Category Archives: Human Genetics

One of the five authors, who all contributed equally, is Dr Adam Rutherford, a prominent science communicator, author, broadcaster and an Honorary Senior Research Associate at UCL.

He announced the new paper, which he says has been accepted by a journal but not yet published, on his Twitter feed.

"I have been working on this a while: sparking a conversation about the lexicon of genetics, which continues to utilise scientifically redundant, confusing and racist terminology,"he said. "We're definitely not prescribing or policing language, but want to prompt a dialogue with colleagues in similar and adjacent fields about our terminology, datasets and tools, and move towards a lexicon that both serves the science and frees us from a racist past."

Dr Ewan Birney, deputy director of the European Molecular Biology Laboratory at the Wellcome Genome Campus in Cambridgeshire, is also a co-author of the article.

He explains that beyond dropping Caucasian, other terms should also be avoided, including ethnicity labels -such as"Native American", "Hispanic"and "White Irish"-and cultural terms such as "European".

Dr Birney and his colleagues advocate for scientists to replace these commonly used words and phrases with more complex language, based around a two-step genetic analysis.

As a result, he says this more technical language would see the label of "European replaced with "The European-associated PCA cluster, which aims to minimise variation in non-genetic factors and genetic factors".

This suggestion is, by Dr Birneys own admission, "bamboozling"and "a bit complex"for non-geneticists.

PCA - orprincipal component analysis - is a tool for analysing genes that picks up similar physical or biochemical characteristics of species,

However, in the article the scientists say they prioritised "technical accuracy over concision".

"Some of these suggestions may meet with disagreement; we present them partly to stimulate discussion of these and other terms, and in the hope that this will lead to better and more accurate language conventions and less misunderstanding, particularly outside of human genetics,"the researchers add.

Dr Aylwyn Scally is another of the authors. Heworks in the genetics department at the University of Cambridge and is based at Darwin College.

Darwin College was set up and named after Sir Charles Galton Darwin -a noted proponent of eugenics and grandson of Charles Darwin -upon his death in 1962.

In a tweet, Dr Scally revealed the opinion piece he co-authored received "constructive input"from Dr Agustin Fuentes, a professor of anthropology at Princeton University, who last month penned a scathing editorial criticisingCharles Darwin.

He accused him of letting his scientific process become "warped" by his prejudices, which included racism, sexism and misogyny.

Dr Michael Inouye, of the University of Cambridge, and Dr Jennifer Raff, of the University of Kansas, also co-authored the article.

The rest is here:
The word Caucasian is racist and must be banned, say academics - Telegraph.co.uk

Humans are testing the limits of most species survival, with their planet-wide changes. As urbanisation, deforestation, loss of wildlife, and human-wildlife conflicts continue to spiral up, there is a need to use every available tool available, to help protect what is left of the natural world. Molecular ecology is one such tool for conservation and can help in wildlife disease management and forensics in illegal trade.

Molecular ecology is a hybrid field that combines molecular biology techniques with ecological data to make sense of natural processes such as the growth or decline of populations, formation of new species, extinctions and invasiveness.

In modern molecular ecology, genetic data is analysed in the context of field and observational studies to address ecological problems.

Molecular ecology is used to estimate population genetic diversities to aid wildlife breeding and conservation efforts, define species for conservation policy, track diseases, and combat poaching.

Genetic data from organisms is collected in the form of molecular markers, which are biological molecules that may be used to distinguish between species, populations, or individuals.

When molecular biologists first began identifying genetic differences between individuals, they extracted proteins from animal or plant tissues, and used them as molecular markers. However, DNA-based markers soon became more popular than protein markers as they could be obtained from very small samples of tissue. They were also easier to handle and showed more variations than protein-based markers. Molecular ecology now relies on extracting DNA from animals using tissue samples (typically hair, scales, skin, bones, horns, or blood) or even fecal matter.

Different individuals within a species can have different forms or variants of a particular gene or molecular marker. A familiar example of this is blood type one of the genes that determine blood type in humans comes in three different forms/variants known as A, B, and O. Such genes are known as polymorphic (poly = many, morphic = form) genes. Genes that are the same in all individuals of a population are called monomorphic (mono = one, morphic = form).

By studying and documenting the variations in the genes and molecular markers, one can measure the genetic diversity of a population of animals with the help of statistics.

Genetic diversity is the fuel for natural selection. It is a source of inheritable variations in characteristics that can allow populations to survive changing environments. Higher the genetic diversity of a population, higher the chance that some individuals in that population can adapt to new environmental conditions. Thus, the population will not go extinct due to any changes.

Large populations typically have high genetic diversities, whereas small populations have low genetic diversities. If the population size of a species drops sharply due to natural disasters or human negligence and anthropogenic activities, its genetic diversity is reduced, creating a genetic bottleneck. When this happens, not only is the population robbed of its potential to survive, it also becomes vulnerable to inbreeding. Inbreeding occurs in small populations, where genetically related individuals are more likely to mate with each other.

Over time, such populations suffer from inbreeding depression, a condition where genetic variants with harmful mutations begin to accumulate.

Cheetahs are a classic example of how inbreeding depression can bring a species to the brink of extinction, despite extensive efforts at conservation through captive breeding programmes. To understand why captive breeding efforts in cheetahs were failing, a series of genetic analyses were done. These analyses showed that due to the combined effects of the past natural disasters and indiscriminate human hunting, cheetahs were highly inbred. The inbreeding not only caused reproductive issues with low fertility and high infant death rates, but also left cheetahs vulnerable to diseases. The cheetahs genetic diversity was so severely decimated, that a crucial immune-related gene complex, which is usually very polymorphic in most species, was monomorphic (had no genetic variation) in cheetahs. This caused feline infectious peritonitis a common viral disease that kills <1% of domestic cats to wipe out nearly 80% of a captive breeding population of cheetahs in the USA.

To offset inbreeding in captive and protected populations of other endangered species (Mexican red wolves, Puerto Rican crested toads, and African lions to name a few), conservationists have attempted genetic rescues. Genetic rescues are carried out by introducing new individuals (which can add more genetic variation) into inbred populations to increase genetic diversity.

However, such measures can backfire in some species like the Ibex and the Arabian oryx, which ironically, suffer from outbreeding depression. Gene flow between populations in such species is usually low, as their populations are insular with very limited immigration and emigration; therefore, each population seems genetically inbred. This, however, is advantageous for the population as it has developed local adaptation and maintains a specific combination of gene variants that allow for better survival in local conditions.

In misplaced attempts at genetic rescue by reversing this local inbreeding to recover genetic diversity in such systems, breeding programmes mate individuals from different populations. The outcomes of these efforts are usually poor. The offspring of such pairings often end up with genetic combinations that leave them unable to survive in either of the two local conditions. For example, in an attempt to genetically rescue the Alpine ibex, Nubian ibex were introduced into the Tatra mountains. Unfortunately, the introduced ibex which were adapted to warmer climates, rutted in autumn and birthed hybrid young in February, the coldest time of the year. Obviously, these offspring did not survive, and the rescue attempt failed.

Based on the lessons learned from both inbreeding and outbreeding depression, it is clear that molecular ecology is essential for successful wildlife conservation.

In India, molecular ecology studies on the critically endangered gharial and blackbuck reveal that the genetic diversities in managed populations of these animals are not high, painting a grim picture for their chances of survival.

Recent work using genome-wide data on tigers suggests that compared to the tigers from Amur, Sumatran, and Malayan populations, Indian tigers have very high genetic diversity. However, this data also indicates that certain tiger populations in India are so isolated and small, that local inbreeding is occurring.

Although we have many tigers in Indiaroughly two-thirds of all the worlds tigerstheir populations in some parts of India are fragmented, which has caused local inbreeding. The Amur tigers, on the other hand, are much fewer in numbers, but they are not inbred because they are not isolated from each other, says Uma Ramakrishnan a molecular ecologist from the National Centre for Biological Sciences (NCBS), Bangalore.

Ramakrishnan and her team have worked on tigers for over 15 years, and their molecular data is now being used to formulate plans for genetically rescuing some of Indias inbred tiger populations. Our work can help collecting data regarding which tigers are least inbred and which ones can be moved between populations, she adds.

Defining a species seems more like an esoteric academic undertaking rather than a serious and practical conservation issue. However, the conservation status of a species and the legal protection it is accorded is based on its taxonomic classification. Therefore, any ambiguity in how or what constitutes a particular species can have a major impact on that organisms survival.

Traditional methods of defining a species based on physical characteristics and behavioral observations are no longer considered reliable. Molecular taxonomy, which depends on genetic information, is now being increasingly used to resolve taxonomic disagreements and correct misclassifications.

Errors in taxonomy have resulted in the mismanagement of conservation efforts of many species. Two examples that stand out, are the cases of the colonial pocket gophers and the dusky seaside sparrow.

A single population of pocket gophers (<100 in number) within a tiny range in the State of Georgia, USA, was managed as an endangered species for more than 10 years as it was described as a distinct species (Geomys colonus) based on physical characteristics. Molecular ecology later proved that this population was genetically no different from Geomys pinetus, a pocket gopher species that is common in southeastern USA.

Similarly, when a darker form of the seaside sparrow (Ammodramus maritimus) was discovered in Florida, USA, it was identified as a separate species (A. nigrensis) and listed as endangered due to its low numbers and restricted range. After a seven-year long unsuccessful captive breeding program, the last dusky sparrow died in captivity. Two years later, however, molecular data revealed that this species had been genetically indistinct from the seaside sparrow.

In both these cases, conservation efforts were wasted on populations that had been misclassified as distinct species.

Another area in which molecular taxonomy is becoming important is in identifying areas rich in endemic species.

India has a huge amount of biodiversity, but many of its landscapes, like savannahs, and organisms, like arthropods, have hardly been studied. Now, with more field expeditions across these landscapes, and better taxonomic tools based on DNA that complement traditional morphology-based classification, we are making some surprising discoveries in the field of systematics, says Jahnavi Joshi, a molecular ecologist and taxonomist from the Centre for Cellular and Molecular Biology (CCMB), Hyderabad.

Recent studies on the molecular taxonomies of geckos and centipedes have shown that previously ignored regions like peninsular India, the Eastern Ghats, and the drier northern parts of the Western Ghats are unexpectedly rich in endemic species. Such areas need to be protected to conserve the range-restricted flora and fauna that are exclusively found there.

Molecular ecology has now become an important part of wildlife disease management. Rapid detection of even low intensities of viral, bacterial, and parasitic infections is now possible using tests based on PCR (polymerase chain reaction a technique that amplifies or makes more copies of specific DNA regions). Currently, PCR-based diagnostic tests allow for the swift detection of a number of diseases in wildlife such as the Kyasanur forest disease (a tick-borne viral disease in South India), Ebola, Nipah, tuberculosis, rabies, and malaria, all of which are directly responsible for endangering wildlife and spilling over into domestic livestock and human populations.

By studying molecular interactions between pathogens and their vectors (insects like ticks and mosquitoes, or wildlife like raccoons), scientists can even track routes of transmission and reservoir hosts for diseases such as monkey fever, avian malaria, and rabies. In addition, molecular ecology studies on host-pathogen interactions can help conservationists understand how some species or individuals are more tolerant, resistant, or susceptible to certain diseases. For example, molecular genetics work on frogs is showing that individuals with stronger immune systems are actually more likely to die of chytridomycosis, a fungal skin infection that has caused mass die-offs and extinctions in amphibians globally.

When law enforcement authorities seize illegal wildlife products, the first problem they encounter is identification what animal does a pelt, skin, hair, horn, flesh, or bone belong to? Molecular forensics using DNA barcoding has been used to identify species even from processed samples such as dried meat and powdered bones or horns. Similar to how supermarket scanners can identify products from a series of black and white stripes using the universal product code, DNA barcoding matches short sequences from samples with those in a reference database to identify which species the sample belongs to. For animals, sequences from the mitochondrial gene COX1 or CO1 (cytochrome oxidase 1) are usually used. Currently, reference databases such as the Barcode of Life Data System (BOLD) and the International Barcode of Life contain nearly 9.5 million DNA barcodes for thousands of species of animals, plants, and other organisms.

The usefulness of molecular tools does not end there. Other molecular markers such as microsatellites, minisatellites, and SNPs (single nucleotide polymorphisms), as well as techniques such as DNA profiling/fingerprinting (which has been used in criminal investigations), can be applied to identify which country or population the poached animal came from. Researchers have used microsatellite data to identify the species, sex, and even geographic origins of seized tiger parts, elephant tusks, and a variety of other animal parts.

Banner image: Although Amur tigers have much smaller population sizes and genetic diversity than Indian tigers, they are not isolated from one another, and so, do not suffer from inbreeding. In India, however, some tiger populations are so small and isolated, that local inbreeding has occurred. Photo by S. Brickman/Flickr.

Excerpt from:
What is molecular ecology and how does it help in conservation? - Mongabay-India

The obvious problem with the lab-leak theory, though, is that there remains no concrete evidence for it. Chan has no particular view about how exactly an accident might have happenedwhether a student got sick in a bat cave, say, or secret research to infect mice with a novel virus went awry. After reading Chans posts, I noticed that many of her claims dont even relate to direct evidence at all; more often, they revolve around its absence. She tends to point out things that Chinese researchers didnt do or say, important facts they did not quickly reveal, the infected market animal they never found, or a database thats no longer online. Shes plainly suggesting there is a cover-upand, therefore, a plot to conceal the truth.

Last February, when leading scientists convened to analyze the virus genome, they ended up publishing two letters. One, in The Lancet, dismissed the lab-accident possibility outright as a conspiracy theory (its authors included a scientist who funded research at the Wuhan lab). The other was the Proximal Origins letter in Nature Medicine, coauthored by Kristian Andersen, an evolutionary biologist at the Scripps Research Institute in La Jolla, California. Andersen and his coauthors looked at the genome of the virus and marshaled arguments for why it was very likely a natural occurrencebacked by evidence that it was similar to others found in nature.

The 30,000 genetic letters in that genome remain the most widely studied clue to the viruss origin. Coronaviruses frequently swap partsa phenomenon called recombination. Andersen found that all the components of the virus had been seen before in samples collected over the years from animals. Evolution could have produced it, he believed. The Wuhan Institute had been genetically engineering bat viruses for scientific experiments, but the SARS-CoV-2 genome did not match any of the favorite chassis viruses used in those experiments, and it did not contain any other obvious sign of engineering.

According to Clarivate, an analytics company, the Nature Medicine letter was the 55th most cited article of 2020, with over 1,300 citations in the journals tracked. Email records would later show that starting in January 2020, the letter had been the subject of urgent, high-level messages and conference calls between the letters authors, Anthony Fauci, head of the National Institute of Allergy and Infectious Diseases; top virologists; and the head of the Wellcome Trust, a major pharmaceutical research funding organization in the United Kingdom. Early on, the authors had worried that the virus looked suspicious before quickly coming together around a scientific analysis supporting a natural cause. Initially one of their aims was to quash rumors that the virus was a bioweapon or a result of engineering gone wrong, but they ended up going further, writing: We do not believe that any type of laboratory-based scenario is plausible.

Working from her home in Massachusetts, Chan soon found a way to revive the lab-accident theory by looking for differences with SARS, a similar virus that broke out in 2002 but caused only about 8,000 illnesses. With Shing Zhan, a bioinformatics specialist at the University of British Columbia, Chan looked at the early human cases of covid and saw that the new virus hadnt mutated as fast as SARS had. If it were an animal virus from a market, she thought, its genome would show signs of adjusting more quickly to fit its brand-new human host. She prepared an analysis arguing that the virus was pre-adapted to humans and offered some theories as to why. Maybe it had been spreading undetected in people elsewhere in China. Or maybe, she thought, it had been growing in a lab somewhere, perhaps multiplying in human cells or in transgenic mice that had had human genes spliced into them.

The chance that a non-engineered virus could have adapted to humans while being studied in a laboratory, she wrote, should be considered, regardless of how likely or unlikely.

On May 2, 2020, Chan posted a preprint paper, coauthored with Deverman and Zhan, to the website bioRxiv, an online venue for quickly communicating results that havent yet been reviewed by other scientists. Our observations suggest that by the time SARS-CoV-2 was first detected in late 2019, it was already pre-adapted to human transmission, they wrote. The Broad Institute communications department also pointed Chan to examples of how to compose a tweetorial, a daisy chain of posts, with pictures, that present a compact scientific argument to a wider public. She posted her first tweetorial the following day.

For journalists suspicious about Chinas handling of the virus, the threadand those that followedwere dynamite. Here was an actual scientist at Americas biggest gene center who was explaining why the official story might be wrong. Coronavirus did NOT come from animals in Wuhan market, screamed a Mail on Sunday headline, in what became Chans first breakout into the public conversation.

While her report was a media success, what the Daily Mail described as Chans landmark paper has still never been formally accepted by a scientific journal. Chan says thats because of censorship due to her raising the lab-origin possibility. Eisen of UC Davis, however, thinks Chans expectations for how the covid-19 virus should have behaved remain conjecture. He doesnt think weve traced enough outbreaks in enough molecular detail to really know what's normal. And, he notes, covid-19 has continued to change and adapt.

My colleagues said, This is a conspiracydont bother. I said, No, I am going to treat this like any other paper, says Eisen, who took time to study the manuscript. I think its interesting what she tried to do, but I am not convinced by the conclusion, and I think the inferences were wrong. I do commend her for posting it. Many of the people pushing the lab-origin theory are not making claims based on logic, but she presented her evidence. I dont agree with it, but that is science.

Wrong or right, though, the word Chan usedpre-adaptedsent shivers up the spine of people like author Nicholson Baker. We were dealing with a disease that was exceptionally good, right out of the gate, at chewing up human airways, says Baker, who got in touch with Chan to learn more. Several months later, in January of this year, Baker would publish a lengthy report in New York magazine saying hed become convinced a laboratory accident was to blame. He cited a variety of sources, including Chan.

Chan wasnt done knocking holes in the natural-origins narrative. She next took on four papers that had been rapidly published early in 2020, two of them in Nature, describing viruses in pangolinsendangered scale-covered mammals sometimes eaten as delicacies in Chinathat shared similarities to SARS-CoV-2. If researchers could find all the components of the pandemic virus, especially in wild animals illegally trafficked as food, they could cinch the case for a spillover from nature, given the way coronaviruses swap parts. The pangolin papers, published in quick succession in early 2020, were a promising start. To the authors of Proximal Origins, these similar viruses offered strong and parsimonious evidence for natural emergence.

Chan and Zhan noticed that all the papers described the same batch of animalseven though some failed to acknowledge the overlap. One even relabeled the data, which made it appear novel. To Chan, that wasnt just sloppy work or scientific misconduct. There could, she believed, have been coordination between the overlapping authors of all these papers, some of whom had published together before. She created the hashtag #pangolinpaperscalling to mind the Panama Papers, documents that exposed secret offshore financial dealings.

Maybe, she thought, researchers were now laundering data to make it seem that nature was swimming with similar viruses.

Chan started emailing authors and journals to get the raw data she needed to more fully analyze what they had done. Making such data available is usually a condition of publication, but it can still be hard to obtain. After what she calls months of stonewalling, Chan finally lost her cool and blasted an accusation out from her browser. I need the scientists + editors who are directly or indirectly covering up severe research integrity issues surrounding some of the key SARS-2-like viruses to stop and think for a bit, she posted to Twitter. If your actions obscure SARS2 origins, you're playing a hand in the death of millions of people.

Eddie Holmes, a prominent Australian virologist and coauthor of one of those papers (as well as Proximal Origins), called the tweet one of most despicable things I read on the origins issue. He felt accused, but he wondered what he was being accused of, since his paper had correctly accounted for its pangolin data sources. Holmes then circulated an intricate time line prepared by Chan of the publication dates and past connections between the authors. The charts dense web of arrows and connections bore an unmistakable resemblance to an obsessives cork board covered with red string and thumbtacks.

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They called it a conspiracy theory. But Alina Chan tweeted life into the idea that the virus came from a lab. - MIT Technology Review

A symposium organized by the Food and Agriculture Organization of the United Nations (FAO) and the International Atomic Energy Agency (IAEA) opened today focusing on the prevention of animal disease outbreaks that can cause human pandemics like COVID-19, as well as ways to boost sustainable animal production to feed growing populations.

The week-long International Symposium on Sustainable Animal Production and Health virtually brings together over 2000 experts in veterinary medicine, genetics and biochemistry, among other scientific fields, to discuss topics such as emergency preparedness and response to outbreaks, advances in animal disease vaccine development and the latest tools to improve livestock production, breeding and feed.

The IAEAs mandate to promote nuclear technologies and their peaceful applications is especially important in health, food and agriculture, IAEA Director General Rafael Mariano Grossi said in his opening remarks.

Sustainable animal production and animal health systems are essential to attain the Four Betters better production, better nutrition, a better environment, and a better life, leaving no one behind, said FAO Director General Qu Dongyu. Protecting animal health under the One Health framework is at the core of our work. This Symposium is an excellent platform to discuss progress, but more importantly, to envisage the future, he added.

The IAEA Animal Production and Health Laboratory plays a critical role in implementing the programmes of the Joint FAO/IAEA Centre of Nuclear Techniques in Food and Agriculture, and has supported vital research and development work to help countries tackle animal and zoonotic diseases such as Avian flu, African swine fever, Zika and Ebola in the past decade. More recently, it has been at the centre of the IAEAs assistance to 130 Member States in their efforts to contain the spread of COVID-19.

Building on this experience, last year the IAEA launched the Zoonotic Disease Integrated Action (ZODIAC) initiative to support countries in the use of nuclear and nuclear-derived techniques for the timely detection and control of pathogens at the animal-human interface. The IAEA is staying present and offering this platform with a nuclear-specific component, Director General Grossi said while recalling past Agency assistance to the international community in battles against significant outbreaks. The IAEA, together with FAO and the Paris-based World Organisation for Animal Health (OIE), will continue to tackle zoonoses, he said.

The world is looking to us to produce synergies and provide leadership for a One Health approach that prevents future pandemics originating from animal sources, FAO Director General Qu Dongyu said.

With livestock production systems becoming more intensified in many parts of the world to meet demands for animal-based foods, the symposium will address the challenges and potential strategies for controlling emerging and re-emerging infectious diseases, especially with the One Health approach. One Health recognizes the interconnectedness of the health of people, animals and the environment, and this multidisciplinary approach is essential to achieve optimal planetary health and the Sustainable Development Goals by 2030.

Ten-year anniversary of the eradication of rinderpest disease

The Symposium marks ten years since the successful eradication of rinderpest the second viral disease to have been defeated globally after smallpox was eliminated in 1980. For centuries, the cattle and wild animal pest seriously threatened food security, especially in Africa and Asia. Its eradication was declared in 2011 by the OIE, following an international effort that benefited from FAO and IAEA support to develop tools to quickly detect and efficiently monitor rinderpest cases in the field.

"The eradication of rinderpest is a perfect example of the effectiveness of well-built partnerships, OIE Director General Monique Eloit said in her opening remarks. Surveillance, she added, is an essential component of disease prevention along with vaccines, and the Joint FAO/IAEA Centre plays a key role in this regard, supporting the overarching goals of the OIE and FAO.

Joint FAO/IAEA Centre of Nuclear Techniques in Food and Agriculture

First established in 1964, the Joint FAO/IAEA Centre operates five laboratories that help countries in the use of nuclear and isotopic techniques to improve global food security and sustainable agriculture worldwide. Located at the IAEA Seibersdorf facility, 35 km south of the Austrian capital Vienna, these laboratories carry out research and development, and provide guidance and training to scientists from around the world.

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Improving Zoonotic Disease Prevention and Livestock Production through Nuclear-derived Techniques Discussed at FAO/IAEA Meeting | IAEA - International...

This article first appeared on The Journalists Resource and is republished here under a Creative Commons license.

Titled Socioeconomic Inequality in Respiratory Health in the U.S. from 1959 to 2018, the study isnt the first to show that lower income and education are associated with respiratory diseases like asthma or poorer lung health. But its noteworthy in that it looks at these trends over a long span of time, showing that even though air qualityhas improvedand smoking rateshave droppedover the past 60 years, disparities in respiratory health have persisted and the improvements havent been equitably enjoyed, according to the study.

Poor lung health reduces quality of life and is associated with an increased risk of death due todisease or harmful exposure, so a widening gap in lung function based on income and education can also mean a widening gap in life expectancy between poorer and richer Americans in the 21st century, the authors write.

"Our lungs can be a mirror of the inequalities in our society and they reflect the hazards that we face because of our (socioeconomic) position."Dr. Adam Gaffney

Our lungs can be a mirror of the inequalities in our society and they reflect the hazards that we face because of our [socioeconomic] position, says the studys lead authorDr. Adam Gaffney, a pulmonary and critical care physician at the Cambridge Health Alliance and an instructor in medicine at Harvard Medical School.

The study doesnt include data from 2020, when the COVID-19 pandemic arrived and shined a light on existing disparities. But it highlights the magnitude of this problem and I think its an important first step to develop more solutions and address these disparities, saysDr. Sarath Raju, an assistant professor of medicine at Johns Hopkins, who wasnt involved in the study but wrote aninvited commentaryon it inJAMA Internal Medicinealong withDr. Emily Brigham, also an assistant professor at Johns Hopkins.

NHANESis an annual survey of about 7,000 randomly selected residents across the U.S. each year. Itcombines interviews and physical exams of participants. The survey, which is a representative of the U.S. population, is a major part of the National Center for Health Statistics, under the Centers for Disease Control and Prevention.

In total, the study included 215,399 individuals between ages 6 and 74 years old.

The researchers defined socioeconomic status by family income and adult educational achievement. They used thresholds from the U.S. Census Bureau to create family income quintiles. They categorized education as less than high school, high school, some college and college.

They looked at three types of pulmonary outcomes: Respiratory symptoms including shortness of breath, persistent cough and wheezing; respiratory diseases including asthma and chronic obstructive pulmonary disease (COPD); and lung volumes, measured by a standard clinical device called a spirometer.

They also looked at trends in socioeconomic disparities and prevalence of tobacco smoking among adults.

Researchers thenexamined time trends for each income and education group in the prevalence of current or former smoking, each respiratory symptom, asthma and COPD, and lung function.

Their analysis showed that income and education disparities in smoking behavior widened between 1971 and 2018.

Between 1971 and 1975, 63% of adults in the top-fifth of the income scale were current/former smokers, compared with 56% in the bottom fifth. By the 2017 to 2018 time period, the corresponding figures were 34% for the top fifth and 58% for the bottom fifth, the authors write.

The new study adds to the existing body of research linking lower socioeconomic status to worse respiratory health outcomes.

Socioeconomic disparities for respiratory symptoms like shortness of breath and wheezing also widened.

Between 1971 and 1975, 44.5% of those in the bottom fifth of the income scale had shortness of breath compared with 26% in the highest income individuals, an 18% difference. In 2017 to 2018, the corresponding proportions were 48% and 28%, a 20% difference, the authors write. They found similarly persistent disparities by education.

Researchers also found that income and education-based disparities in persistent cough widened, and even though wheezing rates fell among the highest income and education group, they remained relatively stable among people with lowest levels of income and education.

Among children, asthma prevalence rose in all income groups after 1980, but increased more sharply among poorer children, researchers found.

Among children aged 6 to 11 years, asthma prevalence was 3% to 4% in all income groups between 1976 to 1980, and the difference between the poorest and wealthiest was nonsignificant. By 2017 to 2018, asthma prevalence among younger children was 14.8% in the poorest group, compared with 6.8% in the wealthiest.

Researchers found a similar pattern among adults with asthma.

For COPD, disparities based on income also widened, from 4.5% difference in 1971 to 11.3% in 2018.

Disparities in most lung function measurements also widened, the analysis showed.

The new study adds to theexistingbody of research linking lower socioeconomic status to worse respiratory health outcomes.

Dr. Juan Celedn, the immediate past-president of the American Thoracic Society, isnt surprised by these findings, given the economic trends in recent decades.

Economic data shows that the gap between the rich and the poor has widened, says Celedn, division chief of pulmonary medicine at UPMC Childrens Hospital of Pittsburgh and a professor of medicine, epidemiology and human genetics at the University of Pittsburgh.

The study did not include race, although theres evidence that those gaps have also continued to persist.

In the 2015 study, Time Trends in Racial and Ethnic Disparities in Asthma Prevalence in the United States From the Behavioral Risk Factor Surveillance System (BRFSS) Study (19992011), published in theAmerican Journal of Public Health, researchers showed that disparities in asthma prevalence by race and ethnicity increased between minority groups and whites in that decade. Blacks and Puerto Rican Hispanics were most affected, the study showed.

(Generocity graphic)

Several studies have shown an association between respiratory health andsocioeconomic status,race and ethnicity, and place of living, includingrural versus urban areas.

Some of the drivers for these disparities are smoking, air pollution, exposure to dust and gases in the workplace, nutritional deficiencies and lack of access to health care, Gaffney and colleagues write.

Add to those education and income.

Education signifies familial and personal resources, material and intellectual; education may also influence occupation and promote health literacy, Raju and Brigham write in their invited commentary Lung Health Disparities in Time.

Income often mirrors education and also increases access to health resources and allows for adjustment of personal and family environment, they write.

Meanwhile, even though air quality has improved and so have occupational exposures with the establishment ofOccupational Safety and Health Administration(OSHA) in 1971, individuals with lower socioeconomic status and racial and ethnic minorities still face more workplace hazards and reside in more polluted neighborhoods, according to the study authors.

"Minorities and the poor are more likely to live close to a highway. And why do they live there? It goes back to things like poverty, segregation and redlining."Dr. Juan Celedn

Think about air pollution, says Celedn, who wasnt involved in the newJAMAstudy. In this country, minorities and the poor are more likely to live close to a highway. And why do they live there? It goes back to things like poverty, segregation andredlining.

In the May 2021 study Racial Segregation and Respiratory Outcomes among Urban Black Residents with and at Risk of COPD, published in theAmerican Journal of Respiratory and Critical Care Medicine, researchers write that when two or more racial groups live separately,kept apartby housing policies, legislations, racism and discrimination, it may lead to worse health outcomes due to economic opportunities, social isolation, discrimination and environmental exposure.

In the 2017 National Bureau of Economic Research working paper Is It Who You Are or Where You Live? Residential Segregation and Racial Gaps in Childhood Asthma, Diane Alexander and Janet Currie show that place of living plays an important role in explaining disparities in childhood asthma rates, in addition to low birth weight, poverty and smoking.

Clearly, understanding what aspects of neighborhoods contribute most to these disparities is key to reducing the racial gap in asthma, and potentially in other health conditions, they write.

There also appear to be respiratory health disparities in rural versus urban areas.

In their 2019 study, Rural Residence and Poverty Are Independent Risk Factors for Chronic Obstructive Pulmonary Disease in the United States, Raju and colleagues show that people living in rural communities were more likely to have COPD than their urban counterparts, even after accounting for poverty and health insurance status.

Development of respiratory diseases including COPD and asthma have to do with lifetime exposures to factors that can happen early in life and impact lung development much later, says Raju.

Low-income communities historically have had a higher prevalence of exposure to indoor and outdoor air pollution, poor nutrition, low birth weight and childhood respiratory infections, all of which can contribute to increase risk of COPD and poor lung health, Raju and colleagues write.

Smoking is another driver of lung health disparities.

In the 2020 study Disparities in current cigarette smoking among US adults, 20022016, published in the journalTobacco Control, researchers show that even though smoking rates had declined over the study period, overall disparities in prevalence of cigarette smoking grew even wider or remained unchanged.

Some of these disparities are driven by a higher density of tobacco stores in low-income neighborhoods, tobacco advertising thats targeted to low-income communities,including menthol cigarettes, and barriers in accessing smoking cessation resources.

People in these communities try just as hard to quit smoking but theyre much less successful, says Raju, due to barriers such as access to resources for smoking cessation programs.

Lack of funding for research is another source of persisting disparities, says Celedn, citing the example of funding forsickle cell disease, which affects mostly Black people, andcystic fibrosis, which affects mostly white people. Both have genetic causes.

In the 2020 study Comparison of U.S. Federal and Foundation Funding of Research for Sickle Cell Disease and Cystic Fibrosis and Factors Associated with Research Productivity, published inJAMA Network Open, researchers found that even though sickle cell disease is three times as prevalent as cystic fibrosis, affecting nearly100,000 Americans, federal funding for both was about the same between 2008 and 2018.

The study also showed disparities in funding from foundations and philanthropy.

The study also showed disparities in funding from foundations and philanthropy. Between 2008 and 2017, the mean expenditure by cystic fibrosis foundations were $231 million, compared with $9 million by sickle cell foundations. The total funding per cystic fibrosis patient was $10,600, compared with $942 for patients with sickle cell disease.

Another issue is lack of diversity among researchers and health-care professionals. People who are minorities tend to do more research on minority groups, Celedn says. Also, minority physicians are more likely to practice in underserved communities.

The American Thoracic Society, for instance, created the Health Equality Subcommittee in 2013 and since then has held workshops and published several papers, including one about its role inaddressing the racial and ethnic disparitiesin the pandemic.

Meanwhile, in April, the Food and Drug Administrationannouncedthat its planning to ban all menthol and flavored cigarettes within the next year.The agency didnt announce a specific date.

With these actions, the FDA will help significantly reduce youth initiation, increase the chances of smoking cessation among current smokers, and address health disparities experienced by communities of color, low-income populations, and LGBTQ+ individuals, all of whom are far more likely to use these tobacco products, said acting FDA Commissioner Dr. Janet Woodcock in astatement.

While the COVID-19 pandemic has shineda light on health disparitiesin the U.S., it has also helped the medical community to rethink the way it can deliver care and how it can reach out to different communities, researcher says.

COVID revealed pulmonary inequalities, says Gaffney. I would hope that this experience and this kind of research help push us towards the policies that we need to ensure that everyone can live a healthier life and bring us to a state of health equity.

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New research: Disparities in respiratory health have persisted or widened in the US in the last 60 years - Generocity

REYKJAVIK, Iceland, June 18, 2021 /PRNewswire/ -- Scientists from deCODE genetics have developed a predictor based on protein measurements in blood samples that predicts the time to all-cause death better than traditional risk factors.

In a paper published today in Communications Biology, scientists from deCODE genetics, a subsidiary of Amgen, describe how they developed predictor of how much is left of the life of a person.

Using a dataset of ~5000 protein measurements in 22,913 Icelanders, of whom 7,061 died during the study period, the scientists developed a predictor of the time to death that can outperform predictors based on multiple known risk factors. The predictor can identify the 5% at highest risk in a group of 60-80 year olds, where 88% died within ten years and the 5% at lowest risk where only 1% died within ten years.

The scientists explored how individual proteins associate with mortality and various causes of death and found most causes of death to have similar protein profiles. In particular, they found growth/differentiation factor 15 (GDF15), which has been associated with mortality and ageing before, to be an important predictor of all-cause mortality. Furthermore, they found that, on average, participants predicted at high risk of death within a short period of time had less grip strength and performed worse on an exercise tolerance test and a test of cognitive function than those predicted at lower risk.

"The predictor gives a good estimate of general health from a single blood draw," says Thjodbjorg Eiriksdottir scientist at deCODE genetics and author on the paper.

"This is pretty cool but also scary and hopefully somewhat useful", says Kari Stefansson a senior author on the paper . "This shows that our general health is reflected in the plasma proteome. Using just one blood sample per person you can easily compare large groups in a standardized way, for example, to estimate treatment effects in clinical trials."

Based in Reykjavik, Iceland, deCODE is a global leader in analyzing and understanding the human genome. Using its unique expertise in human genetics combined with growing expertise in transcriptomics and population proteomics and vast amount of phenotypic data, deCODE has discovered risk factors for dozens of common diseases and provided key insights into their pathogenesis. The purpose of understanding the genetics of disease is to use that information to create new means of diagnosing, treating and preventing disease. deCODE is a wholly-owned subsidiary of Amgen (NASDAQ: AMGN).

Contact:

Thora Kristin AsgeirsdottirPR and CommunicationsdeCODE geneticsthoraa@decode.is354 894 1909

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SOURCE deCODE genetics

Company Codes: NASDAQ-NMS:AMGN

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deCODE genetics: Predicting the probability of death - BioSpace

Reading a breathless account of an amazing new medical treatment, lured in by an exciting headline, only to discover a few paragraphs in that the findings are in rodents, can at best be annoying, and at worst raise false hopes for patients and their families. A new study, long overdue, pins down one source of this common error of omission: leaving out mice in the titles of technical articles.

A chain reaction of mangled communication is at fault.

Leaving Out the Rodents

Missing mice happen at several points in the medical news trajectory.

Failure to mention that an experiment was done on non-human animals in a technical articles title can reverberate as a news release and then echo in media reports, tweets, and memes. Or, the headline of a news release or its content can ignore the mice, even if the journal article mentions them.

In yet another scenario, the reporter can omit the rodents. Journalists are sometimes so rushed with deadlines that they may modify a news release rather than take the time to read the technical report behind it that may indeed credit the mice and rats. Another source of the error: editors who write the headlines of news articles, omitting the mention (writers rarely write the headlines).

Many science journalists get ideas from the dozens of news releases posted daily at Eurekalert.org, from institutions and companies all over the world. And some releases only mention mice a few paragraphs in or not at all.

Hype resulting from mouse-deficient headlines has bugged me for a long time. When I edit abstracts for a medical journal, one of my regular gigs, I alert authors who leave out model organisms from article titles.

So I was happy to read, ironically in a news release, that Marcia Triunfol at Humane Society International in Washington, DC and Fabio Gouveia at the Oswaldo Cruz Foundation in Rio de Janeiro have investigated whether mention of mice in news release headlines dampens media coverage.

The findings described in Whats not in the news headlines or titles of Alzheimer disease articles? #InMice, published in PLOS Biology, arent surprising: when a scientific papers title omits the rodent connection, journalists reporting on the paper tend to do the same. And reporters are more likely to cover papers without mice in their titles.

Id never pitch an idea based only on mouse work to Medscape or MedPage Today, whose readers are clinicians. And I dont include such studies in my human genetics textbook.

A Mouse Isnt a Little Human

Mice are terrific models of some human diseases. Their anatomical, physiological, and genomic similarities to us make them useful in preclinical studies emphasis on the PRE.

Testing a new treatment in mice is great for amassing large numbers, implementing several control groups, and doing things that one wouldnt or couldnt do to people, like yanking out a liver or slicing up a brain to study effects of a drug. Mice in particular are useful for studying aging, collapsing the timeframe of a lifetime from 80 years to 2.

For some diseases, exploring treatments first in a model organism makes sense. But the differences among species must be considered to jump from preclinical study to clinical trial. The correspondence can come down to a single gene. According to Why Mouse Matters at the NIHs Genome.gov, on average, the protein-coding regions of the mouse and human genomes are 85 percent identical; some genes are 99 percent identical while others are only 60 percent identical.

Evolution has conserved large swathes of mammalian genomes. We use versions of the same molecules for the same things. But even when human genes are swapped into or added to rodent or monkey genomes, creating humanized creatures, differences in development impinge upon the extrapolation and interpretation of experimental results. This is particularly true for syndromes that unfurl according to a distinctive timetable, like genetic diseases with characteristic developmental delays or loss of milestones, and common chronic diseases that emerge and worsen over a lifetime, like diabetes and cardiovascular disease.

The imperfection of animal models isnt a new idea.

A study of studies from 2005, Of Mice and Men, by Lloyd Demetrius, published in EMBO Reports, has a one-sentence abstract: When it comes to studying ageing and the means to slow it down, mice are not just small humans.

Demetrius examined the misplaced use of rodents in investigating aging and caloric restriction the idea that near-starvation extends life. Theres evidence for the connection if youre a rat. For people, not so much, although reducing eating may lower weight and blood pressure and cholesterol and glucose levels in the blood, which lowers risk of chronic conditions. He argued that the different developmental timetables of rodents and us reflect differences in the aging process itself, specifically metabolic responses to stress.

So you cant extrapolate from mice living longer on a kale diet compared to littermates eating regular grub, to people making different dietary choices.

Considering Alzheimers

The new study probes the effect on media coverage of including, or not including, in mice in the title of a technical report about Alzheimers disease. They chose Alzheimers because its an exclusively human condition, but for which hundreds of mouse models have been developed to probe specific physiological responses not related to the passage of time.

The investigators divided 623 scientific reports published in 2018 and 2019 that used mice in Alzheimers disease research into those that outed the rodents in the title and those that didnt. Then they tracked the news stories appearing in the wake of publication of each study.

The papers that left out mice received more media coverage and were significantly more highly tweeted. The authors expressed concern at the misleading of the public, even if unintentional.

Most people only read the headlines of news stories. If the headline omits that the Alzheimers study was done in mice, most keep the impression that the study findings apply to humans, which is not true. We now know that virtually all findings obtained in animal studies in Alzheimers disease do not replicate to humans, said Triunfol in the news release.

Alzheimers is only one example, but the failure to identify model organisms is pervasive and a practice not likely to fade away anytime soon. In fact, when I saw the news release that inspired this post, on EurekAlert, I read another, guilty of the mouse sin: Plant-based diet protects from hypertension, preeclampsia.

But heres the first two sentences: A plant-based diet appears to afford significant protection to rats bred to become hypertensive on a high-salt diet, scientists report. When the rats become pregnant, the whole grain diet also protects the mothers and their offspring from deadly preeclampsia.

Will that headline alone trickle into news reports? Inspire tweets or Facebook memes? Probably. But the example of hypertension is less disturbing than Alzheimers blood pressure is controllable in many ways, altering diet among them.

Headlines and news reports sensationalized, perhaps inadvertently, by errors of omission, will continue. So its up to readers to realize that dramatic claims of medical advances might not apply to people caveat emptor.

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Tracing the Origins of Medical Media Hype: Failing to Mention Mice - DNA Science - PLoS Blogs

Dr. Deon Miles 97 has been a member of the faculty at Sewanee, the University of the South, since 2002, where his current course offerings include Instrumental Analysis, General Chemistry, Advanced Topics in Analytical Chemistry, Solution and Solid-State Chemistry, and the Science of Food and Cooking.

He talks about teaching, his experiences in the classroom and lab, and his path from Gary, Indiana, to a tenured professorship atop the Cumberland Plateau.

Q: Were you always interested in chemistry?

Miles: No, and its probably a story that a lot of students have. I started out to be a doctor and intended to be a biology major. The class that got me out of the biology track was genetics. I really did not enjoy it. At the same time during my sophomore year, I was taking a chemistry class, and found that material to be more interesting. I always had a love for math and science. Those two fields merged well in chemistry. The challenge in starting a chemistry major my sophomore year was how to get it done. Thankfully, the professors were very helpful in navigating that, especially Dr. (David) Phillips, and I got it done in three years.

Q: As you departed Wabash 1997, did you feel prepared for graduate school?

DM: The time at Wabash was really important. Learning how to study, not only with peers, but also on my own, to develop that hunger for knowledge, to develop those problem-solving skills, was essential. Those skills werent fully developed on day one. The molding, all that experience, helped get me to where I was ready and prepared for graduate school.

Q: What was the fall 2020 semester like for you? How did you deal with labs and the normal teaching responsibilities?

DM: I saw COVID-19 as more of an opportunity. One of the things that I did in preparation for my analytical chemistry course was to make sure students could still get a lab experience, regardless of where they were. You can record lectures, but it was the hands-on lab I was most concerned about. What I did starting in April 2020 was ask, How can we design a laboratory experience that a student can do right in their home kitchen? How can we give them an analytical chemistry experience in their homes, and do it safely? I tried very carefully to think about the kind of big picture experiments and concepts we could cover safely. We ended up coming up with seven experiments that could be done at home, and then adding three dry lab experiences things that didnt need reagents or equipment. Once finished, you then could dump them down the drain or throw things in the trash. We called them Lab in a Box. We actually used these in the labs when the students returned.

I also flipped my classroom. We didnt know if we would have students that would have to quarantine for two weeks, so I wondered how they would get the lecture content? I redesigned and recorded all my lectures, putting them in more digestible chunks. I did that throughout the semester. It was a good experience. Im going to continue to do that kind of going forward because it gives me the opportunity to do more things in class that I didnt have the opportunity to do before because of the lecture content.

Q: Did you find it harder to engage with your students?

DM: There were moments, yes, when it was more challenging to stay engaged with the students. Thankfully, all my students this past semester were in person. Because I flipped the classroom, I would come in and ask if there were any questions. A lot of times there were, but there were times I didnt have another activity planned, so we would meet, go over questions, and 10-15 minutes later, we were leaving.

We were so focused on physical distancing and not spending a lot of time together. All those informal interactions went away. Those informal interactions are the things I missed the most.

Q: Did you hear from your students about mental health concerns, or perhaps sense moments where questions unrelated to chemistry might alleviate some stress?

DM: Those moments happened one-on-one. Im in my 19th year as a professor. I can see when a student wants to have that kind of conversation. They put their things away slowly, they linger a little bit. Everybody else is running out of the class. I had opportunities to ask, how are things going? A student might have needed a couple of more days to do a lab report after staring at the same four walls for the last three days. We recognized that and we got through the semester.

Q: Did some of those informal conversations and the questions that were on students minds outside of class allow you to talk of chemistry in timely, topical, or different ways?

DM: When we think about chemistry, we dont necessarily think about social justice. Its almost like, just stick with atoms and molecules and then move on. But thats not entirely true. Ive tried to lead by example and have started to incorporate some aspects of social justice in my classes. When you think about social justice and think about this from a chemistry perspective, its about getting students to think beyond their immediate circles of influence. How do you do that with chemistry?

The water crisis in Flint, Michigan, is a great example. What happened with the lead pipes? How did the water get lead in it? From an analytical chemistry perspective, we can talk about the instruments that are used to detect the lead. We can also talk about the human side of it. We can talk about the impact of lead water on children under the age of six and how it slows development in a number of ways. Thats one way analytical chemistry can enter into conversations about social change. I want my colleagues to find more examples and see how we can incorporate those into our courses. We still get the chemistry, but lets think about the human aspect as well.

For more stories about alumni making a difference in education, check out the upcoming issue of the Wabash Magazine, available in early July.

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Deon Miles '97: Think About the Human Aspect - Wabash College

Its estimated 150 million Americans 57 per cent of the country watched the verdict in the 1995 OJ Simpson trial.

The case dominated news bulletins around the world and in the stand as an expert witness was Kiwi mathematician Bruce Weir.

For three days, the world-renowned authority on biostatistics discussed the blood samples taken from Simpsons car and glove. The DNA evidence was overwhelming ... and it all pointed in the same direction, he says.

He faced a grilling from Simpsons lawyer, and at one stage conceded an error in his calculations. Having spent months working on the complex equations with a colleague, he was asked by the judge to provide additional data.

I went back to my hotel room and did them overnight. I left out one term, so the numbers were not correct. Unfortunately for me, and maybe fortunately for the defence, they spotted this. I dont think it was a crucial element.

Simpson was found not guilty, and the extensive media coverage of the trial made Weir a recognisable figure on American streets. I couldnt go anywhere without being recognised. When you are on national TV for an extended period you get known.

The 77-year-old now lives and works on Americas northwest coast, 11,000 kilometres from where he grew up in Christchurch.

Last month he became a Fellow of the Royal Society, the oldest and most prestigious national scientific institution in the world.

READ MORE:* Fifty years of asteroid hunting for Kiwi couple* National Portrait: Antarctic archaeologist Dr David Harrowfield * Poet and writer Mohamed Hassan on searching for home* New headmaster chosen for Christchurch's Shirley Boys' High School

Its a huge honour, he says, but he feels most proud to be one of the 50 or so New Zealanders who have been elected.

Lord Rutherford and a couple of Nobel Prize winners. I don't even think of being at that level, but it's nice to be in a group which has those.

Biostatistics is an area of expertise that has played a vital role in the fight against Covid-19.

Data analysis was used during the clinical trials for the coronavirus vaccines and to study mutations in the virus, he says.

When there's an outbreak they can see which variant and where it came from. It's the numbers which are so crucial.

And he praises New Zealands response to the pandemic, especially the sequencing, which has been world class.

Born in 1943, Weir was raised in the Christchurch suburb of Shirley with his four siblings.

Most of his family worked in the trades and his dad hoped he would become a plumber.

My father worked in a factory, he rose through the hierarchy, but he worked with his hands, Weir says.

My mother had been secretarial and that was typical for our family. My aunts and uncles all had good jobs but not what we'd call professionals.

Supplied

Shirley Boys' High School headmaster Charles Gallagher with First-Day third formers Trevor Purver, Neville Burnby, Peter Cox, Robert Clarke, Grant Webley, and Robert Dollan. Image taken around 1957.

In November 1957, Shirley Boys High School opened and Weir was one of 156 form three students, now known as First-Day Pupils.

He remembers it being an exciting time.

It was a brand new school, new building, new staff who were very enthusiastic.

I was one of the boys who got to unpack the chemistry equipment, and I'd never seen a test tube or a beaker. It was a whole new world.

Nearby Christchurch Boys' High was founded in 1881 and a healthy rivalry was quickly established between the two schools.

We were on a mission, he says. We were the second public boys' school and we had a rival. There was also the other private boys' schools, Christ's College, St Andrews, St Bedes, and we tried very hard to be part of that scene.

Weirs time at Shirley Boys was instrumental, especially the guidance he received from the amazing headmaster Charles Gallagher, who helped him launch his academic career.

Supplied

Shirley Boys' High School. Back L-R Graeme Hern, Cyril Morris, Ross Nicholas Front L-R Alex Wilson, Max Wright, Headteacher Charles Gallagher, James Barrie and Bruce Weir. Image taken in 1959.

His degree was in maths and he was personally very encouraging.

Weir was made head boy and in 1961 became the schools first dux.

But despite the plaudits, the following week he was working a summer job on the rubbish trucks.

I got all the prizes and then a week later I was on D and R dust and rubbish.

After winning a scholarship, he attended the University of Canterbury (UC), the first of his family to go to university.

It was a bit daunting. It was hard work, but that was fine.

Whilst at UC he began an internship at the Department of Scientific and Industrial Research under acclaimed statistician Brian Hayman, who worked in genetics.

I had no idea what genetics was, Weir says.

Hayman told him to read Genetics by biologist Hans Kalmus and the book sparked an interest that would shape his career.

I read that and thought wow. Who knew we had genes and they seem to obey some mathematical rules? I thought that was neat.

At that point, genetics was largely concerned with plants and animals and most statistical work was used for improving crop or milk yield, he says.

After graduating in 1965 with a first class degree in mathematics, Weir undertook a PhD in statistics with a minor in genetics at North Carolina State University, in the US.

There he met Columbus Clark Cockerham who developed the language for statistical genetic data and the pair would undertake pioneering work over the next three decades.

During his post-doctoral studies in California in the late 1960s, Weir was part of a team that studied human genes a field which was still in its infancy.

We were so excited, we had information on four genes, this was unprecedented. In the work I'm doing now, we have a billion.

He returned to New Zealand in 1970, working as a senior lecturer at Massey University.

And he could be seen driving around Palmerston North in a 1966 Ford Mustang, which he shipped back from America.

In those days you couldn't travel to the US by air, unless you were extremely rich, so everybody sailed.

Coming back, my checked luggage was my Mustang.

Supplied

Bruce and Beth Weir's wedding in August 1971. The couple drove away in his 1966 Ford Mustang.

While at Massey he met his wife Elizabeth Swainson, his American car having caught her eye.

I think it helped attract my wife. We sold it at a huge profit and it helped us buy our first house.

The couple would have two children together, Claudia and Henry, and in 1976 they moved to the States, with Weir becoming the founding director of the Bioinformatics Research Centre at North Carolina State University.

Today, he is an honorary professor at the University of Aucklands Department of Statistics but is primarily based in Seattle, where he is a professor of biostatistics, epidemiology and genome sciences at the University of Washington Schools of Public Health and Medicine.

As a lecturer, he has been prolific supervising more than 35 PhD students but he is best known for his groundbreaking research.

The book he co-wrote on interpreting DNA evidence is considered the definitive text for lawyers and judges.

And his biostatistical studies have resulted in the publication of more than 200 peer-reviewed articles.

By the early 1990s, DNA profiling was increasingly being used in criminal investigations and Weir was approached by the FBI to help ensure its calculations were rigorous.

He provided testimonies in about 20 trials, before prosecutors in Los Angeles County asked him to assist in the trial of Simpson,

the American actor and former NFL player who was arrested and charged in 1994 with the murders of his ex-wife Nicole Brown Simpson and her friend Ron Goldman.

Reed Saxon/AP

OJ Simpson and defence attorney F. Lee Bailey during the double murder trial in Los Angeles on June 30, 1995.

Though he was acquitted, he would later serve nine years for a robbery-kidnapping conviction in Las Vegas.

Weir hopes his own work will one day lead to cures for a range of illnesses.

Conditions like Alzheimer's disease could be better treated with the identification of what gene causes it.

We could then maybe give the person a drug to compensate for what that person's gene was not doing. It all rests on the data.

Supplied

Bruce and Beth Weir (centre). Their daughter Claudia Weir and son Henry Weir, with his children Zoe and Spencer.

In May, Weir became a Fellow of the Royal Society, which was founded in 1660 and is made up of the most eminent scientists, engineers and technologists from throughout the Commonwealth.

He was recognised for his contributions to the theory of population and quantitative genetics and to forensic science.

Each year 52 new Fellows are elected and for the 2021 elections there were almost 700 candidates.

Current members include around 75 Nobel Prize winners, while past Fellows include Isaac Newton, Charles Darwin and Alan Turing.

Weir says its a huge honour but he feels most proud to be one of the 50 or so New Zealanders who have been elected.

Lord Rutherford and a couple of Nobel Prize winners. I don't even think of being at that level, but it's nice to be in a group which has those.

One of the things he is especially delighted about is that his election means Shirley Boys' High School now has a fellow of the Royal Society.

We have joined Christ's College and Christchurch Boys'. Thats a big deal.

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National Portrait: New Royal Society fellow Bruce Weir on DNA and that OJ Simpson trial - Stuff.co.nz

Special purpose acquisition companies (SPACs) have been the talk of Wall Street for more than a year now. And although 2020 was deemed the year of the SPAC, 2021 also has welcomed a few of their own. That said, business mogul Richard Branson and 23andMe are getting in on the action.

Source: Sergei Bachlakov / Shutterstock.com

What do these two have going on, and why should investors care?

Lets dive in and take a closer look at the latest SPAC move featuring Richard Branson and 23andMe.

Shares of VGAC stock rose nearly 10% the day of the announcement but are down about 4.7% as of Tuesday afternoon.

On the date of publication, Nick Clarkson did not have (either directly or indirectly) any positions in the securities mentioned in this article.

Nick Clarkson is a web editor at InvestorPlace.

Article printed from InvestorPlace Media, https://investorplace.com/2021/06/vgac-stock-everything-you-need-to-know-about-richard-branson-23andme-and-this-weeks-spac-merger/.

2021 InvestorPlace Media, LLC

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VGAC Stock: Everything You Need to Know About Richard Branson, 23andMe and This Week's SPAC Merger - InvestorPlace