StemCell Therapy

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

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/

Continued here:
Genesis and Genetics | We look at Genetics in Genesis

A new study by UCLA researchers reveals the range of reactions from rejection to reinterpretation to acceptance after white nationalists learn that DNA ancestry test results indicate they may not be as white or European as they previously thought.

Thestudy,When Genetics Challenges a Racists Identity: Genetic Ancestry Testing Among White Nationalists, is the work of UCLA researchersAaron Panofskyand Joan Donovan, who presented their findings at the annual meeting of the American Sociological Association held Aug. 14, 2017, in Montreal, Canada.

Upon receiving genetic evidence of non-white or non-European ancestry, those posting online expend considerable energy to repair identities by rejecting or reinterpreting genetic ancestry testing results, said the researchers, who studied discussion threads on the topic posted on the white nationalist online forum Stormfront.

UCLA Luskin School of Public Affairs

Aaron Panofsky

In their study, Donovan and Panofsky, an associate professor with appointments in Public Policy at UCLA Luskin School of Public Affairs, the Institute for Society and Genetics, and Sociology, looked at more than 3,000 posts in 70 discussion threads on topics related to test reveals. These included posts by individuals who revealed results of non-white/non-European ancestry on Stormfront, a website that requires members to be white or European with non-Jewish ancestry. Responses also included the comments on those test results.

Panofsky and Donovan, a postdoctoral fellow at the Institute for Society and Genetics, report that while ancestry tests promote the capacity to reveal ones genetic ties to ethnic groups, ancient populations and historical migrations, and even famous historical figures this opportunity to know thyself can come with significant risks.

Panofsky points out that based on white nationalists responses to genetic information upon learning their test results, there is no reason to believe that they would give up their racial ideology, and, more importantly, that genetic information cannot be relied on to change the views of white nationalists.

In addition, Panofsky said that, as a group, white nationalists appear to have a combination of sophisticated and unsophisticated methods of interpreting the data from statistical and genetic viewpoints, as well as on their own historical reasoning or reinterpretation.

In this framework, the repair strategy is not to reject scientific or historical knowledge, but to educate oneself to understand the construction of [genetic test] results and to explain those results in alternate terms, the researchers conclude.

In parsing responses to genetic ancestry test results posted on Stormfront, Panofsky and Donovan created a decision tree consisting of good news responses, or confirmation of white identity, or bad news, revealing results of non-white or non-European ancestry.

Good news served a confirming purpose and was well-received, but bad news elicited responses of rejection of the test results. Alternatives to the rejected responses included championing traditional methods, citing family history or using a mirror test, whereby individuals evaluated their outward appearance as a gauge of racial identity.

Many of the responses to bad news are about how to repair the damage, rather than latching onto the ideology of Stormfront, Panofsky said. Even though they have that idea of purity, they help people explain away or dismiss the result.

The researchers also found that some who reject unfavorable genetic test results interpret them as the product of companies with an anti-white bias, or Jewish ownership invested in sowing racial doubt and confusion among whites. They also attribute a small percentage of non-white or non-European markers as being part of a multicultural conspiracy, according to the study.

Another way the posters dealt with bad news, Panofsky and Donovan reported, was to discount indications of non-white ancestry as a statistical error or noise to engage in scientific reinterpretation of the results.

The findings also indicate that white nationalists are using genetic ancestry test results to rethink the boundaries of whiteness. Panofsky and Donovan point out that a great deal of discussion on Stormfront focuses on what are the genetic markers of legitimate whiteness or European-ness, and how to think about white nationalism in an era of genetic ancestry testing.

Go here to read the rest:
Study reveals white nationalists' reactions when genetics test results challenge their identity - UCLA Newsroom

August 23, 2017 - By Stan Paul - A new study by UCLA researchers reveals the range of reactions from rejection to reinterpretation to acceptance after white nationalists learn that DNA ancestry test results indicate they may not be as white or European as they previously thought.

Thestudy,When Genetics Challenges a Racists Identity: Genetic Ancestry Testing Among White Nationalists, is the work of UCLA researchersAaron Panofskyand Joan Donovan, who presented their findings at the annual meeting of the American Sociological Association held Aug. 14, 2017, in Montreal, Canada.

Upon receiving genetic evidence of non-white or non-European ancestry, those posting online expend considerable energy to repair identities by rejecting or reinterpreting genetic ancestry testing results, said the researchers, who studied discussion threads on the topic posted on the white nationalist online forum Stormfront.

(Right) Aaron Panofsky - Credit: UCLA Luskin School of Public Affairs

In their study, Donovan and Panofsky, an associate professor with appointments in Public Policy at UCLA Luskin School of Public Affairs, the Institute for Society and Genetics, and Sociology, looked at more than 3,000 posts in 70 discussion threads on topics related to test reveals. These included posts by individuals who revealed results of non-white/non-European ancestry on Stormfront, a website that requires members to be white or European with non-Jewish ancestry. Responses also included the comments on those test results.

Panofsky and Donovan, a postdoctoral fellow at the Institute for Society and Genetics, report that while ancestry tests promote the capacity to reveal ones genetic ties to ethnic groups, ancient populations and historical migrations, and even famous historical figures this opportunity to know thyself can come with significant risks.

Panofsky points out that based on white nationalists responses to genetic information upon learning their test results, there is no reason to believe that they would give up their racial ideology, and, more importantly, that genetic information cannot be relied on to change the views of white nationalists.

In addition, Panofsky said that, as a group, white nationalists appear to have a combination of sophisticated and unsophisticated methods of interpreting the data from statistical and genetic viewpoints, as well as on their own historical reasoning or reinterpretation.

In this framework, the repair strategy is not to reject scientific or historical knowledge, but to educate oneself to understand the construction of [genetic test] results and to explain those results in alternate terms, the researchers conclude.

In parsing responses to genetic ancestry test results posted on Stormfront, Panofsky and Donovan created a decision tree consisting of good news responses, or confirmation of white identity, or bad news, revealing results of non-white or non-European ancestry.

Good news served a confirming purpose and was well-received, but bad news elicited responses of rejection of the test results. Alternatives to the rejected responses included championing traditional methods, citing family history or using a mirror test, whereby individuals evaluated their outward appearance as a gauge of racial identity.

Many of the responses to bad news are about how to repair the damage, rather than latching onto the ideology of Stormfront, Panofsky said. Even though they have that idea of purity, they help people explain away or dismiss the result.

The researchers also found that some who reject unfavorable genetic test results interpret them as the product of companies with an anti-white bias, or Jewish ownership invested in sowing racial doubt and confusion among whites. They also attribute a small percentage of non-white or non-European markers as being part of a multicultural conspiracy, according to the study.

Another way the posters dealt with bad news, Panofsky and Donovan reported, was to discount indications of non-white ancestry as a statistical error or noise to engage in scientific reinterpretation of the results.

The findings also indicate that white nationalists are using genetic ancestry test results to rethink the boundaries of whiteness. Panofsky and Donovan point out that a great deal of discussion on Stormfront focuses on what are the genetic markers of legitimate whiteness or European-ness, and how to think about white nationalism in an era of genetic ancestry testing.Source: UCLA

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UCLA Researchers Study Reveals White Nationalists' Reactions When Genetics Test Results Challenge Their Identity - Sierra Sun Times

When Katy Neese and Olivia Sacopulos jumped into their research this summer, they did it with all heart mice hearts, that is.

Neese and Sacopulos used the Summer Undergraduate Research Experience at Indiana State University to conduct preliminary research on the Foxhead BOX (FOX) gene expression, which encodes transcription factor proteins that switch genes on or off as the heart forms. Its a critical process the body has to get right for proper heart development. But when some Forkhead genes are mutated or dysfunctional, they fail to produce proteins that can correctly turn on or off other genes. The result is a congenital heart defect.

The project by Neese and Sacopulos used two approaches: further analysis of previously published available gene expression microarray data and the collection of FOX gene expression analyses curated by genomic databases and published in scientific literature.

They charted their findings to see when and where FOX genes are expressed or unexpressed using the Mouse Genome Informatics Database as a primary resource for a spectrum of genetic, genomic and biological data, which archives bioinformatic and experimental data of the mouse as an experimental model system for understanding human biology and disease.

The comparison of the curated gene expression databases validate the microarray dataset by identifying sever FOX genes with known expression during heart development, said Neese, a junior biology with a medical lab specialization major from Martinsville, Ind. Several of the FOX genes that are significantly changed in the heart according to the microarray data set have not been characterized in using conventional gene expression analysis techniques.

Sacopulos curated a list of FOX genes, looking at all 44 of the genes and used the Mouse Genome Informatics database to see the expression of each gene during different stages of development. She found that 22 genes were expressed, 22 were undefined and 11 were not expressed and used the data to validate Neeses findings.

My part involved coding and using the Bio conductor package to pull out the statistically significant FOX genes and create a heat map to show when the genes are expressed, said Socaphales, a junior biology major from Terre Haute. If we can determine if heart defects are caused by the genes, there may be a way to correct the problem.

Their preliminary findings will ultimately aid Indiana State biology instructor Kristopher Schwab with his research on the FOX genes functions when cardiac muscular tissue is formed, particularly during embryonic development.

Research exposes students to new areas of science, allowing them to explore the language, concepts and tools of research. Rather than just reading from a book, the research allowed them to get involved in the process and learn at a greater depth by going through data analysis, hypothesizing and investigating, Schwab said. Once they have that basic skill set, that they can transfer to other areas of science and apply it.

Read more:
Sycamores investigate genetics behind congenital heart defects - Indiana Statesman

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

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.

See the rest here:
Genetics, Not Laziness, Might Be Why You Hate Exercising - Medical Daily

Human history is often something modern man only sees as through a glass, darkly. This is particularly the case when that history did not occur in the Mediterranean, the Nile Valley, India, or China, or when there is no written record on which scholars can rely. Exacerbating the disrupting effects of time on history can be when that history occurs in a region where extensive migration has disrupted whatever temporarily stable civilization happened to have taken root at that place at any particular time.

But humans leave traces of themselves in their history and a variety of such traces have been the source of reconstructions outside conventional sources. Luigi Cavalli-Sforza began the study of human population genetics as a way to understand this history in 1971 in The Genetics of Human Populations, and later extended these studies to include language and how it influences gene flow between human populations. More recent efforts to use genetics to reconstruct history include Deep Ancestry: The Landmark DNA Quest to Decipher Our Distant Past by Spencer Wells (National Geographic: 2006), and The Seven Daughters of Eve: The Science that Reveals our Genetic Ancestry by Brian Sykes (Carrol & Graf: 2002). And even more recently, genetic studies have illuminated the "fine structure" of human populations in England (see "Fine-structure Genetic Mapping of Human Population in Britain").

Two recent reports illustrate how genetics can inform history: the first, in the American Journal of Human Genetics entitled "Continuity and Admixture in the Last Five Millennia of Levantine History from Ancient Canaanite and Present-Day Lebanese Genome Sequences"; and a second in the Proceedings of the National Academy of Sciences USA, entitled "Genomic landscape of human diversity across Madagascar." In the first study, authors* from The Wellcome Trust Sanger Institute, University of Cambridge, University of Zurich, University of Otago, Bournemouth University, Lebanese American University, and Harvard University found evidence of genetic admixture over 5,000 years of a Canaanite population that has persisted in Lebanese populations into the modern era. This population is interesting for historians in view of the central location of the ancestral home of the Canaanites, the Levant, in the Fertile Crescent that ran from Egypt through Mesopotamia. The Canaanites also inhabited the Levant during the Bronze Age and provide a critical link between the Neolithic transition from hunter gatherer societies to agriculture. This group (known to the ancient Greeks as the Phoenicians) is also a link to the great early societies recognized through their historical writings and civilizations (including the Egyptians, Assyrians, Babylonians, Persians, Greeks, and Romans); if the Canaanites had any such texts or other writings they have not survived. In addition, the type of genetic analyses that have been done for European populations has not been done for descendants of inhabitants of the Levant from this historical period. This paper uses genetic comparisons between 99 modern day residents of Lebanon (specifically, from Sidon and the Lebanese interior) and ancient DNA (aDNA) from ~3,700 year old genomes from petrous bone of individuals interred in gravesites in Sidon. For aDNA, these analyses yielded 0.4-2.3-fold genomic DNA coverage and 53-264-fold mitochondrial DNA coverage, and also compared Y chromosome sequences with present-day Lebanese, two Canaanite males and samples from the 1000 Genomes Project. Over one million single nucleotide polymorphisms (SNPs) were used for comparison.

These results indicated that the Canaanite ancestry was an admixture of local Neolithic populations and migrants from Chalcolithic (Copper Age) Iran. The authors estimate from these linkage disequilibrium studies that this admixture occurred between 6,600 and 3,550 years ago, a date that is consistent with recorded mass migrations in the region during that time. Perhaps surprisingly, their results also show that the majority of the present-day Lebanese population has inherited most of their genomic DNA from these Canaanite ancestors. These researchers also found traces of Eurasian ancestry consistent with conquests by outside populations during the period from 3,750-2,170 years ago, as well as the expansion of Phoenician maritime trade network that extended during historical time to the Iberian Peninsula.

The second paper arose from genetic studies of an Asian/African admixture population on Mozambique. This group** from the University of Toulouse, INSERM, the University of Bordeaux, University of Indonesia, the Max Plank Institute for Evolutionary Anthropology, Institut genomique, Centre Nacional de Genotypage, University of Melbourne, and the Universite de la Rochelle, showed geographic stratification between ancestral African (mostly Bantu) and Asian (Austronesean) ancestors. Cultural, historical, linguistic, ethnographic, archeological, and genetic studies supports the conclusion that Madagascar residents have traits from both populations but the effects of settlement history are termed "contentious" by these authors. Various competing putative "founder" populations (including Arabic, Indian, Papuan, and/or Jewish populations as well as first settlers found only in legend, under names like "Vazimba," "Kimosy," and "Gola") have been posited as initial settlers. These researchers report an attempt to illuminate the ancestry of the Malagasy by a study of human genetics.

These results showed common Bantu and Austronesian descent for the population with what the authors termed "limited" paternal contributions from Europe and Middle Eastern populations. The admixture of African and Austronesian populations occurred "recently" (i.e., over the past millennium) but was gender-biased and heterogeneous, which reflected for these researchers independent colonization by the two groups. The results also indicated that detectable genetic structure can be imposed on human populations over a relatively brief time (~ a few centuries).

Using a "grid-based approach" the researchers performed a high-resolution genetic diversity study that included maternal and paternal lineages as well as genome-wide data from 257 villages and over 2,700 Malagasy individuals. Maternal inheritance patterns were interrogated using mitochondrial DNA and patterns of paternity assayed using Y chromosomal sequences. Non-gender specific relationships were assessed through 2.5 million SNPs. Mitochondrial DNA analyses showed maternal inheritance from either African or East Asian origins (with one unique Madagascar variant termed M23) in roughly equal amounts, with no evidence of maternal gene flow from Europe or the Middle East. The M23 variant shows evidence of recent (within 900-1500 years) origin. Y chromosomal sequences, in contrast are much more prevalent from African origins (70.7% Africa:20.7% East Asia); the authors hypothesize that the remainder may reflect Muslim influences, with evidence of but little European ancestry.

Admixture assessments support Southeast Asian (Indonesian) and East African source populations for the Malagasy admixture. These results provide the frequency of the African component to be ~59%, the Asian component frequency to be ~37%, and the Western European component to have a frequency of about 4% (albeit with considerable variation, e.g., African ancestry can range from ~26% to almost 93%). Similar results were obtained when the frequency of chromosomal fragments shared with other populations were compared to the Malagasy population (finding the closest link to Asian populations from south Borneo, and excluding Indian, Somali, and Ethiopian populations, although the analysis was sensitive in one individual to detect French Basque ancestry). The split with ancestral Asian populations either occurred ~2,500 years ago or by slower divergence between ~2,000-3,000 years ago, while divergence with Bantu populations occurred more recently (~1,500 years ago).

There were also significant differences in geographic distribution between descendants of these ancestral populations. Maternal African lineages were found predominantly in north Madagascar, with material Asian lineages found in central and southern Madagascar (from mtDNA analyses). Paternal lineages were generally much lower overall for Asian descendants (~30% in central Madagascar) based on Y chromosome analyses. Genome-wide analyses showed "highlanders" had predominantly Asian ancestry (~65%) while coastal inhabitants had predominantly (~65%) African ancestry; these results depended greatly on the method of performing the analyses which affected the granularity of the geographic correlates. Finally, assessing admixture patterns indicated that the genetic results are consistent with single intermixing event (500-900 years ago) for all but one geographic area, which may have seen a first event 28 generations ago and a second one only 4 generations ago. These researchers also found evidence of at least one population bottleneck, where the number of individuals dropped to a few hundred people about 1,000-800 years ago.

These results are represented pictorially in the paper:

In view of the current political climate, the eloquent opening of the paper deserves attention:

Ancient long-distance voyaging between continents stimulates the imagination, raises questions about the circumstances surrounding such voyages, and reminds us that globalization is not a recent phenomenon. Moreover, populations which thereby come into contact can exchange genes, goods, ideas and technologies.

* Marc Haber, Claude Doumet-Serhal, Christiana Scheib, Yali Xue, Petr Danecek, Massimo Mezzavilla, Sonia Youhanna, Rui Martiniano, Javier Prado-Martinez, Micha Szpak, Elizabeth Matisoo-Smith, Holger Schutkowski, Richard Mikulski, Pierre Zalloua, Toomas Kivisild, Chris Tyler-Smith

** Denis Pierrona, Margit Heiskea, Harilanto Razafindrazakaa, Ignace Rakotob, Nelly Rabetokotanyb, Bodo Ravololomangab, Lucien M.-A. Rakotozafyb, Mireille Mialy Rakotomalalab, Michel Razafiarivonyb, Bako Rasoarifetrab, Miakabola Andriamampianina Raharijesyb, Lolona Razafindralambob, Ramilisoninab, Fulgence Fanonyb, Sendra Lejamblec, Olivier Thomasc, Ahmed Mohamed Abdallahc, Christophe Rocherc,, Amal Arachichec, Laure Tonasoa, Veronica Pereda-lotha, Stphanie Schiavinatoa, Nicolas Brucatoa, Francois-Xavier Ricauta, Pradiptajati Kusumaa,d,e, Herawati Sudoyod,e, Shengyu Nif, Anne Bolandg, Jean-Francois Deleuzeg, Philippe Beaujardh, Philippe Grangei, Sander Adelaarj, Mark Stonekingf, Jean-Aim Rakotoarisoab, Chantal Radimilahy, and Thierry Letelliera

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Using Genetics to Uncover Human History - JD Supra (press release)

A white supremacist wears a shirt with the slogan European Brotherhood at a rally in Charlottesville, Virginia, U.S., August 12, 2017. Photo by Joshua Roberts/Reuters

Whether youre a white supremacist, a white nationalist or a member of the alt-right, much of your ideology centers around a simple principle: being white. The creation of a white ethnostate, populated and controlled by pure descendants of white Europeans, ranks high on your priority list.

Yet, when confronted with genetic evidence suggesting someone isnt pure blood, as white supremacists put it, they do not cast the person out of online communities. They bargain.

A new study from UCLA found when genetic ancestry tests like 23andMe spot mixed ancestry among white supremacists, most respond in three ways to discount the results and keep members with impure genealogy in their clan. Their reactions range from challenging the basic math behind the tests to accusing Jewish conspirators of sabotage.

Some argued their family history was all the proof they needed. Or they looked in the mirror and clung to the notion that race and ethnicity are directly visible, which is false.

But the real takeaway centers on a new, nuanced pattern within white supremacist groups to redefine and solidify their ranks through genetic ancestry testing, said Aaron Panofsky, a UCLA sociologist who co-led the study presented Monday at the American Sociological Associations 112th annual meeting in Montreal.

Once they start to see that a lot of members of their community are not going to fit the all-white criteria, they start to say, Well, do we have to think about what percentage [of white European genealogy] could define membership? said Aaron Panofsky, a UCLA sociologist who co-led the study presented Monday at the American Sociological Associations 112th annual meeting in Montreal.

And this co-opting of science raises an important reminder: The best way to counter white supremacists may not be to fight their alternative facts with logical ones, according to people who rehabilitate far-right extremists.

To catalog white supremacists reactions to genetic ancestry results, this study logged onto the website Stormfront. Launched in 1995, Stormfront was an original forum of white supremacy views on the internet. The website resembles a Reddit-style social network, filled with chat forums and users posting under anonymous nicknames. By housing nearly one million archived threads and over twelve million posts by 325,000 or more members, Stormfront serves as a living history of the white nationalist movement.

Over the course of two years, Panofsky and fellow UCLA sociologist Joan Donovan combed through this online community and found 153 posts where users volunteered the results of genetic ancestry tests. They then read through the subsequent discussion threads 2,341 posts wherein the community faced their collective identities.

No surprise, but white supremacists celebrate the test results that suggest full European ancestry. One example:

67% British isles18% Balkan15% Scandinavian100% white! HURRAY!

On the flip side, Panofsky and Donovan found that bad news was rarely met with expulsion from the group.

So sometimes, someone says, Yeah, this makes you not white. Go kill yourself,' Panofsky said. Much more of the responses are what we call repair responses where theyre saying, OK, this is bad news. Lets think about how you should interpret this news to make it to make it right.'

These repair responses fell into two categories.

Reject! One coping mechanism involved the outright rejection of genetic tests validity. Some argued their family history was all the proof they needed. Or they looked in the mirror and clung to the notion that race and ethnicity are directly visible, which is false, University of Chicago population geneticist John Novembre told NewsHour.

Genetically, the idea of white European as a single homogenous group does not hold up.

Though the genetics of whiteness are not completely understood, the gene variants known to influence skin color are more diluted across the globe than any random spot in the human genome. That is to say, humans appear, based on our skin pigmentation, to be much more different from each other than we actually are on a genomic level, Novembre said.

Others accused the ancestry companies of being run and manipulated by Jews, in an attempt to thwart white nationalism, but even other Stormfront users pointed out the inaccuracy of this idea.

Reinterpret:The biggest proportion of responses 1,260 posts tried to rationalize the result by offering an educational or scientific explanation for the genetic ancestry results. Many in the online community played a numbers game. If a genetic ancestry test stated someone was 95 percent white European, they would merely count the remaining 5 percent as a statistical error.

Many adapted this line of thinking to make exceptions for those with mixed ancestry. Nearly 500 posts made appeals by misapplying theories of genetics or by saying whiteness is a culture, not just biology an apparent contradiction to the mission of forming a pure ethnostate. This trend led some white supremacists to debate the boundaries of their ethnostate, Panofsky said.

They start to think about the genetic signs and markers of white nationalism that might be useful for our community, Panofsky said. [They say] maybe there are going to be lots of different white nations, each with slightly different rules for nationalism? Or an overlapping set of nations, that are genetically defined in their own ways?

But these arguments are moot, because these genetic ancestry boundaries are inherently built on shaky ground.

If it seems white supremacists are making arbitrary decisions about their ancestry tests, its hard to blame them. Direct-to-consumer ancestry testing is a slippery, secretive industry, built largely upon arbitrary scientific definitions.

Its black box because its corporate, said Jonathan Marks, biological anthropologist at the University of North Carolina at Charlotte. The way these answers are generated depends strongly on the sampling, the laboratory work that you do and the algorithm that you use to analyze the information. All of this stuff is intellectual property. We cant really evaluate it.

White nationalists carry torches on the grounds of the University of Virginia, on the eve of a planned Unite The Right rally in Charlottesville, Virginia, U.S. August 11, 2017. Picture taken August 11, 2017. Photo by Alejandro Alvarez/News2Share via REUTERS

Genetic ancestry companies assess a persons geographic heritage by analyzing DNA markers in their autosomal DNA (for individual variation), mitochondrial DNA (for maternal history) or their Y chromosome (for paternal history). The latter two sources of DNA remain unchanged from parent to child to grandchild, aside from a relatively small number of mutations that occur naturally during life. These mutations can serve as branch points in the trees of human ancestry, Panofsky and Donovan wrote, and as DNA markers specific to different regions around the world.

When genetic anthropologists examine the full scope of humans, they find that historical patterns in DNA markers make the case that everyone in the world came from a common ancestor who was born in East Africa within the last 100,000 to 200,000 years. Plus, groups intermingled so much over the course of history that genetic diversity is a continuum both within American and Europe, through to Asia and Africa, Novembre of the University of Chicago said.

WATCH: Years after transatlantic slavery, DNA tests give clarity

Genetically, the idea of white European as a single homogenous group does not hold up. The classic geographic boundaries of the Mediterranean, Caucasus, and Urals that have shaped human movement and contact are all permeable barriers, said Novembre. Most of the genetic variants you or I carry, we share with other people all across the globeIf you are in some ethnic group, there are not single genetic variants that you definitely have and everyone outside the group does not.

Commercial ancestry companies know these truths, but bend them to draw arbitrary conclusions about peoples ancestry, researchers say. They compare DNA from a customer to the genomes of people or reference groups whose ancestries they claim to already know.

23andMe, for instance, uses reference dataset that include genomes from 10,418 people who were carefully chosen to reflect populations that existed before transcontinental travel and migration were common (at least 500 years ago). To build these geographic groups, they select individuals who say all four of their grandparents were born in the same country, and then remove outliers whose DNA markers do not match well within the group.

These choices willfully bias the genetic definitions for both geography and time. They claim that a relatively small group of modern people can reveal the past makeup of Europe, Africa and Asia and the ancestral histories for millions of customers. But their reference groups skew toward the present and overpromise on the details of where people came from.

While 23andMe denounces the use of their services to justify hateful ideologies, they do not actively ban known white supremacists from their DNA testing.

A study by 23andMe reported that with their definition of European ancestry, there is an average of 98.6 percent European ancestry among self-reported European-Americans. But given all Ive said, we should digest this with caution, Novembre said. An individual with 100 percent European ancestry tests is simply someone who looks very much like the European reference samples being used.

Though ancestry companies cite research that claims genetic tests can pinpoint someone within 100 miles of their European ancestral home, thats not always the case. Marks offered the recent example of three blond triplets who took an ancestry test for the TV show The Doctors. The test said the triplets were 99 percent European. But one sister had more English and Irish ancestry, while another had more French and German. Did we mention they are identical triplets?

That shows you just how much slop there is in these kinds of of ancestry estimates, Marks said.

Marks described commercial ancestry testing as recreational science because its proprietary nature lacks public, academic oversight, but uses scientific practices to validate stereotypical notions of race and ethnicity.

While 23andMe denounces the use of their services to justify hateful ideologies, they do not actively ban known white supremacists from their DNA testing, BuzzFeed reported.

But white supremacists arent the only ones to buy into these wayward notions when genetic ancestry tests support their self-prescribed identities or reject the science when things dont pan out as expected. African-Americans do it too, as Columbia University sociologist Alondra Nelson found in 2008.

Consumers have what I call genealogical aspiration, Nelson told NewsHour. They often make choices among dozens of companies based on the kind of information theyre seeking. If youre interested in finding whether or not youre a member of the small group that has, for example, some trace of Neanderthal DNA, then youre going to go to a company that focuses on that.

She said Panofsky and Donovans study shows that white nationalists will engage in a process of psychic and symbolic negotiation when genetic ancestry results fail to satisfy their impossible idea for racial purity.

But Panofsky, who doesnt support or sympathize with white nationalists, believes these negotiations are not a reason to dismiss white nationalists as ignorant and stupid.

I think that is actually a dangerous view, Panofsky said. Our study reveals that these white nationalists are often engaging with genetic information in extraordinarily sophisticated ways.

Many white supremacists are dealing with toxic shame, a perpetual subconscious belief system where their sense of identity is negative.

White supremacists are trying to deal with the issue of identity as an intellectual problem, said Tony McAleer, the co-founder and board chair of Life After Hate, a counseling organization that rehabs white supremacists. But he said the rehab of white nationalist views doesnt start with challenging their mental gymnastics with data.

We need to deal with the emotional drivers first, McAleer said. University of Maryland did a study of violent extremists and what they found was the number one correlated factor with someone joining a violent extremist group was childhood trauma.

But McAleer continued that the emotional trauma fueling white supremacy extends past physical and sexual abuse. Many white supremacists are dealing with toxic shame, a perpetual subconscious belief system where their sense of identity is negative.

The person feels at a subconscious level theyre not good enough, McAleer said. One way to react to that is to perpetually spend all of your efforts to prove to the world that you are a winner.

So, Life After Hates antidote to this shame is compassion and empathy, he said. Rather than toss statistics about how Muslims arent flooding the country and do not lead to spikes in crime, they will take a white supremacist to an Islamic center and have them sit down and spend time there.

A personal connection is a much more powerful way to change the dynamics within a person, than it is to re-educate the dataset thats in their head, McAleer said.

Continued here:
How white supremacists respond when their DNA says they're not ... - PBS NewsHour

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.

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

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

On Aug 11, we issued an updated research report on Salt Lake City, UT-based molecular diagnostics provider,Myriad Genetics, Inc.(MYGN - Free Report). The company currently carries a Zacks Rank #3 (Hold).

For the past three months, Myriad has been trading above the broader industry. The company has rallied 24.7%, compared with the industrys 3.7% gain.

Myriad ended fiscal 2017 on a solid note, with its fourth-quarter numbers exceeding the Zacks Consensus Estimate. The company particularly observed strong growth in EndoPredict and GeneSight testing revenues. Also, Myriad witnessed a third consecutive quarter of rise in hereditary cancer volumes. Also, it received provincial reimbursement in Quebec for EndoPredict.

Notably, at the European League Against Rheumatism (EULAR) meeting held in June in Spain, Crescendo Bioscience, a wholly-owned subsidiary of Myriad, released new data from a meta-analysis of clinical studies. The data has demonstrated the Vectra DA tests ability to predict a joint damage.

The same month, the company announced that its BRACAnalysis CDxcompanion diagnostic test has successfully identified BRCA-mutated patients with HER2- metastatic breast cancer in the OlympiAD trial, who have responded to treatment with olaparib better than standard chemotherapy.

Myriads collaborations with AstraZeneca and BeiGene for development of companion diagnostics also raise optimism. Moreover, Myriad continues to make progress with its kit-based versions of Prolaris and myPath Melanoma in the international market and expects to file for CE Mark for Prolaris by 2018.

Moreover, the company has introduced its Elevate 2020 program that targets to achieve $50 million of incremental operating income by fiscal 2020. Per management, the company has selected the projects that are anticipated to deliver $17 million of operating income in fiscal 2018 and another $24 million in fiscal 2019.

On the flip side, unfavorable currency translation continues to be a major dampener for the stock. Management fears that further strengthening of the dollar against foreign currencies will lead to deteriorating operating results.

Intensifying competition as well as the possibility that Myriads new test might not generate meaningful profits to outweigh the costs associated with its development continues to raise concern.

Zacks Rank and Key Picks

Some better-ranked medical stocks are Edwards Lifesciences Corp. (EW - Free Report), Steris Plc (STE - Free Report) and Align Technology, Inc. (ALGN - Free Report). Edwards Lifesciences and Align Technology sport a Zacks Rank #1 (Strong Buy), while Steris carries a Zacks Rank #2 (Buy). You can seethe complete list of todays Zacks #1 Rank stocks here.

Edwards Lifesciences has a positive earnings surprise of 10.75% over the trailing four quarters. The stock has gained around 0.9% over the last three months.

Align Technology has a long-term expected earnings growth rate of 26.6%. The stock has rallied roughly 25.4% over the last three months.

Steris has a positive earnings surprise of 0.78% over two of the trailing four quarters. The stock has gained 13.1% over the last three months.

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Myriad Genetics (MYGN) Grows on Higher Cancer Test Volumes - Zacks.com

FORTY FORT, LUZERNE COUNTY (WBRE/WYOU) -- In a time when many wonder about career opportunities of the future, there is one that's showing signs of significant growth. It has to do with helping patients understand and address personal health risk factors.

The U.S. Bureau of Labor Statistics reports nearly 40,000 jobs were created last month in the health sector. Of that sector, one particular field is showing tremendous employment opportunity more than any other job.

What you're witnessing is the future of medicine: unlocking genetic code secrets to personalize treatment and even prevention of certain illnesses and conditions. Both in and out of these DNA labs are genetic counselors who gather and analyze family history and inheritance patterns to help identify individuals and families who may be at risk. "It's so such on the cutting edge of science and technology that it's continuously changing and there are always new things to really keep on top of and excite me," said Geisinger Genomic Medicine Institute Genetic Counselor Marci Schwartz.

Ms. Schwartz works in both cardiovascular and cancer genetics. By the end of 2024, the demand for genetic counselors like her is expected to grow by nearly 30 percent which is greater than any other job sector in the nation. So what's driving that demand? "We are now getting to the point where genetic information is really becoming relevant to clinical care," said Geisinger Genomic Medicine Institute Director Marc Williams, MD.

That care also includes targeted medicine in neurology, pediatrics, and prenatal genetics. Home to the 11 years and counting genome project "MyCode", Geisinger anticipates needing hundreds of genetic counselors in the next few years. "We have a huge opportunity but also this deficit in terms of training personnel," said Dr. Williams. Part of the genetic field job explosion is a recently created position by Geisinger called a genetic counseling assistant.

Geisinger Commonwealth School of Medicine in Scranton will soon offer a masters program in genomics but exploring career possibilities in this field can begin much sooner. "Some of the shadowing and volunteer experience can certainly be started in high school," said Ms. Schwartz.

You don't need to be a doctor to become a genetic counselor but you do need a masters degree. The starting salary for this growing profession is roughly $65,000 a year. You can learn more about career opportunities in genetic counseling by clicking here.

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Career Opportunity Explosion in Genetics - PA home page

Doing challenges in The Sims 4 can be a lot of fun but a lot of them also require a lot of work. Thats fun when youre looking for a more involved challenge but sometimes you just want quick and easy fun. Thats where the Random Genetic Challenge comes in. Creating your Sims is certainly one of the most fun aspects of playing The Sims 4 but sometimes its justfun to see if lady luck is on your side.Plenty of Sims 4 players have been taking to forums and social media to share the results of their own Random Genetics Challenge and heres how you can get in on the action.

You just start out by randomizing two adult Sims. You will do this by going through each of the different customizable features and clicking the dice icon for a pre-determined amount of times that you should decide on before starting the challenge. For example, if you decide your lucky number is three you will click on the dice icon three times for each of the features. Once you do this for both parent Sims you will want to use the Play With Genetics feature to create their child. Technically, you are welcome to use any age Sim youd like for this challenge but the most common and highly recommended Life Stage to use is the Teen.

The next step is incredibly simpletry to make your new offspring as beautiful as possible without actually changing any of their genetics. So you cant simply do awaywith any features you dont like but youre more than welcome to try to cover them up with different hairstyles and makeup. Now take your new family into the world and see if your Sim will become an Adult that grew into their looks or if theyll be relying on a good personality for the rest of their life.

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The Sims 4: How to Do the Random Genetics Challenge - Twinfinite

With the usual mix of anticipation and apprehension, Kaitlyn Johnson is getting ready to go to her first summer camp. She's looking forward to meeting new friends and being able to ride horses, swim and host tea parties. She's also a little nervous and a little scared, like any 7-year-old facing her first sleepaway camp.

But the wonder is that Kaitlyn is leaving the house for anything but a medical facility. Diagnosed with leukemia when she was 18 months old, her life has been consumed with cancer treatments, doctors' visits and hospital stays.

Acute lymphoblastic leukemia is the most common cancer among young children, accounting for a quarter of all cancer cases in kids, and it has no cure. For about 85% to 90% of children, the leukemia can, however, be effectively treated through chemotherapy.

If it is not eliminated and comes back, it is, more often than not, fatal. Rounds of chemotherapy can buy patients time, but as the disease progresses, the periods of remission get shorter and shorter. "The options for these patients are not very good at all," says Dr. Theodore Laetsch, a pediatrician at the University of Texas Southwestern Medical Center.

When Kaitlyn's cancer wasn't controlled after three years and round after round of chemotherapy drugs, her doctors had little else to offer. "They said, 'This did nothing, it didn't touch it,'" says Kaitlyn's mother Mandy, a dental assistant from Royce City, Texas. "My stomach just dropped." Kaitlyn could receive a bone-marrow transplant, but only about half of those procedures are successful, and there was a good chance that she would reject the donor cells. If that happened, her chances of surviving were very small.

In a calculated gamble, her doctors suggested a radical new option: becoming a test subject in a trial of an experimental therapy that would, for the first time, use gene therapy to train a patient's immune system to recognize and destroy their cancer in the same way it dispatches bacteria and viruses. The strategy is the latest development in immunotherapy, a revolutionary approach to cancer treatment that uses a series of precision strikes to disintegrate cancer from within the body itself. Joining the trial was risky, since other attempts to activate the immune system hadn't really worked in the past. Mandy, her husband James and Kaitlyn traveled from their home in Texas to Children's Hospital of Philadelphia (CHOP), where they stayed in a hotel for eight weeks while Kaitlyn received the therapy and recovered. "The thought crossed my mind that Kaitlyn might not come home again," says Mandy. "I couldn't tell you how many times I would be in the bathroom at the hospital, spending an hour in the shower just crying, thinking, What are we going to do if this doesn't help her?"

But it did. After receiving the therapy in 2015, the cancer cells in Kaitlyn's body melted away. Test after test, including one that picks up one cancer cell in a million, still can't detect any malignant cells lurking in Kaitlyn's blood. What saved Kaitlyn was an infusion of her own immune cells that were genetically modified to destroy her leukemia. "You take someone who essentially has no possibility for a cure--almost every single one of these patients dies--and with [this] therapy, 90% go into remission," says Dr. David Porter, director of blood and bone-marrow transplantation at the University of Pennsylvania. Such radical immune-based approaches were launched in 2011 with the success of intravenous drugs that loosen the brakes on the immune system so it can see cancer cells and destroy them with the same vigor with which they attack bacteria and viruses. Now, with the genetically engineered immune cells known as chimeric antigen receptor (CAR) T cells that were used in Kaitlyn's study, doctors are crippling cancer in more precise and targeted ways than surgery, chemotherapy and radiation ever could. While the first cancer immunotherapies were broadly aimed at any cancer, experts are now repurposing the immune system into a personalized precision treatment that can not only recognize but also eliminate the cancer cells unique to each individual patient.

What makes immune-based therapies like CAR T cell therapy so promising--and so powerful--is that they are a living drug churned out by the patients themselves. The treatment isn't a pill or a liquid that has to be taken regularly, but a one-hit wonder that, when given a single time, trains the body to keep on treating, ideally for a lifetime.

"This therapy is utterly transformative for this kind of leukemia and also lymphoma," says Stephan Grupp, director of the cancer immunotherapy program at CHOP and one of the lead doctors treating patients in the study in which Kaitlyn participated.

Eager to bring this groundbreaking option to more patients, including those with other types of cancers, an advisory panel for the Food and Drug Administration voted unanimously in July to move the therapy beyond the testing phase, during which several hundred people have been able to take advantage of it, to become a standard therapy for children with certain leukemias if all other treatments have failed. While the FDA isn't obligated to follow the panel's advice, it often does, and it is expected to announce its decision in a matter of weeks.

Across the country, doctors are racing to enroll people with other cancers--breast, prostate, pancreatic, ovarian, sarcoma and brain, including the kind diagnosed in Senator John McCain--in hundreds of trials to see if they, too, will benefit from this novel approach. They are even cautiously allowing themselves to entertain the idea that this living drug may even lead to a cure for some of these patients. Curing cancers, rather than treating them, would result in a significant drop in the more than $120 billion currently spent each year on cancer care in the U.S., as well as untold suffering.

This revolutionary therapy, however, almost didn't happen. While the idea of using the body's immune cells against cancer has been around for a long time, the practical reality had proved daunting. Unlike infection-causing bacteria and viruses that are distinctly foreign to the body, cancer cells start out as healthy cells that mutate and grow out of control, and the immune system is loath to target its own cells.

"Only a handful of people were doing the research," says Dr. Carl June, director of the Center for Cellular Immunotherapy at the University of Pennsylvania's Abramson Cancer Center and the scientist who pioneered the therapy. A graduate of the U.S. Naval Academy, June is all too familiar with the devastating effects of cancer, having lost his first wife to ovarian cancer and battled skin cancer himself. Trial after trial failed as reinfusions of immune cells turned out to be more of a hit-or-miss endeavor than a reliable road to remission.

After spending nearly three decades on the problem, June zeroed in on a malignant fingerprint that could be exploited to stack the deck of a cancer patient's immune system with the right destructive cells to destroy the cancer.

In the case of leukemias, that marker turned out to be CD19, a protein that all cancerous blood cells sprout on their surface. June repurposed immune cells to carry a protein that would stick to CD19, along with another marker that would activate the immune cells to start attacking the cancer more aggressively once they found their malignant marks. Using a design initially developed by researchers at St. Jude Children's Research Hospital for such a combination, June and his colleague Bruce Levine perfected a way to genetically modify and grow these cancer-fighting cells in abundance in the lab and to test them in animals with leukemia. The resulting immune platoon of CAR T cells is uniquely equipped to ferret out and destroy cancer cells. But getting them into patients is a complex process. Doctors first remove a patient's immune cells from the blood, genetically tweak them in the lab to carry June's cancer-targeting combination and then infuse the modified cells back into the patient using an IV.

Because these repurposed immune cells continue to survive and divide, the therapy continues to work for months, years and, doctors hope, perhaps a lifetime. Similar to the way vaccines prompt the body to produce immune cells that can provide lifelong protection against viruses and bacteria, CAR T cell therapy could be a way to immunize against cancer. "The word vaccination would not be inappropriate," says Dr. Otis Brawley, chief medical officer of the American Cancer Society.

June's therapy worked surprisingly well in mice, shrinking tumors and, in some cases, eliminating them altogether. He applied for a grant at the National Cancer Institute at the National Institutes of Health to study the therapy in people from 2010 to 2011. But the idea was still so new that many scientists believed that testing it in people was too risky. In 1999, a teenager died days after receiving an experimental dose of genes to correct an inherited disorder, and anything involving gene therapy was viewed suspiciously. While such deaths aren't entirely unusual in experimental studies, there were ethical questions about whether the teenager and his family were adequately informed of the risks and concerns that the doctor in charge of the study had a financial conflict of interest in seeing the therapy develop. Officials in charge of the program acknowledged that important questions were raised by the trial and said they took the questions and concerns very seriously. But the entire gene-therapy program was shut down. All of that occurred at the University of Pennsylvania--where June was. His grant application was rejected.

It would take two more years before private funders--the Leukemia and Lymphoma Society and an alumnus of the university who was eager to support new cancer treatments--donated $5 million to give June the chance to bring his therapy to the first human patients.

The date July 31 has always been a milestone for Bill Ludwig, a retired corrections officer in New Jersey. It's the day that he joined the Marines as an 18-year-old, and the day, 30 years later, that he married his wife Darla.

It was also the day he went to the hospital to become the first person ever to receive the combination gene and CAR T cell therapy, in 2010. For Ludwig, the experimental therapy was his only remaining option. Like many people with leukemia, Ludwig had been living on borrowed time for a decade, counting the days between the chemotherapy treatments that would hold the cancer in his blood cells at bay for a time. Inevitably, like weeds in an untended garden, the leukemia cells would grow and take over his blood system again.

But the periods of reprieve were getting dangerously short. "I was running out of treatments," says Ludwig. So when his doctor mentioned the trial conducted by June and Porter at the University of Pennsylvania, he didn't hesitate. "I never thought that the clinical trial was going to cure me," he says. "I just wanted to live and to continue to fight. If there was something that would put me into the next month, still breathing, then that's what I was looking for."

When Ludwig signed the consent form for the treatment, he wasn't even told what to expect in terms of side effects or adverse reactions. The scientists had no way of predicting what would happen. "They explained that I was the first and that they obviously had no case law, so to speak," he says. So when he was hit with a severe fever, had difficulty breathing, showed signs of kidney failure and was admitted to the intensive care unit, he assumed that the treatment wasn't working.

His condition deteriorated so quickly and so intensely that doctors told him to call his family to his bedside, just four days after he received the modified cells. "I told my family I loved them and that I knew why they were there," he says. "I had already gone and had a cemetery plot, and already paid for my funeral."

Rather than signaling the end, Ludwig's severe illness turned out to be evidence that the immune cells he received were furiously at work, eliminating and sweeping away the huge burden of cancer cells choking up his bloodstream. But his doctors did not realize it at the time.

It wasn't until the second patient, Doug Olson, who received his CAR T cells about six weeks after Ludwig, that Porter had a eureka moment. When he received the call that Olson was also running a high fever, having trouble breathing and showing abnormal lab results, Porter realized that these were signs that the treatment was working. "It happens when you kill huge amounts of cancer cells all at the same time," Porter says. What threw him off initially is that it's rare for anything to wipe out that much cancer in people with Ludwig's and Olson's disease. June and Porter have since calculated that the T cells obliterated anywhere from 2.5 lb. to 7 lb. of cancer in Ludwig's and Olson's bodies. "I couldn't fathom that this is why they both were so sick," says Porter. "But I realized this is the cells: they were working, and working rapidly. It was not something we see with chemotherapy or anything else we have to treat this cancer."

Ludwig has now been in remission for seven years, and his success led to the larger study of CAR T cell therapy in children like Kaitlyn, who no longer respond to existing treatments for their cancer. The only side effect Ludwig has is a weakened immune system; because the treatment wipes out a category of his immune cells--the ones that turned cancerous--he returns to the University of Pennsylvania every seven weeks for an infusion of immunoglobulins to protect him from pneumonia and colds. Olson, too, is still cancer-free.

While the number of people who have received CAR T cell therapy is still small, the majority are in remission. That's especially encouraging for children, whose lives are permanently disrupted by the repeated cycles of treatments that currently are their only option. "It's a chance for these kids to have a normal life and a normal childhood that doesn't involve constant infusions, transfusions, infections and being away from their home, family and school," says Dr. Gwen Nichols, chief medical officer of the Leukemia and Lymphoma Society.

The hope is that while CAR T cell therapy will at first be reserved for people who have failed to respond to all standard treatments, eventually they won't have to wait that long. As doctors learn from pioneers like Kaitlyn, Ludwig and Olson, they will have more confidence in pushing the therapy earlier, when patients are stronger and the cancer is less advanced--perhaps as a replacement for or in combination with other treatments.

The severe immune reaction triggered by the therapy remains a big concern. While it can be monitored in the hospital and managed with steroids or antibodies that fight inflammation, there have been deaths in other trials involving CAR T cells. One drug company put one of its studies on hold due to the toxic side effects. "I am excited by CAR T therapy, but I'm also worried that some people might get too excited," says the American Cancer Society's Brawley. "It's important that we proceed slowly and do this meticulously so that we develop this in the right way."

For now, CAR T cells are expensive--some analysts estimate that each patient's batch of cells would cost hundreds of thousands of dollars--because they require a bespoke production process. If approved, Novartis, which licensed the technology from the University of Pennsylvania, will provide the therapy in about 35 cancer centers in the U.S. by the end of the year. Other companies are already working toward universal T cells that could be created for off-the-shelf use in any patient with cancer. "This is just the beginning," says June.

Since Ludwig's cancer has been in remission, he and his wife have packed their RV and taken the vacations they missed while he was a slave to his cancer and chemotherapy schedule. This year, they're visiting Mount Rushmore, Grand Teton National Park and Yellowstone National Park before taking their granddaughter to Disney World in the fall. "When they told me I was cancer-free, it was just like someone said, 'You won the lottery,'" he says. "If somebody else with this disease has the chance to walk in my shoes and live past it, that would be the greatest gift for me."

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Cancer's Newest Miracle Cure - TIME

A scientist from The University of Manchester has hit upon an innovative way to control greenflies which infest our gardens and farms.

Dr Mouhammad Shadi Khudr, discovered that living lacewing insects- which are used as a way to biocontrol greenflies are also effective after they have died.

Dr Khudr, an evolutionary ecologist based at the University's Division of Evolution and Genomic Sciences, discovered how genetic variations in greenflies' respond to the fear of predation by lacewing known as aphid lions.

The greenflys' genetic variation and life history influenced how they responded to traces of their predator.

He hit upon the discovery while looking at how different lineages of one species of greenfly responded to lacewings on a crop.

Even though each greenfly line had a distinct way of responding to the exposure to the traces of the aphid lion they all suffered from dramatic reduction in their reproduction, he says.

Dr khudr designed and lead the collaborative research, which was funded by the Freie Universitt Berlin (Free University of Berlin).

The research is published in the journal Scientific Reports today.

He said: "Whether alive or dead, lacewings make it more difficult for aphids to reproduce.

"The smell and visual impact of dead predators reduce the greenflies' capacity to give offspring and the way they clump together on the plants they infest."

He added: "This approach is at the crossroads of agricultural, evolutionary and ecological science.

"It is a unique way of understanding the effect of genetic variability corresponding with the risk of predation and thus should receive much more attention.

"It has organic, easy to produce and affordable applications and thus has a promising potential to help solve an age old problem which frustrates many gardeners.

"And it would be most interesting to see if this approach might also work with other pests and biocontrol agents in other agricultural systems."

Explore further: The genetics of life and death in an evolutionary arms-race

More information: Mouhammad Shadi Khudr et al. Fear of predation alters clone-specific performance in phloem-feeding prey, Scientific Reports (2017). DOI: 10.1038/s41598-017-07723-6

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Genetics takes fight to gardeners' green foe - Phys.Org

DURHAM Millions of people die every year from dehydration as a result of exposure and illness. In humans, even the most minor dehydration can compromise the kidneys causing lifelong, irreparable issues or even death. However, some animals living in desert environments are able to survive both acute and chronic dehydration. While these animals, like cactus mice, have evolved over time to deal with environmental stressors like dehydration, researchers at the University of New Hampshire have found its not the physical makeup that is helping them survive, but rather their genetic makeup.

Initially, we thought that maybe their kidneys are structurally different from people, but theyre not, said Matt MacManes, assistant professor of genome enabled biology at UNH and lead author of the study. However, when exposed to acute dehydration, no kidney injury was apparent, which would definitely be the case for humans exposed to similar levels of dehydration, suggesting their genes may be whats preventing widespread kidney damage.

The kidney is the canary in the coal mine when it comes to dehydration, continues MacManes. The exciting outcome of this research is that the molecular toolkit of the cactus mouse has orthologues, or related genes, in humans. These provide the potential for development of drugs or other therapies that could help protect the human body from the damages of dehydration. Such a response could be extremely valuable in a wide variety of situations for people with renal failure, where water is severally limited due to geography or possibly global climate change, for troops deployed in the desert, and perhaps even in space travel.

To understand how desert-adapted cactus mice (Peromyscus eremicus) survive, the study recently published in the American Journal of Renal Physiology outlines how the researchers modeled a desert-like condition. The mice that went without water for 72 hours lost on average 23 percent of their body weight, which would be fatal for humans. Even though dehydrated, the mice continued to be active, eat, and interact normally. Researchers analyzed several other factors including serum electrolytes (sodium, calcium, bicarbonate ion) as well as blood urea nitrogen (BUN) and creatinine. While both were slightly elevated, gene-based biomarkers for kidney injury, were not, which suggests kidney injury is not occurring.

Further analysis found genes that are important in modulating electrolytes were very active, as were genes responsible for maintaining kidney blood pressure.

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UNH research: Genetics mechanism preventing kidney injury after severe dehydration - Foster's Daily Democrat

George Frey | AFP | Getty Images

A lab technician at Myriad Genetics in Salt Lake City, Utah.

Thousands of people are getting genetic tests, for everything from their cancer risk to their likelihood of passing on a disease to a child.

But many doctors aren't adequately trained to interpret these results, or tell patients how to act on them. And genetic counselors -- who do have that knowledge -- are in short supply. There are only about 4,000 genetic counselors in the country today. That's one for every 80,000 Americans. That means some patients have to wait months to get a consultation.

Start-up Clear Genetics, which launches this week after raising $2.5 million in financing, is trying to make genetic expertise more widely available.

The start-up has developed a conversational chatbot to guide a user through their results, collect information and review options for genetic testing, and answer questions about things like whether the test will be covered by insurance. If there's a need for additional support, the patient can then schedule a consultation with a human expert via video or in-person.

"We're finding that it's working really well with patients," said Moran Snir, Clear Genetics' CEO, who was previously a software engineer with the Israeli military.

Clear Genetics is working with several large health systems in the United States to test out a beta version of its product.

"I think this is a very good use for AI," said David Ledbetter, executive vice president and chief scientific officer at hospital network Geisinger Health System, in an interview with CNBC.

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You're getting a DNA test start-up Clear Genetics is building chatbots to help you understand the results - CNBC

Genes carry the information that make you you. So it's fitting that, when sequenced and stored in a computer, your genome takes up gobs of memoryup to 150 gigabytes. Multiply that across all the people who have gotten sequenced, and you're looking at some serious storage issues. If that's not enough, mining those genomes for useful insight means comparing them all to each other, to medical histories, and to the millions of scientific papers about genetics.

Sorting all that out is a perfect task for artificial intelligence. And plenty of AI startups have bent their efforts in that direction. On August 3, sequencing company Veritas Genetics bought one of the most influential: seven-year old Curoverse. Veritas thinks AI will help interpret the genetic risk of certain diseases and scour the ever-growing databases of genomic, medical, and scientific research. In a step forward, the company also hopes to use things like natural language processing and deep learning to help customers query their genetic data on demand.

It's not totally surprising that Veritas bought up Curoverse. Both companies spun out of George Church's prolific Harvard lab. Several years ago, Church started something called the Personal Genomics Project, with the goal of sequencing 100,000 human genomesand linking each one to participants' health information. Veritas' founders helped lead the sequencing partstarting as a prenatal testing service and launching a $1,000 full genome product in 2015while Curoverse worked on academic strategies to store and sort through all the data.

But more broadly, genomics and AI practically call out for one another. As a raw data format, a single person's genome takes up about 150 gigabytes. How!?! OK so, yes, storing a single base pair only takes up around two bits. Multiply that by roughly 3 billionthe total number of base pairs in your 23 chromosome pairsand you wind up with around 750 megabytes. But genetic sequencing isn't perfect. Mirza Cifric, Veritas Genetics cofounder and CEO, says his company reads each part of the genome at least 30 times in order to make sure their results are statistically significant. "And you gotta keep all that data, so you can refer back to it over time," says Cifric.

That's just storage. "Everything after that is going to specific areas and asking questions: Theres a variant at this location, a substitution of this base, a deletion here, or multiple copies of this same gene here, here, and here," says Cifric. Now, interpret all that. Oh, and do it across a thousand, hundred thousand, or million genomes. Querying all those genetic variations is how scientists get leads to find new drugs, or figure out how existing drugs work differently on different people.

But cross-referencing all those genomes is just the beginning. Curoverse, which was focusing on projects to store and sort genomic data, also has its work cut out for it in searching through the 6 millionand countingjargon-filled academic papers detailing gene behavior, including visual information found in charts, graphs, and illustrations.

That's pretty ambitious. Natural language processing is one of the stickiest problems in AI. "Look, I am a computer scientist, I love AI and machine learning, and no amount of coding makes sense to solve this," says Atul Butte, the director of UCSF's Institute of Computational Health Sciences. At his former job at Stanford University, Butte actually tried to do the same thinguse AI to dig through genetics research. He says in the end, it was way cheaper to hire people to read the papers and input the findings into his database manually.

But hey, never say never, right? However they accomplish it, Veritas wants to move past what companies like 23andMe and Color offer: genetic risk based on single-variant diseases. Some of America's biggest dangers come from diseases like diabetes and heart disease, which are activated by interactions between multiple genesin addition to environmental factors like diet and exercise. With AI, Cifric believes Veritas will be able to not only dig up these various genetic contributors, but also assign each a statistical score showing how much it contributes to the overall risk.

Again, Butte hates to be a spoilsport, but ... there's all sorts of problems with doing predictive diagnostics with genetic data. He points to a 2013 study that used polygenic testing to predict heart disease using the Framingham Heart Study dataabout as good as you can get, when it comes to health data and heart disease. "They authors showed that yes, given polygenic risk score, and blood levels, and lipid levels, and family history, you can predict within 10 years if someone will develop heart disease," says Butte. "But doctors could do the same thing without using the genome!"

He says the problems come down to just how messy it is trying to square up all the different research on each gene alongside the environmental risks, and all the other compounding factors that come up when you try to peer into the future. "Its been the holy grail for a long time, structured genome reporting," says Butte. Even attempts to get researchers to write and report data in a standard, machine-readable way, have fallen flat. "You get into questions that never go away. One researcher defines autism different from another one, or high blood pressure, or any number of things," he says.

Butte isn't a total naysayer. He says partnerships like the one between Veritas and Curoverse are becoming more commonlike the data processing deal between genetic sequencing giant Illumina and IBM Watsonbecause there's a clear need for new computing methods in this area. "You want to get to a point where you are developing stuff that improves clinical care," he says.

Or how about directly to the owners of the genomes? Cifric hopes the merger will improve the consumer experience of using genetic data, even seamlessly integrating it into daily life. For instance, linking your genome and health records to your digital assistant. Alexa, should I eat this last piece of pizza? Maybe you should skip it, depending on your baseline genetic risk for cholesterol and latest blood test results. Diet isn't the only area where genomics could help improve your day to day life. Some people are more or less sensitive to over the counter drugs. A quick query might tell you whether you should take a little less Tylenol than is recommended.

Cifric thinks this acquisition could position Veritas as a global powerhouse of genomic data. "Apple recently announced that they had shipped 41 million iPhones in a quarter, right? I think in not too distant future, well be doing 41 million genomes in a quarter," he says. That might seem ambitious, given that the cost to consumers is nearly $1,000. But that cost is bound to come down. And artificial intelligence will make paying for the genome a matter of common sense.

This story has been updated to reflect that the company is named Veritas Genetics, not Veritas Genomics.

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Veritas Genetics Scoops Up an AI Company to Sort Out Its DNA - WIRED

In genetics, a mosaic (or mosaicism) means the presence of two different genotypes in an individual which developed from a single fertilized egg. As a result, the individual has two or more genetically different cell lines derived from a single zygote.[1]

Mosaicism may result from:

The phenomenon was discovered by Curt Stern. In 1936, he demonstrated that recombination, normal in meiosis, can also take place in mitosis.[2] When it does, it results in somatic (body) mosaics. These are organisms which contain two or more genetically distinct types of tissue.[3]

A genetic chimera is an organism composed of two or more sets of genetically distinct cells. Dispermic chimeras happen when two fertilized eggs fuse together. Mosaics are a different kind of chimerism: they originate from a single fertilized egg.

This is easiest to see with eye colours. When eye colours vary between the two eyes, or within one or both eyes, the condition is called heterochromia iridis (= 'different coloured iris'). It can have many different causes, both genetic and accidental. For example, David Bowie had the appearance of different eye colours due to an injury that caused one pupil to be permanently dilated.

On this page, only genetic mosaicism is discussed.

The most common cause of mosaicism in mammalian females is X-inactivation. Females have two X chromosomes (and males have only one). The two X chromosomes in a female are rarely identical. They have the same genes, but at some loci (positions) they may have different alleles (versions of the same gene).

In the early embryo, each cell independently and randomly inactivates one copy of the X chromosome.[4] This inactivation lasts the lifetime of the cell, and all the descendants of the cell inactivate that same chromosome.

This phenomenon shows in the colouration of calico cats and tortoiseshell cats. These females are heterozygous for the X-linked colour genes: the genes for their coat colours are carried on the X chromosome. X-inactivation causes groups of cells to carry either one or the other X-chromosome in an active state.[5]

X-inactivation is reversed in the female germline, so that all egg cells contain an active X chromosome.

Mosaicism refers to differences in the genotype of various cell populations in the same individual, but X-inactivation is an epigenetic change, a switching off of genes on one chromosome. It is not a change in the genotype.[6] Descendent cells of the embryo carry the same X-inactivation as the original cells. This may give rise to mild symptoms in female 'carriers' of X-linked genetic disorders.[7]

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Mosaic (genetics) - Simple English Wikipedia, the free ...