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Archive for the ‘Genetics’ Category

New ‘hit-and-run’ gene editing tool temporarily rewrites genetics to treat cancer and HIV – GeekWire

Thursday, August 31st, 2017

Nanoparticles (orange) deliver temporary gene therapy to immune cells (blue) to give them disease-fighting tools. (Fred Hutch Illustration / Kimberly Carney)

CAR T immunotherapies are all the rage in the medical community, reprogramming a patients immune system to fight cancer. For some patients, theyve produced near-miraculous recoveries, and they could be a huge breakthrough in cancer treatment.

The business community is taking note as well: Kite Pharma, a biotech company developing these therapies, announced a deal to be acquired for $11.9 billion on Monday, sending stock prices of Seattle immunotherapy developer Juno Therapeuticsskyrocketing.

But there are still giant pitfalls to using the therapies on a large scale because they are incredibly complex and expensive to produce. Researchers from Seattles Fred Hutchinson Cancer Research Center are taking the problem head-on with new hit-and-run gene editing technology.

In a study published Wednesday in the journal Nature Communications, researchers led by Dr.Matthias Stephan reported they have developed a nanoparticle delivery system that can temporarily alter cells so they are able to fight cancer and other diseases.

The best part? The treatment is a powder that just needs to be mixed with water to activate and even better, it could be an essential breakthrough in making cutting-edge medical technology affordable for patients.

Stephan told GeekWire in a previous piece on the technology that his goal is to make immunotherapy so easy to access that it replaces chemotherapy as the front-line treatment for cancer.

What I envision is like the Walgreens flu shot scenario, or you go to your doctor and you get hepatitis B shot, he said at the time. You go there every Friday, and thats it.

We realized in order to outcompete chemotherapy, we have to design something that is at least as affordable and can be manufactured at large scale by one biotech company and shipped out to local infusion centers, Stephan said. At the moment, CAR T cell therapies must be made individually for each patient in specialized labs.

Heres how the new tech works: The nanoparticles designed by Stephan and his team act like shipping containers for bundles of mRNA, the molecules that tell cells how to build disease-fighting proteins. The nanoparticles also have molecules attached to the outside to help them find the right kind of cells, like a shipping label on a package.

When the mRNA is delivered to the cell, it prompts the cell to grow disease-fighting features, like the chimeric antigen receptor in CAR T cells that help them identify and kill cancer.Researchers said the technology could potentially be used to develop treatments for HIV, diabetes and other immune-related diseases.

In the short run, the tech could help researchers discover new treatments and therapies in the lab. It could one day be used in hospitals and clinics around the world, but will first need to undergo extensive clinical trials to ensure the tech is effective and safe to use in humans.

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Genetics could be behind statin side effects – World First Travel Insurance

Thursday, August 31st, 2017

31 August 2017 08:22

Almost all men over 60 and women over 75 are eligible for statins

A common genetic variant could be the reason some people suffer from aches and pains when taking statins, according to new research.

The study could lead to a screening method to help identify those patients who are most likely to have a bad reaction to the drugs.

Statin intolerance doubles

Millions of Britons take statins every year to lower cholesterol and reduce their risk of heart attacks and strokes. However, between 7% and 29% of users suffer from sore muscle symptoms, which can in some cases stop them using the pills.

Research undertaken at the University of Dundee found that statin intolerance was doubled when patients carried two identical copies of a common variant of the LILRB5 gene, which has an immune system and muscle repair role.

The team also confirmed that some people are genetically more likely to suffer from aching muscles regardless of whether they are taking statins.

Lead scientist Professor Colin Palmer said: "We found that there are people in the general population who carry a genetic factor that predisposes them to muscle aches. If these people are put on statins, they might discontinue their medication in the erroneous belief that it is the statin that is making their muscles ache."

Sub-group of patients

He added that the researchers also identified a genetic sub-group of patients who are susceptible to statin-specific muscle ache, however, at this stage the reason for this is not understood.

Professor Palmer suggested that in the future prospective statin users could be tested for key genetic variants, including LILRB5.

Almost 12,000 statin users took part in the Genetics of Diabetes Audit and Research Tayside Scotland (GoDARTS) study. The findings will appear in the European Heart Journal.

People with long-term, pre-existing conditions can arrange medical travel insurance should they need to travel.

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Genetics put some older women at higher risk than men for Alzheimer’s – USC News

Tuesday, August 29th, 2017

White women whose genetic makeup puts them at higher risk for Alzheimers disease are more likely than white men to develop the disease during a critical 10-year span in their lives, according to a study headed by Keck School of Medicine of USC researchers.

The findings from one of the worlds largest big-data studies on Alzheimers counter long-held beliefs about who is at greatest risk for the disease and when, suggesting new avenues for clinical trials.

Study results show genetically vulnerable 55- to 85-year-old white men and women have the same odds of developing the memory-erasing disease. One exception: From their mid-60s to mid-70s, these women still face significantly higher risk. That may provide clues to disease causes and potential interventions among these women.

Our discovery is important because it highlights how clinical trials could be weighted toward women a susceptible part of the population to help scientists more rapidly identify effective drug interventions to slow or cure Alzheimers, said Arthur Toga, director of the USC Stevens Neuroimaging and Informatics Institute at the Keck School of Medicine among the nations leaders in innovative scientific discovery.

The study was published Aug. 28 in the Journal of the American Medical Association Neurology. It included data from 57,979 North Americans and Europeans in the Global Alzheimers Association Interactive Network (GAAIN). This big-data project provides scientists around the world with shared data and sophisticated analysis tools to address a disease that makes up about 65 percent of the 47 million cases of dementia worldwide.

The results contradict a seminal 20-year-old study that found women with one copy of ApoE4, a gene variant linked to Alzheimers, were diagnosed with the disease 50 percent more often than men with the same genetic profile.

The findings presented in the USC-led study expand the number of participant data by ninefold and indicate the critical decade falls between 65 and 75, more than 10 years after the start of menopause. Previous studies in animals and humans have reported a relationship between ApoE4, menopause and cognitive decline.

So much work has been dependent on one 1997 finding, but with tools like GAAIN, we now have the ability to reinvestigate with increased statistical power, Toga said.

The new findings are significant because almost two-thirds of the more than 5 million Americans now with Alzheimers disease today are women.

The new findings are significant because almost two-thirds of the more than 5 million Americans now living with Alzheimers disease are women, according to the Alzheimers Association.

Many attribute the imbalance in disease risk to the fact that women, on average, live longer than men. However, a growing body of evidence suggests other reasons also contribute to the difference. For instance, men have higher rates of heart disease and stroke. So, men who live longer may be healthier than women of the same age and may face less risk of developing Alzheimers, according to the USC-led study.

In the future, doctors who want to prevent Alzheimers may intervene at different ages for men and women, said Judy Pa, co-author of the study and an assistant professor of neurology at the USC Stevens Neuroimaging and Informatics Institute.

Menopause and plummeting estrogen levels, which on average begins at 51, may account for the difference, Pa said. However, scientists still dont know what is responsible. Researchers need to study women 10, 15 or even 20 years before their most vulnerable period to see if there are any detectable signals to suggest increased risk for Alzheimers in 15 years.

Only some women are at increased risk of developing Alzheimers in their mid-60s to mid-70s compared to men. To find out, women could have their DNA analyzed. However, Pa cautions that genetic testing for the ApoE4 variant is no crystal ball.

There is controversy in terms of whether people should know their ApoE status because it is just a risk factor, Pa said. It doesnt mean youre going to get Alzheimers disease. Even if you carry two copies of ApoE4, your chances are greatly increased, but you could still live a long life and never have symptoms.

Even if some women discover they are at heightened risk, they can improve their odds by making life changes.

Get more exercise. Work out your mind, especially in old age.

Judy Pa

Get more exercise. Work out your mind, especially in old age, Pa said. Pick up hobbies that are cognitively or physically challenging. Reduce processed sugar intake because its linked to obesity, which is associated with many chronic diseases.

Alzheimers disease is the fifth-leading cause of death for Americans 65 and older, but it may one day outpace the nations top two killers heart disease and cancer. Alzheimers-related deaths increased by nearly 39 percent between 2000 and 2010 while heart disease-related deaths declined 31 percent and cancer deaths fell 32 percent, according to the Centers for Disease Control and Prevention.

Because Alzheimers disease has a huge impact on lifelong health, USC has more than 70 researchers dedicated to the prevention, treatment and potential cure of the memory-erasing disease. Big data projects like this require experts across disciplines computer science, biology, pathophysiology, imaging and genetics to coordinate.

For this study, the researchers examined data from 27 different studies that assessed participants ApoE gene variation, as well as characteristics such as sex, race, ethnicity, diagnosis (normal, mild cognitive impairment or Alzheimers disease) and age at diagnosis.

The records of nearly 58,000 people were scrutinized. Meta-analyses were performed on 31,340 whites who received clinical diagnoses sometime between ages 55 and 85.

The proportion of minorities was so small that analysts could not draw statistically significant conclusions about their disease risk. Because of this, the study focused on whites only.

Most of the archives around the world have insufficient numbers of underrepresented groups, Toga said. One of the take-home messages from our study is people of all races and ethnicities need to be involved in Alzheimers clinical trials because this disease is a problem that affects all of us.

The current findings need to be confirmed in more diverse study populations.

USC is working to build more diverse population studies related to Alzheimers. Established in 1984, the Alzheimer Disease Research Center at the Keck School of Medicine reaches out to communities in the greater Los Angeles area to educate the citys diverse population about Alzheimers and the clinical trials they might be interested in joining. Previous studies, for example, have focused on Latinos.

Historically, women have not been adequately represented in clinical trials, especially in studies on heart disease. Women need to be represented equally to men or even overrepresented, Pa said.

The bottom line is women are not little men, Pa said. A lot more research needs to target women because gender-specific variations can be so subtle that scientists often miss them when they control for gender or use models to rule out gender differences. Most research today is ignoring a big part of the equation.

The study was made possible because of lead author Scott Neu, a leader in the development of a federated approach to analyzing metadata and assistant professor of research at the Laboratory of Neuro Imaging at the Keck School of Medicine.

GAAIN the free resource we created in conjunction with the Alzheimers Association allows anyone to explore data sets around the world and conduct preliminary analyses to test scientific hypotheses, Neu said. Our goal is to connect scientists with those who have collected data to create new collaborations to further research and understanding of Alzheimers disease.

Analysts excluded people with a history of stroke, cerebrovascular disease, abnormal proteins that contribute to Parkinsons disease and dementia, gene mutations leading to higher levels of toxic amyloid brain plaques and any known neurological diseases.

Scientists did not adjust for known Alzheimers risk factors such as education, family history of Alzheimers or dementia because that information was not provided in all data sets. They also were unable to adjust for sex-dependent differences such as cigarette smoking, hormonal changes with age and alcohol usage.

The study was supported by the Alzheimers Association through the Global Alzheimers Association Interactive Network initiative (GAAIN-14-244631) via a $5 million grant and a portion of two National Institutes of Health grants: $12 million from Big Data to Knowledge (U54-EB020406) and $5 million from neuroimaging and genetics (P41-EB015922).

More stories about: Alzheimer's Disease, Research

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The Genetics of Eating Disorders – Scientific American (blog)

Tuesday, August 29th, 2017

Thirty million American women and men will struggle with eating disorders in their lifetime, and these life-threatening conditions have a higher mortality rate than any other psychiatric illness. For example, someone struggling with anorexia for five years has a 5 per cent, or one in20 chance, of dying.

While more and more people have come to understand that eating disorders are diseases of the brain, there's still awidespreadbeliefthat people with these devastating conditionsare vain, attention-seeking, or lacking in will power. But apaperjust published in Plos One makes it clear that this isn't true. The studyevaluated the genomes of95 individuals with diagnosed eating disorders andidentified 430 genes, clustered into two large groups, that are more likely to be damaged than in people without those disorders.

This adds to a growing body of research shows that eating disorders are powerful, biologically-driven illnesses. The new studysupports previous findings that the risk of developing an eating disorder is 50-80 per cent geneticthatpatientshave inherited damaged copies of genes that increase their risk of developing disordered eating. And understanding which genes are damaged can practitioners create better treatment treatment protocols.

In the PlosOne study, patients with eating disorders were clustered into two main groups. In the first, the damaged genes fell into a class of gut neuropeptides affecting that control appetite,food intakeand digestion/absorption of nutrients, making patients more likely to binge. Roughly half of this group struggled with restricted eating patterns, and the other half were binge eaters. The research confirms reports by our patients who believe their behavior is biologically driven.

The second group of patients had a cluster of genes involved in the function of the immune system and inflammation, which has long been known to suppress appetite. Patients with damaging mutations in the inflammation cluster are much more likely to have restricted-eating patterns. More research is needed to test a possible connection between eating disorders and auto-immune conditions like irritable bowel disease.

The new findings are consistent with known environmental eating disorder triggers. Faddieting, excessive exercise, or medical illness, are examples of negative energy states that have long been seen as possible eating disorder triggers. Negative energy states can set up behavioral changes like food binges or restricted food intake, triggering preexisting genetic drivers for eating disorders. Based on these findings, we argue that eating disorders are biologically driven illnesses that alter mood and behavior, similar to how the lack of thyroid hormone can result in depression in a patient with hypothyroidism.

Failure to understand the underlying causes of eating disorders creates stigma, making it less likely for those who struggle to get treatment. People with any medical condition deserve support and access to the best treatment. Someone with cancer wouldnt be denied treatment for their illness. Likewise, patients with eating disorders shouldnt feel guilty about their illness and they should have access to safe, effective treatment.

Biology isnt destiny. Eating disorders treatment is most effective if its accompanied by a general understanding that eating illnesses are biologically driven.

Lasting recovery from an eating disorder is possibleand those who struggle deserve understanding and support without guilt or judgment.

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Hospital to boost genetic testing for newborn babies – Belfast Telegraph

Tuesday, August 29th, 2017

Hospital to boost genetic testing for newborn babies

BelfastTelegraph.co.uk

One of the UK's largest women's hospitals is to increase its ability to genetically test newborn babies 12-fold.

http://www.belfasttelegraph.co.uk/news/northern-ireland/hospital-to-boost-genetic-testing-for-newborn-babies-36079324.html

http://www.belfasttelegraph.co.uk/news/northern-ireland/article36079323.ece/c3338/AUTOCROP/h342/PANews%20BT_P-013b5e7c-4e66-4b0a-b8d6-04b3c11abd37_I1.jpg

One of the UK's largest women's hospitals is to increase its ability to genetically test newborn babies 12-fold.

Liverpool Women's NHS Foundation Trust will be able to screen all infants for inherited conditions or illnesses and plan for early treatment as part of a major new IT project.

It will also contribute to a major population health programme in Liverpool analysing genetic information by location, identifying and enabling work to prevent localised health issues.

IT firm Novosco will introduce the computing system.

Novosco managing director Patrick McAliskey said: "We are delighted to secure this contract which will enable the trust to take genetic testing to the next level and play an important role in the identification and prevention of conditions and illnesses in new-born babies and the wider population."

This role of genetics in healthcare is one of the most rapidly expanding areas of development for Liverpool Women's.

It provides a regional clinical genetics service based at Alder Hey Hospital, covering a population of around 2.8 million people from across Merseyside, Cheshire and the Isle of Man, chief executive Kathryn Thomson posted on the trust's website.

She added: "To discover that you or any child you have or plan to have may be at risk of a genetic disorder which could cause disability or a rare condition is traumatic.

"People are sometimes shocked and anxious and wonder what the future might hold.

"They need as much information and support as possible to help them cope.

"That is why the often unsung work of our clinical genetics team is so important, providing diagnosis and supporting families when they need it most."

Liverpool Women's NHS Foundation Trust specialises in the health of women and their babies - both within the hospital and in the community. It is one of only two such specialist trusts in the UK - and the largest women's hospital of its kind.

Novosco is an IT infrastructure and managed cloud computing company and employs over 150 people. It has its headquarters in Belfast, with offices in Manchester, Dublin, and Cork.

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Introduction to genetics – Wikipedia

Monday, August 28th, 2017

This article is a non-technical introduction to the subject. For the main encyclopedia article, see Genetics.

A long molecule that looks like a twisted ladder. It is made of four types of simple units and the sequence of these units carries information, just as the sequence of letters carries information on a page.

They form the rungs of the DNA ladder and are the repeating units in DNA. There are four types of nucleotides (A, T, G and C) and it is the sequence of these nucleotides that carries information.

A package for carrying DNA in the cells. They contain a single long piece of DNA that is wound up and bunched together into a compact structure. Different species of plants and animals have different numbers and sizes of chromosomes.

A segment of DNA. Genes are like sentences made of the "letters" of the nucleotide alphabet, between them genes direct the physical development and behavior of an organism. Genes are like a recipe or instruction book, providing information that an organism needs so it can build or do something - like making an eye or a leg, or repairing a wound.

The different forms of a given gene that an organism may possess. For example, in humans, one allele of the eye-color gene produces green eyes and another allele of the eye-color gene produces brown eyes.

The complete set of genes in a particular organism.

When people change an organism by adding new genes, or deleting genes from its genome.

An event that changes the sequence of the DNA in a gene.

Genetics is the study of geneswhat they are, what they do, and how they work. Genes inside the nucleus of a cell are strung together in such a way that the sequence carries information: that information determines how living organisms inherit various features (phenotypic traits). For example, offspring produced by sexual reproduction usually look similar to each of their parents because they have inherited some of each of their parents' genes. Genetics identifies which features are inherited, and explains how these features pass from generation to generation. In addition to inheritance, genetics studies how genes are turned on and off to control what substances are made in a cellgene expression; and how a cell dividesmitosis or meiosis.

Some phenotypic traits can be seen, such as eye color while others can only be detected, such as blood type or intelligence. Traits determined by genes can be modified by the animal's surroundings (environment): for example, the general design of a tiger's stripes is inherited, but the specific stripe pattern is determined by the tiger's surroundings. Another example is a person's height: it is determined by both genetics and nutrition.

Chromosomes are tiny packages which contain one DNA molecule and its associated proteins. Humans have 46 chromosomes (23 pairs). This number varies between speciesfor example, many primates have 24 pairs. Meiosis creates special cells, sperm in males and eggs in females, which only have 23 chromosomes. These two cells merge into one during the fertilization stage of sexual reproduction, creating a zygote. In a zygote, a nucleic acid double helix divides, with each single helix occupying one of the daughter cells, resulting in half the normal number of genes. By the time the zygote divides again, genetic recombination has created a new embryo with 23 pairs of chromosomes, half from each parent. Mating and resultant mate choice result in sexual selection. In normal cell division (mitosis) is possible when the double helix separates, and a complement of each separated half is made, resulting in two identical double helices in one cell, with each occupying one of the two new daughter cells created when the cell divides.

Chromosomes all contain DNA made up of four nucleotides, abbreviated C (cytosine), G (guanine), A (adenine), or T (thymine), which line up in a particular sequence and make a long string. There are two strings of nucleotides coiled around one another in each chromosome: a double helix. C on one string is always opposite from G on the other string; A is always opposite T. There are about 3.2 billion nucleotide pairs on all the human chromosomes: this is the human genome. The order of the nucleotides carries genetic information, whose rules are defined by the genetic code, similar to how the order of letters on a page of text carries information. Three nucleotides in a rowa tripletcarry one unit of information: a codon.

The genetic code not only controls inheritance: it also controls gene expression, which occurs when a portion of the double helix is uncoiled, exposing a series of the nucleotides, which are within the interior of the DNA. This series of exposed triplets (codons) carries the information to allow machinery in the cell to "read" the codons on the exposed DNA, which results in the making of RNA molecules. RNA in turn makes either amino acids or microRNA, which are responsible for all of the structure and function of a living organism; i.e. they determine all the features of the cell and thus the entire individual. Closing the uncoiled segment turns off the gene.

Heritability means the information in a given gene is not always exactly the same in every individual in that species, so the same gene in different individuals does not give exactly the same instructions. Each unique form of a single gene is called an allele; different forms are collectively called polymorphisms. As an example, one allele for the gene for hair color and skin cell pigmentation could instruct the body to produce black pigment, producing black hair and pigmented skin; while a different allele of the same gene in a different individual could give garbled instructions that would result in a failure to produce any pigment, giving white hair and no pigmented skin: albinism. Mutations are random changes in genes creating new alleles, which in turn produce new traits, which could help, harm, or have no new effect on the individual's likelihood of survival; thus, mutations are the basis for evolution.

Contents

Genes are pieces of DNA that contain information for synthesis of ribonucleic acids (RNAs) or polypeptides. Genes are inherited as units, with two parents dividing out copies of their genes to their offspring. This process can be compared with mixing two hands of cards, shuffling them, and then dealing them out again. Humans have two copies of each of their genes, and make copies that are found in eggs or spermbut they only include one copy of each type of gene. An egg and sperm join to form a complete set of genes. The eventually resulting offspring has the same number of genes as their parents, but for any gene one of their two copies comes from their father, and one from their mother.[1]

The effects of this mixing depend on the types (the alleles) of the gene. If the father has two copies of an allele for red hair, and the mother has two copies for brown hair, all their children get the two alleles that give different instructions, one for red hair and one for brown. The hair color of these children depends on how these alleles work together. If one allele dominates the instructions from another, it is called the dominant allele, and the allele that is overridden is called the recessive allele. In the case of a daughter with alleles for both red and brown hair, brown is dominant and she ends up with brown hair.[2]

Although the red color allele is still there in this brown-haired girl, it doesn't show. This is a difference between what you see on the surface (the traits of an organism, called its phenotype) and the genes within the organism (its genotype). In this example you can call the allele for brown "B" and the allele for red "b". (It is normal to write dominant alleles with capital letters and recessive ones with lower-case letters.) The brown hair daughter has the "brown hair phenotype" but her genotype is Bb, with one copy of the B allele, and one of the b allele.

Now imagine that this woman grows up and has children with a brown-haired man who also has a Bb genotype. Her eggs will be a mixture of two types, one sort containing the B allele, and one sort the b allele. Similarly, her partner will produce a mix of two types of sperm containing one or the other of these two alleles. When the transmitted genes are joined up in their offspring, these children have a chance of getting either brown or red hair, since they could get a genotype of BB = brown hair, Bb = brown hair or bb = red hair. In this generation, there is therefore a chance of the recessive allele showing itself in the phenotype of the childrensome of them may have red hair like their grandfather.[2]

Many traits are inherited in a more complicated way than the example above. This can happen when there are several genes involved, each contributing a small part to the end result. Tall people tend to have tall children because their children get a package of many alleles that each contribute a bit to how much they grow. However, there are not clear groups of "short people" and "tall people", like there are groups of people with brown or red hair. This is because of the large number of genes involved; this makes the trait very variable and people are of many different heights.[3] Despite a common misconception, the green/blue eye traits are also inherited in this complex inheritance model.[4] Inheritance can also be complicated when the trait depends on interaction between genetics and environment. For example, malnutrition does not change traits like eye color, but can stunt growth.[5]

Some diseases are hereditary and run in families; others, such as infectious diseases, are caused by the environment. Other diseases come from a combination of genes and the environment.[6]Genetic disorders are diseases that are caused by a single allele of a gene and are inherited in families. These include Huntington's disease, Cystic fibrosis or Duchenne muscular dystrophy. Cystic fibrosis, for example, is caused by mutations in a single gene called CFTR and is inherited as a recessive trait.[7]

Other diseases are influenced by genetics, but the genes a person gets from their parents only change their risk of getting a disease. Most of these diseases are inherited in a complex way, with either multiple genes involved, or coming from both genes and the environment. As an example, the risk of breast cancer is 50 times higher in the families most at risk, compared to the families least at risk. This variation is probably due to a large number of alleles, each changing the risk a little bit.[8] Several of the genes have been identified, such as BRCA1 and BRCA2, but not all of them. However, although some of the risk is genetic, the risk of this cancer is also increased by being overweight, drinking a lot of alcohol and not exercising.[9] A woman's risk of breast cancer therefore comes from a large number of alleles interacting with her environment, so it is very hard to predict.

The function of genes is to provide the information needed to make molecules called proteins in cells.[1] Cells are the smallest independent parts of organisms: the human body contains about 100 trillion cells, while very small organisms like bacteria are just one single cell. A cell is like a miniature and very complex factory that can make all the parts needed to produce a copy of itself, which happens when cells divide. There is a simple division of labor in cellsgenes give instructions and proteins carry out these instructions, tasks like building a new copy of a cell, or repairing damage.[10] Each type of protein is a specialist that only does one job, so if a cell needs to do something new, it must make a new protein to do this job. Similarly, if a cell needs to do something faster or slower than before, it makes more or less of the protein responsible. Genes tell cells what to do by telling them which proteins to make and in what amounts.

Proteins are made of a chain of 20 different types of amino acid molecules. This chain folds up into a compact shape, rather like an untidy ball of string. The shape of the protein is determined by the sequence of amino acids along its chain and it is this shape that, in turn, determines what the protein does.[10] For example, some proteins have parts of their surface that perfectly match the shape of another molecule, allowing the protein to bind to this molecule very tightly. Other proteins are enzymes, which are like tiny machines that alter other molecules.[11]

The information in DNA is held in the sequence of the repeating units along the DNA chain.[12] These units are four types of nucleotides (A,T,G and C) and the sequence of nucleotides stores information in an alphabet called the genetic code. When a gene is read by a cell the DNA sequence is copied into a very similar molecule called RNA (this process is called transcription). Transcription is controlled by other DNA sequences (such as promoters), which show a cell where genes are, and control how often they are copied. The RNA copy made from a gene is then fed through a structure called a ribosome, which translates the sequence of nucleotides in the RNA into the correct sequence of amino acids and joins these amino acids together to make a complete protein chain. The new protein then folds up into its active form. The process of moving information from the language of RNA into the language of amino acids is called translation.[13]

If the sequence of the nucleotides in a gene changes, the sequence of the amino acids in the protein it produces may also changeif part of a gene is deleted, the protein produced is shorter and may not work any more.[10] This is the reason why different alleles of a gene can have different effects in an organism. As an example, hair color depends on how much of a dark substance called melanin is put into the hair as it grows. If a person has a normal set of the genes involved in making melanin, they make all the proteins needed and they grow dark hair. However, if the alleles for a particular protein have different sequences and produce proteins that can't do their jobs, no melanin is produced and the person has white skin and hair (albinism).[14]

Genes are copied each time a cell divides into two new cells. The process that copies DNA is called DNA replication.[12] It is through a similar process that a child inherits genes from its parents, when a copy from the mother is mixed with a copy from the father.

DNA can be copied very easily and accurately because each piece of DNA can direct the creation of a new copy of its information. This is because DNA is made of two strands that pair together like the two sides of a zipper. The nucleotides are in the center, like the teeth in the zipper, and pair up to hold the two strands together. Importantly, the four different sorts of nucleotides are different shapes, so for the strands to close up properly, an A nucleotide must go opposite a T nucleotide, and a G opposite a C. This exact pairing is called base pairing.[12]

When DNA is copied, the two strands of the old DNA are pulled apart by enzymes; then they pair up with new nucleotides and then close. This produces two new pieces of DNA, each containing one strand from the old DNA and one newly made strand. This process is not predictably perfect as proteins attach to a nucleotide while they are building and cause a change in the sequence of that gene. These changes in DNA sequence are called mutations.[15] Mutations produce new alleles of genes. Sometimes these changes stop the functioning of that gene or make it serve another advantageous function, such as the melanin genes discussed above. These mutations and their effects on the traits of organisms are one of the causes of evolution.[16]

A population of organisms evolves when an inherited trait becomes more common or less common over time.[16] For instance, all the mice living on an island would be a single population of mice: some with white fur, some gray. If over generations, white mice became more frequent and gray mice less frequent, then the color of the fur in this population of mice would be evolving. In terms of genetics, this is called an increase in allele frequency.

Alleles become more or less common either by chance in a process called genetic drift, or by natural selection.[17] In natural selection, if an allele makes it more likely for an organism to survive and reproduce, then over time this allele becomes more common. But if an allele is harmful, natural selection makes it less common. In the above example, if the island were getting colder each year and snow became present for much of the time, then the allele for white fur would favor survival, since predators would be less likely to see them against the snow, and more likely to see the gray mice. Over time white mice would become more and more frequent, while gray mice less and less.

Mutations create new alleles. These alleles have new DNA sequences and can produce proteins with new properties.[18] So if an island was populated entirely by black mice, mutations could happen creating alleles for white fur. The combination of mutations creating new alleles at random, and natural selection picking out those that are useful, causes adaptation. This is when organisms change in ways that help them to survive and reproduce. Many such changes, studied in evolutionary developmental biology, affect the way the embryo develops into an adult body.

Since traits come from the genes in a cell, putting a new piece of DNA into a cell can produce a new trait. This is how genetic engineering works. For example, rice can be given genes from a maize and a soil bacteria so the rice produces beta-carotene, which the body converts to Vitamin A.[19] This can help children suffering from Vitamin A deficiency. Another gene being put into some crops comes from the bacterium Bacillus thuringiensis; the gene makes a protein that is an insecticide. The insecticide kills insects that eat the plants, but is harmless to people.[20] In these plants, the new genes are put into the plant before it is grown, so the genes are in every part of the plant, including its seeds.[21] The plant's offspring inherit the new genes, which has led to concern about the spread of new traits into wild plants.[22]

The kind of technology used in genetic engineering is also being developed to treat people with genetic disorders in an experimental medical technique called gene therapy.[23] However, here the new gene is put in after the person has grown up and become ill, so any new gene is not inherited by their children. Gene therapy works by trying to replace the allele that causes the disease with an allele that works properly.

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Warnings over shock dementia revelations from ancestry DNA tests – The Guardian

Monday, August 28th, 2017

People who use genetic tests to trace their ancestry only to discover that they are at risk of succumbing to an incurable illness are being left to suffer serious psychological problems. Dementia researchers say the problem is particularly acute for those found to be at risk of Alzheimers disease, which has no cure or effective treatment. Yet these people are stumbling upon their status inadvertently after trying to find their Viking, Asian or ancient Greek roots.

These tests have the potential to cause great distress, said Anna Middleton, head of society and ethics research at the Wellcome Genome Campus in Cambridge. Companies should make counselling available, before and after people take tests. The issue is raised in a paper by Middleton and others in the journal Future Medicine.

A similar warning was sounded by Louise Walker, research officer at the Alzheimers Society. Everyone has a right to know about their risk if they want to, but these companies have a moral responsibility to make sure people understand the meaning and consequences of this information. Anyone considering getting genetic test results should do so with their eyes open.

Alzheimers is linked to the build-up in the brain of clumps of a protein called amyloid. This triggers severe memory loss, confusion and disorientation. One gene, known as ApoE, affects this process and exists in three variants: E2, E3 and E4. Those possessing the last of these face an increased chance of getting the disease in late life.

About 3% of the population has two copies of the E4 variant one inherited from each parent, Professor John Hardy, of University College London, said. They have about an 80% chance of getting Alzheimers by the age of 80. The average person has a 10% risk.

The gene test company has made its profit and walks away. They should be made to pay for their customers' counselling

The link with ApoE was made in 1996 and Hardy recalled the reaction in his laboratory. We went around testing ourselves to see which variant we possessed. I found I have two low-risk E3 versions on my genome. But if I had found two E4 versions? By now, having reached my 60s, I would be facing the prospect that I had a serious chance of getting Alzheimers disease in 10 years. I would be pretty fed up.

The ability to find a persons ApoE status has become even easier as a result of the development of genetic tests that provide information about a persons ancestry, health risks and general traits. Dozens of companies offer such services and adverts portray happy individuals learning about their roots 43% African or 51% Middle Eastern often to the sound of Julie Andrews singing Getting to Know You or a similarly happy-sounding track. All you have to do is provide a sample of spittle.

The resulting information about predilections to disease is not stressed but it is given. Kelly Boughtflower, from London, took a gene test with the company 23andMe because she wanted to prove her mothers family came from Spain. The results provided no evidence of her Iberian roots but revealed she carried one E4 version of the ApoE gene, which increases her chances of getting Alzheimers, though not as drastically as a double dose.

I didnt think about it at the time, said Boughtflower. Then, when I took up work as an Alzheimers Society support worker, I learned about ApoE4 and the information has come to sit very heavily with me. Did I inherit the ApoE4 from my mother? Is she going to get Alzheimers very soon? Have I passed it on to my daughter? I have tried to get counselling on the NHS but that is not available for a person in my particular predicament, I was told.

Other examples appear on the ApoE4 Info site, a forum for those whose gene tests show an Alzheimers susceptibility. Have stumbled upon my 4/4 ApoE status. Im still in shock, writes one. Another states: I got paid a $50 Amazon gift-card to take part in a genetic study. I was naive and unprepared.

There is no drug or treatment for Alzheimers and although doctors advise that having a healthy lifestyle will help, the baseline risk for E4 carriers remains high. That is a real problem, said Middleton. Genetic test companies say they offer advice about counselling but that usually turns out to be a YouTube video outlining your risks. Affected people needed one-to-one counselling.

For their part, gene test companies say results about Alzheimers and other such as breast cancer and Parkinsons are often hidden behind electronic locks. A person has to answer several questions to show they really want to open these and is informed of potential risks. But Middleton dismissed these precautions. You know there is medical information about you online and so you will go and find it. It is human nature.

Margaret McCartney, a GP and author of The Patient Paradox, agreed. What worries me is the aggressive way these tests are marketed. People are told all the benefits but there is no mention of the downsides. The NHS is expected to mop these up.

Meanwhile, the gene test company has made its profit and walks away from the mess they have created. I think that is immoral. They should be made to pay for counselling for their customers.

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UNL partners with University of Montana to study plant adaptation genetics – Daily Nebraskan

Monday, August 28th, 2017

A new research partnership at the University of Nebraska-Lincoln will focus on how genetic adaptations in plants and animals have helped animals evolve and withstand environmental challenges.

A four-year, $4 million National Science Foundation study will partner UNL with the University of Montana.

Species of both plants and animals can be present in vastly different local conditions, and learn to adapt to their conditions, said Jay Storz, a UNL Susan J. Rosowski professor of biological sciences.

Were looking at ways to figure out the causal connections between information encoded in the genome and the traits involved in those adaptations, he said.

The team will analyze genomes of animals and plants that have shown they can adapt to different conditions. Researchers will compare the genomes to those of the same species and of species that do not adapt to other climates to establish a link between genetic changes and environment-specific traits.

It might help you narrow down your search of the whole genome to a more targeted set of candidate genes, said Kristi Montooth, associate professor of biological sciences at UNL. If you can kind of back track from the physiology and try to match physiological changes to changes in gene expression, then you may be able to better localize in the genome what changes might be responsible for that [trait].

Colin Meiklejohn, an assistant professor of biological sciences at UNL, said this will give them the potential to help populations that are going extinct and give them the ability to survive. If there is a closely related species, scientists could breed the two species together and save a population while also potentially giving the species the ability to adapt better than before.

A yearly meeting will give researchers a chance to discuss their progress and debate questions they find during their research. Each institution will be hiring four postdoctoral researchers and full-time research assistants to help with the project. The positions will be funded by the project.

Montooth said a majority of the money from the project fund will be used toward training the next generation of evolutionary geneticists.

news@dailynebraskan.com

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Magnetothermal Genetics: A Fourth Tool in the Brain-Hacking Toolbox – IEEE Spectrum

Saturday, August 26th, 2017

A scientist wanting to hack into an animals brain used to have three different tools to choose from: electriccurrent, drugs, and light. Now theres a fourth: magnetic fields. In a paper published last week in the open-access journal eLife, scientists at the University at Buffalo used magneto-thermal genetics to manipulate brain cells in mice, enabling the researchers to control the animals behavior.

Magneto-thermal genetics has been previously shownto activate neurons in anesthetized rodent brains, but this is the first time anyone hasreported using the tool to manipulate animal behavior, says Arnd Pralle, the University at Buffalo biophysicist who led the research.

Brain hacking tools help scientists better understand the wiring of the brainthe arrangement of neural circuits and which onescontrol different movements and behaviors. These tools could someday lead to the development of artificial human eyes and ears, or treatments for paralysis,traumatic brain injury, and diseases such as Parkinsons and depression.

Over the past few years, major funding agencieshave encouraged scientists and bioengineers to focus their work on the bodys internal wiring. The U.S. National Institutes of Health (NIH) and DARPA have been doling out grants for work on both the peripheral and central nervous systems.

Engineers play a key role in the research. The bodys nervous systems communicate, after all, in a language of electrical signals. Researchers must not only map those signals, but also figure out how to interface with them, and override them when they malfunction.

Magnetic fields can do the job (following some complicated, multi-step bioengineering). In Pralles experiments, he and his team injected a virus containing a gene and some helper genetic elementsinto the brains of mice. This genetic material gets incorporated into the DNA of the mouses brain cells, or neurons. The foreign gene makes the neurons heat sensitive. Next, they injected magnetic nanoparticlesinto a specific region of the mouse brain that latch onto the neurons in that region. They then applied alternating magnetic fields, which cause the nanoparticles to heat up a couple of degrees. The rise in temperature triggers the heat-sensitive neurons to open ion channels. Positively-charged ions flow into the neuron, causing it to fire.

Pralle demonstrated proof of the concept in 2010, and others, such as Polina Anikeeva, a professor of materials science and engineering at MIT, have since improved upon it. Those studies confirmed that the technique could indeed activate neurons in the rodent brain.

In the new study, Pralle and his team show how magneto-thermal genetics can manipulate behavior in mice that are awake and freely moving. In their experiments, they activated regions of the brain that made the mice run faster around the perimeter of their cages, spin in circles, and, eerily, freeze the motion of all four paws.

Those same behaviors have been induced in rodents by activating neurons using other brain hacking tools, including optogenetics (in which neurons are genetically sensitized to respond to light), and chemogenetics (in which neurons are genetically sensitized to respond to designer drugs).

Those three toolsmagneto-thermal genetics, optogenetics, and chemogeneticsare new and purely experimental. A fourth toolelectrical stimulationhas been around for decades, with some success in treating Parkinsons, depression, memory loss, paralysis, and epilepsy in humans.

None of the tools has made a dent, relatively speaking, in the range of functions that the brain, spinal cord and peripheral nerves control. Its like owning four different musical instruments and knowing how to play onlya few rudimentary toddler songs on each of them. That untapped potential has inspired scientists to continue to test and develop the tools.

That means overcomingthe shortcomings of each tool. Electrical stimulation of deep brain regions requires, at least for now, an invasive surgical procedure to implant electrodes. That limits the number of patients willing to undergo the surgery. The method is also limited in how specifically it can target small brain regions or cell types.

Optogenetic techniques can target specific neurons, but animals in these experiments usually have to be tethered to an optical fiber or other kind of implant that delivers the light, which can affect their behavior. Study animals undergoing chemogenetic modulation can run free, but their response to the drugs is much slower than to light or electrical stimulation.

Magneto-thermal genetic toolsare non-invasive, tetherless, and induce a response within seconds of turning on the magnetic fields. But theres controversy over how the tool works.

Pralles team has shown that the magnetic nanoparticles injected into the mouse brains latch onto the membranes of the neurons, thus restricting the heating to those membranes rather than diffusing out to the surrounding liquid. This makes little sense from a physics point of view, and contradicts basic principles of heat transfer, saysMarkus Meister, a bioengineer at the California Institute of Technology in Pasadena.

Meister has also argued that previous experiments in magnetogeneticsa sister tool to magneto-thermal geneticsthat involves a different mechanismcontradict the laws of physics.He laid out his back-of-the-envelope calculations last year ina paper ineLife, whichgarnered a lot of attentionin the field of neuromodulation.

However, Pralles main claim, that he successfully used magnetic heating to control animal behavior, looks well supported, Meister says. Bottom line, the reported effects on behavior look real, but just what the mechanism is behind them remains to be understood.

Pralle says his work clearly demonstrates and measures local heating at the cell membrane, showing that it does indeed occur. Why thats happening, however, is unclear, he says.We cannot completely explain why the increase in heat stays within a few tenths or hundredths of nanometers of the neuronal membrane, Pralle says. The heat should diffuse more quickly into the [surrounding] water solution, so it shouldnt have much of a local heating effect.

Several theorists and experimentalists, including Anikeeva, have formulated and are testingmodels to explain the phenomenon. Similar effects have been seen, measured and correctly predicted for laser heating of gold nanoparticles in water, Pralle says.

Anikeeva says she sees nocontroversy in Pralles latest work. Meisters argument is based on a model that isnot applicable to nanoscale heat transport, she says.

Next, Pralle plans to develop, in collaboration with Anikeeva,a magneto-thermal genetics tool that can modulate multiple areas of the brain simultaneously, allowing the researchers to more fully control behavior, or multiple behaviors at one time. If we dream about it we can overcome the technical hurdles, Pralle says.

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Magnetothermal Genetics: A Fourth Tool in the Brain-Hacking Toolbox - IEEE Spectrum

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Genetics for everyone – The Boston Globe

Saturday, August 26th, 2017

Illustration by cristina span/for the boston globe

The Greeks asked their oracles to predict future fortunes and future losses. The Romans studied the entrails of sacrificed animals for similar reasons. In modern-day medicine, though, soothsayers come in the form of genetic tests.

Ever since the human genome was sequenced almost 15 years ago, tens of thousands of genetic tests have flooded the marketplace. By analyzing someones DNA, often through a blood sample or cheek swab, these tests promise to foretell whether a patient is prone to certain cancers, blessed with the potential to become a star soccer player, or at an elevated risk of having an opioid addiction.

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These types of genetic tests are finding an eager audience. The North American genetic testing market, already the largest in the world, was worth $11.9 billion in 2016, by one estimate, and is expected to grow at more than 15 percent a year for the foreseeable future. Companies such as LabCorp, which offer genetic tests via doctor recommendations, and the healthcare giant Roche have moved aggressively into the field. The company 23andMe, a household name because of its ancestry tests, sells health-related tests directly to consumers.

But for a source of medical information to be legally sold in the United States, just how accurate does it need to be?

Like a prediction from a crystal ball, genetic test results are sometimes wrong. Some tests that predict the likelihood a young pregnant woman will have a child with a genetic condition such as Down syndrome may only be correct only 60 percent of the time. Most genetic tests, and many other lab tests, go unvetted by the Food and Drug Administration. That means these tests may not undergo any independent review to make sure they accurately pick up the disease or genetic conditions they claim to be seeking.

Using the worlds first portable DNA lab to sequence beer is a cool thing to do.

The FDA has been wrestling for years with whether and how to do more. During the Obama administration, the agency proposed a new set of draft limits on a whole class of tests, and then put them on hold immediately after Donald Trumps election. This spring, the FDA gave 23andMe permission to market genetic screenings for susceptibility to Alzheimers, Parkinsons, and other conditions. It was the first time the agency blessed direct-to-consumer tests for genetic health risks.

While the debate over genetic testing often follows a pattern familiar from countless other industries business groups want less regulation, and consumer advocates favor more it also raises more cosmic questions: Is a medical test just a piece of information? Or is it something more, if its result leads to dramatic or irreversible action such as chemotherapy or an abortion? And if a data point is factually suspect, or ripe for misinterpretation, when and how should it be offered to consumers?

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Especially if regulators stand aside, Americans may soon be swimming in even more tests that vary greatly in their reliability. Yet for some people contemplating a current ailment or their future well-being, getting an answer even an unreliable one may be better than no answer at all.

Especially for people expecting a baby, genetic tests can be hard to resist. I think we all are wanting to know our child doesnt have something... we want them to be healthy, said Mischa Livingstone, a filmmaker and professor who lives in California. Without asking for it, his pregnant wife, Jessica, was given a genetic test that predicted a 99 percent chance their child would have Turner syndrome, a genetic condition that can lead to short stature, heart defects, and other symptoms. But genetic tests for Turner are more often wrong than right a fact the couple didnt know at the time.

They were devastated, and immediately went for more invasive testing, which showed the fetus was fine. But their sense of dread didnt lift until their daughter, now 2 1/2, was born perfectly healthy.

Despite the heartache a faulty genetic test result caused, Livingstone says hed consider asking for one again. I think it feeds into that need for certainty, he said.

Both individuals and society as a whole are intolerant of the unknown, medical sociologists say.

Long before genetic screenings, there was a critical relationship between lab tests and medical treatment. Doctors often wont prescribe drugs or treatment without a positive test result. Insurance payments are rarely processed without diagnostic codes. The rise of genetic testing wont change, and may even amplify, that dynamic.

While some diagnoses may still carry social stigma think schizophrenia, for example they more often may confer legitimacy. Having a gene for alcoholism, for example, can make people view the problem as biological, as opposed to a character flaw. For patients, genetic tests promote a therapeutic optimism a hope that they can be treated and cured for an immediate problem or a future one, according to Michael Bury, professor emeritus at Royal Holloway, University of London, who studies society and illness.

A test alone can feel like a step forward. Undergoing a screening, said Natalie Armstrong, professor of healthcare improvement research at the University of Leicester, can make people feel that at least they are doing something proactive.

Interestingly, one study indicated that certain direct-to-consumer genetic tests dont affect users behavior or anxiety levels, bolstering the argument that people may use the information as data points, not a surefire prediction of their own fate.

Many bioethicists are unpersuaded. On an individual basis, it is tempting to discount the pitfalls of a little extra information, says Beth Peshkin, an oncology professor and genetic counselor at Georgetown Lombardi Comprehensive Cancer Center in Washington, D.C. But on a population level the implications of inaccurate results can be costly and, sometimes, deadly.

One of the most cited examples of this harm is from a 2008 genetic test for ovarian cancer that misdiagnosed women, some of whom had their ovaries removed unnecessarily before the test was pulled from the market. Because test makers do not have to report when a test turns out to be wrong in fact many people may never know when a test result is a false positive or negative FDA officials have said it has been almost impossible to assess the overall harm from all unregulated tests.

Cost is another concern that may arise from the overuse of genetic tests that proliferate without meaningful oversight. Tests often beget more tests that cost an ever-escalating amount of money. Enough testing, will invariably pick up something abnormal in a patient, even though it may not harm them, some experts believe.

In some ways its easy for us to try and find something definitive and act on that even though it has nothing to do with what is wrong with the patient, said H. Gilbert Welch, a cancer research at Dartmouth College who has written extensively on the dangers of overtesting. Genetics is an amazing tool... but to what extent does that data predict something that you care about? Is it useful knowledge?

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The American Clinical Laboratory Association, the key trade group for genetic test makers, and other advocates of lighter regulation argue that bad tests are rare, and that its more important for the free market to allow innovation. With more tests in place to identify disease, cures come next, they say.

So far, the public has shown little concern about the fallout of genetic testing. While a 2016 poll showed only 6 percent of American adults have undergone genetic testing, 56 percent of them said they would want to if it could predict cancer or a disease like Alzheimers. Most Americans, the poll found, believe genetic tests for predicting disease are mostly accurate and reliable.

Safety advocates best chance to tighten regulation may have already passed. The world of genetic testing becomes more free-wheeling and consumer-driven all the time. By one industry estimate, 10 new genetic testing products enter the market each day. Despite considerable skepticism from medical experts, new apps purport to use data from gene sequencing to develop personalized diet plans and fitness routines.

The FDAs now-shelved rules would have classified genetic and other tests according to how much harm they could cause if their result was wrong. For example, a new genetic test for colon cancer, which requires intrusive and costly treatment, likely would have been subject to full FDA review; the maker of a test that predicts mere baldness might only have had to register it with the agency and report any known problems with it. Under the Trump administration, the agency appears less likely to draw such distinctions or impose new restrictions at all.

People want answers soon, and their inclination is to believe what appears to be solid, unassailable medicine, said Robert Klitzman, a Columbia University bioethicist. Individuals will need to evaluate these tests carefully. The notion of being able to tell your fortune has great lure. But its a little bit of hubris. We still dont know so much.

Genetic testing, still in its infancy, promises a measure of clarity about the future of our bodies. But as genetic science rapidly evolves, that modern-day crystal ball raises vexing new questions and creates its own kind of uncertainty.

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Genetics for everyone - The Boston Globe

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Hendrix Genetics expand layer distribution in the US – Poultry World (subscription)

Saturday, August 26th, 2017

Eggs

News Aug 25, 2017481views

Hendrix Genetics has officially opened a new $18.5m hatchery in Nebraska, creating 45 jobs, as it aims to expand its share of the market.

The new layer hatchery has a capacity to produce 24m female chicks per year.

Key contract growers located near the new hatchery will rear and house the birds during production. The company is already working with 8 contract growers in the Grand Island area who have invested in new barns with a capacity of 40,000 birds per barn.

The Grand Island contract growers will complete the new national production hub for Hendrix Genetics in the US, enabling the firm to meet another 10% of the total US layer market needs.

Ron Joerissen, Hendrix Genetics production director layers, said: The new hatchery signifies a major step in supplying the US layer market with top quality laying hens. We are dedicated to breed for the egg producing industry of today and tomorrow.

Nebraskas Governor Pete Ricketts described the plant as a great example of value-added agriculture.

It is not only a $20m investment here that will create between 40 to 50 jobs but it is going to allow area farmers to put up these barns for the eggs that will supply this hatchery and a diversified revenue stream for those farmers who are participating, he said.

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YHS Teacher Attends Genetics Workshop – Yankton Daily Press

Saturday, August 26th, 2017

Sanford Health and Harvard Medical School have collaborated to bring information and education about personal genetics and research to classrooms and communities in Massachusetts and South Dakota.

One such program the two facilities have created is the Personal Genetics Education Project (pgEd), which offers workshops that bring awareness and create community understanding about development in genetics and how they affect health.

Lindsay Kortan, who teaches ninth-grade physical science at Yankton High School (YHS), jumped at the chance to learn more about genetics by attending the pgEd Genetics and Social Justice Summer Institute in Brockton, Massachusetts this summer.

A member of the South Dakota Science Teachers Association, Kortan is also a Sanford ambassador and has done research with the organization for several years. It was through this involvement that she was invited to attend the weeklong pgEd conference.

"The setup was them showing (the attendees) their lesson plans, allowing us to experience what type of content is in the lesson and what kind of discussions/questions we might have in the classroom," she explained. "It covered a wide range of things, everything from the eugenics movement to ethics in genetics testing to personal genetics testing."

As someone who developed a strong interest in genetics through her studies at the University of South Dakota, all of this was right up Kortans alley.

"(Genetics) was one of my favorite topics to teach in a biology classroom," she said.

Prior to coming to YHS, Kortan had taught grades 10-12 science biology, physiology, physics and chemistry in the Bon Homme school district for five years.

She admitted that introducing what she learned at the conference into her current class will be difficult, but plans to spread her newfound information in other ways.

"Ive shared my knowledge with some of the other teachers and offered to help them incorporate it into their classrooms if theyre interested," she said.

She plans to be part of next summers workshop in Sioux Falls, which will be hosted by Sanford PROMISE and pgEd.

"From an education perspective, the pgED information is great for teaching our kids those critical-thinking and difficult life-decision questions they might have to encounter in their lifetime, especially now with the way genetic testing and technology is advancing," she said. "Its getting more prevalent in making decisions, even down to doctors looking at your genetic code to know what drugs they should prescribe to you, or whether the drug will be effective or not. Its important for kids to know that information before they get into those critical situations where they have to make an (important) decision. The process of going through that critical thinking and seeing different viewpoints is always a good thing in the classroom.

"Im currently pregnant, so some of those genetic questions that you get asked because of pregnancy and fertility treatments (that) I received really brought it to a personal level for me."

Follow @ReillyBiel on Twitter.

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YHS Teacher Attends Genetics Workshop - Yankton Daily Press

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Head to Head Survey: Signal Genetics (MGEN) & BioTelemetry (BEAT) – TrueBlueTribune

Saturday, August 26th, 2017

Signal Genetics (NASDAQ: MGEN) and BioTelemetry (NASDAQ:BEAT) are both small-cap medical companies, but which is the superior business? We will contrast the two companies based on the strength of their valuation, earnings, profitability, analyst recommendations, risk, institutional ownership and dividends.

Profitability

This table compares Signal Genetics and BioTelemetrys net margins, return on equity and return on assets.

Earnings & Valuation

This table compares Signal Genetics and BioTelemetrys top-line revenue, earnings per share and valuation.

BioTelemetry has higher revenue and earnings than Signal Genetics.

Insider and Institutional Ownership

16.5% of Signal Genetics shares are owned by institutional investors. Comparatively, 76.7% of BioTelemetry shares are owned by institutional investors. 44.4% of Signal Genetics shares are owned by company insiders. Comparatively, 9.6% of BioTelemetry shares are owned by company insiders. Strong institutional ownership is an indication that large money managers, hedge funds and endowments believe a stock will outperform the market over the long term.

Volatility & Risk

Signal Genetics has a beta of 1.91, meaning that its share price is 91% more volatile than the S&P 500. Comparatively, BioTelemetry has a beta of 0.76, meaning that its share price is 24% less volatile than the S&P 500.

Analyst Recommendations

This is a breakdown of recent ratings and price targets for Signal Genetics and BioTelemetry, as provided by MarketBeat.com.

Signal Genetics currently has a consensus price target of $23.00, suggesting a potential upside of 179.81%. BioTelemetry has a consensus price target of $45.75, suggesting a potential upside of 28.87%. Given Signal Genetics higher probable upside, equities analysts plainly believe Signal Genetics is more favorable than BioTelemetry.

Summary

BioTelemetry beats Signal Genetics on 7 of the 11 factors compared between the two stocks.

About Signal Genetics

Signal Genetics, Inc. is a commercial stage, molecular genetic diagnostic company. The Company is focused on providing diagnostic services that help physicians to make decisions concerning the care of cancer patients. The Companys diagnostic service is the Myeloma Prognostic Risk Signature (MyPRS) test. The MyPRS test is a microarray-based gene expression profile (GEP), assay that measures the expression level of specific genes and groups of genes that are designed to predict an individuals long-term clinical outcome/prognosis, giving a basis for personalized treatment options. The Companys MyPRS test provides a whole-genomic expression profile of a patients multiple myeloma (MM). The Company offers MyPRS test in its laboratory located in Little Rock, Arkansas. The Company is licensed to sell its test in all 50 states.

About BioTelemetry

BioTelemetry, Inc. (BioTelemetry), formerly CardioNet, Inc., provides cardiac monitoring services, cardiac monitoring device manufacturing, and centralized cardiac core laboratory services. The Company operates in three segments: patient services, product and research services. The patient services business segments principal focus is on the diagnosis and monitoring of cardiac arrhythmias or heart rhythm disorders, through its core Mobile Cardiac Outpatient Telemetry(MCOT), event and Holter services in a healthcare setting. The product business segment focuses on the development, manufacturing, testing and marketing of medical devices to medical companies, clinics and hospitals. The Companys research services focuses on providing cardiac safety monitoring services for drug and medical treatment trials in a research environment. In August 2012, the Company completed the acquisition of Cardiocore Lab, Inc. (Cardiocore).

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Genesis and Genetics | We look at Genetics in Genesis

Thursday, August 24th, 2017

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

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Heritability of IQ – Wikipedia

Thursday, August 24th, 2017

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

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Study reveals white nationalists’ reactions when genetics test results challenge their identity – UCLA Newsroom

Thursday, August 24th, 2017

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.

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Study reveals white nationalists' reactions when genetics test results challenge their identity - UCLA Newsroom

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

Thursday, August 24th, 2017

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

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

Thursday, August 24th, 2017

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

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Sycamores investigate genetics behind congenital heart defects – Indiana Statesman

Thursday, August 24th, 2017

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.

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Sycamores investigate genetics behind congenital heart defects - Indiana Statesman

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

Tuesday, August 22nd, 2017

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

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

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

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

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

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

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

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

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