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99 Sentences With "monozygotic twins"

How to use monozygotic twins in a sentence? Find typical usage patterns (collocations)/phrases/context for "monozygotic twins" and check conjugation/comparative form for "monozygotic twins". Mastering all the usages of "monozygotic twins" from sentence examples published by news publications.

But the 14-week ultrasound showed they were different genders -- making it impossible for them to be monozygotic twins.
De Cramer and his colleagues conducted several tests on the pups, named Cullen and Romulus, and found that the two were indeed monozygotic twins.
They found that monozygotic twins (with nearly identical genetics) were more likely to have autism in common than dizygotic (or non-identical) twins who shared less in common genetically.
The Jealous Machines and Quazarz: Born On A Gangster Star aren't a part one/part two series, Butler says, but "monozygotic twins" that were recorded in different settings and situations.
Unlike monozygotic twins, dizygotic twins result from the fertilization of two eggs by two separate sperms within the same pregnancy. This causes the set of twins to have genetic variations, so their genetic information is unique from one another. Considering the pathological left handedness syndrome, it was also assumed that monozygotic twins have a higher prevalence for left handedness than dizygotic twins because monozygotic twins experience more birth complications than dizygotic twins. In studies conducted between 1924 and 1976 there were more left-handed monozygotic twins.
Comparison of zygote development in monozygotic and dizygotic twins. In the uterus, a majority of monozygotic twins (60–70%) share the same placenta but have separate amniotic sacs. In 18–30% of monozygotic twins each fetus has a separate placenta and a separate amniotic sac. A small number (1–2%) of monozygotic twins share the same placenta and amniotic sac.
Phenotypically concordant and discordant monozygotic twins display different DNA copy-number-variation profiles.
Monozygotic twins are genetically nearly identical and they are always the same sex unless there has been a mutation during development. The children of monozygotic twins test genetically as half-siblings (or full siblings, if a pair of monozygotic twins reproduces with another pair or with the same person), rather than first cousins. Identical twins do not have the same fingerprints however, because even within the confines of the womb, the fetuses touch different parts of their environment, giving rise to small variations in their corresponding prints and thus making them unique. Monozygotic twins always have the same genotype.
For example, monozygotic twins usually have exactly same genomes. Scientists have focused on comparison studies of such twins for evaluating the heritability of genes and the roles of epigenetics in divergences and similarities between monozygotic twins, and have found that epigenetics plays an important part in human behaviors, including the stress response.
Normally due to an environmental factor or the deactivation of different X chromosomes in female monozygotic twins, and in some extremely rare cases, due to aneuploidy, twins may express different sexual phenotypes, normally from an XXY Klinefelter syndrome zygote splitting unevenly. Monozygotic twins, although genetically very similar, are not genetically exactly the same. The DNA in white blood cells of 66 pairs of monozygotic twins was analyzed for 506,786 single-nucleotide polymorphisms known to occur in human populations. Polymorphisms appeared in 2 of the 33 million comparisons, leading the researchers to extrapolate that the blood cells of monozygotic twins may have on the order of one DNA-sequence difference for every 12 million nucleotides, which would imply hundreds of differences across the entire genome.
Among monozygotic twins, in extremely rare cases, twins have been born with different sexes (one male, one female). When monozygotic twins are born with different sexes it is because of chromosomal defects. The probability of this is so small that multiples having different sexes is universally accepted as a sound basis for in utero clinical determination that the multiples are not monozygotic. Another abnormality that can result in monozygotic twins of different sexes is if the egg is fertilized by a male sperm but during cell division only the X chromosome is duplicated.
A gene may become switched on, switched off, or could become partially switched on or off in an individual. This epigenetic modification is triggered by environmental events. Monozygotic twins can have markedly different epigenetic profiles. A study of 80 pairs of monozygotic twins ranging in age from three to 74 showed that the youngest twins have relatively few epigenetic differences.
Monozygotic twins provide information on epigenetic differences that are not from genetic factors. Epigenetic markers differ the most in monozygotic twins who spend time apart or have a very different medical history. As twins age, their methylation and acetylation of histone H3 and H4 increasingly vary. These marks are specific to the environmental changes between the twins and not changes in methylation from general aging.
Monozygotic twins are identical twins. Twin studies help to reveal epigenetic differences related to various aspects of psychology. In a small clinical study in humans published in 2008, epigenetic differences were linked to differences in risk-taking and reactions to stress in monozygotic twins. The study identified twins with different life paths, wherein one twin displayed risk-taking behaviours, and the other displayed risk-averse behaviours.
Monozygotic twins carry identical genomic information. Therefore, if they are discordant for a particular disease or phenotype it is likely a result of epigenetic differences. However, unless the twins are studied longitudinally it is impossible to determine if epigenetic variation is the cause of or consequence of disease. Another limitation is recruiting a large enough cohort of discordant monozygotic twins with the disease of interest.
An Isograft is a graft of tissue between two individuals who are genetically identical (i.e. monozygotic twins). Transplant rejection between two such individuals virtually never occurs, making isografts particularly relevant to organ transplanations; patients with organs from their identical twins are incredibly likely to receive the organs favorably and survive. Monozygotic twins have the same major histocompatibility complex, leading to the low instances of tissue rejection by the adaptive immune system.
According to the theory, genes play a strong role in the development of alcoholism. Twin studies, adoption studies, and artificial selection studies have shown that a person's genes can predispose them to developing alcoholism. Evidence from twin studies show that concordance rates for alcoholism are higher for monozygotic twins than dizygotic twins—76% for monozygotic twins and 61% for dizygotic twins. However, female twin studies demonstrate that females have much lower concordance rates than males.
The strong genetic component is borne out in studies on monozygotic twins, with a concordance of 38–55%, with an even higher concordance of circulating thyroid antibodies not in relation to clinical presentation (up to 80% in monozygotic twins). Neither result was seen to a similar degree in dizygotic twins, offering strong favour for high genetic aetiology. Hashimoto's thyroiditis is associated with CTLA-4 (cytotoxic T-lymphocyte antigen-4) gene polymorphisms. CTLA-4 downregulates.
Monozygotic twins also known as identical twins are siblings that share the same genetic information because of their prenatal development. Monozygotic twins result from the fertilization of one egg and the division of that single embryo forming two embryos. However, just because a set of twins share the same genetic information, it does not mean they will exhibit the same traits and behaviors. There are different versions of a gene, which are called alleles.
This study is not the first case of different phenotypes occurring between monozygotic twins. Possible causes of phenotypic variability include variations in the intrauterine environment, epigenetic differences, or chance effects.
Specifically, 15 percent of monozygotic twins were left-handed while 13 percent of dizygotic twins were left-handed. In another study the frequency of right-handed and left-handed pairs of dizygotic twins is about 23%, while twins with both individuals displaying left-handedness is less than 4% and the frequency of pairs of monozygotic twins in which only one twin is left-handed is about 21% and in which both twins are left-handed is less than 4%. However, there was no difference in the handedness frequency between monozygotic and dizygotic twins. Currently there is not much evidence to further prove the idea that monozygotic twins have a higher prevalence for left handedness using the pathological left-handedness syndrome because of the improvements within medicine causing a decrease in birth defects and complications.
A major disadvantage is the long timeline of the studies as well as the expense. Longitudinal studies using disease-discordant monozygotic twins gives the added benefit of ruling out genetic influences on epigenetic variation.
Synesthetic color experiences influence memory. Psychological Science, 13, 548-552.Smilek, D., Moffatt, B. A., Pasternak, J., White, B. N., Dixon, M. J., & Merikle, P. M. (2002). Synaesthesia: A case study of discordant monozygotic twins.
Monochorionic placentation occurs when monozygotic twins develop with only one placenta and bears a higher risk of complications during pregnancy. Abnormal placentation can lead to an early termination of pregnancy, for example in pre-eclampsia.
Regarding spontaneous or natural monozygotic twinning, a recent theory proposes that monozygotic twins are probably formed when a blastocyst contains two inner cell masses (ICM), each of which will lead to a separate fetus, rather than by the embryo splitting while hatching from the zona pellucida (the gelatinous protective coating around the blastocyst). Monozygotic twins may also be created artificially by embryo splitting. It can be used as an expansion of in vitro fertilization (IVF) to increase the number of available embryos for embryo transfer.
This heritable variation is estimated from heritability studies based on monozygotic twins. For example, it is known that 80-90% of variance in height can be explained by hereditary differences, but GWA studies only account for a minority of this variance.
There is some evidence that it affects the variance in IQ test findings among identical twins, that is, monochorionic identical twins display less IQ variance one from another than do dichorionic identical twins. There is weak evidence that monozygotic twins sharing a placenta have a higher concordance rate for schizophrenia than monozygotic twins with separate placentas. Sharing a placenta increases the risk for infection, and infection in pregnancy has been shown to be a risk factor for schizophrenia. Equally striking is evidence for increasing difference in genomic expression between identical twins as they are once again implicating environmental intercession.
Individual twin studies and meta-analyses of twin studies have estimated the heritability of risk for schizophrenia to be approximately 80% (this refers to the proportion of variation between individuals in a population that is influenced by genetic factors, not the degree of genetic determination of individual risk), but the heritability estimate varies from 41 to 87%. Concordance rates between monozygotic twins vary in different studies, approximately 50%; whereas dizygotic twins was 17%. Some twin studies have found rates as low as 11.0%-13.8% among monozygotic twins, and 1.8%-4.1% among dizygotic twins, however. Family studies indicate that the closer a person's genetic relatedness to a person with schizophrenia, the greater the likelihood of developing the disorder.
There is a great deal of evidence to show that schizophrenia is a heritable disease. One key piece of evidence is a twin study that showed that the likelihood of developing the disease is 53% for one member of monozygotic twins (twins with same genetic code), compared to the 15% for dizygotic twins, who don't share the exact DNA. Others question the evidence of heritability due to different definitions of schizophrenia and the similar environment for both twins."The Missing Gene: Psychiatry, Heredity, and the Fruitless Search for Genes" Author Jay Joseph The fact that even monozygotic twins don't share a 100% concordance rate suggests environmental factors play a role in the vulnerability and development of the disorder.
Monozygotic twins can develop differently, due to their genes being differently activated. More unusual are "semi-identical twins", also known as "sesquizygotic". , only two cases have been reported. These "half-identical twins" are hypothesized to occur when an unfertilized egg cleaves into two identical attached ova, both of which are viable for fertilization.
The monozygotic twins also chose spouses and best friends who were more similar to their co-twins' friends and spouses than did dizygotic twins. The authors said there was a substantial genetic contribution to these effects in the twins. Similarity to social partners was higher on more heritable characteristics than on less.
The rate of disease discordance between monozygotic twins is usually over 50%, including heritable diseases. This does not correlate to the disease prevalence rate. There are more phenotypic methylation differences in twins discordant for bipolar, schizophrenia, or systemic lupus erythematosus than in unrelated cases. There is no difference between twins discordant for rheumatoid arthritis or dermatomyositis.
Monozygotic twins who share a placenta can develop twin-to-twin transfusion syndrome. This condition means that blood from one twin is being diverted into the other twin. One twin, the 'donor' twin, is small and anemic, the other, the 'recipient' twin, is large and polycythemic. The lives of both twins are endangered by this condition.
If the parents are both right-handed, in dizygotic and monozygotic twins there is a 21% chance of one being left-handed. If one parent is left handed, in DZ and MZ twins there is a 57% chance of one being left-handed. If both parents are left-handed, it is almost certain one twin will be left-handed.
This condition is found in approximately one out of every 100,000 live births; studies produce rates from 1 in 68,741 to 1 in 97,807. It is 100 to 150 times more likely in identical (monozygotic) twins than in singletons or fraternal twins. Sirenomelia is not associated with any ethnic background, but fetuses with sirenomelia are more likely to have testes.
Due to the prevalence of synesthesia among the first-degree relatives of synesthetes, there is evidence that synesthesia might have a genetic basis, however the monozygotic twins case studies indicate there is an epigenetic component. Synesthesia might also be an oligogenic condition, with Locus heterogeneity, multiple forms of inheritance (including Mendelian in some cases), and continuous variation in gene expression.
No two humans are genetically identical. Even monozygotic twins (who develop from one zygote) have infrequent genetic differences due to mutations occurring during development and gene copy-number variation. Differences between individuals, even closely related individuals, are the key to techniques such as genetic fingerprinting. As of 2017, there are a total of 324 million known variants from sequenced human genomes.
The exact development of craniopagus parasiticus is not well known. However, it is known that the underdeveloped twin is a parasitic twin. Parasitic twins are known to occur in utero when monozygotic twins start to develop as an embryo, but the embryo fails to completely split. When this happens, one embryo will dominate development, while the other's development is severely altered.
Discordance, in genetics typically means that a similar trait is not shared between twin members. Studies of twins have shown that genetic traits of monozygotic twins are fully concordant whereas in dizygotic twins, half of genetic traits are concordant, while the other half are discordant. Discordant rates that are higher than concordant rates express the influence of the environment on twin traits.
Conjoined twins (or the once-commonly used term "siamese") are monozygotic twins whose bodies are joined together during pregnancy. This occurs when the zygote starts to split after day 12 following fertilization and fails to separate completely. This condition occurs in about 1 in 50,000 human pregnancies. Most conjoined twins are now evaluated for surgery to attempt to separate them into separate functional bodies.
Partial splitting of the primitive node and streak may result in formation of conjoined twins. These twins are classified according to the nature and degree of their union. Occasionally, monozygotic twins are connected only by a common skin bridge or by a common liver bridge. The type of twins formed depends on when and to what extent abnormalities of the node and streak occurred.
The mutations producing the differences detected in this study would have occurred during embryonic cell-division (after the point of fertilization). If they occur early in fetal development, they will be present in a very large proportion of body cells. Another cause of difference between monozygotic twins is epigenetic modification, caused by differing environmental influences throughout their lives. Epigenetics refers to the level of activity of any particular gene.
As of yet, evidence of its etiology has not been discovered and is not well understood. In 2011, a case of monozygotic twins with divergent ROHHAD phenotypes was reported. One twin was affected with ROHHAD and developed symptoms, while the other twin developed normally. This report questioned the theory that ROHHAD is genetically inherited, and the authors suggest that the disease may have an autoimmune or epigenetic etiology.
Subsequent advances in molecular biology have led to the current terminology of gastrointestinal stromal tumors (GISTs).Boccon-Gibod L, Boman F, Boudjemaa S, Fabre M, Leverger G, Carney AJ. "Separate occurrence of extra-adrenal paraganglioma and gastrointestinal stromal tumor in monozygotic twins: probable familial Carney syndrome." Pediatr Dev Pathol. 2004;7(4):380-4. However, there is limited evidence to suggest that the gastrointestinal stromal tumors (GIST) in Carney triad lack CD117 (c-kit) mutations (i.e.
The decidual plate is tightly attached to the chorion frondosum and goes on to form the actual placenta. Endometrium on the opposite side to the decidua basalis is the decidua parietalis. This fuses with the chorion laevae, thus filling up the uterine cavity.T.W. Sadler, Langman's Medical Embryology, 11th edition, Lippincott & Wilkins In the case of twins, dichorionic placentation refers to the presence of two placentas (in all dizygotic and some monozygotic twins).
Several circumstances have been identified that are associated with an increased risk of sleep paralysis. These include insomnia, sleep deprivation, an erratic sleep schedule, stress, and physical fatigue. It is also believed that there may be a genetic component in the development of RISP, because there is a high concurrent incidence of sleep paralysis in monozygotic twins. Sleeping in the supine position has been found an especially prominent instigator of sleep paralysis.
The many causes of scoliosis include neuromuscular problems and inherited diseases or conditions caused by the environment. An estimated 65% of scoliosis cases are idiopathic, about 15% are congenital, and about 10% are secondary to a neuromuscular disease. About 38% of variance in scoliosis risk is due to genetic factors, and 62% is due to the environment. The genetics are likely complex, however, given the inconsistent inheritance and discordance among monozygotic twins.
Genetic and hereditary causes are being considered and several epidemiologic findings indicate considerable genetic influence especially for early onset cases. First degree relatives have a 2.5-fold risk, and nearly 6-fold risk when considering early onset cases. Monozygotic twins have double concordance rate for hysterectomy compared to dizygotic twins. Expansion of uterine fibroids occurs by a slow rate of cell proliferation combined with the production of copious amounts of extracellular matrix.
Einar Kringlen (born 6 June 1931) is a Norwegian physician and psychiatrist. He was born in Høyanger; the son of teachers Andreas Kringlen and Enbjørg Lotsberg. Among his early research works are Schizophrenia in male monozygotic twins from 1964, and his thesis Heredity and environment in the functional psychoses from 1967. He was professor at the University of Bergen from 1970 to 1971, and at the University of Oslo from 1977 to 2001.
Twin studies manipulate the environmental factors of behavior by examining if identical twins raised apart are different from twins raised together. Before the advancement of molecular genetics, twin studies were almost the only mode of investigation of genetic influences on personality. Heritability was estimated as twice the difference between the correlation for identical, or monozygotic, twins and that for fraternal, or dizygotic, twins. Early studies indicated that personality was fifty percent genetic.
New York: Wiley-Liss, p. 23. . There seems to be some variation in usage of this term. #Transferred components are immune cells and autologous as above. #Transfer of immune cells is made between different individuals of monozygotic twins in human or of the same pure line in experimental animals from immunologically sensitized to naive host, where transferred cells are engrafted without rejection or GVHD in the new host.Tada T, Taniguchi M, Okumura Y, Miyasaka M, eds. (1993).
Esteller works in the field of epigenetics of health and disease. Starting from identical genetic sequences, changes in histone modifications and DNA methylation can produce organisms with different features and distinct susceptibility to sickness. An example is monozygotic twins. To have a complete picture of what is going on with the epigenetic tapestry of our cells, Esteller has advocated the development of a comprehensive Human Epigenome Project (HEP) to map all the epigenetic marks in our genetic material.
Monozygotic, or identical, twins share 100% of their genes, while dizygotic, or fraternal, twins share on average 50% of their genes. The classic twin study compares monozygotic and dizygotic twins. If the monozygotic twins resemble each other much more closely than the dizygotic twins, then it is likely that genetics play a strong role in the development of the trait of interest. These studies showed that the genetic influences on obsessive- compulsive symptoms were 45 to 65% in children.
Identical twins have identical genomes in the immediate aftermath of twinning. Two-thirds of monozygotic twins share the same placenta, arising by cleavage before the fourth day of development; the other third have separate placentas because cleavage has taken place after the fourth day after choriogenesis has begun. Placentas vary with respect to the transport of nutrients and hormones, a variance that may influence epigenesis. For example, the pattern of X chromosome inactivation is affected by placental status.
In a number of publications, Schönemann argued that the statistical heritability estimates used in most twin studies rest on restrictive assumptions which are usually not tested, and if they are, often are found to be violated by the data.Schönemann, P. H. & Schönemann, R. D. (1994). Environmental versus genetic models for Osborne's personality data on identical and fraternal twins. Cahiers de Psychologie Cognitive – Current Psychology of Cognition 13, 141–167: He argued that this was true for the monozygotic twins raised apart vs.
Just as all researched human behavioural phenotypes are influenced by genes (i.e., are heritable), all such phenotypes are also influenced by the environment. The basic fact that monozygotic twins are genetically identical but are never perfectly concordant for psychiatric disorder or perfectly correlated for behavioural traits, indicates that the environment shapes human behaviour. The nature of this environmental influence, however, is such that it tends to make individuals in the same family more different from one another, not more similar to one another.
Referencing the mean proportions of left handedness singletons are 8.5 percent, dizygotic twins are 14 percent and monozygotic twins are 14.5 percent. Using this data, it is theorized that twins have higher prevalence for left handedness because of prenatal complications. For example, the pathological left-handedness syndrome has been speculated to contribute to why twins having a higher prevalence for left handedness. Pathological left-handedness syndrome states that when an injury occurs during early development it effects lateralization and ultimately handedness.
Epigenetic alterations arising during the lifetime of monozygotic twins in Alu repeats resulted in an increase in genomic s instability, and consequently cause insulin resistance and type 2 diabetes. show that methylation levels at all four CpG sites displayed an increase in Alu methylation. This study provides the first evidence that alteration in global DNA hypermethylation is associated with increased risk of IR independent of established risk factors. Because epigenetic modifications are possibly reversible, this research suggests the potential for lifestyle or therapeutic interventions for insulin resistance.
Russell, Wells, and Rushton (1985) reanalyzed several previous studies on similarities between spouses and concluded there is higher similarity on the more heritable characteristics. Rushton examined blood group genes and found that sexually interacting couples had more similar blood group genes than randomly paired individuals. Rushton and Bons (2005) examined personality, attitude, and demographic characteristics for similarity among different groups of people. Monozygotic twins resembled one another (r = 0.53) more than dizygotic twins (r = 0.32), pairs of spouses (r = 0.32), and pairs of best friends (r = 0.20).
Lee Anne Thompson is an American psychology professor known for her work in behavior genetics and the biological processes involved in intelligence. Thompson earned her B.A. from Case Western Reserve University in 1982, then attended University of Colorado at Boulder, earning an M.A. in 1985 and her Ph.D. in 1987. She currently teaches at Case Western and is on the editorial board of Intelligence. Thompson co-authored a widely cited twin study on communication disorders which found higher concordance in monozygotic twins than dizygotic twins.
Epigenetic changes may help to facilitate the development and maintenance of eating disorders via influences in the early environment and throughout the life- span. Pre-natal epigenetic changes due to maternal stress, behaviour and diet may later predispose offspring to persistent, increased anxiety and anxiety disorders. These anxiety issues can precipitate the onset of eating disorders and obesity, and persist even after recovery from the eating disorders. Epigenetic differences accumulating over the life-span may account for the incongruent differences in eating disorders observed in monozygotic twins.
Critics of twin studies argue that they are based on false or questionable assumptions, including that monozygotic twins share 100% of their genes and the equal environments assumption. On this basis, critics contend that twin studies tend to generate inflated estimates of heritability due to biological confounding factors and consistent underestimation of environmental variance. Other critics take a more moderate stance, arguing that the equal environments assumption is typically inaccurate, but that this inaccuracy tends to have only a modest effect on heritability estimates.
For current fiscally available testing, "identical" twins cannot be easily differentiated by the most common DNA testing, but it has been shown to be possible. While other siblings (including fraternal twins) share about 50% of their DNA, monozygotic twins share virtually 99.99%. Beyond these more recently discovered twinning-event mutation disparities, since 2008 it has been known that people who are identical twins also each have their own set of copy number variants, which can be thought of as the number of copies they each personally exhibit for certain sections of DNA.
However, dizygotic twins may also look very different from each other (for example, be of opposite sexes). Studies show that there is a genetic proclivity for dizygotic twinning. However, it is only the mother who has any effect on the chances of having such twins; there is no known mechanism for a father to cause the release of more than one ovum. Dizygotic twinning ranges from six per thousand births in Japan (similar to the rate of monozygotic twins) to 14 and more per thousand in some African countries.
Monozygotic twins had the most overlap in their peer networks (82%), followed by same-sex dizygotic twins (67%), same-sex virtual twins (e.g., unrelated peers matched on certain characteristics; 62%), friend-friend pairs (48%), opposite-sex dizygotic twins (42%), same-sex full siblings (39%), opposite sex virtual twins (37%), and opposite-sex full siblings (27%). Genetics, sex (same- or opposite-sex), age, and relationship intimacy affected rates of peer overlap. Another example used pairs of corporations engaged in a business alliance as the focal unit, and found that the more common partners (i.e.
Some of the susceptibility genes may be population specific. Genetic studies of the rates of disease in families supports the genetic basis of this disease with a heritability of >66%. Identical (monozygotic) twins were found to share susceptibility to the disease at >35% rate compared to fraternal (dizygotic) twins and other full siblings who only showed a 2–5% concordance in shared inheritance. Since SLE is associated with many genetic regions, it is likely an oligogenic trait, meaning that there are several genes that control susceptibility to the disease.
Hypothetically, global hypomethylation should be associated with global increases in transcription, since CpG islands are most prevalent in gene promoters; gene-specific hypermethylation, however, would indicate that these hypermethylated genes are repressed by the methylation marks. Generally, repressive hypermethylation of genes related to learning and memory has been observed in conjunction with derepressive hypomethylation of neuroinflammatory genes and genes related to pathological expression of Alzheimer's disease. Reduced methylation has been found in the long-term memory-associated temporal neocortex neurons in monozygotic twins with Alzheimer’s disease compared to the healthy twin.
Epigenetics can be studied and researched through various methods. One of the most common methods is looking at postmortem brain tissue of patients with schizophrenia and analyzing them for biomarkers. Other common methods include tissue culture studies of neurons, genome-wide analysis of non-brain cells in living patients (see PBMC), and transgenic and schizophrenic animal models. Other studies that are currently being done or that can be done in the future include longitudinal studies of patients, "at-risk" populations, and monozygotic twins, and studies that examine specific gene-environment interactions and epigenetic effects.
Like other mammals, humans have an XY sex-determination system, so that females have the sex chromosomes XX and males have XY. No two humans—not even monozygotic twins—are genetically identical. Genes and environment influence human biological variation in visible characteristics, physiology, disease susceptibility and mental abilities. The exact influence of genes and environment on certain traits is not well understood. Compared to the great apes, human gene sequences—even among African populations—are remarkably homogeneous. On average, genetic similarity between any two humans is 99.5%-99.9%.
The influence that genetics has had on a variety of individual differences is well documented. Some research suggests genetics also play a role in the intrinsic, direct experiences of job satisfaction like challenge or achievement (as opposed to extrinsic, environmental factors like working conditions). One experiment used sets of monozygotic twins, reared apart, to test for the existence of genetic influence on job satisfaction. While the results indicate the majority of the variance in job satisfaction was due to environmental factors (70%), genetic influence is still a minor factor.
This skewing can then be inherited by progeny cells, or increased by secondary selection. The X-chromosome controlling element (Xce) gene in mice has been found to influence genetically mediated skewing. It is unknown whether a similar gene plays a role in human X-inactivation, although a 2008 study found that skewing in humans is mostly caused by secondary events rather than a genetic tendency. There is a much higher concordance rate in genetically identical (monozygotic) twins compared to non-identical (dizygotic) twins, which suggests a strong genetic input.
Twin studiesClassical Twin Studies and Beyond, www.nature.com provide a way to understand how genotype affects an observable characteristic (called a phenotype). In short, identical (monozygotic) twins carry the same alleles for 100% of their genes whereas fraternal (dizygotic) twins will carry different alleles at 50% of the genes for which their parents had different genotypes. So if some characteristic (say, depression) that is observed in one identical twin is always observed in the other one, but this does not hold for fraternal twins, then one can conclude that heredity plays an important role in causing the condition.
Over time, this can result in measurable differences between biological and chronological age. Epigenetic changes have been found to be reflective of lifestyle and may act as functional biomarkers of disease before clinical threshold is reached. A more recent study, where 114 monozygotic twins and 80 dizygotic twins were analyzed for the DNA methylation status of around 6000 unique genomic regions, concluded that epigenetic similarity at the time of blastocyst splitting may also contribute to phenotypic similarities in monozygotic co-twins. This supports the notion that microenvironment at early stages of embryonic development can be quite important for the establishment of epigenetic marks.
Non- conjoined monozygotic twins form up to day 14 of embryonic development, but when twinning occurs after 14 days, the twins will likely be conjoined. Some argue that an early embryo cannot be a person because "If every person is an individual, one cannot be divided from oneself." However, Fr. Norman Ford stated that "the evidence would seem to indicate not that there is no individual at conception, but that there is at least one and possibly more." He went on to support the idea that, similar to processes found in other species, one twin could be the parent of the other asexually.
It removes the possible influence of dominance and epistatic effects which, if present, will tend to make monozygotic twins more similar than dizygotic twins and mask the influence of shared environmental effects. This is a limitation of the twin design for estimating c^2. However, the general conclusion that shared environmental effects are negligible does not rest on twin studies alone. Adoption research also fails to find large (c^2) components; that is, adoptive parents and their adopted children tend to show much less resemblance to one another than the adopted child and his or her non-rearing biological parent.
Pillard is also well known for a series of studies he coauthored with the psychologist J. Michael Bailey, which examined the rate of concordance of sexual identity among monozygotic twins, dizygotic twins of the same sex, non- twin siblings of the same sex, and adoptive siblings of the same sex. In all studies they found rates of concordance variantly consistent with the hypothesis that homosexuality has a significant genetic component. The Council for Responsible Genetics and other researchers have criticized this work for using a self-selected sample, a problem which later studies have attempted to remedy.
The genetic mechanism of synesthesia has long been debated. Due to the prevalence of synesthesia among the first-degree relatives of synesthetes, there is evidence that synesthesia might have a genetic basis, however the monozygotic twins case studies indicate there is an epigenetic component. Synesthesia might also be an oligogenic condition, with locus heterogeneity, multiple forms of inheritance (including Mendelian in some cases), and continuous variation in gene expression. It has been found that women have a higher chance of developing Synesthesia, and in the UK, females are 8 times more likely to have it than men (reasons are unknown).
Additionally, the mitochondria in the cytoplasm also contains DNA and during SCNT this mitochondrial DNA is wholly from the cytoplasmic donor's egg, thus the mitochondrial genome is not the same as that of the nucleus donor cell from which it was produced. This may have important implications for cross-species nuclear transfer in which nuclear-mitochondrial incompatibilities may lead to death. Artificial embryo splitting or embryo twinning, a technique that creates monozygotic twins from a single embryo, is not considered in the same fashion as other methods of cloning. During that procedure, a donor embryo is split in two distinct embryos, that can then be transferred via embryo transfer.
The exact cause of the condition is unknown. Although various theories indicate incomplete separation of monozygotic twins as an etiological factor, abnormal adherence between the ectoderm and endoderm during gastrulation, polytopic primary developmental field defects, somatic and germ line mutations in developmental genes, and damage to the caudal cell mass and posterior gut have also been linked to cause structural anomalies in the caudal region. It is speculated that the condition is related to the HOX gene, namely HOX10 and HOX11. Normally coding for the mammalian appendicular and axial skeleton, misexpression of the genetic factors could lead to abnormal proliferation of the caudal mesenchyme.
Monozygotic twinning occurs in birthing at a rate of about 3 in every 1000 deliveries worldwide (about 0.3% of the world population). The likelihood of a single fertilization resulting in monozygotic twins is uniformly distributed in all populations around the world. This is in marked contrast to dizygotic twinning, which ranges from about six per thousand births in Japan (almost similar to the rate of identical twins, which is around 4–5) to 15 and more per thousand in some parts of India and up to over 20 in some Central African countries. The exact cause for the splitting of a zygote or embryo is unknown.
A longitudinal study found that obstetric complications involving hypoxia were one factor associated with neurodevelopmental impairments in childhood and with the later development of schizophreniform disorders. Fetal hypoxia has been found to predict unusual movements at age 4 (but not age 7) among children who go on to develop schizophrenia, suggesting that its effects are specific to the stage of neurodevelopment. A Japanese case study of monozygotic twins discordant for schizophrenia (one has the diagnosis while the other does not) draws attention to their different weights at birth and concludes hypoxia may be the differentiating factor. The unusual functional laterality in speech production (e.g.
In the Minnesota Study of Twins Reared Apart, monozygotic twins separated shortly after birth were reunited in adulthood. These adopted, reared-apart twins were as similar to one another as were twins reared together on a wide range of measures including general cognitive ability, personality, religious attitudes, and vocational interests, among others. Approaches using genome- wide genotyping have allowed researchers to measure genetic relatedness between individuals and estimate heritability based on millions of genetic variants. Methods exist to test whether the extent of genetic similarity (aka, relatedness) between nominally unrelated individuals (individuals who are not close or even distant relatives) is associated with phenotypic similarity.
That is, estimates of shared environmental effects (c^2) in human studies are small, negligible, or zero for the vast majority of behavioural traits and psychiatric disorders, whereas estimates of non-shared environmental effects (e^2) are moderate to large. From twin studies c^2 is typically estimated at 0 because the correlation (r_{MZ}) between monozygotic twins is at least twice the correlation (r_{DZ}) for dizygotic twins. When using the Falconer variance decomposition (1.0 = a^2 + c^2 + e^2) this difference between monozygotic and dizygotic twin similarity results in an estimated c^2=0. It is important to note that the Falconer decomposition is simplistic.
During the early development of monozygotic twins, the time in which the embryo divide have an impact on placentation. If the split of the embryo occurs within three days of fertilization, two individual placentas are formed resulting in monozygotic dichorionic twins. If the split of the embryo occurs between 3 and 12 days after fertilization, a placenta will be shared between the offspring resulting in monozygotic monochorionic twins. Since the zygote of monozygotic monochorionic twins occurs after the establishment of an axis of bilateral symmetry, it was theorized that opposite handedness within the same pair of twins are more frequent than in monozygotic dichorionic twins because of mirror imaging.
The fact that some people affected with this disease have circulating antinuclear antibodies in their serum supports the theory that Parry–Romberg syndrome may be an autoimmune disease, specifically a variant of localized scleroderma. Several instances have been reported where more than one member of a family has been affected, prompting speculation of an autosomal dominant inheritance pattern. However, there has also been at least one report of monozygotic twins in which only one of the twins was affected, casting doubt on this theory. Further, the National Organization for Rare Disorders has stated there is currently no evidence that Parry–Romberg syndrome is genetic or that it can be passed on to children.
Evidence for the genetic basis of facial recognition abilities in the general population, however, comes from studies on face perception in twin participants by Wilmer, J. B. et al. in 2009, in which the facial recognition scores on the Cambridge Face Memory test were twice as similar for monozygotic twins in comparison to dizygotic twins. This finding was supported by a twin study on the genetic bases of facial recognition by Zhu, Q. et al. in (2009) which found a similar difference in facial recognition scores when comparing monozygotic and dizygotic twins and Shakeshaft, N. G. & Plomin, R. (2015), which determined the heritability of facial recognition to be approximately 61%, using a similar set of twin studies.
Moreover, since there are about 12 million monozygotic twins on Earth, the theoretical probability is not accurate. In practice, the risk of contaminated-matching is much greater than matching a distant relative, such as contamination of a sample from nearby objects, or from left-over cells transferred from a prior test. The risk is greater for matching the most common person in the samples: Everything collected from, or in contact with, a victim is a major source of contamination for any other samples brought into a lab. For that reason, multiple control-samples are typically tested in order to ensure that they stayed clean, when prepared during the same period as the actual test samples.
DNA sequence differences that would be abundant in a singleton-based study do not interfere with the analysis. Environmental differences can produce long-term epigenetic effects, and different developmental monozygotic twin subtypes may be different with respect to their susceptibility to be discordant from an epigenetic point of view. A high-throughput study, which denotes technology that looks at extensive genetic markers, focused on epigenetic differences between monozygotic twins to compare global and locus-specific changes in DNA methylation and histone modifications in a sample of 40 monozygotic twin pairs. In this case, only healthy twin pairs were studied, but a wide range of ages was represented, between 3 and 74 years.
For example, in one approach to twin studies, researchers compare the personality scores of monozygotic (MZ) or identical twins reared together to dizygotic (DZ) or fraternal twins reared together. Because both types of twins in this design are reared together, all twin pairs are regarded as having shared a 100% common environment. In contrast, the monozygotic twins share 100% of their genes whereas the dizygotic twins only share about 50% of their genes. Therefore, for any given personality trait, it is possible to parcel out genetic influences by first obtaining the MZ correlation (reflecting 100% common environment and 100% shared genes) and subtracting the DZ correlation (reflecting 100% common environment and 50% shared genes).
Alleles have identity by type (IBT) when they have the same phenotypic effect or, if applied to a variation in the composition of DNA such as a single nucleotide polymorphism, when they have the same DNA sequence. Alleles that are identical by type fall into two groups; those that are identical by descent (IBD) because they arose from the same allele in an earlier generation; and those that are non-identical by descent (NIBD) because they arose from separate mutations. NIBD can also be identical by state (IBS) though, if they share the same mutational expression but not through a recent common ancestor. Parent-offspring pairs share 50% of their genes IBD, and monozygotic twins share 100% IBD.
In a 1991 study, Bailey and Pillard conducted a study of male twins recruited from "homophile publications", and found that 52% of monozygotic (MZ) brothers (of whom 59 were questioned) and 22% of the dizygotic (DZ) twins were concordant for homosexuality. 'MZ' indicates identical twins with the same sets of genes and 'DZ' indicates fraternal twins where genes are mixed to an extent similar to that of non-twin siblings. In a study of 61 pairs of twins, researchers found among their mostly male subjects a concordance rate for homosexuality of 66% among monozygotic twins and a 30% one among dizygotic twins. In 2000, Bailey, Dunne and Martin studied a larger sample of 4,901 Australian twins but reported less than half the level of concordance.
DNAm pattern changes have been extensively studied in complex diseases such as cancer and diabetes. In a normal cell, the bulk genome is highly methylated at CpGs whereas CpG islands (CPI) at gene promoter regions remain highly unmethylated. Aberrant DNAm is the most common type of molecular abnormally in cancer cells, where the bulk genome because globally ‘hypomethylated’ and CPIs in promoter regions become ‘hypermethylated’, usually leading to silencing of tumour suppressor genes. More recently, studies on diabetes have uncovered further evidence to support an epigenetic component of diseases, including differences in disease-associated epigenetic marks between monozygotic twins, the rising incidence of type 1 diabetes in the general population, and developmental reprogramming events in which in utero or childhood environments can influence disease outcome in adulthood.
However, he considered the book necessary to bring together the information from such studies. Jones called the book "the latest and most effective among the growing corpus of books and articles arguing for an exclusively biological explanation of sexual orientation", writing that it showed LeVay's "brilliance", "scientific acumen", and "exceptional capacity for the integration of an enormous array of scientific findings." He credited LeVay with "sophistication in outlining the nature of sexual orientation". However, he wrote that LeVay's claim that if one of a pair of monozygotic twins is gay, the other is roughly fifty per cent likely to be gay as well is incorrect, and that research that LeVay himself cites shows that the actual odds are much smaller.
In fact, a jury should consider how likely it is that an individual matching the genetic profile would also have been a suspect in the case for other reasons. Also, different DNA analysis processes can reduce the amount of DNA recovery if the procedures are not properly done. Therefore, the number of times a piece of evidence is sampled can diminish the DNA collection efficiency. Another spurious statistical argument is based on the false assumption that a 1 in 5 million probability of a match automatically translates into a 1 in 5 million probability of innocence and is known as the prosecutor's fallacy. When using RFLP, the theoretical risk of a coincidental match is 1 in 100 billion (100,000,000,000), although the practical risk is actually 1 in 1000 because monozygotic twins are 0.2% of the human population.
While Siemens focused on dermatological phenotypes, he also explored psychological features using twin studies. An example of this research was on the academic performance of identical and fraternal twins: His research found that identical twins were more likely to have a similar performance in school than fraternal twins. Siemens wrote in "Zwillingspathologie" about his findings: > "If an illness is regularly dominant, then both of the identical twins > either suffer from it or are free from it.. the nonidentical twins correlate > as the siblings of a two-child family .... With the help of twin pathology, > we found a possible way to judge hereditary influence on the investigated > features .... The assessment is based on the comparison of the findings in > identical and nonidentical twins." His research included reporting on similarities in skin traits in monozygotic twins, including naevi among other dermatological traits.
Large interfamilial and intrafamilial variability occurs in ADPKD. Most individuals with PKD1 mutations have kidney failure by age 70 years, whereas more than 50% of individuals with PKD2 mutations have adequate renal function at that age (mean age of onset of end-stage renal disease: 54·3 years with PKD1; 74·0 years with PKD2). The significant intrafamilial variability observed in the severity of renal and extrarenal manifestations points to genetic and environmental modifying factors that may influence the outcome of ADPKD, and results of an analysis of the variability in renal function between monozygotic twins and siblings support the role of genetic modifiers in this disease. It is estimated that 43–78% of the variance in age to ESRD could be due to heritable modifying factors, with parents as likely as children to show more severe disease in studies of parent-child pairs.
On September 15, 1991 in Sydney, Australia at the Prince of Wales Children's Hospital, reported on two brothers with a distinct facial appearance, severe mental retardation, short stature, cryptorchidism (undescended testicle), asplenia in one (absent spleen), dramatic failure to thrive, early hypotonia, and later hypertonia, all suggestive of the Smith–Fineman–Myers syndrome. All five of the reported cases have been males, suggesting X-linked inheritance. On September 23, 1998 at the Hospital Injury Research and Rehabilitation at the University of São Paulo in Bauru, Brazil report on two boys, monozygotic twins born to normal and non consanguineous parents, presenting with an unusual facial appearance, cortical atrophy, dolichocephaly, short stature, cleft palate, micrognathia, prominent upper central incisors, bilateral Sidney line, minor foot deformities, unstableness in walking, early hypotonia, hyperreflexia, hyperactivity, psychomotor retardation, and severe delay in language development. These symptoms resemble those previously described in the Smith–Fineman–Myers syndrome.
Monozygotic twins share around 99.99% of their DNA, while other siblings share around 50%. Some next generation sequencing tools are capable of detecting rare de novo mutations in only one of the twins (detectable in rare single nucleotide polymorphisms). Most DNA testing tools would not detect these rare SNPs in most twins. Each person's DNA is unique to them to the slight exception of identical (monozygotic and monospermotic) twins, who start out from the identical genetic line of DNA but during the twinning event have incredibly small mutations which can be detected now (for all intents and purposes, compared to all other humans and even to theoretical "clones, [who would not share the same uterus nor experience the same mutations pre-twinning event]" identical twins have more identical DNA than is probably possible to achieve between any other two humans). Tiny differences between identical twins can now (2014) be detected by next generation sequencing.
Lindon J. Eaves (born 23 September 1944) is a behavior geneticist who has published on topics as diverse as the heritability of religion and psychopathology. His research encompasses the development of mathematical models reflecting competing theories of the causes and familial transmission of human human differences, the design of studies for the resolution, analytical methods for parameter estimation and hypothesis-testing and application to substantive questions about specific (human) traits. He was the first to consider standardized variance components for heritability estimates and was the first (at least in the human context) to consider the effects of living with a relative (with a different genotype or, in the case of monozygotic twins, the same genotype) on the behavior of a person. Furthermore, he was the first to think about genotype x age interaction and set up the algebra to study the effects of genes working in males as well as females, making it possible to use twins pairs of opposite-sex (dizygotic opposite sex).

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