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Zenith Epigenetics Triple Negative Breast Cancer Clinical Data Highlighted in an Oral Discussion at the American Society of Clinical Oncology…

Posted: June 22, 2022 at 2:35 am

CALGARY, Alberta, June 21, 2022 (GLOBE NEWSWIRE) -- Zenith Epigenetics Ltd. (Zenith or the Company) announced today that the data from its Phase 2 Metastatic Triple Negative Breast Cancer (mTNBC) clinical trial combining ZEN-3694 + Pfizer Inc.s Talzenna (talazoparib) was highlighted at an oral session Optimizing Targeted Therapies in Advanced Breast Cancer: Building on Past Success. The discussant presented the novel concept of administering ZEN-3694, a bromodomain and extraterminal (BET) inhibitor (BETi), to sensitize resistant mTNBC tumors to talazoparib, a poly (ADP-ribose) polymerase (PARP) inhibitor (PARPi), and the clinically meaningful response rate and manageable safety profile of the combination from the Phase 2 study. Selection of an abstract for an oral discussion is a very competitive process with only 24 of the more than 125 accepted abstracts selected for this presentation format. The poster can be viewed on Zenith Epigenetics website (Poster) and the discussion can be viewed on the ASCO website (Discussion).

The data from the Phase 2 trial demonstrate that the ZEN-3694 plus talazoparib combination regimen, with a clinically meaningful response rate of 32% in a defined population, has the potential for treating patients whose tumors do not harbor germline mutations in BRCA1/2, said Dr. Philippe Aftimos, a principal investigator and medical oncologist at The Institut Jules Bordet in Brussels, Belgium. This combination is active with a manageable safety profile and warrants continued clinical evaluation. Zenith has expanded the Phase 2 trial to continue to evaluate the combination in an additional 120 mTNBC patients (NCT03901469).

In conjunction with ASCO, Zeniths TNBC poster was also awarded the GRASP Advocate Choice Award and selected to be discussed at theGRASPPoster Walkthroughs. GRASP, which standsfor Guiding Researchers and Advocates for Scientific Partnerships,is a patient-led organization that brings together patients, clinicians, and researchers to exchange ideas and learn from each other to accelerate scientific breakthroughs. GRASP Poster Walkthroughs are small group discussions of selected posters presented at scientific conferences such as ASCO.

We are very pleased that the data from our mTNBC clinical study, conducted in collaboration with Pfizer, was well received and recognized at ASCO, said Don McCaffrey, CEO of Zenith Epigenetics. The combination regimen of ZEN-3694 + talazoparib has shown promising clinical activity in a mTNBC patient population with significant unmet need. We continue to advance this program toward registration and are committed to bring an important therapy to these patients.

About Zenith and ZEN-3694

Zenith Epigenetics Ltd., a wholly-owned subsidiary of Zenith Capital Corp., is a clinical stage biotechnology company focused on the discovery and development of novel therapeutics for the treatment of cancer and other disorders with significant unmet medical need. Zenith Epigenetics is developing various novel combinations of BET inhibitors with other targeted agents. The lead compound, ZEN-3694, is in clinical development for various oncologic indications, specifically:

About Triple Negative Breast Cancer (TNBC)

TNBC is an aggressive form of breast cancer with low survival rates. TNBC accounts for about 10-15%of all breast cancers and it differs from other types of invasive breast cancer in that it tends to grow and spread faster, has fewer treatment options, and tends to have a worse prognosis. The termtriple-negative breast cancerrefers to the fact that the cancer cells have only low or no amount of the receptors ER, PR, and HER2. Approximately 75,000 women in the US, Japan and the major EU countries are diagnosed with TNBC each year.

About ZEN-3694 + Talazoparib Combination

In the United States, talazoparib is currently approved under the brand name TALZENNA, which is a PARP inhibitor indicated for the treatment of adult patients with deleterious or suspected deleterious germline BRCA-mutated (gBRCAm) HER2-negative locally advanced or metastatic breast cancer. ZEN-3694, in combination with talazoparib, is being developed for targeting tumors that do not have a germline BRCA mutation which represent approximately 89% of TNBC tumors. Preclinical and clinical data has shown that BET inhibition may reduce the levels of DNA repair proteins such as BRCA1/2 and RAD51 and thus create synthetic lethality in wildtype BRCA1/2 TNBC tumors when combined with PARP inhibition.

For further information, please contact:

Investor Relations & Communications

Zenith EpigeneticsPhone: 587-390-7865Email: info@zenithepigenetics.comWebsite:www.zenithepigenetics.com

This news release may contain certain forward-looking information as defined under applicable Canadian securities legislation, that are not based on historical fact, including without limitation statements containing the words "believes", "anticipates", "plans", "intends", "will", "should", "expects", "continue", "estimate", "forecasts" and other similar expressions. In particular, this news release includes forward looking information relating to the Companys development activities involving ZEN-3694 in combination with Pfizers PARP inhibitor Talzenna, and other targeted agents used in precision oncology, as well as other planned PARPi based combination therapy clinical trials in other tumor types. Our actual results, events or developments could be materially different from those expressed or implied by these forward-looking statements. We can give no assurance that any of the events or expectations will occur or be realized. By their nature, forward-looking statements are subject to numerous assumptions and risk factors including those discussed in our most recent MD&A which are incorporated herein by reference and are available through SEDAR at http://www.sedar.com. The forward-looking statements contained in this news release are expressly qualified by this cautionary statement and are made as of the date hereof. Zenith disclaims any intention and has no obligation or responsibility, except as required by law, to update or revise any forward-looking statements, whether as a result of new information, future events or otherwise.

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Genetics proposes, epigenetics disposes: how our approach to human health changes in the 21st century and how CRISPR-Cas is involved – Digital Journal

Posted: June 22, 2022 at 2:35 am

Los Angeles, California, United States 06-16-2022 (PR Distribution)

Change your lifestyle and you will initiate a chain of biochemical changes that will imperceptibly but steadily help you and, possibly, all your descendants until the end of their lifeon Earth. This quote belongs to German neurophysiologist P.Spork, who considers epigenetics the breakthrough science that will spearhead progress in the 21st century.

The Greek prefix epi-means over or upon; in other words, we are dealing with something that goes above genetics. It is hardly possible to overestimate the role epigenetic mechanisms play in embryonic development: specialized cells of an adult body grow from embryonic cells sharing the same DNA. Scientists think that genetic activity responds to external stimuli, such as stress levels, physical activities, and diurnal rhythms.

In case epigenetics has already done its dirty deed, it is still possible to use the molecular scissors of the CRISPR/Cas gene editing system, first described by Japanese scientist Y. Ishino.

In nature, CRISPR/Cas is the adaptive immune system used by bacteria to countervarious pathogens. It has the following work principle: once a bacterium gets attacked by a virus,its specialized Cas proteins quickly cut out parts of the virus and insert them into the CRISPR cassette in a certain order.The purpose of this process is to learn the face of the enemy and develop a specialized immune response.

Soon, scientists started to hope they could use the CRISPR-Cas9 system of Streptococcus bacteria to edit genomes of other organisms and fight genetic disorders. CRISPR-Cas9 is already used for treating various diseases. In spring 2020, scientists reported on the first intraretinalinjection of a modified virus to a patient suffering from Leber congenital amaurosis (a disease that causes blindness). The new method involves point base editing of RPE65 gene mutations [8]. Twoyears ago, The New England Journal of Medicinepublished the results of the firstsuccessful editing of ?-Thalassemia sickle cell anemia mutations.

For discovering the CRISPR/Cas9 genetic scissors and their potential for point editing, E. Charpentier (France) and J. Doudna (USA) were awarded the Nobel Prize in Chemistry in 2020.

It seems that genetic or epigenetic research can hardly be imagined without information technologies. We know bioinformatics methods are commonly used in computational epigenetics in addition to experimental studies; given the explosive growth of epigenomic data sets, computational methods are starting to play a greater role.

For instance, experimental ChIP-on-chip, ChIP-seq, and bisulfite sequencing methods are applied for genome-wide mapping of epigenetic data. They all generate large amounts of dataand demand effective ways of processing and quality control. On the one hand, big data is ofimmense help to scientists. Back in the day,complete genome sequencing took years and required millions of dollars. The next-generation sequencing method can provide the sameresults for $1200 within 24 hours.

On the other hand, some experts have a somewhat skeptical attitude to big data, as researchers simply cannot keep up with the enormous volumes of information. Besides, the use of supercomputers overhauls the work of scientists. In 2015, Italian biologist F.Mazzocchi noted that classical scientific methods are getting outdated in the age of data and supercomputing, with theories, hypotheses, and discussions becoming obsolete. Scientists no longer search formodels, while correlations offered by big data are replacing causality. M. Frick warns his colleagues against putting too much trust in the machine. He claims that data-driven science will or would find many spurious connections. Data-driven science could easily lead toapophenia and a wild outbreak of hornswoggling.

Only time will tell how justified these concerns are. Yet one thing is already crystal clear: there will be no going back to the old ways because treatment of the most complex diseases is on the verge of a breakthrough.

About the Author

Rustam Gilfanov is an IT entrepreneur and a venture partner of the LongeVC fund.

Media Contacts:

Company Name: Blacklight agencyFull Name: VladPhone: +74993403383Email Address: Send EmailWebsite: https://blacklight.ru

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Genetics proposes, epigenetics disposes: how our approach to human health changes in the 21st century and how CRISPR-Cas is involved - Digital Journal

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The relationship between P16INK4A and TP53 promoter methylation and the risk and prognosis in patients with oesophageal cancer in Thailand |…

Posted: June 22, 2022 at 2:35 am

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The relationship between P16INK4A and TP53 promoter methylation and the risk and prognosis in patients with oesophageal cancer in Thailand |...

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New Combination Therapy Effective in Pediatric Leukemia – Technology Networks

Posted: June 22, 2022 at 2:34 am

Acute lymphoblastic leukaemia (ALL) is the most common cancer affecting children. The T-ALL form of leukaemia that emerges from early T lineage cells has a poorer prognosis than B-lineage ALL. The prognosis for relapsed T-ALL is very poor and new therapies are sorely needed. A joint study by Tampere Universitys Faculty of Medicine and Health Technology in Finland, the Massachusetts General Research Institute, and the Harvard Stem Cell Institute discovered a new combination of drugs that is effective against T-ALL.

The finding is based on a previous discovery made by the Tampere University research group where the general tyrosine kinase inhibitor dasatinib was found to be effective in approximately one third of the tested patient samples.

In the treatment of leukaemia, the efficacy of a single drug is usually lost quickly, so the new study searched for drug combinations that would have an enhanced synergistic effect with dasatinib. This was the case with temsirolimus, a drug that inhibits a parallel signalling pathway. The combination of the two drugs was more effective in eradicating leukaemia cells in zebrafish and human disease than using a single drug.

During this study, we developed a new drug screening method for the rapid assessment of drug responses in zebrafish leukaemia samples. In this screen, an effective drug combination was found, which was later confirmed by several cell line models, patient samples and human leukemias grown in mice, says PhDSaara Laukkanen, the first author of the study.

This has been a long project, taking 45 years, and as a result, we now understand the mechanism of action of these drugs at molecular level in T-ALL, Laukkanen adds.

During the project, she spent six months as Visiting Researcher in the Department of Pathology at Massachusetts General Hospital in Boston with ProfessorDavid Langenau'sresearch group, with whom the project was carried out. She worked extensively with PhDAlexandra Veloso, a research fellow in the Langenau team and co-lead author on the work.

This is a promising new treatment option for T-acute leukaemia. The next step is to take the discovery into clinical practice for patients with relapsed or refractory disease via early phase clinical trials, says Research DirectorOlli Lohi, MD, PhD, from Tampere University and Tays Hospitals Cancer Centre.

The development of precision treatments is slow and requires accurate knowledge of the molecular mechanisms that cause and maintain disease. Here we utilized a specific dependency of T-ALL cells on certain signalling routes that the combination of dasatinib and temsirolimus shuts off, Lohi says.

The study was published inBlood, the most prestigious scientific journal in the field of haematology. In addition to researchers at Tampere University and Harvard Stem Cell Institute, researchers from the Universities of North Carolina, Eastern Finland and Helsinki also participated in the study.

Reference:Laukkanen S, Bacquelaine Veloso A, Yan C, et al. Combination therapies to inhibit LCK tyrosine kinase and mTOR signaling in T-cell acute lymphoblastic leukemia. Blood. 2022:2021015106. doi: 10.1182/blood.2021015106

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

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MIT Pioneers Technology To Grow Customizable Wood Products in the Lab With Little Waste – SciTechDaily

Posted: June 22, 2022 at 2:34 am

Scientists demonstrate that they can control the properties of lab-grown plant material, which could enable the production of wood products with little waste.

Because of deforestation, the world loses about 10 million hectares of forest an area about the size of Iceland each year. At that rate, some researchers predict the worlds forests could disappear in 100 to 200 years.

A hectare is an area equal to a square with 100-meter sides, or 10,000 m2, and is primarily used in the measurement of land. One hectare contains about 2.47 acres and an acre is about 0.405 hectares. 100 hectares makes one square kilometer.

In an effort to provide an environmentally friendly and low-waste alternative, researchers at MIT have pioneered a tunable technique to generate wood-like plant material in a lab, which could enable someone to grow a wooden product like a table without needing to cut down trees, process lumber, etc.

These researchers have now demonstrated that, by adjusting certain chemicals used during the growth process, they can precisely control the physical and mechanical properties of the resulting plant material, such as its stiffness and density.

They also show that, using 3D bioprinting techniques, they can grow plant material in shapes, sizes, and forms that are not found in nature and that cant be easily produced using traditional agricultural methods.

In an effort to provide an environmentally friendly and low-waste alternative, researchers at MIT have pioneered a tunable technique to generate wood-like plant material in a lab. Credit: Courtesy of the researchers

The idea is that you can grow these plant materials in exactly the shape that you need, so you dont need to do any subtractive manufacturing after the fact, which reduces the amount of energy and waste. There is a lot of potential to expand this and grow three-dimensional structures, says lead author Ashley Beckwith, a recent PhD graduate.

Though still in its early days, this research demonstrates that lab-grown plant materials can be tuned to have specific characteristics, which could someday enable researchers to grow wood products with the exact features needed for a particular application, like high strength to support the walls of a house or certain thermal properties to more efficiently heat a room, explains senior author Luis Fernando Velsquez-Garca, a principal scientist in MITs Microsystems Technology Laboratories.

Joining Beckwith and Velsquez-Garca on the paper is Jeffrey Borenstein, a biomedical engineer and group leader at the Charles Stark Draper Laboratory. The research is published recently in the journal Materials Today.

To begin the process of growing plant material in the lab, the researchers first isolate cells from the leaves of young Zinnia elegans plants. The cells are cultured in liquid medium for two days, then transferred to a gel-based medium, which contains nutrients and two different hormones.

Adjusting the hormone levels at this stage in the process enables researchers to tune the physical and mechanical properties of the plant cells that grow in that nutrient-rich broth.

In the human body, you have hormones that determine how your cells develop and how certain traits emerge. In the same way, by changing the hormone concentrations in the nutrient broth, the plant cells respond differently. Just by manipulating these tiny chemical quantities, we can elicit pretty dramatic changes in terms of the physical outcomes, Beckwith says.

In a way, these growing plant cells behave almost like stem cells researchers can give them cues to tell them what to become, Velsquez-Garca adds.

They use a 3D printer to extrude the cell culture gel solution into a specific structure in a petri dish, and let it incubate in the dark for three months. Even with this incubation period, the researchers process is about two orders of magnitude faster than the time it takes for a tree to grow to maturity, Velsquez-Garca says.

Following incubation, the resulting cell-based material is dehydrated, and then the researchers evaluate its properties.

They found that lower hormone levels yielded plant materials with more rounded, open cells that have lower density, while higher hormone levels led to the growth of plant materials with smaller, denser cell structures. Higher hormone levels also yielded plant material that was stiffer; the researchers were able to grow plant material with a storage modulus (stiffness) similar to that of some natural woods.

Another goal of this work is to study what is known as lignification in these lab-grown plant materials. Lignin is a polymer that is deposited in the cell walls of plants which makes them rigid and woody. They found that higher hormone levels in the growth medium causes more lignification, which would lead to plant material with more wood-like properties.

The researchers also demonstrated that, using a 3D bioprinting process, the plant material can be grown in a custom shape and size. Rather than using a mold, the process involves the use of a customizable computer-aided design file that is fed to a 3D bioprinter, which deposits the cell gel culture into a specific shape. For instance, they were able to grow plant material in the shape of a tiny evergreen tree.

Research of this kind is relatively new, Borenstein says.

This work demonstrates the power that a technology at the interface between engineering and biology can bring to bear on an environmental challenge, leveraging advances originally developed for health care applications, he adds.

The researchers also show that the cell cultures can survive and continue to grow for months after printing, and that using a thicker gel to produce thicker plant material structures does not impact the survival rate of the lab-grown cells.

I think the real opportunity here is to be optimal with what you use and how you use it. If you want to create an object that is going to serve some purpose, there are mechanical expectations to consider. This process is really amenable to customization, Velsquez-Garca says.

Now that they have demonstrated the effective tunability of this technique, the researchers want to continue experimenting so they can better understand and control cellular development. They also want to explore how other chemical and genetic factors can direct the growth of the cells.

They hope to evaluate how their method could be transferred to a new species. Zinnia plants dont produce wood, but if this method were used to make a commercially important tree species, like pine, the process would need to be tailored to that species, Velsquez-Garca says.

Ultimately, he is hopeful this work can help to motivate other groups to dive into this area of research to help reduce deforestation.

Trees and forests are an amazing tool for helping us manage climate change, so being as strategic as we can with these resources will be a societal necessity going forward, Beckwith adds.

Reference: Physical, mechanical, and microstructural characterization of novel, 3D-printed, tunable, lab-grown plant materials generated from Zinnia elegans cell cultures by Ashley L. Beckwith, Jeffrey T. Borenstein and Luis F. Velsquez-Garca, 7 March 2022, .DOI: 10.1016/j.mattod.2022.02.012

This research is funded, in part, by the Draper Scholars Program.

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MIT Pioneers Technology To Grow Customizable Wood Products in the Lab With Little Waste - SciTechDaily

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Where science meets fiction: the dark history of eugenics – The Guardian

Posted: June 22, 2022 at 2:33 am

Its a quirk of history that the foundations of modern biology and as a consequence, some of the worst atrocities of the 20th century should rely so heavily on peas. Cast your mind back to school biology, and Gregor Mendel, whose 200th birthday we mark next month. Though Mendel is invariably described as a friar, his formidable legacy is not in Augustinian theology, but in the mainstream science of genetics.

In the middle of the 19th century, Mendel (whose real name was Johann Gregor was his Augustinian appellation) bred more than 28,000 pea plants, crossing tall with short, wrinkly seeds with smooth, and purple flowers with white. What he found in that forest of pea plants was that these traits segregated in the offspring, and did not blend, but re-emerged in predictable ratios. What Mendel had discovered were the rules of inheritance. Characteristics were inherited in discrete units what we now call genes and the way these units flowed through pedigrees followed neat mathematical patterns.

These rules are taught in every secondary school as a core part of how we understand fundamental biology genes, DNA and evolution. We also teach this history, for it is a good story. Mendels work, published in 1866, was being done at the same time as Darwin was carving out his greatest idea. But this genius Moravian friar was ignored until both men were dead, only to be rediscovered at the beginning of the new century, which resolved Darwinian evolution with Mendelian genetics, midwifing the modern era of biology.

But theres a lesser-known story that shaped the course of the 20th century in a different way. The origins of genetics are inextricably wedded to eugenics. Since Plato suggested the pairing of high-quality parents, and Plutarch described Spartan infanticide, the principles of population control have been in place, probably in all cultures. But in the time of Victorian industrialisation, with an ever-expanding working class, and in the wake of Darwinian evolution, Darwins half-cousin, Francis Galton, added a scientific and statistical sheen to the deliberate sculpting of society, and he named it eugenics. It was a political ideology that co-opted the very new and immature science of evolution, and came to be one of the defining and most deadly ideas of the 20th century.

The UK came within a whisker of having involuntary sterilisation of undesirables as legislation, something that Churchill robustly campaigned for in his years in the Asquith government, but which the MP Josiah Wedgwood successfully resisted. In the US though, eugenics policies were enacted from 1907 and over most of the next century in 31 states, an estimated 80,000 people were sterilised by the state in the name of purification.

American eugenics was faithfully married to Mendels laws though Mendel himself had nothing to do with these policies. Led by Charles Davenport a biologist and Galton devotee the Eugenics Record Office in Cold Spring Harbor, New York, set out in 1910 to promote a racist, ableist ideology, and to harvest the pedigrees of Americans. With this data, Davenport figured, they could establish the inheritance of traits both desirable and defective, and thus purify the American people. Thus they could fight the imagined threat of great replacement theory facing white America: undesirable people, with their unruly fecundity, will spread inferior genes, and the ruling classes will be erased.

Pedigrees were a major part of the US eugenics movement, and Davenport had feverishly latched on to Mendelian inheritance to explain all manner of human foibles: alcoholism, criminality, feeblemindedness (and, weirdly, a tendency to seafaring). Heredity, he wrote in 1910, stands as the one great hope of the human race; its saviour from imbecility, poverty, disease, immorality, and like all of the enthusiastic eugenicists, he attributed the inheritance of these complex traits to genes nature over nurture. It is from Davenport that we have the first genetic studies of Huntingtons disease, which strictly obeys a Mendelian inheritance, and of eye colour, which, despite what we still teach in schools, does not.

One particular tale from this era stands out. The psychologist Henry Goddard had been studying a girl with the pseudonym Deborah Kallikak in his New Jersey clinic since she was eight. He described her as a high-grade feeble-minded person, the moron, the delinquent, the kind of girl or woman that fills our reformatories. In order to trace the origin of her troubles, Goddard produced a detailed pedigree of the Kallikaks. He identified as the founder of this bloodline Martin Kallikak, who stopped off en route home from the war of independence to his genteel Quaker wife to impregnate a feeble-minded but attractive barmaid, with whom he had no further contact.

In Goddards influential 1912 book, The Kallikak Family: A Study in the Heredity of Feeble-Mindedness, he traced a perfect pattern of Mendelian inheritance for traits good and bad. The legitimate family was eminently successful, whereas his bastard progeny produced a clan of criminals and disabled defectives, eventually concluding with Deborah. With this, Goddard concluded that the feeble-mindedness of the Kallikaks was encoded in a gene, a single unit of defective inheritance passed down from generation to generation, just like in Mendels peas.

A contemporary geneticist will frown at this, for multiple reasons. The first is the terminology feeble-minded, which was a vague, pseudopsychiatric bucket diagnosis that we presume included a wide range of todays clinical conditions. We might also reject his Mendelian conclusion on the grounds that complex psychiatric disorders rarely have a single genetic root, and are always profoundly influenced by the environment. The presence of a particular gene will not determine the outcome of a trait, though it may well contribute to the probability of it.

This is a modern understanding of the extreme complexity of the human genome, probably the richest dataset in the known universe. But a meticulous contemporary analysis is not even required in the case of the Kallikaks, because the barmaid never existed.

Martin Kallikaks legitimate family was indeed packed with celebrated achievers men of medicine, the law and the clergy. But Goddard had invented the illegitimate branch, by misidentifying an unrelated man called John Wolverton as Kallikaks bastard son, and dreaming up his barmaid mother. There were people with disabilities among Wolvertons descendants, but the photos in Goddards book show some of the children with facial characteristics that are associated with foetal alcohol syndrome, a condition that is entirely determined not by genetic inheritance, but by exposure to high levels of alcohol in utero. Despite the family tree being completely false, this case study remained in psychology textbooks until the 1950s as a model of human inheritance, and a justification for enforced sterilisation. The Kallikaks had become the founding myth of American eugenics.

The German eugenics movement had also begun at the beginning of the 20th century, and grown steadily through the years of the Weimar Republic. By the time of the rise of the Third Reich, principles such as Lebensunwertes Leben life unworthy of life were a core part of the national eugenics ideology for purifying the Nordic stock of German people. One of the first pieces of legislation to be passed after Hitler seized power in 1933 was the Law for the Prevention of Genetically Diseased Offspring, which required sterilisation of people with schizophrenia, deafness, blindness, epilepsy, Huntingtons disease, and other conditions that were deemed clearly genetic. As with the Americans tenacious but fallacious grip on heredity, most of these conditions are not straightforwardly Mendelian, and in one case where it is Huntingtons the disease takes effect after reproductive age. Sterilisation had no effect on its inheritance.

The development of the Nazis eugenics programmes was supported intellectually and financially by the American eugenicists, erroneously obsessed as they were with finding single Mendelian genes for complex traits, and plotting them on pedigrees. In 1935, a short propaganda film called Das Erbe (The Inheritance) was released in Germany. In it, a young scientist observes a couple of stag beetles rutting. Confused, she consults her professor, who sits her down to explain the Darwinian struggles for life and shows her a film of a cat hunting a bird, cocks sparring. Suddenly she gets it, and exclaims, to roars of laughter: Animals pursue their own racial policies!

The muddled propaganda is clear: nature purges the weak, and so must we.

The film then shows a pedigree of a hunting dog, just the type that you might get from the Kennel Club today. And then, up comes an animation of the family tree of the Kallikaks, on one side Erbgesunde Frau and on the other, Erbkranke Frau genetically healthy and hereditarily defective women. On the diseased side, the positions of all of the miscreants and deviants pulse to show the flow of undesirable people through the generations, as the voiceover explains. Das Erbe was a film to promote public acceptance of the Nazi eugenics laws, and what follows the entirely fictional Kallikak family tree is its asserted legacy: shock images of seriously disabled people in sanatoriums, followed by healthy marching Nazis, and a message from Hitler: He who is physically and mentally not healthy and worthy, may not perpetuate his suffering in the body of his child. Approximately 400,000 people were sterilised under this policy. A scientific lie had become a pillar of genocide in just 20 years.

Science has and will always be politicised. People turn to the authority of science to justify their ideologies. Today, we see the same pattern, but with new genetics. After the supermarket shootings in Buffalo in May, there was heated discussion in genetics communities, as the murderer had cited specific academic work in his deranged manifesto, legitimate papers on the genetics of intelligence and the genetic basis of Jewish ancestry, coupled with the persistent pseudoscience of the great replacement.

Science strives to be apolitical, to rise above the grubby worlds of politics and the psychological biases that we are encumbered with. But all new scientific discoveries exist within the culture into which they are born, and are always susceptible to abuse. This does not mean we should shrug and accept that our scientific endeavours are imperfect and can be bastardised with nefarious purpose, nor does it mean we should censor academic research.

But we should know our own history. We teach a version of genetics that is easily simplified to the point of being wrong. The laws in biology have a somewhat tricksy tendency to be beset by qualifications, complexities and caveats. Biology is inherently messy, and evolution preserves what works, not what is simple. In the simplicity of Mendels peas is a science which is easily co-opted, and marshalled into a racist, fascist ideology, as it was in the US, in Nazi Germany and in dozens of other countries. To know our history is to inoculate ourselves against it being repeated.

This article was amended on 20 June 2022. The mass shooting in Buffalo, US, in May 2022 was at a supermarket, not a school as an earlier version said.

Control: The Dark History and Troubling Present of Eugenics by Adam Rutherford is published by Weidenfeld & Nicolson (12.99). To support the Guardian and Observer order your copy at guardianbookshop.com. Delivery charges may apply

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Should genetics be used to create social policy? – Big Think

Posted: June 22, 2022 at 2:33 am

Eugenics is the practice of using planned breeding for racial improvement.

Because this idea is repulsive, the predominant response has been genome blindness that is, avoiding any study or discussion of genetic differences between people.

But according to geneticist Paige Harden, this is the wrong solution. Instead, we should identify genetic differences between people including those that might affect social outcomes so that we can help provide people with the resources they need to be successful.

KATHRYN PAIGE HARDEN: Eugenics is an interesting word because it could be used to describe a number of different things. So one way to think about eugenics is just as selective breeding or sort of control over reproduction. So, if we think about involuntary sterilization in Virginia in the 1920s, that's saying there's better people, there's worse people; it's on the basis of something "genetic" about them, and we're gonna allocate freedoms on the basis of that hierarchy. Some people have reproductive autonomy: they get to choose to have children, but other people don't- they are involuntarily sterilized.

So it's this control of reproduction that's coercive, and is based on this idea, this hierarchy of people. The predominant response to the eugenic perspective has been what I call 'Genome blindness.' And that's really the idea that we should avoid studying or talking about, scientifically or politically, biological or genetic differences between people. We can't use any genetic information to slot people into eugenic hierarchy if there are no genetic differences or if we insist, they don't matter.

If you ask the average American how much do you think genes influence your intelligence or personality or risk for mental illness, their answer is almost never "zero." So if people already think that genes make a difference for outcomes that they care about, if the only people that are talking about that are the most extreme, sometimes hate-filled voices, that is a problem. I really worry that too much of the conversation is focused right now on the ethics of knowledge production, and not enough on the brass tacks of legislation and policy at the state-by-state level. I have a colleague and friend here at the University of Texas who wrote a fascinating book called "Predict and Surveil."

She embedded herself with the LA Police Department for several years and looked how they saw predictive policing, algorithms, and data aggregation in order to police, and I would say, over-police some communities. And a lot of the data that they're using comes from proprietary software that's provided by for-profit companies. When people think about dystopian scenarios, I actually worry less about the overt white nationalists and more about people who know they can make money using genetic information. So the challenge then is, how do we identify genetic differences between people, even genetic differences that might have a relationship to outcomes we care about socially? So something like intelligence or education or impulsivity, without using them or interpreting them eugenically.

When we think about our own intimate relationships, we can separate what makes someone valuable, worthy of freedom, worthy of resources, worthy of consideration of welfare, from what does our capitalist economy currently value. And I think that's the distinction that we also need to draw between observing genetic differences versus using them eugenically.

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49 Genetic Variants That Increase the Risk of Varicose Veins Identified – Technology Networks

Posted: June 22, 2022 at 2:33 am

Varicose veins are a very common manifestation of chronic venous disease, affecting over 30% of the population in Western countries. In America, chronic venous disease affects over 11 million men and 22 million women aged 4080 years old. Left untreated it can escalate to multiple health complications including leg ulcers and ultimately amputations. A new international study by Oxford researchers published on 2 June 2022 in Nature Communications establishes for the first time, a critical genetic risk score to predict the likelihood of patients suffering with varicose veins to require surgery, as well as pointing the way towards potential new therapies.

In a vasttwo-stage genome-wide association study of varicose veins in 401,656 individuals from UK Biobank, and replication in 408,969 individuals from 23andMe, Oxford researchers identified 49 genetic variants that increase the risk of varicose veins. They highlighted pathways including problems with the connective tissues of the body, and the immune system as key players in varicose vein pathology.

This study was an interdisciplinary collaborative effort across the Medical Sciences Division at the University of Oxford. Researchers from theNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, theNuffield Department of Surgical Sciencesand theNuffield Department of Women's & Reproductive Healthworked withan Americancommercial, direct to consumer genotyping company called23andMeto explore which people were moresusceptible to developingVaricose veins.

Lead authorProfessor Dominic Furnisscommented: 'The inclusion of surgeons in the research team was vital as they enabled the identification of patients whose disease was more severe, and they had therefore had surgery. This lead to the discovery of49 genetic variants at 46 areas into the genome thatpredisposes to Varicose veins. This breakthroughgreatly improves our team's knowledge of the biology of Varicose veins, and it will be the foundation of further research into the biology and potentially new treatment'.

Co-authorProfessor Krina Zondervansaid: 'This large study brings together a great deal of new evidence of the genetics underlying varicose veins, a condition that is highly prevalent in women and in pregnancy. It opens up exciting new avenues for the development of new future treatments.'

Reference:Ahmed WUR, Kleeman S, Ng M, et al. Genome-wide association analysis and replication in 810,625 individuals with varicose veins. Nat Commun. 2022;13(1):3065. doi: 10.1038/s41467-022-30765-y

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

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Genetics project to lift performance of northern cattle herd – Government of Western Australia

Posted: June 22, 2022 at 2:33 am

The three year project is part of the Department of Primary Industries and Regional Developments (DPIRD) Northern Beef Development initiative to assist the Western Australian industry to become more profitable, resilient and sustainable.

DPIRD development officer Rebecca Butcher said the project would work with pastoralists to gather intelligence, share experiences and extend learnings about the use of genetic selection data to drive breeding objectives.

There has been varying use of genetic evaluation and management tools, like Estimated Breeding Values, known as EBVs, in the industry for some time to inform herd breeding programs, she said.

This project will harness that knowledge to get a better understanding of the needs of the production system and how breeding traits, like growth rates, carcase weight and fertility, and heritability can be better integrated to refine breeding programs.

DPIRD has contracted established livestock genetics consultants Animal Genetics and Breeding Unit (AGBU), a joint venture between New South Wales Department of Primary Industries and the University of New England, to deliver the project.

Six Kimberley and seven Pilbara pastoral stations have already signed up to participate in the project, while there is still opportunity for more to join.

Ms Butcher said it was important for pastoralists to make informed decisions when purchasing bulls, which could generate substantial gains to pastoral enterprises.

Bull selection is the single most important factor affecting herd productivity and profitability, she said.

With pastoralists paying $6000 to $8000 for a good bull or up to $60,000 in some cases it is imperative that money is well spent on an animal that has economically important production traits that advance the businesses breeding objectives.

DPIRDs Northern Beef development officers and the AGBU team will discuss the use of EBVs with participating Kimberley and Pilbara pastoralists and how they could be refined to benefit their operation.

The intelligence will be used to develop tailored selection indexes for northern beef producers aimed at cattle destined for the live export market, as well as the emerging north-south supply chain.

The selection indexes will be developed using the BREEDPLAN genetic evaluation system developed for Australian beef cattle breeders.

Future workshops and field days are planned in coming months to share information and experiences.

To participate in DPIRDs Genetics and Breeding project email rebecca.butcher@dpird.wa.gov.au or telephone (08) 9651 0540.

For more information on DPIRDs Northern Beef Development initiative visit http://www.agric.wa.gov.au/northern-beef-development.

Picture caption: DPIRD development officer Rebecca Butcher is involved in a new Northern Beef genetic improvement project to boost the efficiency and marketability of the northern cattle herd.

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‘So lucky to have you and your genetics’, Tiger Shroff wishes his dad on Father’s Day – Devdiscourse

Posted: June 22, 2022 at 2:33 am

Bollywood's newest action star Tiger Shroff shared a picture of his father Jackie Shroff and penned a heartfelt message to mark the occasion of Father's Day. The 'Heropanti' actor took to his Instagram handle and posted a jaw-dropping picture of Jackie Shroff where he can be seen wearing casual outfits with a pair of sunglasses and a watch. He can be seen flaunting his chiselled biceps.

He captioned the post by writing a heartfelt message that read, "Happy Fathers day to the best dad ever so lucky to have you and your genetics." As soon as she shared the post, Bollywood celebrities showered love on Jackie in the comments sections.

Siddhant Chaturvedi dropped a smiling face with heart eyes while Anil Kapoor wrote, "The best dad and best friend too." Arjun Rampal praised Jackie for his chiselled physique, he wrote, "Kya baat hain Jackie Da ripped."

Meanwhile, on the work front, Tiger has wrapped up the shoot of his new film 'Ganpath'. After an arduous schedule in Ladakh, the actor will now begin preparations for his next film, titled 'Rambo', followed by 'Bade Miyan Chote Miyan' alongside Akshay Kumar. 'Ganpath' will be hit the theatres on December 23, 2022. (ANI)

(This story has not been edited by Devdiscourse staff and is auto-generated from a syndicated feed.)

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