How Africa’s genetic diversity can be harnessed to close the continent’s ‘drug and treatment gap’ – Genetic Literacy Project

I have begged to just die.

Those were the words of Sadeh Sophia, a sickle cell disease patient. Although living in the UK, she suffers from the genetic blood disorder that primarily targets Africans, SCD globally affects 25 million people, mostly in equatorial countries across Africa, the Middle East and Asia. The World Health Organization reckons that circa 300, 000 people are born with sickle cell disease. There is no cure.

Sub-Saharan Africa is the diseases epicenter. As many as 40% of the population in some African countries carry the trait. About 1,000 children in Africa are born with SCD every day, and more than half will die before they reach 5 years old.

Yet, the African genome, which could yield critical clues to the development of life-saving malaria drugs and medical treatments, has been vastly understudied. How can this be changed?

The diseases affecting Africans differ significantly in severity, scope and distribution from those that affect inhabitants of other regions. These are due to a variety of factors, including genetics, economic development, political stability and even cultural norms. One example of such a disease is polio which was endemic in Nigeria, Afghanistan, parts of Asia and most countries in Africa (presently, Pakistan and Afghanistan are the only polio-endemic countries).

Malaria, transmitted by the Anopheles mosquito, which disproportionately affects Africans, is largely linked to geographical location, hygiene conditions and economic development. It claims the life of a sub-Saharan African child every two minutes. The haemoglobinopathies and sickle cell trait (HbAS) confers protection from the lethal manifestation of malaria. The vital aspect is the mutation that causes sickle cell disease which leads to a 90% risk reduction of severe Plasmodium falciparum malaria across sub-Saharan Africa.

Africa has the fastest growing and youngest population in the world, with more than 1.14 billion people. Its also the worlds poorest region, According to current population trends, with its most populous country, Nigeria, known as the worlds poverty headquarters. Although the need for advanced drugs is critical, the government and the people are too poor to afford them in the quantities necessary to make a dent in the problem. No wonder many drug makers do not consider the continent when investing in new drug development.

Advances in genetics are opening the door to addressing the African drug desert. Starting about 100,000 years ago, humans began migrating out of Africa, kick-starting a mass exodus to other parts of the world (pre-humans made their way out millions of years earlier). Today, most non-Africans trace their ancestry to their forbears in Africa. The reason why humans emigrated from the continent is not disconnected from the basic human behaviour of moving in search of resources: land, food and water became scarce as the climate changed. According to researchers who have studied various modes of migration movements, humans emigrated based on those universal needs.

The Human Genome Project, initiated in 1991 and completed 13 years later, aimed to map out the entire set of human genes to provide the world with information on the basic set of heritable factors required for the development and functioning of humans. Its been a boon to medical research and drug development. However, a focus on populations in wealthier countries has led to a lack of proper understanding of health issues that affect poor nations, most of which are in sub-Saharan Africa. Less than 2% of human genomes analysed so far have been African, notwithstanding the fact that Africa, where modern humans emerge, harbours more genetic diversity than any other continent.

Previous genomic sequencing projects have not completely captured the immense level of diversity that exists within populations throughout the region. In a bid to further unravel Africas genetic diversity, scientists from the African Society of Human Genetics, the US National Institutes of Health (NIH) and the Wellcome Trust (WT) formed a consortium that led to the founding of what is known as Human Heredity and Health in Africa (H3Africa), which seeks to understand disease susceptibility and how it affects drug responses amongst the African populace. It focused on common, non-communicable disorders such as sickle cell and heart disease, as well as communicable diseases such as tuberculosis.

H3Africa has led to the creation of biorepositories, investigation of non-communicable diseases affecting Africans and training of the next generation of bioinformaticians. Its potential to address diseases disproportionately affecting Africans is enormous.

But there are also tangible benefits to the rest of the world. One of the great mysteries of the current pandemic is why sub-Saharan Africa has emerged as a cold spot for serious COVID despite a fractured and overwhelmed medical infrastructure. Such an initiative could explain the genetic diversity and composition of sub-Saharan Africans who were less impacted from the lethal outcomes of the coronaviruscritical information about human genetic differences that could lead to the development of future treatments for non-African populations as well..

Drug discovery and development is a long, cumbersome, risky and expensive process. Recent studies show that the estimated cost for discovering and developing a drug from laboratory benches to shelves is circa $2.6 billion and rising. As an example, in cancer research, greater than 95% of drug candidates do not successfully pass the testing phases. The industry relies on blockbuster drugs revenues to fuel research future treatments and/or cures. The economics behind this model incentivizes industry players to research diseases that afflict richer nations as opposed to those which burden poorer countries. Thus, this model has seen poorer countries diseases under-studied, which leads to fewer drugs treating ailments that beset their citizens. While some pharmaceutical companies compete in doing good by donating medicines or sub-licensing them to generic firms, this altruism does not address the lack of effective medicines against infirmities that disproportionately affect the poor, the vast majority domiciled in sub-Saharan Africa.

Developing the research capacity of low- and middle-income countries (LMICs) is therefore criticalone of the main impetuses for H3Africa. Wealth is the fundamental driver of drug development, but there is a limit to which poor countries can fund basic medical research. In the US, cystic fibrosis enjoys a 75-fold upper hand in charitable funding for research compared to sickle cell disease, partly because the bulk of the SCD patients live in other regions.

But as more Africans emigrate out of the continent for greener pastures, there has been a rise in diseases common to Africa that are showing up elsewhere. Thus, it behooves philanthropists, especially those of African descent, to donate to research studies that aid in ameliorating the under-study of ailments that affect them. Now one-sixth of the people on Earth, based on current demographic trends, Africa will likely be the home to one-in-three people by 2021, thus implying a significant segment of the worlds populace will be bereft of life-saving drugs.

There is a limit to providing solutions for diseases that disproportionately burden Africans, especially those south of the Sahara Desert, by just conducting studies and collating results. Although the African Genome Project contributes greatly by outlining in depth the genomes of Africans, it does little to address the specific issue of the dearth of medicines for maladies that afflict inhabitants in the sub-region.

Researchers involved in the H3Africa understandably want to ensure that African countries retain the control of the treatments developed. There are concerns about data theft, histories of mistrusts and secrecy regarding the use of such data and samples. But it is also important that pharmaceutical companies and entrepreneurs, regardless of nationality and race, have access to the data to aid in drug development. It would be akin to throwing the baby with the bathwater to not allow access to refine treatments and help develop manufacturing and distribution capacity.

Fortunately, many companies are now entering the space, such as 54Gene, Africas top DNA research start-up, which has received venture capital of more than $45 million since its founding. Efforts are aimed at not just collating samples but developing a pipeline of drugs for conditions that afflict sufferers. Such initiatives will ensure that the genetic diversity of Africans will contribute significantly to drug discovery and development.

Uchechi Moses is an aspiring plant biotechnologist based in Akwa Ibom, Nigeria. He holds a BS in Genetics and Biotechnology and writes about how capitalism and science can provide food security and prosperity for the next generation of Africans. Follow him on Twitter @UchechiMoses_

Read the original:
How Africa's genetic diversity can be harnessed to close the continent's 'drug and treatment gap' - Genetic Literacy Project

Why do we love sugar so much? Here is a genetic connection to your sweet addiction – Economic Times

The sweetness of sugar is one of life's great pleasures. People's love for sweet is so visceral, food companies lure consumers to their products by adding sugar to almost everything they make: yogurt, ketchup, fruit snacks, breakfast cereals and even supposed health foods like granola bars.

Schoolchildren learn as early as kindergarten that sweet treats belong in the smallest tip of the food pyramid, and adults learn from the media about sugar's role in unwanted weight gain. It's hard to imagine a greater disconnect between a powerful attraction to something and a rational disdain for it. How did people end up in this predicament?

Insights into our species' evolutionary history can provide important clues about why it's so hard to say no to sweet.

The basic activities of day-to-day life, such as raising the young, finding shelter and securing enough food, all required energy in the form of calories. Individuals more proficient at garnering calories tended to be more successful at all these tasks. They survived longer and had more surviving children - they had greater fitness, in evolutionary terms.

One contributor to success was how good they were at foraging. Being able to detect sweet things - sugars - could give someone a big leg up.

In nature, sweetness signals the presence of sugars, an excellent source of calories. So foragers able to perceive sweetness could detect whether sugar was present in potential foods, especially plants, and how much.

This ability allowed them to assess calorie content with a quick taste before investing a lot of effort in gathering, processing and eating the items. Detecting sweetness helped early humans gather plenty of calories with less effort. Rather than browsing randomly, they could target their efforts, improving their evolutionary success.

Sweet taste genesEvidence of sugar detection's vital importance can be found at the most fundamental level of biology, the gene. Your ability to perceive sweetness isn't incidental; it is etched in your body's genetic blueprints. Here's how this sense works.

Sweet perception begins in taste buds, clusters of cells nestled barely beneath the surface of the tongue. They're exposed to the inside of the mouth via small openings called taste pores.

Different subtypes of cells within taste buds are each responsive to a particular taste quality: sour, salty, savory, bitter or sweet. The subtypes produce receptor proteins corresponding to their taste qualities, which sense the chemical makeup of foods as they pass by in the mouth.

One subtype produces bitter receptor proteins, which respond to toxic substances. Another produces savory (also called umami) receptor proteins, which sense amino acids, the building blocks of proteins. Sweet-detecting cells produce a receptor protein called TAS1R2/3, which detects sugars. When it does, it sends a neural signal to the brain for processing. This message is how you perceive the sweetness in a food you've eaten.

Genes encode the instructions for how to make every protein in the body. The sugar-detecting receptor protein TAS1R2/3 is encoded by a pair of genes on chromosome 1 of the human genome, conveniently named TAS1R2 and TAS1R3.

Comparisons with other species reveal just how deeply sweet perception is embedded in human beings. The TAS1R2 and TAS1R3 genes aren't only found in humans - most other vertebrates have them, too. They're found in monkeys, cattle, rodents, dogs, bats, lizards, pandas, fish and myriad other animals. The two genes have been in place for hundreds of millions of years of evolution, ready for the first human species to inherit.

Geneticists have long known that genes with important functions are kept intact by natural selection, while genes without a vital job tend to decay and sometimes disappear completely as species evolve. Scientists think about this as the use-it-or-lose-it theory of evolutionary genetics. The presence of the TAS1R1 and TAS2R2 genes across so many species testifies to the advantages sweet taste has provided for eons.

The use-it-or-lose-it theory also explains the remarkable discovery that animal species that don't encounter sugars in their typical diets have lost their ability to perceive it. For example, many carnivores, who benefit little from perceiving sugars, harbor only broken-down relics of TAS1R2.

Sweet taste liking

The body's sensory systems detect myriad aspects of the environment, from light to heat to smell, but we aren't attracted to all of them the way we are to sweetness.

A perfect example is another taste, bitterness. Unlike sweet receptors, which detect desirable substances in foods, bitter receptors detect undesirable ones: toxins. And the brain responds appropriately. While sweet taste tells you to keep eating, bitter taste tells you to spit things out. This makes evolutionary sense.

So while your tongue detects tastes, it is your brain that decides how you should respond. If responses to a particular sensation are consistently advantageous across generations, natural selection fixes them in place and they become instincts.

Such is the case with bitter taste. Newborns don't need to be taught to dislike bitterness - they reject it instinctively. The opposite holds for sugars. Experiment after experiment finds the same thing: People are attracted to sugar from the moment they're born. These responses can be shaped by later learning, but they remain at the core of human behavior.

Sweetness in humans' futureAnyone who decides they want to reduce their sugar consumption is up against millions of years of evolutionary pressure to find and consume it. People in the developed world now live in an environment where society produces more sweet, refined sugars than can possibly be eaten.

There is a destructive mismatch between the evolved drive to consume sugar, current access to it and the human body's responses to it. In a way, we are victims of our own success.

The attraction to sweetness is so relentless that it has been called an addiction comparable to nicotine dependence - itself notoriously difficult to overcome.

It is worse than that. From a physiological standpoint, nicotine is an unwanted outsider to our bodies. People desire it because it plays tricks on the brain. In contrast, the desire for sugar has been in place and genetically encoded for eons because it provided fundamental fitness advantages, the ultimate evolutionary currency.

Sugar isn't tricking you; you are responding precisely as programmed by natural selection.

Go here to read the rest:
Why do we love sugar so much? Here is a genetic connection to your sweet addiction - Economic Times

Helping sheep and goat farmers improve productivity and increase supply with a new genetic services system – Yahoo Finance

Helping sheep and goat farmers improve productivity and increase supply with a new genetic services system

Canada NewsWire

OTTAWA, ON, Jan. 7, 2022

OTTAWA, ON, Jan. 7, 2022 /CNW/ - Today, the Minister of Agriculture and Agri-Food, the Honourable Marie-Claude Bibeau, announced an investment of $495,000 for the Canadian Centre for Swine Improvement (CCSI) to enable stakeholders to work together to increase innovation and resiliency in Canada's sheep and goat industries.

Through this investment, CCSI is collaborating with project partners on developing a Canada-wide integrated genetic services system to help sheep and goat farmers improve productivity and increase supply. Farmers will be able to use the new service system to access new developments and industry information on livestock genomics that can improve breeding and provide a more sustainable supply of high quality products along the sheep and goat value chains.

CCSI is working with a number of partners to integrate genetic services, including the Canadian Sheep Breeders Association, Ontario Sheep Farmers, the Canadian Goat Society, Canadian Livestock Records Corporation, Centre for Genetic Improvement of Livestock, Centre d'expertise en production ovine du Qubec, AgSights, and the Canadian Meat Goat Association. The integrated system will include services such as phenotype measurements on traits such as growth rate and milk yield, training for farmers to adopt new technologies, genetic evaluation, and research and development.

Canada's sheep and goat industries offer many growth opportunities for farmers across several agricultural sectors, including meat, dairy and fibre. Increasing industry collaboration in areas such as genetic services will benefit farmers with improved breeding stock to develop a more adaptable, competitive industry.

Quotes

"Canada has a strong reputation as a leader in livestock genetics and breeding. This investment will enable sheep and goat farmers to benefit from new developments in livestock genetics and improve product quality and productivity."

Story continues

- The Honourable Marie-Claude Bibeau, Minister of Agriculture and Agri-Food

"Better integration of services will enhance these organizations' abilities to deliver on their respective breed improvement mandates, while the breeders and commercial producers will benefit from improved genetics. This will also lead to a more sustainable supply of high quality inputs for other stakeholders in the sheep and goat product value chains."

- Brian Sullivan, Chief Executive Officer, Canadian Centre for Swine Improvement

Quick Facts

The funding announced today is provided through the Canadian Agricultural Strategic Priorities Program (CASPP), a $50.3 million, five-year investment to help the agricultural sector adapt and remain competitive.

The Canadian Centre for Swine Improvement is a national not-for-profit corporation that provides leadership, innovation and coordination in national genetic evaluations, database establishment and maintenance, program standards and research and development for industries such as pork, goats and sheep.

There are more than 1.2 million head of sheep and goats in Canada on approximately 15,000 farms (2016 Census of Agriculture), with over $250 million of farm cash receipts, which in 2020 had a combined annual revenue of more than $263 million. Potential for growth is large and illustrated by the fact that the number of goats has more than doubled in the last 30 years.

Additional Links

Canadian Agricultural Strategic Priorities ProgramCanadian Centre for Swine Improvement

Follow us on Twitter, Facebook, Instagram, and LinkedInWeb: Agriculture and Agri-Food Canada

SOURCE Agriculture and Agri-Food Canada

Here is the original post:
Helping sheep and goat farmers improve productivity and increase supply with a new genetic services system - Yahoo Finance

Coronavirus: Conflicting tests on two AEK players to be settled by genetics institute – Cyprus Mail

What Are Cookies

As is common practice with almost all professional websites, https://cyprus-mail.com (our Site) uses cookies, which are tiny files that are downloaded to your device, to improve your experience.

This document describes what information they gather, how we use it, and why we sometimes need to store these cookies. We will also share how you can prevent these cookies from being stored however this may downgrade or break certain elements of the Sites functionality.

How We Use Cookies

We use cookies for a variety of reasons detailed below. Unfortunately, in most cases, there are no industry standard options for disabling cookies without completely disabling the functionality and features they add to the site. It is recommended that you leave on all cookies if you are not sure whether you need them or not, in case they are used to provide a service that you use.

The types of cookies used on this Site can be classified into one of three categories:

Disabling Cookies

You can prevent the setting of cookies by adjusting the settings on your browser (see your browsers Help option on how to do this). Be aware that disabling cookies may affect the functionality of this and many other websites that you visit. Therefore, it is recommended that you do not disable cookies.

Third-Party Cookies

In some special cases, we also use cookies provided by trusted third parties. Our Site uses [Google Analytics] which is one of the most widespread and trusted analytics solutions on the web for helping us to understand how you use the Site and ways that we can improve your experience. These cookies may track things such as how long you spend on the Site and the pages that you visit so that we can continue to produce engaging content. For more information on Google Analytics cookies, see the official Google Analytics page.

Google Analytics

Google Analytics is Googles analytics tool that helps our website to understand how visitors engage with their properties. It may use a set of cookies to collect information and report website usage statistics without personally identifying individual visitors to Google. The main cookie used by Google Analytics is the __ga cookie.

In addition to reporting website usage statistics, Google Analytics can also be used, together with some of the advertising cookies, to help show more relevant ads on Google properties (like Google Search) and across the web and to measure interactions with the ads Google shows.

Learn more about Analytics cookies and privacy information.

Use of IP Addresses

An IP address is a numeric code that identifies your device on the Internet. We might use your IP address and browser type to help analyze usage patterns and diagnose problems on this Site and improve the service we offer to you. But without additional information, your IP address does not identify you as an individual.

Your Choice

When you accessed this Site, our cookies were sent to your web browser and stored on your device. By using our Site,you agree to the use of cookies and similar technologies.

More Information

Hopefully, the above information has clarified things for you. As it was previously mentioned, if you are not sure whether you want to allow the cookies or not, it is usually safer to leave cookies enabled in case it interacts with one of the features you use on our Site. However, if you are still looking for more information, then feel free to contact us via email at [emailprotected]

Read the original here:
Coronavirus: Conflicting tests on two AEK players to be settled by genetics institute - Cyprus Mail

The genetic lottery: Are our lives determined at birth? – New Zealand Herald

A controversial new book suggests that our success or failure in life is hard-coded in our genes at conception. By Danyl McLauchlan.

It's deeply unfair. Shortly after we're conceived, our genetic material long sequences of chemical codes arranged in a double-helical structure called DNA, tightly bundled into dense thread-like structures called chromosomes is uncoiled and scanned by complex factories of molecular machinery.

These factories use our genes as blueprints for turning a tiny, fertilised egg into a fully grown human, assembling proteins into cells, cells into organs, organs into anatomical systems digestive, muscular, cardiovascular, nervous that allow us to eat, walk, breathe and think. But we have no control over which genes we get, or the type of person they turn us into.

Each of us is genetically unique. We inherit our DNA from our parents, but in each sperm or egg the genetic sequences are recombined, shuffled around, mixed up. Which is why each of us resembles the other members of our family, but none of us is identical to them (even identical twins have minor genetic differences). If two people were able to produce kids carrying every possible combination of their genotypes, they'd have 70 trillion children.

We like to tell ourselves that we're all equal, despite our vast, randomly generated genetic diversity that life is about the choices we make or the world we're born into. These assumptions carry over into our politics. On the right, success or failure is considered meritocratic: people should have equality of opportunity but then take personal responsibility for themselves and work hard to get ahead. Left-wing politics focuses on social or economic injustice: income inequality, exploitation, discrimination. But in the first decades of the 21st century, new findings in the field of behavioural genetics call the premises behind both political projects into question.

Kathryn Paige Harden is a psychologist and behavioural geneticist at the University of Texas. In 2021, she became one of the most controversial scientists in the world when she published her first book, The Genetic Lottery. In it, Harden argues that genes matter. A lot. Social scientists have long known that family income is a strong predictor of educational attainment: if you grow up in a wealthy household, you're more likely to get a degree and a well-paid job. But what Harden is saying is that genetics are just as decisive that an important part of our success or failure is hard-coded at birth.

The sum total of all your DNA across all of your chromosomes is known as your genome. The first human genome was sequenced back in 2003, a 13-year project that cost more than a billion dollars. Today, a whole genome sequence costs about $1000 and takes 24 hours to produce. However, most labs doing behavioural research use a cheaper technique that looks for a known collection of genetic markers. This costs about $100.

There's a gene on your fourth-largest chromosome, called the huntingtin gene. It tells your cells how to create a protein that plays a role in building subcellular structures, especially in the brain. If you have a specific mutation in this gene, you're doomed to develop Huntington's chorea, a terrible neurodegenerative condition that strikes in adulthood. (When biology and medical students first learn about the gene, they worry that they might have this mutation, but if you're a member of one of the rare families that are stricken by the disease, you'll already be very aware of it.)

For a long time, genetics researchers thought that all genes worked like the huntingtin gene, in the sense that it coded for a specific protein, and a mutation caused a specific disorder. So they went in search of other monocausal genes; they looked for drug-addiction genes, depression genes, height genes, cancer genes, gay genes, criminal genes, and schizophrenia genes. Rather embarrassingly, they often announced that they'd found them.

But in 2007, the first large-scale genome-wide association study (GWAS) was published, and it revealed that most genes and gene variants were totally unlike the huntingtin model, and that none of these "depression genes" or "criminal genes" had any scientific validity.

4 Jan, 2022 04:00 PMQuick Read

27 Dec, 2021 04:00 PMQuick Read

GWAS is a suite of statistical tools: it works by comparing huge numbers of individual genomes the first studies used 10,000 people, now they're into the millions to look for differences in life outcomes. Which individuals have heart disease or cancer? How tall are they? What's their highest educational qualification? What's their household income? Researchers then use high-performance computers and sophisticated algorithms to find genes that correlate with those outcomes.

The results show us that most gene effects are tiny a variation in a single gene usually has a minimal impact, and almost all genetic effects are "polygenic", meaning they're the combination of many genes working together.

Instead of a single gene for height, there are about 700 gene variants involved, influencing everything from growth hormones to bone length. GWAS reveals that most genetic diseases or inherited traits are staggeringly complex. Even something as seemingly simple as hair colour is influenced by more than 100 different genes interacting with each other.

Because GWAS is such a powerful technique, it has been taken up by researchers across the life and social sciences. And they're uncovering the genetic origins of thousands of diseases and conditions.

You can look at the health outcomes, hair colour or height of the people in your study and correlate them to which variants they have. And you can calculate a polygenic score in which you add up all the effects of all the gene variants and estimate the likelihood that an individual will have the trait you're investigating that they'll be short or tall, have red hair or be prone to heart disease.

At the heart of Harden's argument in The Genetic Lottery is the claim that academic success in modern educational systems is innate that it's less to do with determination or grit and more like tallness or hair colour. "There are specific types of cognitive skills that are richly rewarded in modern educational systems: the verbal and visuospatial reasoning abilities that are tested by standardised cognitive tests," says Harden. And gene variations and combinations that correlate to those abilities show up in the GWAS results. "Beyond that, we see genes associated with personality traits, such as delay of gratification and openness to new experience, are also associated with going further in school."

When Harden was 22, her boyfriend at the time was a history PhD student, and for her birthday he gave her a copy of Daniel Kevles' horrifying historical study, In the Name of Eugenics. "Not the most romantic present I've ever gotten," she admits, "but certainly one of the most durably influential." So, she gets why people are so sensitive to this conversation: statistics and genetics share a very sinister past. People are right to be apprehensive.

But first, she counters, the way eugenicists and white supremacists talk about race is scientifically incoherent. Humans are a very promiscuous species; none of us are descended from one single group of people. Recent research estimates that the most recent common ancestor of every person currently alive probably lived in East Asia a few thousand years ago. We have superficial differences facial features such as the colour of our skin, eyes and hair based on where the majority of our recent ancestors are from, but we're all fairly recent relatives. "Ironically," Harden says, "genetic data help us see why modern 'race science' is actually pseudoscience."

Second, it's very hard to make racial comparisons with GWAS. This is partly because the biological markers don't line up properly across different ethnic groups and these mismatches confound the analysis. But it's also because the genomes currently available for GWAS analysis are mostly from white people. "I think it's helpful to step back and think about where the data in large-scale genetic studies of education are coming from," says Harden. "The biggest sources are European-ancestry participants from [genetic testing company] 23andMe and the UK Biobank. This is a very particular segment of the American and British populations people who are likely to be racially identified as white and who went to school in the UK and the US in the latter half of the 20th century. The genetic data does give us some clues about what sorts of traits are rewarded by the educational system for this segment of the population."

Third, Harden asks, if there's a cluster of genes that reward educational attainment, at least among people with recent European ancestry, and those people get good qualifications and access to well-paid high-status jobs how is that fair? None of us choose the genes we're born with. It is, quite literally, a lottery. "There is no measure of so-called 'merit' that is somehow free of genetic influence or untethered from biology," she says.

Instead of accepting the outcome of genetic meritocracy, she challenges us in the book with the assumption that a meritocratic society is moral. Shouldn't we be asking ourselves why our education system and labour markets allocate success and status to such a narrow set of attributes and punish others?

When it comes to genetic discrimination and how to address it, Harden says two things that school systems seem to be selecting against are ADHD symptoms and early fertility. "Making schools more inclusive and supportive of children who feel the need to move their body constantly, and of teenagers and young adults who have care responsibilities, would change the pattern of what genes are associated with getting more education."

In 1973, psychologists at the University of Otago began studying the lives of 1037 babies born between April 1, 1972 and March 31, 1973 at Dunedin's Queen Mary Maternity Hospital. In what is known as the Dunedin Study, researchers survey the participants at regular intervals, conducting interviews, physical tests, blood tests and even dental examinations. The Dunedin Study has been running for nearly 50 years and is one of the most respected longitudinal studies in the world.

In 2016, the journal Psychological Science published a paper in which the genomes of 918 non-Mori Dunedin Study participants were subjected to GWAS analysis for educational attainment. And they reported a number of key findings: educational attainment polygenic scores also predicted adult economic outcomes, such as how wealthy the subjects became; genes and environments were correlated in that children with higher polygenic scores were born into better-off homes; children with higher polygenic scores were more upwardly mobile than children with lower scores; polygenic scores predicted behaviour across the life course, from early acquisition of speech and reading skills through to geographic mobility and mate choice and on to financial planning for retirement; polygenic-score associations were mediated by psychological characteristics, including intelligence, self-control and interpersonal skill.

What they found was that children with gene-variant combinations that correlated with educational attainment were more likely to say their first words at younger ages, learn to read at younger ages and have higher aspirations as high school students. All of which sounds like a massive validation of Harden's thesis. But Professor Richie Poulton, a co-author of the paper and director of the Dunedin Study since 2000, cautions strongly against linking these findings to Harden's conclusions.

"A key point, often missed," he says, "is the genetic effects were small. A lot of hot air has been expended without acknowledging this very critical and basic fact. [Genes] are not huge influences by themselves: it's nature-nurture interplay that accounts for the most important outcomes. That's where the real gold (versus fool's gold) lies in understanding how people's lives turn out."

The same point is made by the University of Auckland's Sir Peter Gluckman, an internationally recognised expert in child development. For him, the problem with Harden's approach is that "there's no discussion of developmental plasticity. There's no doubt that genes influence behaviour. We know that genetic associations with educational achievement are very real.

"But we also know a lot of those mechanisms are very indirect. And we know that environmental influences, starting from before birth and acting right through childhood have the biggest outcomes. Take the famous experiment on the cat."

Gluckman is referring to the Harvard "pirate kitten experiment", an influential experiment in the 1960s that biology lecturers still like to shock their undergraduate students with. It involved suturing a kitten's eye closed for the first three months of its life. When the sutures were removed, the kitten was blind in that eye because the animal's brain didn't develop the ability to process data from it. "Yes, we have genes that determine eye growth," says Gluckman, "but if we don't use the eye properly in the first few months after birth, then those genes don't work properly. And at the end of the day, what we can affect is the environment."

Poulton agrees that it's far too early to talk about policy solutions based on behavioural genetics. "The understanding of how you would do this and what you would focus on is far too primitive. But you can focus on some of the 'environmental' factors that mediate the genetic effects Self-regulation abilities play a role here, and trying to strengthen those skills among all young people would have benefits."

Harden acknowledges that environmental factors are hugely important. And she believes that the effect sizes for educational attainment polygenic scores will only increase as the datasets grow and the genomic information becomes more fine-grained. But she doesn't believe you can talk about proper educational intervention without discussing genetics. She points out that most current educational interventions have almost no effect on student outcomes, no matter how well funded they are. "Not talking about genetics means sticking with the status quo," she says.

Read the original here:
The genetic lottery: Are our lives determined at birth? - New Zealand Herald

Human Skin Cell Biology and Disease Research at UCI Expands for The Human Cell Atlas Project – New University

In connection with UCIs Skin Biology Resource Center, a UCI interdisciplinary research team received a three-year, $2 million grant from the Chan Zuckerberg Initiative in November of last year.

According to the Chan Zuckerberg Initiative website, the research team is using this grant to work towards constructing a skin cell atlas that will help explain ancestral differences in skin biology and pathology. The initiative, which was founded in 2015, aims to alleviate some of the toughest challenges presented in society, including science and education. With its contribution to this skin cell atlas, knowledge of all types of cells on human skin will be collected in a revolutionary new way.

Like many of the current cell atlas projects underway, the teams goal is part of a larger initiative: The Human Cell Atlas.

Cells are important to every system that allows the human body to function, they are the basic building blocks of life. According to the Human Cell Atlas goals outlined here, cell biologists hope to expand and transform our current understanding of cells.

As a global project, this initiative aims to map every single cell type in the human body. Cell mapping refers to the process of finding a cells location within tissue or an organ. In this way, molecular information about the cell can be gathered and its functions and behavior with neighboring cells can be described.

With over two thousand members, one thousand institutes and over 75 countries involved, this project will serve as a valuable source of information for health and disease, aiding disease diagnosis and treatment.

In collaboration with professors from the University of Michigan, UCI professors Maksim Plikus and Qing Nie who teach development and cell biology, Bogi Andersen who teaches biological chemistry, Natasha Mesinkovska who specializes in dermatology, and Dara Sorkin who specializes in psychology and social behavior are working on the creation of the skin cell atlas at an ancestral level. This ancestral level, referring to the ancestors in ones family, allows for the analysis of biological characteristics that have been inherited throughout a familial linaeage.

Through a study including 72 adults of ages 18 and above, the principal investigators from both institutions will generate a skin cell atlas with networks composed of gene expression and gene regulatory state data.

Gene expression is an important process that instructs DNA to create functional products in the human body, such as proteins. Gene regulation states allow for the control of gene expression. Here, both processes are fundamental in the functions of particular skin cell types, where these skin cell types will vary based on each individuals ancestry.

Researchers will be collecting samples from individuals of African American, Latinx, Middle Eastern and Asian backgrounds on developmental, anatomical and physiological distinct sites of the human body.

While skin disease today can arise from factors such as skin pigmentation, the color of a persons skin, skin thickness and hair texture, these factors vary among individuals who encompass different ancestries as well. Since these skin and hair characteristics have yet to be known, the skin cell atlas will also be useful in understanding new information about these particular body characteristics.

To learn more about this study and the five UCI and University of Michigan professors that are involved, visit the Chan Zuckerberg Initiative website.

Korintia Espinoza is a STEM Staff Writer for the winter 2022 quarter. She can be reached at korintie@uci.edu.

Related

Go here to see the original:
Human Skin Cell Biology and Disease Research at UCI Expands for The Human Cell Atlas Project - New University

LUMICKS Announces Adoption of z-Movi Cell Avidity Analyzer by Two Major Centres for Cancer Immunology – PRNewswire

AMSTERDAM, Jan. 10, 2022 /PRNewswire/ -- LUMICKS, a next generation life science tools provider, today announced that two major centers of excellence in cancer immunology have adopted LUMICKS' z-Movi Cell Avidity Analyzer instrument.

The first placement is at Fred Hutchinson Cancer Research Center ("Fred Hutch") in Seattle, Washington, USA, a leading research institute dedicated to the eradication of cancer. The instrument is housed at the Immune Monitoring Core Facility and serves multiple immuno-oncology and cell therapy research groups from the Center to accelerate immunotherapy development for cancer treatments.

The second z-Movi is placed at the University of Oxford, in Oxford, UK, in the lab of Prof. Tim Elliott, a world leader in the field of antigen presentation and T cell biology. The teams of Prof. Elliott and Prof. Persephone Borrow are using the instrument to investigate a broad range of T celltarget interactions including the potency and longevity of T cells in solid tumors.

"The z-Movi Cell Avidity Analyzer provides an excellent platform for quantitating the avidity of interactions occurring between T cells and cognate antigen-presenting target cells during the induction and effector phases of an immune response," said Prof. Elliott and Prof. Borrow. "This enables dissection of attributes of both T cells and their interaction partners that influence the response to viral infections and cancer."

"We are delighted that our z-Movi instrument will be adopted into the workflows at Fred Hutch and University of Oxford, two institutions devoted to the development of promising immunotherapeutic strategies," said LUMICKS CSO Dr. Andrea Candelli. "At LUMICKS, we are focused on developing new technologies that help cancer researchers discover new therapies. We believe that cell avidity measurements provide unique insights into the mechanism of action of cell therapy products, ultimately leading to higher success rates for novel cancer immunotherapies."

About LUMICKS

LUMICKS is a leading life science tools company that develops equipment for Dynamic Single-Molecule and Cell Avidity analysis, two rapidly emerging areas in biology research and immuno-oncology. LUMICKS' tools allow researchers to build the crucial and as yet unfinished bridge between structure and function at both a molecular and a cellular level. This is achieved by applying and measuring forces around biological interactions, enabling the detailed real-time analysis of underlying biological mechanisms. LUMICKS' C-Trap Optical Tweezers Fluorescence & Label-free Microscopy, allows scientists to analyze complex biological processes in real-time. Similarly, the z-Movi Cell Avidity Analyzer enables the measurement and selection of immune cells based on their real-time interactions with target cells.

For more information contact:

Kassandra Barbetsea, media contact+31 (0) 63 482 09 48[emailprotected]

Joshua Young, investor contact[emailprotected]

SOURCE LUMICKS

More:
LUMICKS Announces Adoption of z-Movi Cell Avidity Analyzer by Two Major Centres for Cancer Immunology - PRNewswire

Undergrad’s Extensive Research Experience Was Supported by Several Key Programs | | SBU News – Stony Brook News

Samuel Escobar

Samuel Escobar the URECA researcher of the month for January 2022 was in the University Scholars program at Stony Brook University and recently graduated summa cum laude with a BS in Biology from the College of Arts and Sciences. His substantive involvement in research as an undergraduate was supported by several key programs. Escobar participated in a four-week pre-freshman program in the Collegiate Science and Technology Entry Program (CSTEP), and in his freshman year, he participated in the INSPIRE/Include New Students through a Peer Introduction to Research Experience program. In spring semester of his freshman year, Escobar arranged to do research with Assistant Professor Benjamin Martin from the Department of Biochemistry and Cell Biology during Summer 2019 as a participant in the PSEG-Explorations in STEM program, a 10-week summer research program co-administered by the Career Center and URECA.

Escobar continued doing research in the Martin Lab for the rest of his undergraduate years, and was one of two 2021 URECA summer program applicants to be awarded the Chhabra-URECA Fellowship, an award that provides funding for summer research and recognizes students with a passion for research. His work on Cell Cycle Regulation Modulates Tail-Bud Morphogenesis in Zebrafish involves using an R software script to design hybridization chain reaction probes for genes of interest. Escobar will be presenting this research at the Spring 22 URECA poster symposium.

When asked about his research experience, Escobar said, if youre considering doing research, just try it out! You might regret not doing it. Thats why I picked Stony Brook. I always tell people, the price for what youre getting here is insane. I was able to get this awesome research experience, which has been super valuable to me, and to have great mentors.

On campus, Escobar has served as a teaching assistant, vice president of the Latino Medical Student Association Plus+, and a Center for Prevention and Outreach Red Watch Band intern. He volunteers with Good Samaritan Hospital, the NOSH Soup Kitchen and the Eastern Farm Workers Association. During May 2020 to May 2021, Escobar was employed as a contact tracer with the New York Department of Health and is currently employed as a medical scribe with Long Island Urgent Care in West Babylon and Manorville, NY, where he aids in performing intake questions, as well as translation of medical explanations for Spanish-speaking patients. Escobar plans to apply to medical school programs in the next year. He is a first-generation college student from Deer Park, NY.

Read the interview with URECA Director Karen Kernan

View original post here:
Undergrad's Extensive Research Experience Was Supported by Several Key Programs | | SBU News - Stony Brook News

Berkeley Lights and Aanika Biosciences Announce Partnership – GlobeNewswire

EMERYVILLE, Calif., Jan. 10, 2022 (GLOBE NEWSWIRE) -- Berkeley Lights, Inc. (Nasdaq: BLI), a leader in digital cell biology, and Aanika Biosciences, a growing biotech start-up using edible microbial tags to improve food safety, today announced a strategic partnership that will enable faster identification of outbreak sources, reduce incidents of fresh produce contamination and minimize the impact of food borne illness related recalls.

In this partnership, Aanika will use Berkeley Lights' high-throughput, functional screening service to rapidly identify and optimize functional, antimicrobial peptides (AMPs) capable of killing harmful bacteria, including those that cause outbreaks of foodborne illness. In addition, the Beacon Optofluidic Platform will be leveraged to find peptides that are toxic to bacteria to create a new antibacterial tag that will then be applied to their bacterial spore-based barcoding technology to protect the food supply chain.

Berkeley Lights high-throughput, functional screening service, based on our proprietary cell-free expression technology, is accelerating novel discoveries to develop solutions and products in the agricultural space, said Eric Hobbs, Ph.D., chief executive officer of Berkeley Lights. Specifically, applying the Berkeley Lights platform to AMPs allows us to rapidly map and identify the top mutational sites to further optimize AMP performance.

AMPs are gaining popularity as antibacterial agents across a wide range of applications, particularly as microbes are becoming more resistant to antibiotics, and are a growing focus for both companies.

Tracking, tracing and identifying the origin of food borne illnesses is just the beginning of what Aanikas watermark technology can do to help improve and protect our global food system, said Aanika co-founder and CEO Vishaal Bhuyan. The partnership with Berkley Lights will enable us to move faster, and go deeper, into uncovering and unlocking the opportunities to have greater economic, environmental and human health impact.

Berkeley Lights will participate in the downstream economics created by its enabling technology through a royalty arrangement as part of this strategic partnership. Additional terms of the agreement are not disclosed. This is Berkeley Lights second announced high-throughput, functional screening partnership following theBayer Partnership announced in 2021.

About Berkeley Lights

Berkeley Lights is a leading digital cell biology company focused on enabling and accelerating the rapid development and commercialization of biotherapeutics and other cell-based products for our customers. The Berkeley Lights Platform captures deep phenotypic, functional and genotypic information for thousands of single cells in parallel and can also deliver the live biology customers desire in the form of the best cells. Our platform is a fully integrated, end-to-end solution, comprising proprietary consumables, including our OptoSelect chips and reagent kits, advanced automation systems, and application software. We developed the Berkeley Lights Platform to provide the most advanced environment for rapid functional characterization of single cells at scale, the goal of which is to establish an industry standard for our customers throughout their cell-based product value chain.

Berkeley Lights Beacon and Lightning systems and Culture Station instrument are FOR RESEARCH USE ONLY. Not for use in diagnostic procedures.

About Aanika Biosciences

Aanika Biosciences was co-founded in 2018 by Vishaal Bhuyan after he personally experienced the consequences of ordering fresh seeds and receiving stale, contaminated products instead. He made it is his mission to create a safer food supply by finding a way to track, trace and authenticate products. Aanikas customized microbial-based tags help companies gain valuable insights about their supply chains, help their customers make better consumption choices, and create a more sustainable world.

Forward-Looking Statements

To the extent that statements contained in this press release are not descriptions of historical facts regarding Berkeley Lights or its products, they are forward-looking statements reflecting the current beliefs and expectations of management. Such forward-looking statements involve substantial known and unknown risks and uncertainties that relate to future events, and actual results and product performance could differ significantly from those expressed or implied by the forward-looking statements. Berkeley Lights undertakes no obligation to update or revise any forward-looking statements. For a further description of the risks and uncertainties relating to the Companys growth and continual evolution see the statements in the "Risk Factors" sections, and elsewhere, in our filings with the U.S. Securities and Exchange Commission.

Media ContactsMedia @berkeleylights.comLaura.shulman@foodfuturestrategies.com

Investor ContactIR@berkeleylights.com

Read more:
Berkeley Lights and Aanika Biosciences Announce Partnership - GlobeNewswire