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Fulgent Genetics: A Buy If You Believe COVID Testing Is Here To Stay - Seeking Alpha
A new framework which reconciles the roles of behavioural genetics and cultural evolution in inheritance and cuts through the nature/nurture debate has been put forward by researchers at the London School of Economics and Political Science (LSE).
The model, which is set out in a forthcoming paper in Behavioral and Brain Sciences, uses a dual inheritance approach to predict how cultural factors such as technological innovation can affect heritability. Heritability is the extent to which variation in a certain phenotypic trait, such as IQ, can be predicted by genetics as opposed to environmental factors such as access to education.
The new framework highlights how genes and culture are deeply intertwined. For example, humans have jaws too weak and guts too short for a world without controlled fire and cooked food. We lack the genes for fire-making or cooking and instead rely on culture to compensate. Alongside genetic evolution, culture evolves over time in response to ecological, demographic and social factors.
The authors note that when culture overlaps with genes, the impact of genetics on a trait can become masked, unmasked or reversed and the effects of a gene can mistakenly be attributed to the environment or vice versa.
This integrated approach challenges the simple nature/nurture debate and helps resolve controversies in topics such as IQ by revealing that behavioural and cognitive characteristics are reliant on a whole host of evolving interacting factors both genetic and cultural.
The cultural evolutionary approach also helps explain how factors such as rates of innovation impact heritability across different social contexts, helping resolve issues that arise from a disproportionately WEIRD (western, educated, industrialised, rich and democratic) literature.
Commenting on the new framework, paper co-author Ryutaro Uchiyama from the Department of Psychological and Behavioural Science at LSE said: Since its founding, the field of behavioural genetics has quantified the influence of genes by contrasting it with influence from the environment, but it has relied on an impoverished conception of the environment. Human environments are dynamically structured by cultural evolution, and this understanding forces us to reassess the statistical and practical meaning of genetic indices like heritability.
Paper co-author Dr Michael Muthukrishna added: Biological differences dont imply genetic differences culture is also biological. This new framework allows us to better understand how genes and culture interact to create us. As the paper reveals, high heritability does not mean schools and other aspects of the environment dont matter or that there is anything inevitable about who we are and what we become.
The paper Cultural Evolution of Genetic Heritability has been accepted by the journal Behavioral and Brain Sciences as a target article. The journal is currently soliciting reactive commentary on the target article from other researchers. The authors will respond to these commentaries in a follow-up article later in the year.
For a copy of the paper, please visit: https://www.cambridge.org/core/services/aop-cambridge-core/content/view/9CBEB629203EA430B6EE5549C5E729FC/S0140525X21000893a.pdf/cultural-evolution-of-genetic-heritability.pdf
Voter turnout is an important factorperhaps the most important factorin ensuring that the democratic process properly represents a population. Despite this, governments around the world are constantly faced with poor turnout. Understanding how individual differences predict this is important to building meaningful interventions.
While it is known that education and intelligence correlate with voter turnout, the precise mechanism of this relation is unknown. The same goes for the well-established relation between genetics and voter turnout (between 40-50%, according to some studies). The authors of a recent study published in Human Behaviour decided to examine the two factors together, to see to what extent genetic influence on voter turnout was mediated by education and intelligence.
The authors also wanted to create a more robust study than previous experiments which have relied on reared-together twin studies (making it difficult to separate nurture from nature) and voter self-reporting, known to be particularly unreliable. Instead, the present study used a large (Danish) genetic dataset comprising roughly 47 000 individuals, in correlation with actual voter registration records.
The results of the study seem to agree with the authors hypothesis. That is, genotypes that predicted individual differences in education and performance on intelligence tests also predicted differences in voter turnout.
Its important to note, however, that these relations are correlational in nature (not causal), and that their mechanisms are not yet understood. The authors allude to previous studies, for example, which suggest that the influence of genetics on education attainment may be exerted via personality traits or, indirectly, through the family environment.
Nonetheless, the correlation is clear and robust. Individuals with a greater genetic disposition to obtain a degree of education one standard deviation higher than the mean were 2.66 times more likely to vote in municipal elections. Similarly, scoring one standard deviation higher on intelligence testing was correlated with a 1.85x greater likelihood to vote in national elections.
There are some limitations, including the fact that the data is limited to a single nation. Nonetheless, the studys large size and its robust correlational measures obtained through actual voter registration make this a particularly significant study statistically speaking, and lay the groundwork for interventions that will help increase voter turnout, buoying the democratic process.
The article, Genetic predictors of educational attainment and intelligence test performance predict voter turnout, was authored by Lene Aare, Vivek Appadurai, Kasper M. Hansen, Andrew J. Schork, Thomas Werge, Ole Mors, Anders D. Brglum, David M. Hougaard, Merete Nordentoft, Preben B. Mortensen, Wesley Kurt Thompson, Alfonso Buil, Esben Agerbo, and Michael Bang Petersen.
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Genetics may play a role in the link between education, intelligence, and voter turnout - PsyPost
Taken together, the bacteria, viruses, fungi and other microbes that live in our intestines form the gut microbiome, which plays a key role in the health of people and animals. In new research from the University of Minnesota, University of Notre Dame and Duke University, scientists found that genetics nearly always plays a role in the composition of the gut microbiome of wild baboons.
In humans, research has shown that family members share a significant portion of microbes in their gut, but its hard to answer if our microbiome is shaped more by nature, such as those we inherit from our family, or nurture, such as the similar diets, environments and behaviors families share, said lead author Laura Grieneisen, a postdoctoral fellow in the College of Biological Sciences. Many human diseases and other markers of health have a genetic component. The number and types of bacteria in the gut are no different. By understanding the heritability of the gut microbiome will help us better link genes, the gut and health.
To examine consistent data, researchers turned to more than 16,000 microbiome samples collected from 585 wild baboons over the course of 14 years. The size and generational scope of this microbiome data crucial for understanding how the microbiome is affected by genetics (i.e. microbiome heritability) has not yet been collected in humans.
In the research, published in the journal Science, the team tested how host traits (e.g., age, sex), behaviors (e.g., social group membership, grooming), diet, pedigree relatedness, and environmental characteristics (e.g., season, year) predicted 1,034 gut microbiome traits.
Researchers found that:
Our results qualitatively change the fields perspective on the determinants of microbiome composition, said co-author Ran Blekhman, an associate professor in the College of Biological Sciences. From one in which the host genotype plays no role in the majority of microbiome taxa to one in which the host genotype nearly always plays a role. As a result, microbiome traits might evolve via natural selection on the host.
Researchers state that this opens the door to identifying individual microbes that are particularly shaped by host genetics.
As a result, if there are microbes that are heritable and linked to health outcomes, it would allow us to better understand the genetic basis of these outcomes, said Grieneisen. Most of the microbiome may be visible to natural selection on the host genome.
The researchers add that their results are consistent with past work: although the role of a hosts genotype is universal, their environment and behaviors are still much more important than genetics in shaping microbiome composition. The team will continue to work with the wild baboon dataset to pursue questions about the drivers and physiological consequences of long-term changes in the microbiome.
This research was supported by funding from the National Institutes of Health, the University of Minnesota Grand Challenges Biology Postdoctoral Fellowship, the Duke University Population Research Institute and the University of Notre Dames Eck Institute for Global Health.
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Role of host genetics on gut microbiome is near-universal, but environmentally-dependent - UMN News
During the COVID-19 pandemic, Fulgent Genetics (NASDAQ:FLGT) was in the right place at the right time. Fulgent became a key provider of COVID-19 testing in 2020 and saw its revenue explode by almost 1,300% over the prior year. Few companies benefited more during the pandemic -- and few have a bigger cloud of uncertainty hanging over them as investors worry about what comes next.
The good news is that Fulgent isn't a one-trick pony. The company is going through a metamorphosis, strengthened by a reinforced balance sheet and a growing core business in an attractive genetic testing market. Investors should prepare to shift their perspective.
Image source: Getty Images.
Before the COVID-19 testing opportunity came along, Fulgent's core business was a small but fast-growing next generation sequencing (NGS) genetic testing service primarily focused on pediatric rare diseases.
That segment is still expanding fast. In the first quarter ended March 31, NGS volume grew 185% year over year from 13,000 to 38,000 tests, while corresponding revenue grew 115% to $16.7 million. Management is projecting NGS revenue of over $100 million in 2021, representing 170% year-over-year growth.
Fulgent has an efficient technology and operating platform generating gross margins of about 80% and operating margins above 70%. As a result, liquidity is a real bright spot for Fulgent. At the end of Q1, it reported $697 million in cash, cash equivalents, and marketable securities. Management expects to close the year with more than $1 billion in short-term liquidity, excluding any merger- and acquisition-related activity.
The encouraging growth in the core business is understandably offset by a rapid reduction in COVID-19 testing revenue. Unless there is a flare-up of infections from virus variants, COVID-19 testing revenue will continue to fall dramatically. Management is projecting $418 million in COVID-19 testing revenue for the remainder of the year, compared with $312 million in Q1 alone.
This precipitous revenue falloff is an operational challenge, but Fulgent has an experienced management team that over the past year has proven to be strong operators in building and scaling the business.
Fulgent will report quarterly earnings in early August. Smart investors will keep an eye on these three areas for signs management is executing on the long-term growth potential:
1. Continued COVID-19 testing
While testing volumes are declining, the endpoint is not zero. Fulgent has proven to be a high-quality, low-cost, fast-turnaround provider of gold-standard RT-PCR tests. Many screening programs are not allowing less sensitive antigen or rapid molecular tests to be used. As a result, Fulgent has been able to secure contracts for "return to normalcy" testing, particularly with school systems and the government.
The Department of Health and Human Services announced it will invest $12 billion in COVID-19 testing through the American Rescue Plan, with $10 billion going to schools. Fulgent management estimates that more than 1 million tests per day will be needed with this new program. Look for contract wins and continued testing volume in the near term.
2. Growth catalysts
Fulgent is expanding into additional genetic testing areas, including hereditary cancer, which is a high-growth area. There are more than 550 ongoing clinical trials for oncology genetic therapies, which will drive the need for more genetic testing and higher reimbursement over the coming years. Pharma companies are advocating and paying for genetic testing, since it will drive demand for their therapies. Fulgent has also established FF Gene Biotech, a joint venture focused on oncology in China, which is expected to be a $45 billion market. Stay tuned to these critical long-term developments.
3. Mergers and acquisitions
Fulgent's large cash position and strong operating leverage could make acquisitions a way to rapidly generate revenue that is accretive to the bottom line. In last year's Q4 conference call, CEO Ming Hsieh called out his interest in acquisitions to expand the core diagnostic business in Asia and Europe. It's a big world, and billions of people will need the genetic tests Fulgent is developing.
The market doesn't like uncertainty, which has helped push Fulgent shares down 56% from their 52-week high. The share price may go even lower as investors struggle to understand the profit picture in the next few quarters.
For patient long-term buy-and-hold investors with a tolerance for some uncertainty, Fulgent Genetics may actually be the best value biotech stock out there and could be a great addition for your portfolio.
This article represents the opinion of the writer, who may disagree with the official recommendation position of a Motley Fool premium advisory service. Were motley! Questioning an investing thesis -- even one of our own -- helps us all think critically about investing and make decisions that help us become smarter, happier, and richer.
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3 Things About Fulgent Genetics That Smart Investors Know - Motley Fool
Since the human genome was first mapped, scientists have discovered hundreds of genes influencing illnesses like breast cancer, heart disease and Alzheimers disease. Unfortunately, Black people, Indigenous people and other people of color are underrepresented in most genetic studies. This has resulted in a skewed and incomplete understanding of the genetics of many diseases.
We are two researchers who have been working to find genes that affect peoples risk for various diseases. Our team recently found a genetic region that appears to be protective against Alzheimers disease. To do this, we used a method called admixture mapping that uses data from people with mixed ancestry to find genetic causes of disease.
In 2005, researchers first used a groundbreaking method called a genomewide association study. Such studies comb through huge datasets of genomes and medical histories to see if people with certain diseases tend to share the same version of DNA called a genetic marker at specific spots.
Using this approach, researchers have identified many genes involved in Alzheimers disease. But this method can find genetic markers only for diseases that are common in the genomes of the study participants. If, for example, 90% of participants in an Alzheimers disease study have European ancestry and 10% have Asian ancestry, a genome-wide association study isnt likely to detect genetic risks for Alzheimers disease that are present only in individuals with Asian ancestry.
All peoples genetics reflect where their ancestors came from. But ancestry manifests as both genetic variation and social and cultural experiences. All of these factors can influence risk for certain diseases, and this can create problems. When socially caused disparities in disease prevalence appear across racial groups, the genetic markers of ancestry can be mistaken for genetic markers of disease.
African Americans, for example, are up to twice as likely as white Americans to develop Alzheimers disease. Research shows that much of this disparity is likely due to structural racism causing differences in nutrition, socioeconomic status and other social risk factors. A genome-wide association study looking for genes associated with Alzheimers might mistake genetic variations associated with African descent for genetic causes of the disease.
While researchers can use a number of statistical methods to avoid such mistakes, these methods can miss important findings because they are often unable to overcome the overall lack of diversity in genetic datasets.
Disentangling race, ancestry and health disparities can be a challenge in genome-wide association studies. Admixture mapping, on the other hand, is able to make better use of even relatively small datasets of underrepresented people. This method specifically gets its power from studying people who have mixed ancestry.
Admixture mapping relies on a quirk of human genetics you inherit DNA in chunks, not in a smooth blend. So if you have ancestors from different parts of the world, your genome is made of chunks of DNA from different ancestries. This process of chunked inheritance is called admixture.
Imagine color-coding a genome by ancestry. A person who has mixed European, Native American and African ancestry might have striped chromosomes that alternate among green, blue and red, with each color representing a certain region. A different person with similar ancestry would also have a genome of green, blue and red chunks, but the order and size of the stripes would be different.
Even two biological siblings will have locations in their genomes where their DNA comes from different ancestries. These ancestry stripes are how companies like Ancestry.com and 23andMe generate ancestry reports.
Because genome-wide association studies have to compare huge numbers of tiny individual genetic markers, it is much harder to find rare genetic markers for a disease. In contrast, admixture mapping tests whether the color of a certain ancestry chunk is associated with disease risk.
The statistics are fairly complicated, but essentially, because there are a smaller number of much larger ancestral chunks, it is easier to separate the signal from the noise. Admixture mapping is more sensitive, but it does sacrifice specificity, as it cant point to the individual genetic marker associated with disease risk.
Another important aspect of admixture mapping is that it looks at individuals with mixed ancestry. Since two people who have similar socioeconomic experiences can have different ancestry at certain parts of their genomes, admixture mapping can look at the association between this ancestry chunk and disease without mistaking social causes of disease for genetic causes.
Researchers estimate that 58% to 79% of Alzheimers disease risk is caused by genetic difference, but only about a third of these genetic differences have been discovered. Few studies have looked for genetic links to Alzheimers risk among people with mixed ancestry.
Our team applied admixture mapping to a genetic dataset of Caribbean Hispanic people who have a mix of European, Native American and African ancestry. We found a part of the genome where Native American ancestry made people less likely to have Alzheimers disease. Essentially, we found that if you have the color blue in this certain part of your genome, you are less likely to develop Alzheimers disease. We believe that with further research we can find the specific gene responsible within the blue chunk and have already identified possible candidates.
One important note is that the genetic diversity that plays a role in disease risk is not visible to the naked eye. Anyone with Native American ancestry at this particular spot in the genome not just a person who identifies as or looks Native American may have some protection against Alzheimers disease.
Our paper illustrates that gaining a more complete understanding of Alzheimers disease risk requires using methods that can make better use of the limited datasets that exist for people of non-European ancestry. There is still a lot to learn about Alzheimers disease, but every new gene linked to this disease is a step toward better understanding its causes and finding potential treatments.
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Mixed-ancestry genetic research shows a bit of Native American DNA could reduce risk of Alzheimer's disease - The Conversation US
When she isnt pursuing her favorite heart-pumping activities of running, swimming, or cycling, Sharlene M. Day, a presidential associate professor of cardiovascular medicine and director of Translational Research for the Penn Cardiovascular Institute, is focused on the heart in another way; trying to unlock and treat the mysteries of genetic heart disease.
As part of her research at the Day Lab, Day integrates translational and clinical science to understand the full spectrum of genetic heart disease evolution and progression, from gene mutations in heart muscle cells to ways of predicting negative outcomes in patients. Clinically, she sees patients with hypertrophic cardiomyopathy, a condition where the heart muscle becomes thick making it harder for blood to leave the heart, and other genetic heart conditions at the Penn Center for Inherited Cardiac Disease, such as inherited arrhythmias, high blood cholesterol, Marfan syndrome and familial amyloidosis. Her research program primarily focuses on these same conditions.
A physician scientist, Day completed her residency, followed by a cardiology fellowship, and a postdoctoral research fellowship at the University of Michigan before joining the faculty there, and spent 24 years there before coming to Penn. Day was recruited to Penn Medicine to lead initiatives in translational research within the Cardiovascular Institute and to grow the clinical and academic mission in the Penn Center for Inherited Cardiovascular Disease.
Very early on in my training, I became fascinated with the interplay between genetics and cardiac physiology that manifest in very unique observable cardiac traits and complicated disease trajectories including both heart failure and arrhythmias, also known as irregular heartbeats, says Day.
This story is by Sophie Kluthe. Read more at Penn Medicine News.
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Getting to the heart of genetic cardiovascular diseases | Penn Today - Penn Today
Individuals with both attention-deficit/hyperactivity disorder (ADHD) and a disruptive behavior disorder (DBD) share about 80% of genetic variants associated with aggressive and antisocial behaviors, according to new research published in Nature Communications. The study analyzed nearly 4000 patients with these pathologies and 30,000 control individuals, examining the neurobiological basis for aggressive behavior.
Certain people feature 2 or more psychiatric disorders, and this coexistence continues, in many cases, in a chronological axis, in which suffering from a psychiatric disorder such as ADHD involves opening the door to other comorbid pathologies that aggravate the life quality of those who suffer from the disorder, said Marta Ribass, PhD, head of the Laboratory of Genetic Psychiatry of Vall d'Hebrn Research Institute (VHIR), in a press release.
ADHD affects around 5% of children and 2.5% of adults and features hyperactivity, impulsiveness, and attention deficit. It is often associated with additional psychiatric conditions, including DBDs, which can be associated with antisocial and aggressive behaviors.
ADHD and DBD are caused by genetic and environmental factors, said Bru Cormand, professor at the Department of Genetics, Microbiology and Statistics and head of the Research Group on Neurogenetics at the University of Barcelona, in the release. Regarding ADHD, it is estimated that genetics account for 75%, while in DBDs, it would oscillate between 40 and 70%. These clinical pictures are more frequent in boys than girls, and when they come together, people are more likely to fall into risky behaviors, addictive substance use, and premature death.
The investigators identified a genomic segment in chromosome 11 that increases the risk of having ADHD in combination with DBD. This region contains the STIM1 gene, responsible for the regulation of calcium cell levels, neuronal plasticity and learning memory.
Our study shows that genetics are more determining in people with ADHD and DBD than those who only suffer from ADHD, Cormand said in the release. If we compare the genome of patients with ADHD and DBD to that of those patients with only ADHD, we see that people affected by both disorders have a higher genetic correlation with risk genetic variants. These extra correlations of [patients with] ADHD and DBD would probably correspond to alterations other authors had related to aggressive-related behaviors.
According to the investigators, this study will help broaden the understanding of the genetic landscape of ADHD comorbidities, enabling the prediction of potential secondary complications for these patients.
If we consider ADHD to be an open door to a negative trajectory, using genetic information to identify those individuals who are more vulnerable will have a strong impact on prevention, early detection, and treatment, and will shed light on new research studies to find efficient therapies that can be specific for the disorder or shared between several disorders, Ribass said in the release.
REFERENCE
ADHD, DBD and aggressiveness: Risky genetic factors [news release]. EurekAlert; February 17, 2021. Accessed July 13, 2021. https://www.eurekalert.org/pub_releases/2021-02/uob-ada021721.php
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Patients With a Combination of ADHD and DBD Share Genetic Factors Linked to Risky, Aggressive Behavior - Pharmacy Times
School of Science
Location: Medway campusSalary: 33,797 to 49,553 per annumContractType: PermanentClosingDate: Monday 09 August 2021InterviewDate: To be confirmedReference: 2755-E
The School of Science (www.gre.ac.uk/es/science) at the University of Greenwich is a large interdisciplinary School, covering biological sciences, biomedical sciences, food and nutrition, chemistry, pharmaceutical sciences, and forensic science. We have ambitious research and teaching plans as part of our new University Strategy This is our time to ensure that our students are fully prepared for future careers. Collegiality and interdisciplinary research and teaching are key features of the School. Our School is based at the historic Medway campus and boasts amazing learning spaces with state-of-the-art laboratories and lecture theatres.
As part of our ongoing development and expansion of biological, biomedical sciences and forensic science provision within the University, we are seeking to appoint a permanent lecturer/senior lecturer (teaching & research) in genetics (broadest sense). The post holder will have a strong track record at the national and international levels and will establish their own independent research programme. For appointment as Senior Lecturer, you will also have a proven track record of attracting external research and other grants.
Applicants will also be expected to contribute high quality teaching within the School and will be responsible for lectures, tutorials and laboratory classes on the biology, biomedical sciences and forensic sciences degree programmes, as well as academic duties including student assessment, marking and pastoral support. Further, with molecular techniques routinely used for diagnosis and investigation within biosciences and forensics, we seek to appoint a geneticist with knowledge and experience in these methods.
This is an exciting opportunity for a suitably motivated individual to help shape the future of bioscience research and teaching provision within the School.
The post will be based in the School of Science on the Medway campus.
For informal enquiries, please contact the Head of School, Professor Adrian Dobbs onA.Dobbs@gre.ac.uk
Should you have any queries please contact the HR Recruitment Team onHR-Recruitment@gre.ac.uk
We are looking for people who can help us deliver our mission of transforming lives through inspired teaching and research, through ourvalues.
The university welcomes people from diverse and underrepresented communities who can help the university to achieve its mission.
We do this through taking positive action such as encouraging applications from Black, Asian and Minority Ethnic, disabled and LGBT+ people. As part of our commitment to Equality, Diversity and Inclusion, Time to Change Employer Pledge/Mentally Healthy Universities, we are committed to promoting and supporting the physical and mental health of all our staff and removing barriers to improve inclusion.
We encourage applicants to disclose experience of mental health problems so we can support them fully during our recruitment process and make any necessary reasonable adjustments. Any information disclosed will be kept confidential and separate from the job application form.
We are making significant strides to understand and continuously improve our employees experience and we are committed to implementing progressive diversity talent management.
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Lecturer/Senior Lecturer in Genetics job with UNIVERSITY OF GREENWICH | 260037 - Times Higher Education (THE)