of the Department of Preclinical Sciences, Faculty of Medical Sciences at the University of the West Indies, St. Augustine, said its believed that the novel coronavirus may have been transmitted to humans from bats.

Its almost certain that its ancestor was a bat virus but its still not clear whether that virus moved from bats directly to humans or from bats to another species and then to humans.

The real risk comes from wild animals. All the wild animals out there that have a lot of viruses in them. When we encroach on them or we consume them or we butcher them, theres always the chance of getting infected by viruses that they carry.

However, she said wild animals are not to blame, but humans who insist on hunting and eating them.

The problem is our encroachment into their habitats and our destruction of their habitats. What were doing is creating more opportunities for viruses to jump from animal populations into human populations.

She said another factor which led to the rapid spread of the virus is air travel, which allows human hosts to transmit viruses from country to country within hours.

When somebody gets infected the chance of them moving that virus and spreading it to other people is much greater now than it was before.

Armadillos, locally known as tattoos, are a popular wild meat option and can carry leptospirosis and leprosy.

According to Smithsonian, armadillosare the only other animals besides humans to hostthe leprosy bacillus.

Leptospirosisis a bacterial infection obtained from animals including cattle, sheep, goats and deer.

Leprosy (Hansen's disease) is an infectious disease which can affect the nerves of hands, feet, nose, skin and respiratory tract.

In 2011, theNew England Journal of Medicine publishedan articleformally linked the creature to human leprosy casespeople and armadillos tested in the study both shared the same exact strain of the disease.

Studies have shown that red howler monkeys can also become infected by malariaand yellow fever which are transmitted via mosquitos. Red howler monkeys are protected by law.

Hunting is prohibited by law fromMarch 1st to September 30th each year.

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Beware wild meat: UWI doctor looks at connection to virus spread - Loop News Trinidad and Tobago

NewsNarissa FraserYesterdayImage courtesy CDC

CHRISTINE Carrington, UWI professor of molecular genetics and virology, says reports of covid19 re-infection should be looked at "very carefully" as this possibility remains uncertain and unconfirmed.

At the Health Ministry's virtual press briefing on Thursday, Dr Carrington noted international reports of people who recovered from the virus but later tested positive. She said people have been using this as evidence of the possibility of re-infection, but cautioned that scientists are uncertain of this.

"It is possible that some of the genetic material from the virus remains in their body after they have been declared free of the virus itself. And that sort of 'genetic junk' that's left over can be detected by the test."

She said she recently read a study where samples were taken from supposedly re-infected patients to see if the virus detected was infectious, but it was not.

"It does not appear to be a true re-infection, it seems when people are infected they mount an immune response that protects them from further infection.

"What we don't know is how s that immune response is and how long it lasts."

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Virology professor: Possibility of covid19 re-infection still unconfirmed - Trinidad News