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Myriad Genetics (MYGN) versus Quotient (QTNT) Head-To-Head …

Tuesday, June 26th, 2018

Myriad Genetics (NASDAQ: MYGN) and Quotient (NASDAQ:QTNT) are both medical companies, but which is the superior stock? We will contrast the two businesses based on the strength of their profitability, dividends, analyst recommendations, earnings, institutional ownership, risk and valuation.

Risk & Volatility

Myriad Genetics has a beta of 0.55, meaning that its stock price is 45% less volatile than the S&P 500. Comparatively, Quotient has a beta of 0.25, meaning that its stock price is 75% less volatile than the S&P 500.

This table compares Myriad Genetics and Quotients net margins, return on equity and return on assets.

Insider & Institutional Ownership

61.5% of Quotient shares are owned by institutional investors. 6.7% of Myriad Genetics shares are owned by company insiders. Comparatively, 29.0% of Quotient shares are owned by company insiders. Strong institutional ownership is an indication that endowments, large money managers and hedge funds believe a stock is poised for long-term growth.

Analyst Recommendations

This is a summary of current ratings and price targets for Myriad Genetics and Quotient, as reported by MarketBeat.

Myriad Genetics currently has a consensus price target of $30.91, suggesting a potential downside of 20.48%. Quotient has a consensus price target of $11.50, suggesting a potential upside of 30.68%. Given Quotients stronger consensus rating and higher probable upside, analysts plainly believe Quotient is more favorable than Myriad Genetics.

Earnings and Valuation

This table compares Myriad Genetics and Quotients gross revenue, earnings per share and valuation.

Myriad Genetics has higher revenue and earnings than Quotient. Quotient is trading at a lower price-to-earnings ratio than Myriad Genetics, indicating that it is currently the more affordable of the two stocks.

Summary

Myriad Genetics beats Quotient on 8 of the 13 factors compared between the two stocks.

About Myriad Genetics

Myriad Genetics, Inc., a molecular diagnostic company, focuses on developing and marketing novel predictive medicine, personalized medicine, and prognostic medicine tests worldwide. The company offers molecular diagnostic tests, including myRisk Hereditary Cancer, a DNA sequencing test for hereditary cancers; BRACAnalysis, a DNA sequencing test to assess the risk of developing breast and ovarian cancer; BART, a DNA sequencing test for hereditary breast and ovarian cancer; BRACAnalysis CDx, a DNA sequencing test for use as a companion diagnostic with the platinum based chemotherapy agents and poly ADP ribose inhibitor Lynparza; and Tumor BRACAnalysis CDx, a DNA sequencing test that is designed to be utilized to predict response to DNA damaging agents. It also provides COLARIS, a DNA sequencing test for colorectal and uterine cancer; COLARIS AP, a DNA sequencing test for colorectal cancer; Vectra DA, a protein quantification test for assessing the disease activity of rheumatoid arthritis; Prolaris, a RNA expression test for assessing the aggressiveness of prostate cancer; and EndoPredict, a RNA expression test for assessing the aggressiveness of breast cancer. In addition, the company offers myPath Melanoma, a RNA expression test for diagnosing melanoma; myChoice HRD, a companion diagnostic to measure three modes of homologous recombination deficiency; and GeneSight, a DNA genotyping test to optimize psychotropic drug selection for neuroscience patients. Further, it provides biomarker discovery, and pharmaceutical and clinical services to the pharmaceutical, biotechnology, and medical research industries; and operates an internal medicine emergency hospital primarily for internal medicine and hemodialysis. The company has collaboration with AstraZeneca for the development of an indication for BRACAnalysis CDx. Myriad Genetics, Inc. was founded in 1991 and is headquartered in Salt Lake City, Utah.

About Quotient

Quotient Limited, a commercial-stage diagnostics company, develops, manufactures, and commercializes conventional reagent products used for blood grouping in the transfusion diagnostics market worldwide. The company is developing MosaiQ, a proprietary technology platform, which provides tests for blood grouping and serological disease screening. It also develops, manufactures, and commercializes conventional reagent products for blood grouping, including antisera products that are used to identify blood-group antigens; reagent red blood cells, which enable the identification of blood-group antibodies; whole blood control products for use as daily quality assurance tests; and ancillary products that are used to support blood grouping. The company sells its products to donor collection agencies and testing laboratories, hospitals, independent patient testing laboratories, reference laboratories, blood banking operations, and other diagnostic companies, as well as to original equipment manufacturers. Quotient Limited was founded in 2007 and is based in Penicuik, the United Kingdom.

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genetics | History, Biology, Timeline, & Facts …

Thursday, June 21st, 2018

Genetics, study of heredity in general and of genes in particular. Genetics forms one of the central pillars of biology and overlaps with many other areas, such as agriculture, medicine, and biotechnology.

Since the dawn of civilization, humankind has recognized the influence of heredity and applied its principles to the improvement of cultivated crops and domestic animals. A Babylonian tablet more than 6,000 years old, for example, shows pedigrees of horses and indicates possible inherited characteristics. Other old carvings show cross-pollination of date palm trees. Most of the mechanisms of heredity, however, remained a mystery until the 19th century, when genetics as a systematic science began.

Genetics arose out of the identification of genes, the fundamental units responsible for heredity. Genetics may be defined as the study of genes at all levels, including the ways in which they act in the cell and the ways in which they are transmitted from parents to offspring. Modern genetics focuses on the chemical substance that genes are made of, called deoxyribonucleic acid, or DNA, and the ways in which it affects the chemical reactions that constitute the living processes within the cell. Gene action depends on interaction with the environment. Green plants, for example, have genes containing the information necessary to synthesize the photosynthetic pigment chlorophyll that gives them their green colour. Chlorophyll is synthesized in an environment containing light because the gene for chlorophyll is expressed only when it interacts with light. If a plant is placed in a dark environment, chlorophyll synthesis stops because the gene is no longer expressed.

Genetics as a scientific discipline stemmed from the work of Gregor Mendel in the middle of the 19th century. Mendel suspected that traits were inherited as discrete units, and, although he knew nothing of the physical or chemical nature of genes at the time, his units became the basis for the development of the present understanding of heredity. All present research in genetics can be traced back to Mendels discovery of the laws governing the inheritance of traits. The word genetics was introduced in 1905 by English biologist William Bateson, who was one of the discoverers of Mendels work and who became a champion of Mendels principles of inheritance.

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heredity

clear in the study of genetics. Both aspects of heredity can be explained by genes, the functional units of heritable material that are found within all living cells. Every member of a species has a set of genes specific to that species. It is this set of genes that provides

Although scientific evidence for patterns of genetic inheritance did not appear until Mendels work, history shows that humankind must have been interested in heredity long before the dawn of civilization. Curiosity must first have been based on human family resemblances, such as similarity in body structure, voice, gait, and gestures. Such notions were instrumental in the establishment of family and royal dynasties. Early nomadic tribes were interested in the qualities of the animals that they herded and domesticated and, undoubtedly, bred selectively. The first human settlements that practiced farming appear to have selected crop plants with favourable qualities. Ancient tomb paintings show racehorse breeding pedigrees containing clear depictions of the inheritance of several distinct physical traits in the horses. Despite this interest, the first recorded speculations on heredity did not exist until the time of the ancient Greeks; some aspects of their ideas are still considered relevant today.

Hippocrates (c. 460c. 375 bce), known as the father of medicine, believed in the inheritance of acquired characteristics, and, to account for this, he devised the hypothesis known as pangenesis. He postulated that all organs of the body of a parent gave off invisible seeds, which were like miniaturized building components and were transmitted during sexual intercourse, reassembling themselves in the mothers womb to form a baby.

Aristotle (384322 bce) emphasized the importance of blood in heredity. He thought that the blood supplied generative material for building all parts of the adult body, and he reasoned that blood was the basis for passing on this generative power to the next generation. In fact, he believed that the males semen was purified blood and that a womans menstrual blood was her equivalent of semen. These male and female contributions united in the womb to produce a baby. The blood contained some type of hereditary essences, but he believed that the baby would develop under the influence of these essences, rather than being built from the essences themselves.

Aristotles ideas about the role of blood in procreation were probably the origin of the still prevalent notion that somehow the blood is involved in heredity. Today people still speak of certain traits as being in the blood and of blood lines and blood ties. The Greek model of inheritance, in which a teeming multitude of substances was invoked, differed from that of the Mendelian model. Mendels idea was that distinct differences between individuals are determined by differences in single yet powerful hereditary factors. These single hereditary factors were identified as genes. Copies of genes are transmitted through sperm and egg and guide the development of the offspring. Genes are also responsible for reproducing the distinct features of both parents that are visible in their children.

In the two millennia between the lives of Aristotle and Mendel, few new ideas were recorded on the nature of heredity. In the 17th and 18th centuries the idea of preformation was introduced. Scientists using the newly developed microscopes imagined that they could see miniature replicas of human beings inside sperm heads. French biologist Jean-Baptiste Lamarck invoked the idea of the inheritance of acquired characters, not as an explanation for heredity but as a model for evolution. He lived at a time when the fixity of species was taken for granted, yet he maintained that this fixity was only found in a constant environment. He enunciated the law of use and disuse, which states that when certain organs become specially developed as a result of some environmental need, then that state of development is hereditary and can be passed on to progeny. He believed that in this way, over many generations, giraffes could arise from deerlike animals that had to keep stretching their necks to reach high leaves on trees.

British naturalist Alfred Russel Wallace originally postulated the theory of evolution by natural selection. However, Charles Darwins observations during his circumnavigation of the globe aboard the HMS Beagle (183136) provided evidence for natural selection and his suggestion that humans and animals shared a common ancestry. Many scientists at the time believed in a hereditary mechanism that was a version of the ancient Greek idea of pangenesis, and Darwins ideas did not appear to fit with the theory of heredity that sprang from the experiments of Mendel.

Before Gregor Mendel, theories for a hereditary mechanism were based largely on logic and speculation, not on experimentation. In his monastery garden, Mendel carried out a large number of cross-pollination experiments between variants of the garden pea, which he obtained as pure-breeding lines. He crossed peas with yellow seeds to those with green seeds and observed that the progeny seeds (the first generation, F1) were all yellow. When the F1 individuals were self-pollinated or crossed among themselves, their progeny (F2) showed a ratio of 3:1 (3/4 yellow and 1/4 green). He deduced that, since the F2 generation contained some green individuals, the determinants of greenness must have been present in the F1 generation, although they were not expressed because yellow is dominant over green. From the precise mathematical 3:1 ratio (of which he found several other examples), he deduced not only the existence of discrete hereditary units (genes) but also that the units were present in pairs in the pea plant and that the pairs separated during gamete formation. Hence, the two original lines of pea plants were proposed to be YY (yellow) and yy (green). The gametes from these were Y and y, thereby producing an F1 generation of Yy that were yellow in colour because of the dominance of Y. In the F1 generation, half the gametes were Y and the other half were y, making the F2 generation produced from random mating 1/4 Yy, 1/2 YY, and 1/4 yy, thus explaining the 3:1 ratio. The forms of the pea colour genes, Y and y, are called alleles.

Mendel also analyzed pure lines that differed in pairs of characters, such as seed colour (yellow versus green) and seed shape (round versus wrinkled). The cross of yellow round seeds with green wrinkled seeds resulted in an F1 generation that were all yellow and round, revealing the dominance of the yellow and round traits. However, the F2 generation produced by self-pollination of F1 plants showed a ratio of 9:3:3:1 (9/16 yellow round, 3/16 yellow wrinkled, 3/16 green round, and 1/16 green wrinkled; note that a 9:3:3:1 ratio is simply two 3:1 ratios combined). From this result and others like it, he deduced the independent assortment of separate gene pairs at gamete formation.

Mendels success can be attributed in part to his classic experimental approach. He chose his experimental organism well and performed many controlled experiments to collect data. From his results, he developed brilliant explanatory hypotheses and went on to test these hypotheses experimentally. Mendels methodology established a prototype for genetics that is still used today for gene discovery and understanding the genetic properties of inheritance.

Mendels genes were only hypothetical entities, factors that could be inferred to exist in order to explain his results. The 20th century saw tremendous strides in the development of the understanding of the nature of genes and how they function. Mendels publications lay unmentioned in the research literature until 1900, when the same conclusions were reached by several other investigators. Then there followed hundreds of papers showing Mendelian inheritance in a wide array of plants and animals, including humans. It seemed that Mendels ideas were of general validity. Many biologists noted that the inheritance of genes closely paralleled the inheritance of chromosomes during nuclear divisions, called meiosis, that occur in the cell divisions just prior to gamete formation.

It seemed that genes were parts of chromosomes. In 1910 this idea was strengthened through the demonstration of parallel inheritance of certain Drosophila (a type of fruit fly) genes on sex-determining chromosomes by American zoologist and geneticist Thomas Hunt Morgan. Morgan and one of his students, Alfred Henry Sturtevant, showed not only that certain genes seemed to be linked on the same chromosome but that the distance between genes on the same chromosome could be calculated by measuring the frequency at which new chromosomal combinations arose (these were proposed to be caused by chromosomal breakage and reunion, also known as crossing over). In 1916 another student of Morgans, Calvin Bridges, used fruit flies with an extra chromosome to prove beyond reasonable doubt that the only way to explain the abnormal inheritance of certain genes was if they were part of the extra chromosome. American geneticist Hermann Joseph Mller showed that new alleles (called mutations) could be produced at high frequencies by treating cells with X-rays, the first demonstration of an environmental mutagenic agent (mutations can also arise spontaneously). In 1931 American botanist Harriet Creighton and American scientist Barbara McClintock demonstrated that new allelic combinations of linked genes were correlated with physically exchanged chromosome parts.

In 1908 British physician Archibald Garrod proposed the important idea that the human disease alkaptonuria, and certain other hereditary diseases, were caused by inborn errors of metabolism, suggesting for the first time that linked genes had molecular action at the cell level. Molecular genetics did not begin in earnest until 1941 when American geneticist George Beadle and American biochemist Edward Tatum showed that the genes they were studying in the fungus Neurospora crassa acted by coding for catalytic proteins called enzymes. Subsequent studies in other organisms extended this idea to show that genes generally code for proteins. Soon afterward, American bacteriologist Oswald Avery, Canadian American geneticist Colin M. MacLeod, and American biologist Maclyn McCarty showed that bacterial genes are made of DNA, a finding that was later extended to all organisms.

A major landmark was attained in 1953 when American geneticist and biophysicist James D. Watson and British biophysicists Francis Crick and Maurice Wilkins devised a double helix model for DNA structure. This model showed that DNA was capable of self-replication by separating its complementary strands and using them as templates for the synthesis of new DNA molecules. Each of the intertwined strands of DNA was proposed to be a chain of chemical groups called nucleotides, of which there were known to be four types. Because proteins are strings of amino acids, it was proposed that a specific nucleotide sequence of DNA could contain a code for an amino acid sequence and hence protein structure. In 1955 American molecular biologist Seymour Benzer, extending earlier studies in Drosophila, showed that the mutant sites within a gene could be mapped in relation to each other. His linear map indicated that the gene itself is a linear structure.

In 1958 the strand-separation method for DNA replication (called the semiconservative method) was demonstrated experimentally for the first time by American molecular biologist Matthew Meselson and American geneticist Franklin W. Stahl. In 1961 Crick and South African biologist Sydney Brenner showed that the genetic code must be read in triplets of nucleotides, called codons. American geneticist Charles Yanofsky showed that the positions of mutant sites within a gene matched perfectly the positions of altered amino acids in the amino acid sequence of the corresponding protein. In 1966 the complete genetic code of all 64 possible triplet coding units (codons), and the specific amino acids they code for, was deduced by American biochemists Marshall Nirenberg and Har Gobind Khorana. Subsequent studies in many organisms showed that the double helical structure of DNA, the mode of its replication, and the genetic code are the same in virtually all organisms, including plants, animals, fungi, bacteria, and viruses. In 1961 French biologist Franois Jacob and French biochemist Jacques Monod established the prototypical model for gene regulation by showing that bacterial genes can be turned on (initiating transcription into RNA and protein synthesis) and off through the binding action of regulatory proteins to a region just upstream of the coding region of the gene.

Technical advances have played an important role in the advance of genetic understanding. In 1970 American microbiologists Daniel Nathans and Hamilton Othanel Smith discovered a specialized class of enzymes (called restriction enzymes) that cut DNA at specific nucleotide target sequences. That discovery allowed American biochemist Paul Berg in 1972 to make the first artificial recombinant DNA molecule by isolating DNA molecules from different sources, cutting them, and joining them together in a test tube. These advances allowed individual genes to be cloned (amplified to a high copy number) by splicing them into self-replicating DNA molecules, such as plasmids (extragenomic circular DNA elements) or viruses, and inserting these into living bacterial cells. From these methodologies arose the field of recombinant DNA technology that presently dominates molecular genetics. In 1977 two different methods were invented for determining the nucleotide sequence of DNA: one by American molecular biologists Allan Maxam and Walter Gilbert and the other by English biochemist Fred Sanger. Such technologies made it possible to examine the structure of genes directly by nucleotide sequencing, resulting in the confirmation of many of the inferences about genes originally made indirectly.

In the 1970s Canadian biochemist Michael Smith revolutionized the art of redesigning genes by devising a method for inducing specifically tailored mutations at defined sites within a gene, creating a technique known as site-directed mutagenesis. In 1983 American biochemist Kary B. Mullis invented the polymerase chain reaction, a method for rapidly detecting and amplifying a specific DNA sequence without cloning it. In the last decade of the 20th century, progress in recombinant DNA technology and in the development of automated sequencing machines led to the elucidation of complete DNA sequences of several viruses, bacteria, plants, and animals. In 2001 the complete sequence of human DNA, approximately three billion nucleotide pairs, was made public.

A time line of important milestones in the history of genetics is provided in the table.

Classical genetics, which remains the foundation for all other areas in genetics, is concerned primarily with the method by which genetic traitsclassified as dominant (always expressed), recessive (subordinate to a dominant trait), intermediate (partially expressed), or polygenic (due to multiple genes)are transmitted in plants and animals. These traits may be sex-linked (resulting from the action of a gene on the sex, or X, chromosome) or autosomal (resulting from the action of a gene on a chromosome other than a sex chromosome). Classical genetics began with Mendels study of inheritance in garden peas and continues with studies of inheritance in many different plants and animals. Today a prime reason for performing classical genetics is for gene discoverythe finding and assembling of a set of genes that affects a biological property of interest.

Cytogenetics, the microscopic study of chromosomes, blends the skills of cytologists, who study the structure and activities of cells, with those of geneticists, who study genes. Cytologists discovered chromosomes and the way in which they duplicate and separate during cell division at about the same time that geneticists began to understand the behaviour of genes at the cellular level. The close correlation between the two disciplines led to their combination.

Plant cytogenetics early became an important subdivision of cytogenetics because, as a general rule, plant chromosomes are larger than those of animals. Animal cytogenetics became important after the development of the so-called squash technique, in which entire cells are pressed flat on a piece of glass and observed through a microscope; the human chromosomes were numbered using this technique.

Today there are multiple ways to attach molecular labels to specific genes and chromosomes, as well as to specific RNAs and proteins, that make these molecules easily discernible from other components of cells, thereby greatly facilitating cytogenetics research.

Microorganisms were generally ignored by the early geneticists because they are small in size and were thought to lack variable traits and the sexual reproduction necessary for a mixing of genes from different organisms. After it was discovered that microorganisms have many different physical and physiological characteristics that are amenable to study, they became objects of great interest to geneticists because of their small size and the fact that they reproduce much more rapidly than larger organisms. Bacteria became important model organisms in genetic analysis, and many discoveries of general interest in genetics arose from their study. Bacterial genetics is the centre of cloning technology.

Viral genetics is another key part of microbial genetics. The genetics of viruses that attack bacteria were the first to be elucidated. Since then, studies and findings of viral genetics have been applied to viruses pathogenic on plants and animals, including humans. Viruses are also used as vectors (agents that carry and introduce modified genetic material into an organism) in DNA technology.

Molecular genetics is the study of the molecular structure of DNA, its cellular activities (including its replication), and its influence in determining the overall makeup of an organism. Molecular genetics relies heavily on genetic engineering (recombinant DNA technology), which can be used to modify organisms by adding foreign DNA, thereby forming transgenic organisms. Since the early 1980s, these techniques have been used extensively in basic biological research and are also fundamental to the biotechnology industry, which is devoted to the manufacture of agricultural and medical products. Transgenesis forms the basis of gene therapy, the attempt to cure genetic disease by addition of normally functioning genes from exogenous sources.

The development of the technology to sequence the DNA of whole genomes on a routine basis has given rise to the discipline of genomics, which dominates genetics research today. Genomics is the study of the structure, function, and evolutionary comparison of whole genomes. Genomics has made it possible to study gene function at a broader level, revealing sets of genes that interact to impinge on some biological property of interest to the researcher. Bioinformatics is the computer-based discipline that deals with the analysis of such large sets of biological information, especially as it applies to genomic information.

The study of genes in populations of animals, plants, and microbes provides information on past migrations, evolutionary relationships and extents of mixing among different varieties and species, and methods of adaptation to the environment. Statistical methods are used to analyze gene distributions and chromosomal variations in populations.

Population genetics is based on the mathematics of the frequencies of alleles and of genetic types in populations. For example, the Hardy-Weinberg formula, p2 + 2pq + q2 = 1, predicts the frequency of individuals with the respective homozygous dominant (AA), heterozygous (Aa), and homozygous recessive (aa) genotypes in a randomly mating population. Selection, mutation, and random changes can be incorporated into such mathematical models to explain and predict the course of evolutionary change at the population level. These methods can be used on alleles of known phenotypic effect, such as the recessive allele for albinism, or on DNA segments of any type of known or unknown function.

Human population geneticists have traced the origins and migration and invasion routes of modern humans, Homo sapiens. DNA comparisons between the present peoples on the planet have pointed to an African origin of Homo sapiens. Tracing specific forms of genes has allowed geneticists to deduce probable migration routes out of Africa to the areas colonized today. Similar studies show to what degree present populations have been mixed by recent patterns of travel.

Another aspect of genetics is the study of the influence of heredity on behaviour. Many aspects of animal behaviour are genetically determined and can therefore be treated as similar to other biological properties. This is the subject material of behaviour genetics, whose goal is to determine which genes control various aspects of behaviour in animals. Human behaviour is difficult to analyze because of the powerful effects of environmental factors, such as culture. Few cases of genetic determination of complex human behaviour are known. Genomics studies provide a useful way to explore the genetic factors involved in complex human traits such as behaviour.

Some geneticists specialize in the hereditary processes of human genetics. Most of the emphasis is on understanding and treating genetic disease and genetically influenced ill health, areas collectively known as medical genetics. One broad area of activity is laboratory research dealing with the mechanisms of human gene function and malfunction and investigating pharmaceutical and other types of treatments. Since there is a high degree of evolutionary conservation between organisms, research on model organismssuch as bacteria, fungi, and fruit flies (Drosophila)which are easier to study, often provides important insights into human gene function.

Many single-gene diseases, caused by mutant alleles of a single gene, have been discovered. Two well-characterized single-gene diseases include phenylketonuria (PKU) and Tay-Sachs disease. Other diseases, such as heart disease, schizophrenia, and depression, are thought to have more complex heredity components that involve a number of different genes. These diseases are the focus of a great deal of research that is being carried out today.

Another broad area of activity is clinical genetics, which centres on advising parents of the likelihood of their children being affected by genetic disease caused by mutant genes and abnormal chromosome structure and number. Such genetic counseling is based on examining individual and family medical records and on diagnostic procedures that can detect unexpressed, abnormal forms of genes. Counseling is carried out by physicians with a particular interest in this area or by specially trained nonphysicians.

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genetics | History, Biology, Timeline, & Facts ...

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Chimera (genetics) – Wikipedia

Wednesday, June 20th, 2018

This article is about genetic chimrism. For the cartilaginous fish, see Chimaera. For the mythological beast, see Chimera (mythology).

A genetic chimerism or chimera (also spelled chimaera) is a single organism composed of cells with distinct genotypes. In animals, this means an individual derived from two or more zygotes, which can include possessing blood cells of different blood types, subtle variations in form (phenotype), and if the zygotes were of differing sexes then even the possession of both female and male sex organs[1] (this is just one of many different ways that may result in intersexuality). Animal chimeras are produced by the merger of multiple fertilized eggs. In plant chimeras, however, the distinct types of tissue may originate from the same zygote, and the difference is often due to mutation during ordinary cell division. Normally, genetic chimerism is not visible on casual inspection; however, it has been detected in the course of proving parentage.[2]

Another way that chimerism can occur in animals is by organ transplantation, giving one individual tissues that developed from a different genome. For example, transplantation of bone marrow (an organ often not thought of as being such) often determines the recipient's ensuing blood type.

An animal chimera is a single organism that is composed of two or more different populations of genetically distinct cells that originated from different zygotes involved in sexual reproduction. If the different cells have emerged from the same zygote, the organism is called a mosaic. Chimeras are formed from at least four parent cells (two fertilised eggs or early embryos fused together). Each population of cells keeps its own character and the resulting organism is a mixture of tissues. Cases of human chimerism have been documented.[1]

This condition is either inherited or it is acquired through the infusion of allogeneic hematopoietic cells during transplantation or transfusion. In nonidentical twins, chimerism occurs by means of blood-vessel anastomoses. The likelihood of offspring being a chimera is increased if it is created via in vitro fertilisation.[3] Chimeras can often breed, but the fertility and type of offspring depends on which cell line gave rise to the ovaries or testes; varying degrees of intersex differences may result if one set of cells is genetically female and another genetically male.

Tetragametic chimerism is a form of congenital chimerism. This condition occurs through the fertilisation of two separate ova by two sperm, followed by aggregation of the two at the blastocyst or zygote stages. This results in the development of an organism with intermingled cell lines. Put another way, the chimera is formed from the merging of two nonidentical twins (a similar merging presumably occurs with identical twins, but as their genotypes are not significantly distinct, the resulting individual would not be considered a chimera). As such, they can be male, female, or have mixed intersex characteristics.[citation needed]

As the organism develops, it can come to possess organs that have different sets of chromosomes. For example, the chimera may have a liver composed of cells with one set of chromosomes and have a kidney composed of cells with a second set of chromosomes. This has occurred in humans, and at one time was thought to be extremely rare, though more recent evidence suggests that it is not the case.[1][4]

This is particularly true for the marmoset. Recent research shows most marmosets are chimeras, sharing DNA with their fraternal twins.[5] 95% of marmoset fraternal twins trade blood through chorionic fusions, making them hematopoietic chimeras.[6][7]

Most chimeras will go through life without realizing they are chimeras. The difference in phenotypes may be subtle (e.g., having a hitchhiker's thumb and a straight thumb, eyes of slightly different colors, differential hair growth on opposite sides of the body, etc.) or completely undetectable. Chimeras may also show, under a certain spectrum of UV light, distinctive marks on the back resembling that of arrow points pointing downwards from the shoulders down to the lower back; this is one expression of pigment unevenness called Blaschko's lines.[8]

Affected persons may be identified by the finding of two populations of red cells or, if the zygotes are of opposite sex, ambiguous genitalia and intersex alone or in combination; such persons sometimes also have patchy skin, hair, or eye pigmentation (heterochromia). If the blastocysts are of opposite sex, genitals of both sexes may be formed: either ovary and testis, or combined ovotestes, in one rare form of intersex, a condition previously known as true hermaphroditism.[citation needed]

Note that the frequency of this condition does not indicate the true prevalence of chimerism. Most chimeras composed of both male and female cells probably do not have an intersex condition, as might be expected if the two cell populations were evenly blended throughout the body. Often, most or all of the cells of a single cell type will be composed of a single cell line, i.e. the blood may be composed predominantly of one cell line, and the internal organs of the other cell line. Genitalia produce the hormones responsible for other sex characteristics.

Natural chimeras are almost never detected unless they exhibit abnormalities such as male/female or hermaphrodite characteristics or uneven skin pigmentation. The most noticeable are some male tortoiseshells and calicos (although most male tortoiseshells have an extra X chromosome responsible for the colouration) or animals with ambiguous sex organs.[citation needed]

The existence of chimerism is problematic for DNA testing, a fact with implications for family and criminal law. The Lydia Fairchild case, for example, was brought to court after DNA testing apparently showed that her children could not be hers. Fraud charges were filed against her and her custody of her children was challenged. The charge against her was dismissed when it became clear that Lydia was a chimera, with the matching DNA being found in her cervical tissue.[citation needed] Another case was that of Karen Keegan, who was also suspected (initially) of not being her children's biological mother, after DNA tests on her adult sons for a kidney transplant she needed seemed to show she wasn't their mother.[1][9]

The tetragametic state has important implications for organ or stem-cell transplantation. Chimeras typically have immunologic tolerance to both cell lines.[citation needed]

Microchimerism is the presence of a small number of cells that are genetically distinct from those of the host individual. Most people are born with a few cells genetically identical to their mothers' and the proportion of these cells goes down in healthy individuals as they get older. People who retain higher numbers of cells genetically identical to their mothers' have been observed to have higher rates of some autoimmune diseases, presumably because the immune system is responsible for destroying these cells and a common immune defect prevents it from doing so and also causes autoimmune problems. The higher rates of autoimmune diseases due to the presence of maternally-derived cells is why in a 2010 study of a 40-year-old man with scleroderma-like disease (an autoimmune rheumatic disease), the female cells detected in his blood stream via FISH (fluorescence in situ hybridization) were thought to be maternally-derived. However, his form of microchimerism was found to be due to a vanished twin, and whether or not microchimerism from a vanished twin might predispose individuals to autoimmune diseases as well is unknown.[10] Women often also have a few cells genetically identical to that of their children, and some people also have some cells genetically identical to that of their siblings (maternal siblings only, since these cells are passed to them because their mother retained them).[citation needed]

Chimerism occurs naturally in adult Ceratioid anglerfish and is in fact a natural and essential part of their life cycle. Once the male achieves adulthood, it begins its search for a female. Using strong olfactory (or smell) receptors, the male searches until it locates a female anglerfish. The male, less than an inch in length, bites into her skin and releases an enzyme that digests the skin of both his mouth and her body, fusing the pair down to the blood-vessel level. While this attachment has become necessary for the male's survival, it will eventually consume him, as both anglerfish fuse into a single hermaphroditic individual. Sometimes in this process more than one male will attach to a single female as a symbiote. They will all be consumed into the body of the larger female angler. Once fused to a female, the males will reach sexual maturity, developing large testicles as their other organs atrophy. This process allows for sperm to be in constant supply when the female produces an egg, so that the chimeric fish is able to have a greater number of offspring.[11]

Germline chimerism occurs when the germ cells (for example, sperm and egg cells) of an organism are not genetically identical to its own. It has recently been discovered that marmosets can carry the reproductive cells of their (fraternal) twin siblings, because of placental fusion during development. (Marmosets almost always give birth to fraternal twins.)[5][12][13]

In biological research, chimeras are artificially produced by selectively transplanting embryonic cells from one organism onto the embryo of another, and allowing the resultant blastocyst to develop. Chimeras are not hybrids, which form from the fusion of gametes from two species that form a single zygote with a combined genetic makeup. Nor are they Hybridomas which, as with hybrids, result from fusion of two species' cells into a single cell and artificial propagation of this cell in the laboratory. Essentially, in a chimera, each cell is from either of the parent species, whereas in a hybrid and hybridoma, each cell is derived from both parent species. "Chimera" is a broad term and is often applied to many different mechanisms of the mixing of cells from two different species.[citation needed]

As with cloning, the process of creating and implanting a chimera is imprecise, with the majority of embryos spontaneously terminating. Successes, however, have led to major advancements in the field of embryology, as creating chimeras of one species with different physical traits, such as colour, has allowed researchers to trace the differentiation of embryonic cells through the formation of organ systems in the adult individual.[citation needed]

The first known primate chimeras are the rhesus monkey twins, Roku and Hex, with each having six genomes. They were created by mixing cells from totipotent four cell blastocysts; although the cells never fused they worked together to form organs. It was discovered that one of these primates, Roku, was a sexual chimera; as four percent of Roku's blood cells contained two x chromosomes.[6]

A major milestone in chimera experimentation occurred in 1984, when a chimeric geep was produced by combining embryos from a goat and a sheep, and survived to adulthood.[21] The creation of the "geep" revealed several complexities to chimera development. In implanting a goat embryo for gestation in a sheep, the sheep's immune system would reject the developing goat embryo, whereas a "geep" embryo (sharing markers of immunity with both sheep and goats) was able to survive implantation in either of its parent species.[citation needed]

In August 2003, researchers at the Shanghai Second Medical University in China reported that they had successfully fused human skin cells and rabbit ova to create the first human chimeric embryos. The embryos were allowed to develop for several days in a laboratory setting, then destroyed to harvest the resulting stem cells.[22] In 2007, scientists at the University of Nevada School of Medicine created a sheep whose blood contained 15% human cells and 85% sheep cells.[23]

Chimeric mice are important animals in biological research, as they allow the investigation of a variety of biological questions in an animal that has two distinct genetic pools within it. These include insights into such problems as the tissue specific requirements of a gene, cell lineage, and cell potential. The general methods for creating chimeric mice can be summarized either by injection or aggregation of embryonic cells from different origins. The first chimeric mouse was made by Beatrice Mintz in the 1960s through the aggregation of eight-cell-stage embryos.[24] Injection on the other hand was pioneered by Richard Gardner and Ralph Brinster who injected cells into blastocysts to create chimeric mice with germ lines fully derived from injected embryonic stem cells (ES cells).[25] Chimeras can be derived from mouse embryos that have not yet implanted in the uterus as well as from implanted embryos. ES cells from the inner cell mass of an implanted blastocyst can contribute to all cell lineages of a mouse including the germ line. ES cells are a useful tool in chimeras because genes can be mutated in them through the use of homologous recombination, thus allowing gene targeting. Since this discovery occurred in 1988, ES cells have become a key tool in the generation of specific chimeric mice.[26]

The ability to make mouse chimeras comes from an understanding of early mouse development. Between the stages of fertilization of the egg and the implantation of a blastocyst into the uterus, different parts of the mouse embryo retain the ability to give rise to a variety of cell lineages. Once the embryo has reached the blastocyst stage, it is composed of several parts, mainly the trophectoderm, the inner cell mass, and the primitive endoderm. Each of these parts of the blastocyst gives rise to different parts of the embryo; the inner cell mass gives rise to the embryo proper, while the trophectoderm and primitive endoderm give rise to extra embryonic structures that support growth of the embryo.[27] Two- to eight-cell-stage embryos are competent for making chimeras, since at these stages of development, the cells in the embryos are not yet committed to give rise to any particular cell lineage, and could give rise to the inner cell mass or the trophectoderm. In the case where two diploid eight-cell-stage embryos are used to make a chimera, chimerism can be later found in the epiblast, primitive endoderm, and trophectoderm of the mouse blastocyst.[28][29]

It is possible to dissect the embryo at other stages so as to accordingly give rise to one lineage of cells from an embryo selectively and not the other. For example, subsets of blastomeres can be used to give rise to chimera with specified cell lineage from one embryo. The Inner Cell Mass of a diploid blastocyst for example can be used to make a chimera with another blastocyst of eight-cell diploid embryo; the cells taken from the inner cell mass will give rise to the primitive endoderm and to the epiblast in the chimera mouse.[30] From this knowledge, ES cell contributions to chimeras have been developed. ES cells can be used in combination with eight-cell-and two-cell-stage embryos to make chimeras and exclusively give rise to the embryo proper. Embryos that are to be used in chimeras can further be genetically altered in order to specifically contribute to only one part of chimera. An example is the chimera built off of ES cells and tetraploid embryos, tetraploid embryos which are artificially made by electrofusion of two two-cell diploid embryos. The tetraploid embryo will exclusively give rise to the trophectoderm and primitive endoderm in the chimera.[31][32]

There are a variety of combinations that can give rise to a successful chimera mouse and according to the goal of the experiment an appropriate cell and embryo combination can be picked; they are generally but not limited to diploid embryo and ES cells, diploid embryo and diploid embryo, ES cell and tetraploid embryo, diploid embryo and tetraploid embryo, ES cells and ES cells. The combination of embryonic stem cell and diploid embryo is a common technique used for the making of chimeric mice, since gene targeting can be done in the embryonic stem cell. These kinds of chimeras can be made through either aggregation of stem cells and the diploid embryo or injection of the stem cells into the diploid embryo. If embryonic stem cells are to be used for gene targeting to make a chimera, the following procedure is common: a construct for homologous recombination for the gene targeted will be introduced into cultured mouse embryonic stem cells from the donor mouse, by way of electroporation; cells positive for the recombination event will have antibiotic resistance, provided by the insertion cassette used in the gene targeting; and be able to be positively selected for.[33][34] ES cells with the correct targeted gene are then injected into a diploid host mouse blastocyst. These injected blastocysts are then implanted into a pseudo pregnant female surrogate mouse which will bring the embryos to term and give birth to a mouse whose germline is derived from the donor mouse's ES cells.[35] This same procedure can be achieved through aggregation of ES cells and diploid embryos, diploid embryos are cultured in aggregation plates in wells where single embryos can fit, to these wells ES cells are added the aggregates are cultured until a single embryo is formed and has progressed to the blastocyst stage, and can then be transferred to the surrogate mouse.[36]

The distinction between sectorial, mericlinal and periclinal plant chimeras are widely used.[37][38]

These are produced by grafting genetically different parents, different cultivars or different species (which may belong to different genera). The tissues may be partially fused together following grafting to form a single growing organism that preserves both types of tissue in a single shoot.[39] Just as the constituent species are likely to differ in a wide range of features, so the behavior of their periclinal chimeras is like to be highly variable.[40] The first such known chimera was probably the Bizzaria, which is a fusion of the Florentine citron and the sour orange. Well-known examples of a graft-chimera are Laburnocytisus 'Adamii', caused by a fusion of a Laburnum and a broom, and "Family" trees, where multiple varieties of apple or pear are grafted onto the same tree. Many fruit trees are cultivated by grafting the body of a sapling onto a rootstock.[citation needed]

These are chimeras in which the layers differ in their chromosome constitution. Occasionally chimeras arise from loss or gain of individual chromosomes or chromosome fragments owing to misdivision.[41] More commonly cytochimeras have simple multiple of the normal chromosome complement in the changed layer. There are various effects on cell size and growth characteristics.

These chimeras arise by spontaneous or induced mutation of a nuclear gene to a dominant or recessive allele. As a rule one character is affected at a time in the leaf, flower, fruit, or other parts.[citation needed]

These chimeras arise by spontaneous or induced mutation of a plastid gene, followed by the sorting-out of two kinds of plastid during vegetative growth. Alternatively, after selfing or nucleic acid thermodynamics, plastids may sort-out from a mixed egg or mixed zygote respectively. This type of chimera is recognized at the time of origin by the sorting-out pattern in the leaves. After sorting-out is complete, periclinal chimeras are distinguished from similar looking nuclear gene-differential chimeras by their non-mendelian inheritance. The majority of variegated-leaf chimeras are of this kind.[citation needed]

All plastid gene- and some nuclear gene-differential chimeras affect the color of the plasmids within the leaves, and these are grouped together as chlorophyll chimeras, or preferably as variegated leaf chimeras. For most variegation, the mutation involved is the loss of the chloroplasts in the mutated tissue, so that part of the plant tissue has no green pigment and no photosynthetic ability. This mutated tissue is unable to survive on its own but is kept alive by its partnership with normal photosynthetic tissue. Sometimes chimeras are also found with layers differing in respect of both their nuclear and their plastid genes.[citation needed]

There are multiple reasons to explain the occurrence of plant chimera during plant recovery stage:

(1) The process of shoot organogenesis starts form the multicellular origin.[42]

(2) The endogenous tolerance leads to the ineffectiveness of the weak selective agents.

(3) A self-protection mechanism (cross protection). Transformed cells serve as guards to protect the untransformed ones.[43]

(4) The observable characteristic of transgenic cells may be a transient expression of the marker gene. Or it may due to the presence of agrobacterium cells.[citation needed]

Untransformed cells should be easy to detect and remove to avoid chimeras. Because its extremely important to maintain the stable ability of the transgenic plants across different generations. Reporter genes such as GUS and Green Fluorescent Protein[44](GFP) are utilized in combination with plant selective markers (herbicide, antibody etc.) However, GUS expression depends on the plant development stage and GFP may be influenced by the green tissue autofluorescence. Quantitative PCR could be an alternative method for chimera detection.[45]

The US and Western Europe have strict codes of ethics and regulations in place that expressly forbid certain subsets of experimentation using human cells, though there is a vast difference in the regulatory framework.[46] Through the creation of human-chimera comes the question: where does society now draw the line of humanity? This question poses serious legal and moral issues, along with creating controversy. Chimpanzees, for example, are not offered any legal standing, and are put down if they pose a threat to humans. If a chimpanzee is genetically altered to be more similar to a human, it may blur the ethical line between animal and man. Legal debate would be the next step in the process to determine whether certain chimera should be granted legal rights.[47] Along with issues regarding the rights of chimera, individuals have expressed concern whether or not creating human-chimera diminishes the dignity of being human.[48]

In May 2008, a robust debate in the House of Commons of the United Kingdom on the ethics of creating chimeras with human stem cells led to the decision that embryos would be allowed to be made in laboratories, given that they would be destroyed within the first 14 days.[citation needed]

On 11 July 2005 a bill, The Human Chimera Prohibition Act, was introduced into the United States Congress by Senator Samuel Brownback, however it died in Congress sometime in the next year. The bill was introduced based on the findings that science has progressed to the point where the human and nonhuman species can be merged to create new forms of life. Because of this serious ethical issues arise as this blurs the line between humans and other animals, and according to the bill with this blurring of the lines comes a show of disrespect for human dignity. The final claim brought up in The Human Chimera Prohibition Act was that there is an increasing amount of zoonotic diseases and the creation of human-animal chimeras can allow these diseases to reach humans.[48] Since the bill's death in congress there has not been another attempt at setting regulations on chimera research in the United States.

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Artificial breeding bulls in demand as farmers improve genetics – Stuff.co.nz

Monday, September 4th, 2017

RURAL REPORTER

Last updated12:12, September 4 2017

LIC

A good looker, and the best performing bull at LIC is Sierra, a kiwicross bull. The 7-year-old bull might have 100,000 daughters in the next few years.

Father's Day was on Sunday, and many families got together,but there wasone super dad who foundit a struggle meeting all his offspring.

Sierra, one of LIC's top bulls, has fathered 1700 daughters (milking dairy cows).

"We expect that he will have 12,000 more daughters entering the national herd this year, and predict a further 100,000 over the next few years," said Simon Worth, LIC's livestock selection manager.

Farmers needed top quality genetics to get their cows producing top quality heifers in New Zealand and internationally.He said LIC owned24 of the top 30 artificial breeding (AB) bulls in the country, including Sierra - its top kiwicross bull.

READ MORE:

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*Genetics company LIC sells off its deer improvement business

"Bulls like Sierra are shaping the future of dairying in New Zealand. Our bulls provide three out of every four cows in the country, contributing $300 million towards the economy each year," said Dave Hale, LIC's national artificial breeding manager.

During the peak dairy cow mating season in spring LIC collectedsemen from its 73 elite bulls seven days a week, at itsNewstead farm near Hamilton.

Up to five million semen straws will be processed between now and Christmas, with the co-op's exclusive long last liquid semen diluent (LIC proprietary technology) enabling one bull ejaculate to average 7000 fresh semen straws for insemination.

Straws are sentfresh to a team of 775 AB technicians all over the country, for insemination into cows as early as that same afternoon. Top AB technicians inseminate up to 10,000 cows a year, or200-300 a day.

On the peak day in spring 120,000 semen straws are dispatched nationally, internationally the co-op exports one million frozen straws worldwide year-round.

"While only seven years old, Sierra is definitely one of our super dad bulls. Without them Kiwis probably wouldn't have their morning lattes," said Hale.

-Stuff

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Could genetics be the reason behind obesity? – SBS

Sunday, September 3rd, 2017

Twenty-five per cent of Australian adults are estimated to be clinically obese. The common view is that obesity is a self-inflicted condition. But one Melbourne clinic is challenging that perception.

Austin Health Obesity Physician, Professor Joe Proietto says he treats obesity as a chronic genetic disease.

"The view that obesity is genetic is controversial, however the evidence is very strong that there is a genetic predisposition to obesity," said Professor Proietto.

In a new SBS documentary Obesity Myth, doctors are trying to treat patients through a combination of diet, medication and surgery, tailored specifically for their genetic make-up.

Professor Proietto believes the environment has far less bearing on weight than genetics.

But Sydney University Obesity Research Director, Dr Nick Fuller says blaming genetics is only going to make the obesity crisis worse.

"We are finding more and more genes that contribute to obesity but genetics are not the reason for the increase in prevalence of obesity," said Dr Fuller.

Dr Fuller believes dieting is not the most effective solution.He believes weight loss should happen slowly, to trick the body into believing it is at a new set weight point.

"They need to lose a small amount of weight before the usual response to weight loss kicks in and maintain that weight so they can reprogram their set weight before going on to lose weight," said Dr Fuller.

Helene Jagdon has been trying to lose weight for 30 years. She has tried every fad diet and training regime in the book.

Only in the last few years under Dr Fuller's strategy has she been able to lose 14 kilograms and keep it off.

"He didn't make us feel like we were on a diet, he was just guiding us to what foods we can eat and not really saying what foods we can't eat.

"He was just saying if you feel like having a laksa, have a laksa, but maybe limit it to one takeaway treat in a week," said Ms Jagdon.

Now sitting at a comfortable 68 kilograms, Helene has maintained her passion for cooking and is inspiring people half her age to lose weight without dramatically changing their lives.

Preview: The Obesity Myth

The three-part documentary series The Obesity Myth starts September 4 on SBS at 7.30pm.

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Weight Loss Tip: It Ain’t Just About Genetics! – HuffPost

Sunday, September 3rd, 2017

Its a beautiful, sunny, fall-esque day here on Long Island, and I have something personal to share with you. After a nuclear stress test taken earlier in the week, my dads cardiologist recommended he check himself into the hospital on Thursday to have an angiogram. My dads had a couple of heart attacks in the past, and while his doctor didnt think it was anything too too serious, he wanted to make sure.

The angiogram showed a 99% blockage in one of his arteries. Because of this, three stents were put in to open it up. An additional stent is being put in as we speak, and if all goes well, he should be out by tomorrow. My dad is in good spirits and looks pretty good, so Im very optimistic that this will be the last we hear of this for a while.

That being said, something I heard his doctor tell him disturbed me quite a bit. Somehow, the topic of genetics came up in the conversation. My father was essentially told that this was all genetic, there was nothing he could do to improve his condition, and that once he gets out and he rests for about a week, he can resume all regular life activities.

The cardiac wing of the hospital was also feeding him garbage for his heart, like bread (derived from grains, which are inflammatory) and margarine (a trans fat, which is bad for the heart) but we wont even get into that today

While I know genetics can play a role in the acquisition of several diseases, theres a new study called EPIGENETICS. The premise behind this field of study is that based upon your chosen environment and your personal lifestyle habits, you can manipulate your genetic code, and either keep a negative genetic trait like heart disease dormant, or you can completely REVERSE that genes expression, and thus, never develop a hereditary disease in the first place!

Ive heard plenty of would-be clients over the years use genetics as an excuse for their being overweight. My parents, grandparents, aunts and uncles were all fat, so this is just something I have to deal with!

Often, when somebody is overweight, its due to poor diet. Plain and simple. Theres a small percentage of the population that has hormonal imbalances, and thus, theres a bit more to it than that. That being said, most hormone issues can be regulated (and even corrected!) by certain dietary strategies that will get those levels back to normal, and then enable them to both function and lose weight normally.

When the folks who blame genetics review their nutrition with me, Ill tell you one thing: It aint just geneticsIf its even genetics, at all! Their diets tend to be comprised of excessive amounts of sugar, grains and processed foods, which, when ingested in large quantities as they were in these instances, are ALL linked to an increased risk of obesity, Type-2 Diabetes, heart disease, various forms of cancer, and even neurological diseases like Parkinsons and Alzheimers!!

Whether youre dealing with weight issues, whether youre diabetic, or whether youre even suffering from a heart condition like my dad is, youre rarely too far gone!!! There are healthy dietary changes you can make that will not only help you in regulating these conditions, but also help in the REVERSAL of many of these conditions.

Moral of the Story: I was highly DISTURBED to hear this explanation given to my dad. Its never too late to change and improve the quality of your life. The question is: Whatre you going to do to change your circumstances?

pete@weightlossbypete.com

P.S. If you feel you need more help on the nutritional side, then youre definitely going to want to invest in my Food Guide and Healthy Recipe Book!

The Food Guide lays out the three phases of nutrition I use with my Permanent Weight Loss clients. Phase 1 gets you in the habit of making healthier choices, while Phase 2 really cleans up the frequency with which you eat healthier. Phase 3 is a strict macronutrient breakdown that will help expedite the process of weight loss, all while improving your health and making your body a well-oiled machine!

My Healthy Recipe Book includes 72 recipes spanning breakfast,lunch, dinner, snacks, appetizers and desserts. Im constantly adding to it, but these recipes are easy to make, simple and enable you to have your cake and eat it, too!

Normally, I sell each of these books for $10 a piece, but because Im feeling generous today, you can get BOTH for just $13.99!:-)

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Ancient Gut Genetic Core Program Finding May Lead to New … – Genetic Engineering & Biotechnology News

Sunday, September 3rd, 2017

Scientists from the Duke University School of Medicine say they have found a set of genes and regulatory elements in the intestinal lining that has stayed the same from fish to humans. They note that a good number of these genes are linked to human diseases, including inflammatory bowel disorders, diabetes, and obesity.

The research ("Genomic Dissection of Conserved Transcriptional Regulation in Intestinal Epithelial Cells"),which appears in PLOS Biology, marks fish as a model organism for studying how this old genetic information (covering over 420 million years of evolution) controls the development and dysfunction of the intestine.

"The intestinal epithelium serves critical physiologic functions that are shared among all vertebrates. However, it is unknown how the transcriptional regulatory mechanisms underlying these functions have changed over the course of vertebrate evolution. We generated genome-wide mRNA and accessible chromatin data from adult intestinal epithelial cells (IECs) in zebrafish, stickleback, mouse, and human species to determine if conserved IEC functions are achieved through common transcriptional regulation. We found evidence for substantial common regulation and conservation of gene expression regionally along the length of the intestine from fish to mammals and identified a core set of genes comprising a vertebrate IEC signature," write the investigators.

"We define an IEC transcriptional regulatory network that is shared between fish and mammals and establish an experimental platform for studying how evolutionarily distilled regulatory information commonly controls IEC development and physiology."

"Our research has uncovered aspects of intestinal biology that have been well conserved during vertebrate evolution, suggesting they are of central importance to intestinal health," said John F. Rawls, Ph.D., senior author of the study and associate professor of molecular genetics and microbiology. "By doing so, we have built a foundation for mechanistic studies of intestinal biology in nonhuman model systems like fish and mice that would be impossible to perform in humans alone."

According to Dr. Rawls, researchers for years have used animal models to collect information on intestinal epithelial cells that could help combat human diseases. But no one knew how alike these cells were across multiple species. Heand colleagues took a comparative biology approach to address this issue.

Research associate Colin R. Lickwar, Ph.D., and the team obtained genome-wide data from intestinal epithelial cells in four species: zebrafish, stickleback fish, mouse, and human. Dr. Lickwar then created maps for each of the species that showed both the activity level of all of the genes and the location of specific regulatory elements that turned the genes on and off.

The group found a surprising amount of similarity between the different vertebrate species. Dr. Lickwar identified a common set of geneslabeled an intestinal epithelial cell signaturesome of which had shared patterns of activity in specific regions along the length of the intestine. Many of these genes had previously been implicated in a variety of human diseases, and Drs. Lickwar and Rawls wanted to know if this conserved genetic signature was controlled by regulatory elements that might also be shared between species.

They took regulatory elements from fish, mice, and humans and put them into the zebrafish, which are transparent organisms. The scientists then looked under the microscope for color patterns to tell whether a green fluorescent protein or red fluorescent protein, which they had inserted along with the regulatory element, had been turned on in the intestine. They found that this was the case, indicating a very high level of conservation.

"Our findings suggest that intestinal epithelial cells use an ancient core program to do their job in the body of most vertebrates," said Dr. Lickwar, who is lead author of the study. "Now that we have identified this core program, we can more easily translate results back and forth between humans and zebrafish."

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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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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."

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YHS Teacher Attends Genetics Workshop - Yankton Daily Press

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

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

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