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Genesis and Genetics | We look at Genetics in Genesis

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

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

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

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

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

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

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

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

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

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

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

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

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

Key words:

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

Additional Suggested Reading:

Noahs Ark A Fresh Look

Noahs Ark Hermetically Sealed and Safe

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

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

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

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

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

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Genesis and Genetics | We look at Genetics in Genesis

Heritability of IQ – Wikipedia

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Another summary:

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

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

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

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Heritability of IQ - Wikipedia

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Evolutionary Biologists Probe Long-standing Genetics Mystery – Yale News

August 17, 2017

Photo credit: Dreamstime

What makes humans different from chimpanzees? Evolutionary biologists from Howard University and the Yale School of Public Health have developed a unique genetic analysis technique that may provide important answers.

Michael C. Campbell, Ph.D., the papers first author and assistant professor in the Howard University Department of Biology, and co-author Jeffrey Townsend, Ph.D., the Elihu Associate Professor in Biostatistics at Yale, published their findings in the journal Molecular Biology and Evolution.

Their methodModel Averaged Site Selection via Poisson Random Field (MASS-PRF)looks at protein-coding genes to identify genetic signatures of positive selection. These signatures are actually DNA changes that contribute to the development of beneficial traits, or human adaptations, that emerged during human evolutionary history and that are shared across the human species.

It's a quantum leap in our statistical power to detect selection in recently diverged species.

Other approaches have examined this question but analyses have focused on whole genes, typically missing focused evolution that often occurs in small regions of genes. The method Campbell and Townsend created identifies selection within genes, pinpointing sets of mutations that have undergone positive selection.

Our method is a new way of looking for beneficial mutations that have become fixed or occur at 100 percent frequency in the human species, Campbell said. What we are concerned with are mutations within genes and traits that are specific to humans compared to closely related species, such as the chimpanzee. Essentially, we want to know is what are the mutations and traits that make us human and that unite us as a biological species.

Townsend said the technique has far-reaching implications. It helped the research team discover several genes whose evolution appears to have been critical to the divergence of humans from their common ancestor with chimpanzees. The genes play roles in neurological processing, immunity, and reproduction, and the method could eventually help scientists identify many more. It's a quantum leap in our statistical power to detect selection in recently diverged species, Townsend said.

Campbell began the research project with Drs. Zhao and Townsend while they were associate research scientists in the Department of Biostatistics at the Yale School of Public Health, before he arrived at Howard University in 2015. Dr. Zhao, currently a research scientist at The Jackson Laboratory for Genomic Medicine, co-authored the paper.

This article was submitted by Elisabeth Ann Reitman on August 17, 2017.

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Evolutionary Biologists Probe Long-standing Genetics Mystery - Yale News

Grayson’s Anatomy: How did the Sunderland manager rate after Saturday’s defeat at home to Leeds? – Roker Report (blog)

Team Selection

Its pretty simple: we have a squad with a decent amount of quality in it; however, we simply dont have enough quality in reserve if things arent working out or players are feeling somewhat jaded. Both Lee Cattermole and Aiden McGeady looked tired yesterday, and whether you think thats acceptable or not it goes to show that we desperately need quality reinforcements.

This week will give Grayson the chance to experiment in the cup and rest several players/give others a chance to impress, but it really does feel like the side needs several quality additions in order to really push on this season. Yesterdays bench, for example, was bereft of quality - wheres the dynamic striker and the tricky playmaker? Asoro is young and Khazri just hasnt cut the mustard so far this season as he looks for an escape from Wearside.

Verdict: What can you say, we played well until the first goal, but there just seemingly isnt enough quality on the bench to really make a difference when we need it.

Leeds did play well yesterday, but Sunderland could have perhaps played better - or at least smarter.

For once this season we had the lions share of possession (55%) and we had more shots on goal; however, the quality just wasnt there for Sunderland. Only 2/12 of our shots on goal actually hit the target, and it felt like we struggled to consistently create clear chances on goal.

Leeds targeted our full-backs with their pacey forwards, and Jones and Galloway struggled to stand up to their men. Leeds had 8 shots in total and 5 of those found the target - they were efficient with the ball and really gave us a difficult time of it.

The 4-4-2 that has worked so well this season struggled somewhat against Leeds fluid shape that resembled a 4-3-3. Leeds were able to both commit numbers to the middle of the park, and further up the pitch while their defence was steadfast to say the least. They were quicker and smarter than us.

Verdict: I wouldnt be surprised to see Grayson try some new things this week. The 4-4-2 is a decent shape, but we need other options. Perhaps a formation resembling Leeds could suit us well when needed?

Grayson certainly learned from the Sheffield Wednesday game and made changes with plenty of time to spare yesterday as Matthews replaced Galloway after 55 mins (enforced or not, I think that move was coming); Khazri replaced the ineffective Vaughan at the same time, and then Asoro came on for the final 15 minutes.

Unfortunately, as already noted, I just dont think we have enough quality in reserve to really swing a game in our favour. That can change of course; perhaps someone plays well against Carlisle, or maybe we bring in several new faces. Ultimately though, we need more options, and that really isnt Graysons fault as hes not the man in charge of finances and negotiations.

Verdict: Tried to make positive changes, but they just didnt work. Khazri looked inneffective (read to leave?), and Asoro still looks too young while Matthews was definitely an improvement on Galloway. You cant really lay much blame at Graysons feet for this - financially were struggling and bringing new players in isnt an easy task.

Grayson really was spot on in his assessment of the match:

For 20 minutes we were dominant. We asked a lot of questions of them.

I don't think (Liam) Cooper knew too much about it when it hit him on the head and hit the bar - 70 seconds later it's in the back of our next. Those are the fine margins in a football match.

From then onwards, I don't think you can fault the players' effort or commitment, but it was just that final ball that really matters, when you're trying to get back in to a game.

Hes right, we struggled after going behind and couldnt find that bit of quality needed to get back on track.

It really is fine margins in football, but Sunderland need to be a little more capable of making their own luck, and whether thats through new additions, squad rotation, or tactical tweaks, Grayson will work on those weaknesses as he looks to take this club forward.

Verdict: Positive realism as Grayson took the loss on the chin and acknowledges the need to improve. I have every confidence well do just that with him as manager.

Go here to read the rest:
Grayson's Anatomy: How did the Sunderland manager rate after Saturday's defeat at home to Leeds? - Roker Report (blog)

Healthcare Group Invest in R&D Leadership – Labmate Online

Life sciences company Zaluvida has appointed Dr. Graham Dixon as both Group Head of R&D for the entire Swiss-based business and also as Chief Operating Officer at its Welsh-based fundamental research and development arm, Neem Biotech.

With over 25 years of experience across the pharmaceutical and biotechnology industry, Dr. Dixon brings along a wealth of expertise in discovering and developing novel drugs with applications for both orphan and mainstream disease indications. He has steered numerous novel drug candidates from early development through clinical and later stage development processes across multiple indications. These have ranged from anti-infectives to oncology and neurological indications.

Formerly Chief Scientific Officer for Onexo, Dr. Dixon has also held joint Chief Scientific Officer/Head of R&D roles in venture capital funded and publically listed biotechs, including Sensorion, Addex Therapeutics, Galapagos, Entomed and F2G. As Head of R&D at Galapagos, his responsibilities included managing a staff of 260 scientists across three European sites. He started his R&D career as Head of Biochemistry at DowElanco Ltd, moving on later to AstraZeneca as a project leader and later as Global Product Director. Dr Dixon obtained his Ph.D. in biochemistry at Swansea University and his BSc in Applied Biology from the University of Bradford.

Zaluvidas Group CEO, Christoph Staeuble, said: I am very pleased to have Graham on board, both as Head of R&D for the Zaluvida group and as part of the Neem Biotech leadership team. He is a great fit for the organisation and brings with him a valuable wealth of industry experience.

Dr. Michael Graz, Neem Biotechs Managing Director, said: We are delighted to welcome Graham back to Wales, where he started his professional career. Our work in environmental, animal and human health, and, in particular, our developments to fight anti-microbial resistance stand to benefit from his expertise in biotechnology and big pharma.

Dr. Graham Dixon, said: This is an exciting time to join Zaluvida. I am looking forward to being able to play a part in the next phase of the companys evolution and in the development of the impressive pipeline assets of the group.

Link:
Healthcare Group Invest in R&D Leadership - Labmate Online

Two-step process leads to cell immortalization and cancer | Berkeley … – UC Berkeley

A mutation that helps make cells immortal is critical to the development of a tumor, but new research at UC Berkeley suggests that becoming immortal is a more complicated process than originally thought.

The key to immortalization is an enzyme called telomerase, which keeps chromosomes healthy in cells that divide frequently. The enzyme lengthens the caps, or telomeres, on the ends of chromosomes, which wear off during each cell division.

This skin section shows a benign mole or nevus that is transitioning into a melanoma, the most serious type of skin cancer. New experiments by UC Berkeley and UCSF researchers suggest that immortalization of skin cells, which is essential to turning them cancerous, is a two-step process: a mutation in nevus cells slightly raises levels of telomerase, which keep the cells alive long enough for a second change, still unknown, that up-regulates telomerase to make the cells immortal and malignant. (Image by Dirk Hockemeyer/UC Berkeley and Boris Bastian/UCSF)

When the telomeres get too short, the ends stick to one another, wreaking havoc when the cell divides and in most cases killing the cell. The discovery of telomerase and its role in replenishing the caps on the ends of the chromosomes, made by Elizabeth Blackburn and Carol Greider at UC Berkeley and John Szostak at Harvard University in the 1980s, earned them a Nobel Prize in Physiology or Medicine in 2009.

Because telomeres get shorter as cells age, scientists theorized that cancer cells which never age become immortalized by turning on production of telomerase in cells that normally dont produce it, allowing these cells to keep their long telomeres indefinitely. An estimated 90 percent of all malignant tumors use telomerase to achieve immortality, and various proposed cancer therapies focus on turning down the production of telomerase in tumors.

The new research, which studied the immortalization process using genome-engineered cells in culture and also tracked skin cells as they progressed from a mole into a malignant melanoma, suggests that telomerase plays a more complex role in cancer.

Our findings have implications for how to think about the earliest processes that drive cancer and telomerase as a therapeutic target. It also means that the role of telomere biology at a very early step of cancer development is vastly under-appreciated, said senior author Dirk Hockemeyer, a UC Berkeley assistant professor of molecular and cell biology. It is very likely that what we find in melanoma is true for other cancer types as well, which would warrant that people look more carefully at the role of early telomere shortening as a tumor-suppressing mechanism for cancer.

The results were reported online August 17 as a first release publication from the journal Science.

From nevus to cancerHockemeyer and his UC Berkeley colleagues, in collaboration with dermatopathologist Boris Bastian and his colleagues at UCSF, found that immortalization is a two-step process, driven initially by a mutation that turns telomerase on, but at a very low level. That mutation is in a promoter, a region upstream of the telomerase gene referred to as TERT that regulates how much telomerase is produced. Four years ago, researchers reported that some 70 percent of malignant melanomas have this identical mutation in the TERT promoter.

The TERT promoter mutation does not generate enough telomerase to immortalize the pre-cancerous cells, but does delay normal cellular aging, Hockemeyer said, allowing more time for additional changes that turn telomerase up. He suspects that the telomerase levels are sufficient to lengthen the shortest telomeres, but not to keep them all long and healthy.

If cells fail to turn up telomerase, they also fail to immortalize, and eventually die from short telomeres because chromosomes stick together and then shatter when the cell divides. Cells with the TERT promoter mutation are more likely to up-regulate telomerase, which allows them to continue to grow despite very short telomeres. The marginal levels of telomerase in the cell, Hockemeyer said, result is some unprotected chromosome ends in the surviving mutant cells, which could cause mutations and further fuel tumor formation.

Before our paper, people could have assumed that the acquisition of just this one mutation in the TERT promoter was sufficient to immortalize a cell; that any time when that happens, the telomere shortening is taken out of the equation, Hockemeyer said. We are showing that the TERT promoter mutation is not immediately sufficient to stop telomeres from shortening.

It is still unclear, however, what causes the eventual up-regulation of telomerase that immortalizes the cell. Hockemeyer says that its unlikely to be another mutation, but rather an epigenetic change that affects expression of the telomerase gene, or a change in the expression of a transcription factor or other regulatory proteins that bind to the promoter upstream of the telomerase gene.

Nevertheless, we have evidence that the second step has to happen, and that the second step is initiated by or is occurring at a time when telomeres are critically short and when telomeres can be dysfunctional and drive genomic instability, he said.

In retrospect, not a surpriseThough most cancers seem to require telomerase to become immortal, only some 10 to 20 percent of cancers are known to have a single-nucleotide change in the promoter upstream of the telomerase gene. However, these include about 70 percent of all melanomas and 50 percent of all liver and bladder cancers.

Hockemeyer said that the evidence supporting the theory that the TERT promoter mutation up-regulated telomerase has always been conflicting: Cancer cells tend to have chromosomes with short telomeres, yet have higher levels of telomerase, which should produce longer telomeres.

According to the new theory, the telomeres are short in precancerous cells because telomerase is turned on just enough to maintain but not lengthen the telomeres.

Our paper reconciles contradictory information about the cancers that carry these mutations, Hockemeyer said.

The finding also resolves another recent counterintuitive finding: that people with shorter telomeres are more resistant to melanoma. The reason, he said, is that if a TERT promoter mutation arises to push a precancerous lesion the mole or nevus toward a melanoma, the chances are greater in someone with short telomeres that the cell will die before it up-regulates telomerase and immortalizes the cells.

The study also involved engineering TERT promoter mutations in cells differentiated from human pluripotent stem cells and following their progression toward cellular immortality. The results were identical to the progression seen in human skin lesions obtained from patients in UCSFs Helen Diller Family Comprehensive Cancer Center and examined in the Clinical Cancer Genomics Laboratory, which Bastian directs.

Other co-authors of the Science paper are UC Berkeley graduate students Kunitoshi Chiba and Franziska Lorbeer, who contributed equally to the research, Hunter Shain of UCSF, David McSwiggen, Eva Schruf and Xavier Darzacq of UC Berkeley, and Areum Oh and Jekwan Ryu of the Santa Clara firm Optical Biosystems. The work was supported by the Siebel Stem Cell Institute, California Institute of Regenerative Medicine and National Institutes of Health.RELATED INFORMATION

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Two-step process leads to cell immortalization and cancer | Berkeley ... - UC Berkeley

Leo who? Anatomy of a silly-season news story – Irish Times

If you are one of those people who like to type why is this news? beneath stories that arent about earthquakes or civil wars, then let yourself go.

Reports of Taoiseach Leo Varadkar not being recognised in a restaurant will have already sent you into fits of fury. Be aware that proper news makes only incidental appearances in this column. I am here to praise Silly Season, not to bury it. (Though I fear we may have to do a bit of both.)

That charming Leo story was a classic example of Silly Season in action. Young Emma Kelly, a Dublin student with an admirable lack of vanity, is working in a Chicago restaurant for the summer.

Our new Taoiseach who apparently holidays in V-necked tops arrived for a bite of supper. Emma didnt recognise him and, after making the chief wait in a queue, directed him to a small table right beside a bucket of rotting fish heads. (I made up the very last bit. Somebody has to get the fake news rolling.) More power to her.

After realising her mistake, she had a photo taken and gave various amusingly embarrassed interviews for the domestic media. Who expects to see smart-casual taoisigh in midwestern diners?

All the elements are in place. The story has a human-interest angle. It involves important people, but it is not about important things. It comes with a nice photograph that spreads a bit of cheer about the place. With all the foul garbage elsewhere on news feeds this comes as a welcome release.

You could say the same about the story telling us that Walnut Whips are set to lose their walnuts. We actually learnt something from that. Who knew that the price of that nut had risen by 20 per cent over the last year?

It looks as if poor Nestl whose spokesperson claimed British people dont like walnuts anyway will have to market their delicacy as a mere Whip. Whip? The rhythm has gone. Odd connotations are kicked up. How much nicer it is to consider this nonsense than monstrous upheavals across the Atlantic.

The Silly Season has been around longer than you might suspect. British publications were using the phrase as long ago as the 1860s to describe the period covered by the parliamentary recess.

The notion is that reporters all head off for their holidays and allow catastrophes to happen unobserved. If a tree falls in a forest and theres nobody around to write a think piece, does it really make a sound? Giant lizards may, for all we know, have stomped through Toronto in August of 1924. The only thing in the papers was that story about a ferret that looked like Buster Keaton.

In several north and east European languages the period is, rather deliciously, referred to as some variation of cucumber time. When the cucumbers came into season the people that mattered were safely ensconced in quiet resorts far from telegraphs and printing presses. Busy nonsense cluttered headlines displayed in newsagents visited only by stray tufts of tumbleweed.

There is a darker side to Silly Season. Moral panics and confected hysteria occasionally fill the vacuum in the dog days. The British mid-market tabloids like nothing better than rounding on the BBC when August works its sweaty muscles.

The Surrey Panther will be seen haunting the undergrowth as visitors from other planets probe the citizens of Arizona. Last years scary clown sightings began in August. That story grew throughout that month before withering away when the US election loomed.

More often, however, we are dealing with harmless blather such as that surrounding the bare breasts seen on a screen behind Sophie Raworth when she was reading the BBC news.

The actress Anna Paquin expressed herself amused that the clip from True Blood had caused such a fuss. Everybody laughed. Everybody was distracted from the bloody awful mess into which the world seems to be inexorably sliding.

For a month or so the media spreads a coma of triviality that allows brief, blissful oblivion. It is a lovely accidental tradition. You may not be able to afford a real holiday. But you can at least enjoy a holiday from reality.

Well, this is how it used to be. The rise of social media has put us in a weird situation. Every month is Silly Season, but no day is allowed the relief that Silly Season used to bring.

Trivial lies concerning things that dont matter are forever at our elbow. Reminders of genuinely ghastly truths are equally hard to avoid. We are better informed and more poorly informed than ever. No shift in the seasons can halt the endless flow of variously coloured information. That doesnt always feel like a good thing.

Heres a cat that can say marmalade.

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Leo who? Anatomy of a silly-season news story - Irish Times

Eric Dane Only Watched Three Episodes Of ‘Grey’s Anatomy’ – HuffPost

Eric Dane spent six seasons playing Dr. Mark Sloan onGreys Anatomy, but the actor says he barely watched any episodes of the hit ABC series. Ever.

In a recent interview with HuffPost at Build Series, Dane revealed, I watched three episodes of the show while I was on it. After all, he said, I was there when it happened, so I didnt need to see it.

So, its safe to say he doesnt keep up with the series now. But he does keep in touch with some of his former cast members, including Ellen Pompeo and Justin Chambers. Hes also still friendly with series creator Shonda Rhimes.

Shondas great, he said.Im still friends with her to this day. One thing that you do with Shonda is that you dont deviate. Thats one of the biggest lessons you learn is that you stick to the script.

Even though hes been off the series for five years now, Dane still gets called by his Greys nickname, McSteamy. But he doesnt seem to mind too much.

Ive been called a lot worse, he joked. It never did anything bad for me that nickname. So, I dont mind it ... Its not what Im doing now, so it does get a little tiring. But its not something that really upsets me.

Shortly after leaving Greys Anatomy Dane jumped into another big role. He currently stars as Tom Chandler in TNTs The Last Ship, which returns for Season 4 on Sunday. The series follows what happens after a global catastrophe wipes out the bulk of the population. Danes character a Navy captain faced a series of changes at the end of the last season. Season 4 will pick up where that storyline left off.

TNT

Tom Chandler left the Navy after doing something that he felt was morally way against everything he stood for. And hes in a self-imposed exile, Dane said.

Chandler is now in Greece living the life of a fisherman, and Dane says its only a matter of time before he finds some trouble, as he tends to do.

Tom Chandler has to find his way back into the Navy, into the fray, Dane said.

Dane says he really enjoys playing the character and can relate to some of the conflict Chandler experiences on the show. But unlike Greys Anatomy,starring in The Last Ship is physically challenging.

Its a lot of hard work. I enjoy it. But at the end of the day, youre home and you actually feel like you worked.

So, we have one last question: Does Dane watch episodes of The Last Ship?

Sometimes theyll be stupid enough to take my notes when I watch an episode, he said about the shows producers. I always try to offer like, I think theres a better take in there somewhere.

But he admits, its definitely uncomfortable seeing himself on TV, even after all these years.

Im not a big watcher of myself, he said. You start looking at things you shouldnt be looking at that have nothing to do with anything of importance.

The Last Ship returns with a two-hour season premiere this Sunday at 9 p.m. ET on TNT. Check out our full Build interview with Dane below.

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Eric Dane Only Watched Three Episodes Of 'Grey's Anatomy' - HuffPost

Anatomy Of A Play: Preseason Week 1 – Turf Show Times – Turf Show Times

Ive thought of an idea which could be fun to Los Angeles Rams fan, and obviously myself. In this series, we can jump into the tape and breakdown a major play, or any impressive play from the prior week. Ive decided to start during the preseason just to see what you guys think, and to see whether its worth continuing or not. With the intro out of the way, lets get into it.

The play Ive chosen to take a look at was in the first quarter of the game vs the Dallas Cowboys. It was a roll-out on offense that resulted in a 19-yard gain by rookie WR Cooper Kupp, which ultimately put the team in scoring position.

This was the play. The Rams alignment here is a simple 2x2 formation with Robert Woods and Tyler Higbee (in-line) on the left, with Cooper Kupp and Pharoh Cooper on the right side of the formation. Todd Gurley is the singleback making this 11 personnel, which also means that on this play there are only one RB and one TE.

Here is a breakdown of the routes across the board for the Rams weapons. Far left Robert Woods is running a deep comeback. Also on the left, TE Tyler Higbee is running a jerk route breaking back out as opposed to crossing the field. On the right side of the formation, slot WR Cooper Kupp is running a crosser, and far right is Pharoh Cooper running a post route.

This is where things become fun. The Cowboys, theyre lined up in a simple nickel package. Pre-snap, the Cowboys are lined up in man coverage across the board, with two out of three of their CBs playing press-man. With the safeties playing deep on either hash, pre-snap this looks to be a cover-2.

What makes this play fun, is the Cowboys actually disguised their play. Rather than playing a cover-2 man-to-man coverage, the nickel CB (with the red arrow) is actually coming off the edge to blitz. which puts the weakside SS (#38 - creeping up into the box) in man coverage across slot WR Cooper Kupp. This leaves him at a disadvantage because Kupps route takes him to the left side of the field, ultimately leaving the SS to work through a lot of trash as well as starting behind Kupp.

The play does not go as planned for the Cowboys defense. There is a clear miscommunication between the MLB and the SS as to who had to cover Todd Gurley coming out of the backfield, but not only that, there are multiple Cowboys caught peeking into the Rams backfield with a hard sell by Jared Goff on the play action fake. With a well executed fake, and a mistake on the Cowboys part, WR Cooper Kupp is wide open crossing the field, and Jared Goff composes himself outside of the pocket, gathers his feet, and finds his target for a 19-yard completion.

Something this bad camera work doesnt show, is the QB. Now, with the Cowboys rushing five, Jared Goff and the Rams do luck out a bit. The RE on the Cowboys slips on the play, which allows Goff to buy some time and allow Kupp to cross the field and pass the LBs, opening up a passing lane for Goff to find him in.

Heres a different view:

Well, it wasnt anything crazy, but its nice to see the Rams first team move the ball with effectiveness. You see some play-calling that fits Goffs skill-set more favourably, Cooper Kupp being the reliable WR everyone expects him to be, and most importantly, Jared Goff was not fooled by the Cowboys pre-snap defense, re-acclimated himself outside the pocket, and threw a nice accurate pass.

Let me know what you think of the new series Anatomy of a play, and whether we should continue this ride together or not!

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Anatomy Of A Play: Preseason Week 1 - Turf Show Times - Turf Show Times