Category Archives: Genetics

Snowden JA, Ahmedzai SH, Ashcroft J, DSa S, Littlewood T, Low E, et al. Guidelines for supportive care in multiple myeloma 2011. Br J Haematol. 2011;154:76103.

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Association of genetic variants with patient reported quality of life and pain experience in patients in the UK NCRI Myeloma X Relapse [Intensive])...

It would cost less to reduce methane emissions by breeding better sheep, than by offsetting greenhouse gases through carbon forestry, new research shows.

The scientists at AgResearchs Invermay Agriculture Centre who recently made this calculation had already been using portable chambers that could measure the methane sheep belched out for a number of years. This research showed that some sheep emitted less methane than others.

For a recent study by the centres researcher Suzanne Rowe rams that emitted lower levels of methane were bred to low methane-emitting ewes. The study compared the emissions from low emitting sheep to flocks bred from rams and ewes that emitted high levels of methane. The study showed low-methane sheep emitted 10% to 12% less methane than the high-methane animals.

It was calculations from these studies that found it would be cheaper to reduce methane in the agriculture industry through sheep genetics, than through carbon schemes that relied on forestry for offsetting.

READ MORE:* Capturing bulls' breath could help breed lower-methane cows* Lower methane cows... from a catalogue?* Low methane New Zealand sheep coming to a farm near you

John McEwan, animal genomics researcher at AgResearch, said initial calculations showed that the cost to reduce a tonne of methane equivalent through breeding low emitting sheep was $1.72. The calculations were done using conversion factors as used in the emissions trading scheme.

This is markedly less than the $85 per tonne CO2 [equivalent] being paid by the emissions trading scheme currently. It is this $85 per tonne CO2 [equivalent] value in the emission trading scheme which underpins New Zealands forestry conversions and is expected to rise higher in future, McEwan said.

There are limitations to using sheep genetics to lower emissions.

Reduction through better genetics would only mitigate part of the Governments proposed methane emission reductions of 10% by 2030 and 24% to 47% by 2050. Other methods would also be needed and would cost more per tonne of methane emitted, McEwan said.

Gerhard Uys/Stuff

A mix of low and high emitting sheep at Leon Black's farm in Southland.

However, forestry also had defined limitations, McEwan said.

Forests could not continuously absorb the extra methane emitted from fossil fuels for many decades. Forests were a limited short-term fix, while the country transitioned to low carbon energy sources, McEwan said.

Similarly, there were practical limits to reducing methane via sheep genetics. New Zealand had to find a manageable path to being net carbon zero by 2050, or more correctly restricting temperature change to a given agreed value. It had to do this at minimal cost to the economy, and avoid rapid swings in prices especially for leveraged asset values like land, McEwan said

There was untapped potential to make faster genetic gains in the sheep industry and there was a compelling case that this method should be aggressively pursued, McEwan said.

According to the study, low-emitting sheep would not find their way into the national flock immediately and there would be no significant reduction of emissions for the first five years in New Zealands commercial flock as there would be genetic lag effects, and because of low adoption rates of new genetic technologies.

In 2007 Southland sheep breeder Leon Black was one of the first to ask if there were differences between the levels of methane that sheep produced.

Black said it made sense, because there were always many variations in any animal population. Some sheep produce more milk than others, or converted feed into meat more efficiently, he said.

There was therefore the possibility that the internal digestive workings of sheep also differed, Black said.

When the question was first asked, the theory needed to be quantified and answer a number of questions. Firstly, was there variation in how much methane different sheep produced? If there was, was it repeatable. If it was repeatable, was that variation consistent? And importantly, would the variation be passed on to the offspring via genetics, Black said.

To all these questions the answer was yes, Black said.

Gerhard Uys/Stuff

Sheep breeder Leon Black says he hoped that instead of reducing flocks by 10% to meet the Governments climate target, genetics improvements would mean the flock could stay the same size, but produce less methane and still produce meat and wool for a profit.

For farmers who grow wool and meat another question was also important. Would animals bred for lower methane produce better wool or meat, or less wool or meat? The answer was that lower methane producing sheep converted feed into wool and meat much more efficiently, Black said.

Black had now been involved in measuring his flock since 2008. Low methane-emitting rams from his flocks were already finding their way into the flocks of wool and meat farmers and would produce daughters who inherited lower methane-emitting genetics, Black said.

Progress would take time as offspring got half of their genetic traits from their fathers side and half from the mothers side, Black said.

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Better sheep genetics cheaper than trees to get rid of greenhouse gases - Stuff

Mahesh Bhatt is super happy for daughter Alia Bhatt and son-in-law Ranbir Kapoor as they are all set to welcome their first child.

Alia Bhatt and Ranbir Kapoor the good news on June 27.

Father Mahesh Bhatt is over the moon as daughter Alia Bhatt will soon welcome her first child with Ranbir Kapoor. The entire Kapoor-Bhatt clan showed their excitement over the happy news. Mahesh, in an interview, spoke about his to-be-grandchild and said that he would have the genes of two extraordinary kids - Alia and Ranbir.

Mahesh Bhatt is a proud and happy father as daughter Alia Bhatt is all set to welcome her firstborn. Talking to Hindustan Times he said, This is the most challenging role, which life is asking me to play, which is the role of a grandfather. It is a magical moment for the whole family. First of all, Alia has been a magical child since the beginning. She has amazed me with her extraordinary talent, which she has displayed to herself and the world, and then the marriage with Ranbir was a great, high moment, and I love the boy. He is an amazing kid."

He then continued and said that the child would be another universe and would be the best of both worlds. He said, Theres another universe which is going to descend into our backyard and into our lives. It is quite astounding news. I am happy for Alia and Ranbir, and the entire clan. I am certain that the child which is going to be born will have the genetics of these two extraordinary children -- Ranbir and Alia."

While the Kapoor-Bhatt clan celebrate, Alia Bhatt is shooting for her Hollywood film, Heart of Stone, in London. The actress was spotted posing with her friends Manish Malhotra and Karan Johar. What has our attention is her pregnancy glow!

Alia Bhatt and Ranbir Kapoor made the big announcement on Monday, June 27.

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Mahesh Bhatt says Alia, Ranbir Kapoor's 'child will have genetics of two extraordinary people' - India Today

Summary: Mutations in the ASD/intellectual disability genes ADNP and POGZ result in abnormal activation and overexpression of immune response genes and genes for microglia. This results in abnormal brain synaptic function, characteristic of ASD and ID.

Source: University at Buffalo

University at Buffalo scientists have discovered a convergent mechanism that may be responsible for how two top-ranked genetic risk factors for autism spectrum disorder/intellectual disability (ASD/ID) lead to these neurodevelopmental disorders.

While ASD is distinct from ID, a significant proportionapproximately 31%of people with ASD also exhibit ID. Neither condition is well-understood at the molecular level.

Given the vast number of genes known to be involved in ASD/ID and the many potential mechanisms contributing to the disorders, it is exciting to find a shared process between two different genes at the molecular level that could be underlying thebehavioral changes, said Megan Conrow-Graham, Ph.D., first author and an MD/Ph.D. candidate in the Jacobs School of Medicine and Biomedical Sciences at UB.

Published today in the journalBrain, the paper focuses on ADNP and POGZ, the two top-ranked risk factor genes for ASD/ID. The research demonstrates that mutations in these genes result in abnormal activation and overexpression of immune response genes and genes for a type of immune cell in the brain called microglia.

Our finding opens the possibility of targeting microglia and immune genes for treating ASD/ID, but much remains to be studied, given the heterogeneity and complexity of these brain disorders, said Zhen Yan, Ph.D., senior author and SUNY Distinguished Professor in the Department of Physiology and Biophysics in the Jacobs School.

The UB scientists found that mutations in the two genes studied activate microglia and cause immune genes in the brain to be overexpressed. The hypothesized result is the abnormal function of synapses in the brain, a characteristic of ASD/ID.

The research involved studies on postmortem brain tissue from humans with ASD/ID, as well as studies on mice in which ADNP and POGZ were silenced through viral delivery of small interference RNA. These mice exhibited impaired cognitive task performance, such as spatial memory, object recognition memory and long-term memory.

Weakening a repressive function

Under normal conditions, cells in the central nervous system should not express large quantities of genes that activate the immune system, said Conrow-Graham.

ADNP and POGZ both work to repress these genes so that inflammatory pathways are not continuously activated, which could damage surrounding cells. When that repression is weakened, these immune and inflammatory genes are then able to be expressed in large quantities.

The upregulated genes in the mouseprefrontal cortexcaused by the deficiencies in ADNP or POGZ activated the pro-inflammatory response.

This is consistent with what we see in upregulated genes in the prefrontal cortex of humans with ASD/ID, said Conrow-Graham. The prefrontal cortex is the part of the brain responsible for executive function, such as cognition and emotional control.

The mutated genes also activate the glial cells in the brain called microglia, which serve as support cells for neurons and have an immune function in the brain; they comprise 10-15% of all brain cells.

Sensitive microglia

Microglia are very sensitive to pathological changes in the central nervous system and are the main form of active immune defense to maintain brain health, explained Yan. Aberrant activation of microglia, which we demonstrate occurs as a result of deficiency in ADNP or POGZ, could lead to the damage and loss of synapses and neurons.

The researchers are hopeful that future research will determine whether chronic neuroinflammation could be directly contributing to at least some cases of ASD/ID, in which targeting microglia or inflammatory signaling pathways could prove to be a useful treatment.

The researchers pointed out that the clinical presentation of both ASD and ID is incredibly varied. Significant variation also likely is present in the kinds of mechanisms responsible for the symptoms of ASD and/or ID.

We found that changes in two riskgeneslead to a convergent mechanism, likely involving immune activation, said Conrow-Graham. However, this probably isnt the case for all individuals with ASD/ID. When designingclinical trialsto evaluate treatment effectiveness, I think our research underscores the importance of considering the genetic factors involved in an individuals ASD/ID.

The research is the culmination of Conrow-Grahams Ph.D. work; she has now returned to complete the last two years of the MD degree in the Jacobs School. She described her experience pursuing both an MD and a Ph.D. as extremely complementary.

The immune system has a role

My training at each level was super helpful to supplement the other, she said. When I began my Ph.D., I had completed two years of MD training, so I was familiar with the basics of physiology, anatomy and pathology.

Because of this, I was able to bring a broader perspective to my neuroscience research, identifying how the immune system might be playing a role. Prior to this, our lab had not really investigated immunology-related pathways, so having that background insight was really beneficial.

She added that she learned so much from all of her colleagues in Yans lab, including faculty members, lab technicians and other students. I learned so many technical skills that I had never used before joining the lab, thanks to the dedication of lab co-workers for my training, she said.

Her experience at the lab bench working on the basic science underlying neuropsychiatric disorders will definitely influence her work as a clinician.

I plan to pursue a career as a child and adolescent psychiatrist, so I may be able to work directly with this patient population, she said.

Were learning now that better care may be able to be provided by taking a personalized medicine approach, taking into account genetics, psychosocial factors and others. Being able to take a very deep dive into the field of psychiatric genetics was a privilege that I hope will help me to provide the best care for patients.

Author: Ellen GoldbaumSource: University at BuffaloContact: Ellen Goldbaum University at BuffaloImage: The image is in the public domain

Original Research: Closed access.A convergent mechanism of high risk factors ADNP and POGZ in neurodevelopmental disorders by Megan Conrow-Graham et al. Brain

Abstract

A convergent mechanism of high risk factors ADNP and POGZ in neurodevelopmental disorders

ADNPandPOGZare two top-ranking risk factors for autism spectrum disorder and intellectual disability, but how they are linked to these neurodevelopmental disorders is largely unknown. BothADNPandPOGZare chromatin regulators, which could profoundly affect gene transcription and cellular function in the brain.

Using post-mortem tissue from patients with autism spectrum disorder, we found diminished expression ofADNPandPOGZin the prefrontal cortex, a region highly implicated in neurodevelopmental disorders.

To understand the functional role of these neurodevelopmental disorder risk factors, we used viral-based gene transfer to investigate howAdnporPogzdeficiency in mouse prefrontal cortex affects behavioural, transcriptomic and synaptic function. Mice with prefrontal cortex deficiency ofAdnporPogzexhibited specific impairment of cognitive task performance.

RNA-sequencing revealed thatAdnporPogzdeficiency induced prominent upregulation of overlapping genes enriched in neuroinflammation, similar to the elevation of pro-inflammatory genes in humans with neurodevelopmental disorders. Concomitantly,AdnporPogzdeficiency led to the significant increase of pro-phagocytic microglial activation in prefrontal cortex, as well as the significant decrease of glutamatergic transmission and postsynaptic protein expression.

These findings have uncovered the convergent functions of two top risk factors for autism spectrum disorder and intellectual disability in prefrontal cortex, providing a mechanism linking chromatin, transcriptional and synaptic dysregulation to cognitive deficits associated with neurodevelopmental disorders.

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When ASD Occurs With Intellectual Disability, a Convergent Mechanism for Two Top-Ranking Risk Genes May Be the Cause - Neuroscience News

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

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

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

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

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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'So lucky to have you and your genetics', Tiger Shroff wishes his dad on Father's Day - Devdiscourse

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10 traits you may not know can be tied to genetics - The Albany Herald