Category Archives: Genetics

Oxford Genetics secures investment; expands UK facility and eyes US market – BioPharma-Reporter.com

Oxford Genetics will expand its bioproduction services in the UK and target the US market through an office in Boston after receiving a 7.5m ($9.6m) investment.

The investment comes from existing investor Mercia Technologies PLC, and Invesco Perpetual and will help the bioprocessing support firm expand its global presence and increase its DNA, protein, viral and cell line service offerings.

The UK extension adds another floor in its building in Oxford which will be fitted out to increase capacity across the firms entire service offering, allowing the segregation of material flow and the isolation of individual projects, a spokesperson from Oxford Genetics told us.

This will allow us to continue to exceed regulatory requirements and provide quality assurance for our clients. We will also add more analytical, purification and process development equipment, for instance small scale bioreactors, to enable us to fully support our clients from research up to the point of GMP bioproduction.

The 6,000 sq ft extension is expected to be ready by November, and will include cell line engineering capabilities, viral vector production and purification suites, high-throughput robotic screening systems and process development facilities.

The US expansion, meanwhile, will see the firm open an office in Boston to target the large US market.

A US office is integral because it is the single largest market for our technologies and services, we were told. There has been a significant increase in the demand for our viral expression systems and cell line development for virus production.

The firm, founded in 2011, licenses its technology platforms on a non-exclusive basis to all biopharma and according to the spokesperson has had tremendous interest from firms looking for bioproduction optimisation solutions.

We have already begun to sign licenses and collaboration deals. The latter agreements are particularly interesting since they are allowing our collaborators accelerated access to some of our virus production platform technologies, which will fully mature over the next 18 months.

In the past year, Oxford Genetics has benefitted from several funding projects including a 1.6m and 1m, both from Innovate UK, to explore computational and synthetic biology approaches for optimising mammalian biomanufacturing processes, and to overcome the inefficient and costly scale-up of viral vector production, respectively.

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Oxford Genetics secures investment; expands UK facility and eyes US market - BioPharma-Reporter.com

Genetics, Not Laziness, Might Be Why You Hate Exercising – Medical Daily

For some, the hardest part of hitting the gym is lacing up their shoes. But for others, its the actual exercise that makes working out so excruciating. The labored breathing, sore muscles, and sweat dripping into your eyes can be a high or just one step above torture depending on which type of person you are. A new study aimed to determine what accounts for these differences, and it turns out your genetics might be to blame for how much you dread going for a run.

The British Psychological Societys Research Digest reports on a study at the Vrije Universiteit Amsterdam in the Netherlands, which enlisted 115 pairs of identical twins, 111 pairs of non-identical twins, 35 siblings related to the twins and 6 sibling pairs not from families with twins. Everyone rode an exercise bike for 20 minutes and completed a 20-minute run, both at a comfortable pace. Researchers monitored breathing to ensure the workouts were low intensity, and a warm up and cool down accompanied the routines. Subjects also completed a second short ride on the exercise bike that was more vigorous.

The siblings completed assessments while exercising, answering how they felt while working out, how much effort they put in, and whether they were energetic, lively, jittery or tense. Additionally, participants were interviewed about how often they exercised and to what intensity. Using the responses, researchers determined the participants psychological state during physical activity.

Then, scientists looked at the data to determine whether identical twins, who also have identical genes, had similar responses to exercising compared to fraternal twins and non-twin siblings. This allowed them to theorizehow much genetics actually played a role in someone's mental state during physical fitness. They concluded that genetics could account for up to 37 percent of the differences in the way people experienced exercise. Unsurprisingly, people who enjoyed fitness were prone to doing it more. However, its important to note that the study doesnt show a cause and effect relationship.

While this new research indicates that somemay not be born to love fitness, theres no denying that we should still do it. Aside from helping maintain weight, working out can lift your mood, reduce stress and anxiety, strengthen bones and and reduce risk of certain diseases.

Thankfully, it is possible to actually enjoy physical activity. Health reports that the most important thing is to take up an activity you actually like (and yes, there is bound to be something). "Too often I see people who sign up to do something like running, even though they know they hate running," Shavise Glascoe, exercise physiologist at the Johns Hopkins Weight Management Center, explained to the magazine. Even non-vigorous activities like walking your dog or dancing in your room count as exercise.

Finding a workout buddy is an easy way to instantly make jogging, walking or lifting weights more interesting. A study from 2013 found that people who worked out with a spouse, friend or family member reported more enjoyment than doing it alone. If the activity took place around nature, people reported even more enjoyment and better moods. So, stop reading this, grab a buddy and hit your nearest walking trail.

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Genetics, Not Laziness, Might Be Why You Hate Exercising - Medical Daily

Hendrix Genetics is an economic ‘win-win’ for GI – Grand Island Independent

The opening of Hendrix Genetics in Grand Island on Aug. 15 is an excellent example of the power of markets supplemented by appropriate government policy.

Feeding a growing world population now estimated to be 7.5 billion provides both a challenge and an opportunity as food producers endeavor to meet the growing demand for food. For Hendrix Genetics this demand represents opportunity as it is a world leader in turkey, layer and trout breeding as well as a major player in swine, salmon and guinea fowl production.

The numbers connected with Hendrix Genetics are impressive. They currently have 25 percent of the United States egg hatchery market and the new hatchery in Grand Island will serve 10 percent of the U.S. market. With good science and management, poultry production is an excellent way to provide quality food for both domestic and world markets.

Hendrix Genetics was willing and able to create the Grand Island plant because essential markets were available to meet their needs. After a nationwide search they determined that Grand Island was an excellent location. It provided needed isolation that was essential for the required biosecurity. In our area they found infrastructure for transportation needs, access to willing, affordable and capable labor and area producers to build and manage outlying barns as well as to provide feed.

For each component in the production process, prices, profits and wages had to be sufficient to bring together all the resources necessary to open and operate the plant.

Government policies had to align with needs of Hendrix Genetics and our community gave them an excellent invitation to grow our economy. The work of the Grand Island Area Economic Development Corporation was very important and we would add necessary and effective. Government and private enterprise had an effective partnership.

Also to be noted is that Hendrix Genetics is based in Holland and joins other industries in our community that are based in other countries such as New Holland-Italy and JBS-Brazil. Global interdependence is a reality and a plus for all those ready and willing to participate in the global economy.

America first may be effective political rhetoric in some parts of our country, but it is not good long term economic policy. Free trade and open borders will serve us better, particularly the food producers in the Midwest who are willing and able to feed the growing world population and rely on world markets.

This confluence of markets has added an $18 million investment to the city of Grand Island, more than 40 permanent jobs and an economic infusion estimated at $40 million.

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Hendrix Genetics is an economic 'win-win' for GI - Grand Island Independent

Oxford Genetics Secures 7.5M Investment – FinSMEs (blog)

Oxford Genetics, a UK-based developer of innovative synthetic biology-based technologies for biologics discovery, development and delivery, received a 7.5m investment.

Backers included existing investor Mercia Technologies and Invesco Perpetual.

The company intends to use the funds to open a new office in Boston, US and extend its UK facility at the Oxford Science Park by November 2017, which includes cell line engineering capabilities, viral vector production and purification suites, high-throughput robotic screening systems and process development facilities, invest in its research and development capabilities to increase its intellectual property (IP) portfolio and grow its of technology-enabled licensing business.

Led by Ryan Cawood, CEO, Oxford Genetics is a UK based biotechnology company specializing in the production of versatile cloning plasmids for research in academic and biotechnology institutions. The company also provides custom cloning and DNA synthesis.During the latest year, the company has increased the number of clients, key appointments, and market momentum in the growth areas of cell and gene therapy. It has also signed a number of licenses for use of its technologies, including two collaborative partnerships with gene therapy companies designed to develop its IP offering further, as well as filing five new patents intended to improve the discovery, development or delivery of biotherapeutics.

FinSMEs

22/08/2017

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Oxford Genetics Secures 7.5M Investment - FinSMEs (blog)

ETMC Cancer Institute to host women’s luncheon Sept. 12 – Jacksonville Daily Progress

The ETMC Cancer Institute will host Cancer, Genetics and You, a luncheon addressing what every woman should know about how genetics is changing cancer detection, on Tuesday, Sept. 12, at the CrossWalk Conference Center, located on the campus of Green Acres Baptist Church.

The event will feature keynote speaker Damini Desai Morah, MS, CGC, a genetic counselor and specialist from Myriad Genetics.

Science now identifies cancer as a genetic disease, meaning that cancer is caused by certain changes to genes that control the way our cells grow and divide, said Dianne Adelfio, vice president of the ETMC Cancer Institute. The speaker will discuss how your genetic makeup can affect your likelihood of developing cancers specific to women, as well as other cancers.

Attendees will be given a cancer genetic questionnaire to see if they should consider future testing. Cancer physicians and genetic specialists also will be on hand to answer questions.

Since 2015 the ETMC Breast Care Center has offered forms of genetic testing that involve taking a sample of blood or cheek mucosa to analyze a womans genes. The results can help women with breast cancer make treatment decisions, and alert them to risks of developing other cancers. Genetic testing for those who have not had cancer provides a better understanding of their own cancer risks including risks that can impact other family members.

Genetics is leading the way in medical advancements in cancer detection and targeted treatment, said Adelfio. This luncheon is designed to inform and inspire women to be healthcare advocates as they understand more about how the genetic code is providing a deeper understanding of cancer and helping save lives.

Tickets for the event are $20 per person or a table of eight for $150. Doors open at 11 a.m., with the program taking place from 11:30 a.m. to 1 p.m. Reservations are required and may be made online at etmc.org or by calling 903-535-6302.

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ETMC Cancer Institute to host women's luncheon Sept. 12 - Jacksonville Daily Progress

TPR Lifeline: Clinical Genetics Is A Growing Field – Texas Public Radio

We all have about 24,000 genes. How those genes are structured and interact can determine our current health and our future health.

Modern medicine includes specialists in this field called Clinical Geneticists. In todays TPR Lifeline, Bioscience-Medicine reporter Wendy Rigby talks to Baylor College of Medicines Scott McLean, MD, about his work at the Childrens Hospital of San Antonio.

Rigby: Dr. McLean, what is clinical genetics?

McLean: Clinical genetics is the medical specialty that uses genetic information to improve your genetic health or to understand the basis for a variety of medical conditions.

Those of us who have had children in Texas know that while youre still in the hospital, you get some genetic testing done. What is that called and what are you looking for?

We have newborn screening which is actually a blood test that is given to all babies 24 and 48 hours of age. The blood test involves collecting that blood on a piece of paper, filter paper, and sending that to the Texas State Department of Health Services in Austin where they do a series of tests.

This is the foot prick?

This is where you prick the heel. It seem awfully cruel. Babies cry. Parents dont like it. But its actually a wonderful test because it allows us to screen for over 50 conditions.

Give us some examples. What are some of the genetic conditions we might have heard of?

Well, the initial condition that was screened for in newborn screening in the United States was PKU which stands for Phenylketonuria. This is a condition that results in intellectual disability and seizures. We can change that outcome if we are able to identify the condition early enough and change the diet.

Lets say a child comes in to Childrens Hospital of San Antonio. Doctors are having trouble figuring out whats going on. Are you called in to consult?

Most of our patients that we see in the outpatient clinic are sent to us by consultation from physicians in the community or from nurseries, neonatal intensive care units. They range from situations such as multiple birth defects, to autism, intellectual disability, seizures, encephalopathy, blindness, deafness. Theres a whole gamut of reasons that folks come to see us.

When these children become grownups, does that information that youve learned about them help them out if theyre planning to have their own children in the future?

So when pediatric patients make the transition from pediatric care to adult care, its very common for information and ideas to get lost. And we certainly would hope that people remember that. Sometimes when we have identified a situation in a little baby, I tell the parents that I want them to put a sticky note on the last page of their baby book so that when they are showing the baby book to their childs fiance and they get to the last page, it reminds them you need to go back to see the geneticist because theres this genetic situation that you need to have a nice long chat about so that you can plan your family as carefully as possible.

Right. So the work youre doing today could help someone 30 years in the future.

Well, genetics is a very unique specialty in that regard because when we see a patient were not thinking about their next year of life or their next two years of life or the next month. We do think about that. But this is a lifelong diagnosis and a lifelong situation. So I often joke with my patients that Im going to try to put them on the 90-year plan. What we figure out now about their genetics is going to be helpful for them throughout their entire lifespan, at least up until 90 years. And then after that theyre on their own. But well get them to 90.

So its an exciting time to be in the field.

Very exciting. I think the era of gene therapy which for many people we thought was never going to happen, its very promising because we have new technologies that I think are going to allow for advances in that area.

Dr. Scott McLean with Baylor College of Medicine and the Childrens Hospital of San Antonio, thanks for the information.

Youre quite welcome.

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TPR Lifeline: Clinical Genetics Is A Growing Field - Texas Public Radio

Just the Facts on Atossa Genetics Inc. (ATOS) – StockNewsJournal

Atossa Genetics Inc. (ATOS) is an interesting player in the Healthcare space, with a focus on Diagnostic Substances. The stock has been active on the tape, currently trading at $0.43, up from yesterdays close by 7.50%. Given the stocks recent action, it seemed like a good time to take a closer look at the companys recent data.

Technical Analysis

Sometimes, we can understand most about a stock by simply looking at how it has been trading. Looking at the stocks movement on the chart, Atossa Genetics Inc. recorded a 52-week high of $3.97. It is now trading 3.54% off that level. The stock is trading $0.43 its 50-day moving average by 0%. The stock carved out a 52-week low down at $0.32.

In recent action, Atossa Genetics Inc. (ATOS) has made a move of +7.50% over the past month, which has come on Strong relative transaction volume. Over the trailing year, the stock is underperforming the S&P 500 by 99.86, and its gotten there by action that has been more volatile on a day-to-day basis than most other stocks on the exchange. In terms of the mechanics underlying that movement, traders will want to note that the stock is trading on a float of 7.46% with $10.93 Million sitting short, betting on future declines. That suggests something of the likelihood of a short squeeze in shares of ATOS.

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Just the Facts on Atossa Genetics Inc. (ATOS) - StockNewsJournal

Heritability of IQ – Wikipedia

Research on heritability of IQ infers, from the similarity of IQ in closely related persons, the proportion of variance of IQ among individuals in a study population that is associated with genetic variation within that population. This provides a maximum estimate of genetic versus environmental influence for phenotypic variation in IQ in that population. "Heritability", in this sense, "refers to the genetic contribution to variance within a population and in a specific environment".[1] In other words, heritability is a mathematical estimate that indicates how much of a traits variation can be attributed to genes. There has been significant controversy in the academic community about the heritability of IQ since research on the issue began in the late nineteenth century.[2]Intelligence in the normal range is a polygenic trait, meaning it's influenced by more than one gene.[3][4]

The general figure for the heritability of IQ, according to an authoritative American Psychological Association report, is 0.45 for children, and rises to around 0.75 for late teens and adults.[5][6] In simpler terms, IQ goes from being weakly correlated with genetics, for children, to being strongly correlated with genetics for late teens and adults. The heritability of IQ increases with age and reaches an asymptote at 1820 years of age and continues at that level well into adulthood.[7] Recent studies suggest that family and parenting characteristics are not significant contributors to variation in IQ scores;[8] however, poor prenatal environment, malnutrition and disease can have deleterious effects.[9][10]

"Heritability" is defined as the proportion of variance in a trait which is attributable to genetic variation within a defined population in a specific environment.[1] Heritability takes a value ranging from 0 to 1; a heritability of 1 indicates that all variation in the trait in question is genetic in origin and a heritability of 0 indicates that none of the variation is genetic. The determination of many traits can be considered primarily genetic under similar environmental backgrounds. For example, a 2006 study found that adult height has a heritability estimated at 0.80 when looking only at the height variation within families where the environment should be very similar.[11] Other traits have lower heritabilities, which indicate a relatively larger environmental influence. For example, a twin study on the heritability of depression in men calculated it as 0.29, while it was 0.42 for women in the same study.[12] Contrary to popular[citation needed] belief, two parents of higher IQ will not necessarily produce offspring of equal or higher intelligence. In fact, according to the concept of regression toward the mean, parents whose IQ is at either extreme are more likely to produce offspring with IQ closer to the mean (or average).[13][14]

There are a number of points to consider when interpreting heritability:

Various studies have found the heritability of IQ to be between 0.7 and 0.8 in adults and 0.45 in childhood in the United States.[6][18][19] It may seem reasonable to expect that genetic influences on traits like IQ should become less important as one gains experiences with age. However, that the opposite occurs is well documented. Heritability measures in infancy are as low as 0.2, around 0.4 in middle childhood, and as high as 0.8 in adulthood.[7] One proposed explanation is that people with different genes tend to seek out different environments that reinforce the effects of those genes.[6] The brain undergoes morphological changes in development which suggests that age-related physical changes could also contribute to this effect.[20]

A 1994 article in Behavior Genetics based on a study of Swedish monozygotic and dizygotic twins found the heritability of the sample to be as high as 0.80 in general cognitive ability; however, it also varies by trait, with 0.60 for verbal tests, 0.50 for spatial and speed-of-processing tests, and 0.40 for memory tests. In contrast, studies of other populations estimate an average heritability of 0.50 for general cognitive ability.[18]

In 2006, The New York Times Magazine listed about three quarters as a figure held by the majority of studies.[21]

There are some family effects on the IQ of children, accounting for up to a quarter of the variance. However, adoption studies show that by adulthood adoptive siblings aren't more similar in IQ than strangers,[22] while adult full siblings show an IQ correlation of 0.24. However, some studies of twins reared apart (e.g. Bouchard, 1990) find a significant shared environmental influence, of at least 10% going into late adulthood.[19]Judith Rich Harris suggests that this might be due to biasing assumptions in the methodology of the classical twin and adoption studies.[23]

There are aspects of environments that family members have in common (for example, characteristics of the home). This shared family environment accounts for 0.25-0.35 of the variation in IQ in childhood. By late adolescence it is quite low (zero in some studies). There is a similar effect for several other psychological traits. These studies have not looked into the effects of extreme environments such as in abusive families.[6][22][24][25]

The American Psychological Association's report "Intelligence: Knowns and Unknowns" (1995) states that there is no doubt that normal child development requires a certain minimum level of responsible care. Severely deprived, neglectful, or abusive environments must have negative effects on a great many aspects of development, including intellectual aspects. Beyond that minimum, however, the role of family experience is in serious dispute. There is no doubt that such variables as resources of the home and parents' use of language are correlated with children's IQ scores, but such correlations may be mediated by genetic as well as (or instead of) environmental factors. But how much of that variance in IQ results from differences between families, as contrasted with the varying experiences of different children in the same family? Recent twin and adoption studies suggest that while the effect of the shared family environment is substantial in early childhood, it becomes quite small by late adolescence. These findings suggest that differences in the life styles of families whatever their importance may be for many aspects of children's lives make little long-term difference for the skills measured by intelligence tests.

Although parents treat their children differently, such differential treatment explains only a small amount of non-shared environmental influence. One suggestion is that children react differently to the same environment due to different genes. More likely influences may be the impact of peers and other experiences outside the family.[6][24] For example, siblings grown up in the same household may have different friends and teachers and even contract different illnesses. This factor may be one of the reasons why IQ score correlations between siblings decreases as they get older.[26]

Certain single-gene genetic disorders can severely affect intelligence. Phenylketonuria is an example,[27] with publications demonstrating the capacity of phenylketonuria to produce a reduction of 10 IQ points on average.[28] Meta-analyses have found that environmental factors, such as iodine deficiency, can result in large reductions in average IQ; iodine deficiency has been shown to produce a reduction of 12.5 IQ points on average.[29]

The APA report "Intelligence: Knowns and Unknowns" (1995) also stated that:

"We should note, however, that low-income and non-white families are poorly represented in existing adoption studies as well as in most twin samples. Thus it is not yet clear whether these studies apply to the population as a whole. It remains possible that, across the full range of income and ethnicity, between-family differences have more lasting consequences for psychometric intelligence."[6]

A study (1999) by Capron and Duyme of French children adopted between the ages of four and six examined the influence of socioeconomic status (SES). The children's IQs initially averaged 77, putting them near retardation. Most were abused or neglected as infants, then shunted from one foster home or institution to the next. Nine years later after adoption, when they were on average 14 years old, they retook the IQ tests, and all of them did better. The amount they improved was directly related to the adopting family's socioeconomic status. "Children adopted by farmers and laborers had average IQ scores of 85.5; those placed with middle-class families had average scores of 92. The average IQ scores of youngsters placed in well-to-do homes climbed more than 20 points, to 98."[21][30]

Stoolmiller (1999) argued that the range of environments in previous adoption studies were restricted. Adopting families tend to be more similar on, for example, socio-economic status than the general population, which suggests a possible underestimation of the role of the shared family environment in previous studies. Corrections for range restriction to adoption studies indicated that socio-economic status could account for as much as 50% of the variance in IQ.[31]

On the other hand, the effect of this was examined by Matt McGue and colleagues (2007), who wrote that "restriction in range in parent disinhibitory psychopathology and family socio-economic status had no effect on adoptive-sibling correlations [in] IQ"[32]

Turkheimer and colleagues (2003) argued that the proportions of IQ variance attributable to genes and environment vary with socioeconomic status. They found that in a study on seven-year-old twins, in impoverished families, 60% of the variance in early childhood IQ was accounted for by the shared family environment, and the contribution of genes is close to zero; in affluent families, the result is almost exactly the reverse.[33]

In contrast to Turkheimer (2003), a study by Nagoshi and Johnson (2005) concluded that the heritability of IQ did not vary as a function of parental socioeconomic status in the 949 families of Caucasian and 400 families of Japanese ancestry who took part in the Hawaii Family Study of Cognition.[34]

Asbury and colleagues (2005) studied the effect of environmental risk factors on verbal and non-verbal ability in a nationally representative sample of 4-year-old British twins. There was not any statistically significant interaction for non-verbal ability, but the heritability of verbal ability was found to be higher in low-SES and high-risk environments.[35]

Harden and colleagues (2007) investigated adolescents, most 17 years old, and found that, among higher income families, genetic influences accounted for approximately 55% of the variance in cognitive aptitude and shared environmental influences about 35%. Among lower income families, the proportions were in the reverse direction, 39% genetic and 45% shared environment."[36]

Rushton and Jensen (2010) criticized many of these studies for being done on children or adolescents. They argued that heritability increases during childhood and adolescence, and even increases greatly between 1620 years of age and adulthood, so one should be cautious drawing conclusions regarding the role of genetics from studies where the participants are not adults. Furthermore, the studies typically did not examine if IQ gains due to adoption were on the general intelligence factor (g). When the studies by Capron and Duyme were re-examined, IQ gains from being adopted into high SES homes were on non-g factors. By contrast, the adopted children's g mainly depended on their biological parents SES, which implied that g is more difficult to environmentally change.[17] The most cited adoption projects that sought to estimate the heritability of IQ were those of Texas,[37] Colorado[38] and Minnesota[39] that were started in the 1970s. These studies showed that while the adoptive parents' IQ does correlate with adoptees' IQ in early life, when the adoptees reach adolescence the correlation has faded and disappeared. The correlation with the biological parent seemed to explain most of the variation.

A 2011 study by Tucker-Drob and colleagues reported that at age 2, genes accounted for approximately 50% of the variation in mental ability for children being raised in high socioeconomic status families, but genes accounted for negligible variation in mental ability for children being raised in low socioeconomic status families. This gene-environment interaction was not apparent at age 10 months, suggesting that the effect emerges over the course of early development.[40]

A 2012 study based on a representative sample of twins from the United Kingdom, with longitudinal data on IQ from age two to age fourteen, did not find evidence for lower heritability in low-SES families. However, the study indicated that the effects of shared family environment on IQ were generally greater in low-SES families than in high-SES families, resulting in greater variance in IQ in low-SES families. The authors noted that previous research had produced inconsistent results on whether or not SES moderates the heritability of IQ. They suggested three explanations for the inconsistency. First, some studies may have lacked statistical power to detect interactions. Second, the age range investigated has varied between studies. Third, the effect of SES may vary in different demographics and different countries.[41]

A 2017 King's College London study suggests that genes account for nearly 50 per cent of the differences between whether children are socially mobile or not.[42]

A meta-analysis by Devlin and colleagues (1997) of 212 previous studies evaluated an alternative model for environmental influence and found that it fits the data better than the 'family-environments' model commonly used. The shared maternal (fetal) environment effects, often assumed to be negligible, account for 20% of covariance between twins and 5% between siblings, and the effects of genes are correspondingly reduced, with two measures of heritability being less than 50%. They argue that the shared maternal environment may explain the striking correlation between the IQs of twins, especially those of adult twins that were reared apart.[2] IQ heritability increases during early childhood, but whether it stabilizes thereafter remains unclear.[2][old info] These results have two implications: a new model may be required regarding the influence of genes and environment on cognitive function; and interventions aimed at improving the prenatal environment could lead to a significant boost in the population's IQ.[2]

Bouchard and McGue reviewed the literature in 2003, arguing that Devlin's conclusions about the magnitude of heritability is not substantially different from previous reports and that their conclusions regarding prenatal effects stands in contradiction to many previous reports.[43] They write that:

Chipuer et al. and Loehlin conclude that the postnatal rather than the prenatal environment is most important. The Devlin et al. (1997a) conclusion that the prenatal environment contributes to twin IQ similarity is especially remarkable given the existence of an extensive empirical literature on prenatal effects. Price (1950), in a comprehensive review published over 50 years ago, argued that almost all MZ twin prenatal effects produced differences rather than similarities. As of 1950 the literature on the topic was so large that the entire bibliography was not published. It was finally published in 1978 with an additional 260 references. At that time Price reiterated his earlier conclusion (Price, 1978). Research subsequent to the 1978 review largely reinforces Prices hypothesis (Bryan, 1993; Macdonald et al., 1993; Hall and Lopez-Rangel, 1996; see also Martin et al., 1997, box 2; Machin, 1996).[43]

Dickens and Flynn (2001) argued that the "heritability" figure includes both a direct effect of the genotype on IQ and also indirect effects where the genotype changes the environment, in turn affecting IQ. That is, those with a higher IQ tend to seek out stimulating environments that further increase IQ. The direct effect can initially have been very small but feedback loops can create large differences in IQ. In their model an environmental stimulus can have a very large effect on IQ, even in adults, but this effect also decays over time unless the stimulus continues. This model could be adapted to include possible factors, like nutrition in early childhood, that may cause permanent effects.

The Flynn effect is the increase in average intelligence test scores by about 0.3% annually, resulting in the average person today scoring 15 points higher in IQ compared to the generation 50 years ago.[44] This effect can be explained by a generally more stimulating environment for all people. The authors suggest that programs aiming to increase IQ would be most likely to produce long-term IQ gains if they taught children how to replicate outside the program the kinds of cognitively demanding experiences that produce IQ gains while they are in the program and motivate them to persist in that replication long after they have left the program.[45][46] Most of the improvements have allowed for better abstract reasoning, spatial relations, and comprehension. Some scientists have suggested that such enhancements are due to better nutrition, better parenting and schooling, as well as exclusion of the least intelligent, genetically inferior, people from reproduction. However, Flynn and a group of other scientists share the viewpoint that modern life implies solving many abstract problems which leads to a rise in their IQ scores.[44]

More recent research has illuminated genetic factors underlying IQ stability and change. Genome-wide association studies have demonstrated that the genes involved in intelligence remain fairly stable over time.[47] Specifically, in terms of IQ stability, "genetic factors mediated phenotypic stability throughout this entire period [age 0 to 16], whereas most age-to-age instability appeared to be due to non-shared environmental influences".[48][49] These findings have been replicated extensively and observed in the United Kingdom,[50] the United States,[48][51] and the Netherlands.[52][53][54][55] Additionally, researchers have shown that naturalistic changes in IQ occur in individuals at variable times.[56]

Spatial ability has been shown to be unifactorial (a single score accounts well for all spatial abilities), and is 69% heritable in a sample of 1,367 twins from the ages 19 through 21.[57] Further only 8% of spatial ability can be accounted for by a shared environmental factors like school and family.[58] Of the genetically determined portion of spacial ability, 24% is shared with verbal ability (general intelligence) and 43% was specific to spatial ability alone.[59]

A 2009 review article identified over 50 genetic polymorphisms that have been reported to be associated with cognitive ability in various studies, but noted that the discovery of small effect sizes and lack of replication have characterized this research so far.[60] Another study attempted to replicate 12 reported associations between specific genetic variants and general cognitive ability in three large datasets, but found that only one of the genotypes was significantly associated with general intelligence in one of the samples, a result expected by chance alone. The authors concluded that most reported genetic associations with general intelligence are probably false positives brought about by inadequate sample sizes. Arguing that common genetic variants explain much of the variation in general intelligence, they suggested that the effects of individual variants are so small that very large samples are required to reliably detect them.[61] Genetic diversity within individuals is heavily correlated with IQ.[62]

A novel molecular genetic method for estimating heritability calculates the overall genetic similarity (as indexed by the cumulative effects of all genotyped single nucleotide polymorphisms) between all pairs of individuals in a sample of unrelated individuals and then correlates this genetic similarity with phenotypic similarity across all the pairs. A study using this method estimated that the lower bounds for the narrow-sense heritability of crystallized and fluid intelligence are 40% and 51%, respectively. A replication study in an independent sample confirmed these results, reporting a heritability estimate of 47%.[63] These findings are compatible with the view that a large number of genes, each with only a small effect, contribute to differences in intelligence.[61]

The relative influence of genetics and environment for a trait can be calculated by measuring how strongly traits covary in people of a given genetic (unrelated, siblings, fraternal twins, or identical twins) and environmental (reared in the same family or not) relationship. One method is to consider identical twins reared apart, with any similarities which exists between such twin pairs attributed to genotype. In terms of correlation statistics, this means that theoretically the correlation of tests scores between monozygotic twins would be 1.00 if genetics alone accounted for variation in IQ scores; likewise, siblings and dizygotic twins share on average half of their alleles and the correlation of their scores would be 0.50 if IQ were affected by genes alone (or greater if, as is undoubtedly the case, there is a positive correlation between the IQs of spouses in the parental generation). Practically, however, the upper bound of these correlations are given by the reliability of the test, which is 0.90 to 0.95 for typical IQ tests[64]

If there is biological inheritance of IQ, then the relatives of a person with a high IQ should exhibit a comparably high IQ with a much higher probability than the general population. In 1982, Bouchard and McGue reviewed such correlations reported in 111 original studies in the United States. The mean correlation of IQ scores between monozygotic twins was 0.86, between siblings, 0.47, between half-siblings, 0.31, and between cousins, 0.15.[65]

The 2006 edition of Assessing adolescent and adult intelligence by Alan S. Kaufman and Elizabeth O. Lichtenberger reports correlations of 0.86 for identical twins raised together compared to 0.76 for those raised apart and 0.47 for siblings.[66] These number are not necessarily static. When comparing pre-1963 to late 1970s data, researches DeFries and Plomin found that the IQ correlation between parent and child living together fell significantly, from 0.50 to 0.35. The opposite occurred for fraternal twins.[67]

Another summary:

Although IQ differences between individuals are shown to have a large hereditary component, it does not follow that mean group-level disparities (between-group differences) in IQ necessarily have a genetic basis. The Flynn effect is one example where there is a large difference between groups(past and present) with little or no genetic difference. An analogy, attributed to Richard Lewontin,[70] illustrates this point:

Suppose two handfuls are taken from a sack containing a genetically diverse variety of corn, and each grown under carefully controlled and standardized conditions, except that one batch is lacking in certain nutrients that are supplied to the other. After several weeks, the plants are measured. There is variability of growth within each batch, due to the genetic variability of the corn. Given that the growing conditions are closely controlled, nearly all the variation in the height of the plants within a batch will be due to differences in their genes. Thus, within populations, heritabilities will be very high. Nevertheless, the difference between the two groups is due entirely to an environmental factordifferential nutrition. Lewontin didn't go so far as to have the one set of pots painted white and the other set black, but you get the idea. The point of the example, in any case, is that the causes of between-group differences may in principle be quite different from the causes of within-group variation.[71]

Arthur Jensen has written in agreement that this is technically correct, but he has also stated that a high heritability increases the probability that genetics play a role in average group differences.[72][73]

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Heritability of IQ - Wikipedia

Genesis and Genetics | We look at Genetics in Genesis

One lingering mystery concerning Noahs ark is: How many animals were on board? Since DNA has a very good reputation for solving mysteries in the courtroom, now its time to unleash its powers and reveal Noahs passenger list.

As we look about the earth we see a multitude of animals reproducing after their kind, each retaining their distinction as a kind/specie. How does this happen? Two things are required for kinds/species to remain distinct:

(1) They must have the desire (instincts coded in their DNA) to mate with their own kind/species and

(2) They must have the ability (compatible DNA) to produce viable offspring like themselves.

These two requirements are the basis for both the Biblical and secular scientific definition of species/kinds. The words species and kinds are synonyms, but usually species is used by the secular scientific community and kinds is used by the Biblical community. Nonetheless, both words should define the same creatures, and our conclusion is that they do. Our position is as follows:

Fundamentally, all of the species currently defined by modern science were on the Ark

Consider humans, we have the desire and ability to produce more humans like ourselves. We know that we cannot produce a pig or a chimpanzee because we do not have the genetic ability in our DNAto do so.

Next, consider the great horned owls, they desire to mate with other great horned owls and they have the ability to produce other great horned owls. However, their DNA does not produce the desire or the ability to create a bluebird, a barn owl, or even an eagle owl which is the same genus as the great horned owl.

We wrote a technical paper, The Genetics of Kinds Ravens, Owls, and Doves, and found that not one of the owl kinds/species we examined could possibly produce any other owl kinds/species. That is also true for the ravens and doves. They differ from one another by too much genetic information. We also wrote a technical paper, A Study of Biblical Kinds Using 62 Species of Mice; which showed the various species/kinds of mouse DNA differed from one another by significant amounts with distinct DNA gaps between the kinds/species. It would be impossible to bridge these gaps by means of any natural process.

Our study of the mouse was very interesting in that we found that there are more than one hundredmouse kinds/species and they all remain distinct. How do they do it? They have been magnificently designed with the desire and ability to reproduce after their kinds. Here are a few facts: They can read each others genetics like a barcode (Ref 1). They mate only with their own species (Ref 2). They dont breed with close relatives (Ref 3) and the males do not mate with under aged females (Ref 4). All of this is coded in the DNA and not only does it preserve their distinctiveness, but also maintains good genetic health. You may read all about it, get all of the references, and gain access to all of the DNA sequences at: A Study of Biblical Kinds Using 62 Species of Mice.

If only a few kinds would have been on the Ark, there would only be a few kinds now. The scriptures are clear: every kind was created (Genesis 1); every kind was loaded on the Ark (Genesis 6:19-20); and every kind disembarked from the Ark (Genesis 8:17-20). The kinds were distinct and remain distinct.

Our conclusion would necessitate that on the order of 6000 amphibian, 10,000 bird, 6,000 mammal, and 8,000 reptile kinds/species were aboard the Ark. Accounting for pairs, sevens of clean animals, and those that have gone extinct since the flood, the total number aboard the Ark would be on the order of 100,000. This would be no problem for the very large Ark with all of the animals in Biblical deep sleep (Ref 5)

As we look at this glorious creation, we see that the kinds are distinct. They are distinct because they have both the desire and ability to mate with their own kind and produce offspring of like kind. God always does things right, and in order to replenish the earth properly, He gave every kind a berth on the Ark. All of the passengers were peacefully asleep being transported to a new world filled with adventure and hope.

Key words:

Animals of the Ark, Species on the Ark, Kinds on the Ark, Noahs Ark, Noahs Ark, species vs. kinds, and DNA Noahs Ark

Additional Suggested Reading:

Noahs Ark A Fresh Look

Noahs Ark Hermetically Sealed and Safe

References:1. Beynon, R.J. and Hurst, J.L., 2003. Multiple roles of major urinary proteins in the house mouse, Mus domesticus., Biochem Soc Trans. 2003 Feb;31(Pt 1):142-6. PMID:12546672.

2. Lane, R.P., Young, J., Newman, T., and Trask, B.J., 2004. Species specificity in rodent pheromone receptor repertoires. Genome Res. 14: 603-608. [PMC free article] [PubMed]

3. Sherborne, A.L., Michael D., Thom, M.D., Paterson, S., Jury, F., Ollier, W.E.R., Stockley, P., Beynon, R.J. and Hurst, J.L., 2007. The Genetic Basis of Inbreeding Avoidance in House Mice, Current Biology 17, 20612066, December 4, 2007.

4. Ferrero, D.M., Moeller, L.M., Osakada T., Horio, N., Li, Q., Dheeraj S.R., Cichy, A., Spehr, M. Touhara, K. Liberles, S.D., 2013. A juvenile mouse pheromone inhibits sexual behaviour through the vomeronasal system.Nature, 2013; DOI: 10.1038/nature12579

5. http://www.genesisandgenetics.org/2013/07/20/122/

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Genesis and Genetics | We look at Genetics in Genesis

Does genetics make me what I am? – Sunbury Daily Item

Two timely issues call into question our use of genetics, both in science and popular usage: CRISPR technology used in the pre-natal state to genetically edit-out/repair potentially fatal genes, and the Google controversy.

CRISPR Clustered Regularly Interspersed Short Palindromic Repeats technology, discovered by scientists at UC Berkeley and modified by those at MIT, will almost certainly result in a Nobel Prize. Berkeley scientists discovered that these repeats were used by bacteria to protect themselves against viral infections. Between the repeats, they found pieces of the viral DNA that had previously attacked the bacterium. If, and when, the same virus again attacked, the intruder viral DNA would be compared to the DNA stored between the repeats. If it is recognized as a repeat offender, the bacterium sends in proteins to destroy the viral DNA. They additionally noted that in non-virally infected bacteria, CRISPR could be used to delete some bacterial genes and replace them with others.

Our use of this technology in human cells allows injection of the DNA-modifying proteins into a human egg while it is being fertilized in a test-tube. Fatal genetic conditions identified in the mother or father in the recent report this was a cardiac abnormality, hypertrophic cardiomyopathy can potentially be corrected pre-natally and, after the correction, the fertilized egg implanted into the mother. An incredibly promising technology, it may allow, as with this cardiac abnormality, children at-risk for sudden death to grow old.

Of course, there are ethical concerns related to this technology. Will it be used to create perfect people, eliminating the diversity that makes us better and stronger? That is up to us. A head-in-the-sand refusal to engage with this is not the answer.

The scientific use of genetics and the concept of diversity, above, is tied to its non-scientific use in the Googles James Damore controversy.

Damore spent 3,400 words to say three things: Women and ethnic minorities are genetically different than (select) men; Those genetic differences are why there are more men than women (and minorities) in positions of power; Refusing to acknowledge this creates all sorts of difficulties and controversy, and is bad for business.

Google, he argues, doesnt allow ideas such as his from being discussed, as people are shamed into silence.

The differences between men and women in the workplace are due to inherent, genetic differences, he claims. What?

There are differences between men and women phenotypic (hair color, eye color) and genotypic (a slight variation in genes coding for gender) for which I am always pleased. Do these explain workplace differences? Pay differences? IQ? No. What we term Intelligence Quotient is heavily influenced by surroundings and upbringing, including social class. Not that inherent ability is meaningless, but environment matters. It is not nurture versus nature, it is nurture and nature.

There is a thoughtful part of Damores thesis, meriting consideration. Diversity is right because it makes us better and stronger; we should welcome diverse voices. He muddles this logical point by claiming women are paid less than men for the same job because they spend more money and, somehow, this is genetic; so much for diversity.

Genetics both does and does not make us who we are. Yes, there are genetic elements within us that make us phenotypically what we are: Brown eyes rather than green; black hair rather than blond. But brilliance? Thoughtfulness? Humanity? Empathy? The ability to work together to solve a problem? To work on a problem day after day until the solution appears?

If there is a genetics to this, it is the ability of multiple genes to be turned on by stimulation in a young person. These on-switches are flipped by parents and a society that loves and provides for the child, allows the child to explore and ask questions. A society that takes the child seriously. A society that does not think of the child, the sum of her phenotype, what she looks like.

The danger from CRISPR technology is it could be used to create the perfect human, eliminating the diversity that makes us better, and our world more beautiful. Damores paper, without using such technology, does just that. He turns women and ethnic minorities into caricatures of themselves, while asserting that it is he who is not appreciated or valued.

Peoples opinions vary, but facts suggest we are surrounded by conservative voices, of which I am a multi-faceted one.

CRISPR technology has downsides; we need international guardrails for its use. But the misuse of genetics to explain our societys flaws is an error of the highest magnitude. Much more dangerous than the CRISPR tool-set, we see it in action every day. In papers such as Mr. Damores, and in the way we think of, and treat, our children, boys and girls.

Our world view, ideology, is like the air we breathe: invisible, almost indescribable. It is this ideological view that allows Damore and sometimes us to simultaneously argue for diversity, while doing all in our power to eliminate it.

Follow Dr. A. Joseph Layon on Twitter @ajlayon or on his health blog, also titled Notes from the Southern Heartland (ajlayon.com). Letters may be sent to: LettersNFTSH@gmail.com.

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Does genetics make me what I am? - Sunbury Daily Item